Primary Care Guidelines (Juan Fernando Florido Santana)

The video version of this podcast can be found here:

·      https://youtu.be/BnwK2Vts3gY

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in September 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only. I also cover the guideline on Adrenal insufficiency published on 28th August 2024.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for September 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-09-01&to=2024-09-31&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here:

Vibegron for treating symptoms of overactive bladder syndrome:

·      https://www.nice.org.uk/guidance/ta999

Adrenal insufficiency: identification and management:

·      https://www.nice.org.uk/guidance/ng243

The Imperial Centre for Endocrinology prednisolone withdrawal regimen can be found here:

·      https://www.impendo.co.uk/prednisolone/prednisolone-withdrawal

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• Music provided by Audio Library Plus 
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Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in September 2024, focusing on what is relevant in Primary Care only.

We are going to cover just two areas, the treatment of overactive bladder and the guideline on adrenal insufficiency, which was published late in August 2024 and did not make it into last month’s episode.

Right, let’s get started.

The first area is a technology appraisal on Vibegron for treating the symptoms of overactive bladder syndrome in adults. It is very similar to the technology appraisal on mirabegron.

Before looking at the recommendation, let’s have a quick overview of Overactive bladder syndrome. It is a condition characterized by a frequent and urgent need to pass urine, sometimes with urinary incontinence. It is often caused by involuntary contractions of the bladder wall.

Treatment for OAB involves lifestyle changes, behavioural therapies, and medications. NICE recommends that bladder training and lifestyle advice should be offered as first-line treatments. Then an antimuscarinic drug should be offered second-line and beta 3 agonists should be offered third line.

So, let’s look at the two types of drug treatment:

1. Antimuscarinic Agents (or Anticholinergics) are the most commonly prescribed drugs and they work by blocking muscarinic receptors in the bladder, reducing the involuntary contractions of the detrusor muscle.

• Examples are:
• Oxybutynin
• Tolterodine
• Solifenacin
• Darifenacin and
• Fesoterodine
• Since muscarinic receptors are also found in other parts of the body (e.g., the salivary glands, eyes, and intestines), antimuscarinic agents can cause side effects such as dry mouth, constipation, blurred vision, and cognitive dysfunction, especially in elderly patients.

1. Beta-3 Adrenergic Agonists are drugs like mirabegron and vibegron which offer an alternative to antimuscarinics. These drugs specifically stimulate beta-3 receptors on the detrusor muscle, causing the muscle to relax. This increases the bladder’s capacity and reduces the urgency and frequency of urination.

• Beta-3 agonists tend to have fewer side effects compared to antimuscarinic agents. Some common side effects are mild increases in blood pressure, arrythmias, headache, and urinary tract infections.

So, in summary, the main difference between these Drug Classes are that Antimuscarinics work by reducing involuntary bladder contractions whereas Beta-3 agonists relax the bladder, improving bladder storage.

Vibegron, as a beta 3 agonist, works in a similar way to mirabegron and an indirect comparison suggests that it is equally effective at a lower cost. So, vibegron is recommended if antimuscarinic medicines are not suitable, do not work well enough or have unacceptable side effects.

The next section is a brand-new guideline on adrenal insufficiency.

And before we look into it, let’s give a very brief overview on the subject.

Adrenal insufficiency is a disorder where the adrenal glands do not produce sufficient amounts of cortisol, and sometimes aldosterone. It's classified into primary, secondary, and tertiary, each with different causes and pathophysiology.

• Primary adrenal insufficiency is caused by a problem in the adrenal glands. Possible causes include autoimmune conditions, infection, and malignancy. The autoimmune condition Addison's disease is the most common cause in adults, and congenital adrenal hyperplasia is the most common cause in children
• Secondary adrenal insufficiency is caused by a problem in the pituitary gland which limits the secretion of ACTH, leading to reduced adrenal stimulation. Possible causes include pituitary tumours, and damage to the pituitary gland secondary to trauma, surgery or radiation.
• And Tertiary adrenal insufficiency is caused by a problem in the hypothalamus which reduces the levels of corticotropin-releasing hormone (or CRH). Possible causes include tumours in the hypothalamus or adjoining structures, or more commonly the use of prolonged glucocorticoids which suppress the hypothalamic-pituitary-adrenal axis.

The physiopathology in each case is also different:

• In primary adrenal insufficiency, the adrenal cortex is unable to produce both glucocorticoids, and mineralocorticoids, leading to cortisol and aldosterone deficiency.
• In secondary and tertiary adrenal insufficiency, the adrenal glands themselves are functional, but low levels of ACTH and / or corticotropin-releasing hormone (or CRH) impair the production of cortisol. However, mineralocorticoid production is usually preserved because it is regulated primarily by the renin-angiotensin system, not ACTH.

Adrenal insufficiency requires treatment with glucocorticoids and, in primary adrenal insufficiency, mineralocorticoids too. Failure to manage it can lead to life-threatening adrenal crises, especially during stress.

NICE states that we should suspect adrenal insufficiency when there are unexplained suggestive symptoms, bearing in mind that many of these symptoms are non-specific. They include:

• weight loss and lack of appetite
• nausea, vomiting or diarrhoea
• dizziness, hypoglycaemia and hypotension
• salt craving, hyponatraemia and hyperkalaemia and
• lethargy, and muscle weakness

We should also suspect adrenal insufficiency in people with unexplained hyperpigmentation, although hyperpigmentation may not be seen on black or brown skin. In these cases, we should ask the person if they have noticed a change in their skin colour and we should assess the buccal mucosa or any surgical scars.

When do we get this hyperpigmentation? This only happens in the case of primary adrenal insufficiency, when ACTH levels are high. ACTH and melanocyte-stimulating hormone (of MSH) share the same precursor, so when ACTH levels are high, MSH levels also increase with the subsequent increase in melanin.

One common cause of adrenal insufficiency occurs due to adrenal suppression in people who have recently stopped prolonged glucocorticoids by any route. Prolonged means 4 weeks in adults and 3 weeks in children.  However, it can also happen to those who are still taking steroids and have had an episode of physiological stress

Considering this, how should we taper off steroids to prevent adrenal insufficiency?

Well, the first thing that we need to understand is the concept of physiological equivalent dose, which is the dose of glucocorticoid that is equivalent to the amount that a healthy adrenal gland would normally produce. For adults this is a total daily dose of 3 mg to 5 mg of prednisolone, or of 0.5 mg of dexamethasone. In children the calculation requires the use of a complex formula.

So, for someone taking steroids for more than 4 weeks (or 3 weeks in the case of children), in order to taper off the dose safely, we should first reduce the dose gradually to a daily physiological equivalent dose. Then, we should give that dose every other day for 2 weeks, then then twice a week for 2 weeks and then stop, always taking into account that this decision should be made by the clinical team who initiated the treatment for whichever condition the steroids were prescribed for.

However, for people taking steroids for more than 12 weeks, a slower dose-tapering regimen is recommended. For example, for people taking prednisolone, once the daily dose is 3 mg, we are advised to follow the Imperial Centre for Endocrinology prednisolone withdrawal regimen. I have put the link to this in the episode description but the regimen looks like this, where we give patients, a schedule indicating what dose to take each day of the week depending on whether they are in week 1, 2, 3, etc. It takes 7 weeks to reduce the dose from 3 mg to 2 mg using this schedule and, similarly, thereafter, so a total of 21 weeks to reduce from 3 mg to zero. If the starting dose is 5 mg of prednisolone, then a slightly different regimen is followed where the reduction of the dose to zero is over 24 weeks.

As the initial investigations for adrenal insufficiency, we will offer an 8 am to 9 am serum cortisol test, bearing in mind that we should not do this test if taking oral glucocorticoids at physiological equivalent doses or above, because the cortisol levels will be suppressed.

In addition, other routes such as inhaled, intramuscular or topical steroids, may also cause a low cortisol level.

People taking oral oestrogen will have a falsely elevated cortisol so we should stop oral oestrogens for 6 weeks before checking it. If the oral oestrogen is taken for HRT, we will be able to switch to a transdermal preparation.

Once we get the results, if the cortisol level is:

Below 150 nmol/L, then the person may have adrenal insufficiency and we should refer them to endocrinology, urgently in the case of children.

If it is between 150 nmol/L and 300 nmol/L, then the probability of adrenal insufficiency is uncertain and we should repeat the test. If it remains at this level, we will seek specialist advice.

If it is above 300 nmol/L then adrenal insufficiency is very unlikely

The Routine pharmacological management is with Corticosteroid replacement, offering hydrocortisone or prednisolone, and we will add a mineralocorticoid like fludrocortisone for people with primary adrenal insufficiency or congenital adrenal hyperplasia. We will be seeking specialist advice so I will not cover any more of the treatment here.

If there are symptoms of adrenal insufficiency while tapering the dose below a physiological equivalent dose, we will prescribe double the physiological equivalent glucocorticoid dose daily until symptoms resolve, then we will reduce to a daily physiological equivalent dose for 1 week and then use a slower tapering regimen. If symptoms still develop using this slower regimen, then we will need further investigations such as checking serum cortisol levels.

Patients with adrenal insufficiency should be given an emergency kit containing an intramuscular hydrocortisone injection for emergency use in the case of a suspected adrenal crisis.

People having an adrenal crisis should immediately go to hospital by ambulance without needing a referral.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I go through a real-life case of a patient with abnormal Liver Function Tests and non- alcoholic fatty liver disease or NAFLD. I will describe a recommended approach to diagnose and manage them according to guidelines. 

I am not giving medical advice; this podcast is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here: 

·      The NICE GP YouTube Channel: NICE GP - YouTube 

The links to the websites that can calculate these scores are in the episode description:

·      The NAFLD Fibrosis Score (NFS) is available at https://www.thecalculator.co/health/NAFLD-Fibrosis-Score-Calculator-969.html 

·      The Fibrosis 4 (FIB-4) Score available at https://www.mdcalc.com/calc/2200/fibrosis-4-fib-4-index-liver-fibrosis 

You can download a summary of the episode here:  

·      Summary of NAFLD patient case: https://1drv.ms/b/s!AiVFJ_Uoigq0mBYIbok6DSu5vTnY?e=2W11Jd

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Transcript

Hello everyone and welcome. My name is Fernando and I am a GP in the United Kingdom. 

In today’s episode I go through a real-life case of a patient with abnormal Liver Function Tests and non- alcoholic fatty liver disease or NAFLD, describing the recommended approach for its diagnosis and management according to guidelines.

By the way, I am not giving medical advice; this is for health care professionals and it is only my interpretation of the various guidelines consulted so you must use your own clinical judgement.

If you want to download a summary of the episode, the link is in the episode description.

Remember that there is also a YouTube version of these episodes so have a look in the episode description. 

Right, so let’s get straight into it.

Our patient is a 55-year-old man of Hispanic family background who consults you following a routine blood test done one week earlier. This was a repeat blood test because 4 months previously he had been found to have a mildly raised alanine aminotransferase or ALT of 75 (NR 0-55).

The results of all his blood tests were normal with the exception of the ALT which was still high at 65.

His PMH includes:

·      Prediabetes

·      Hyperlipidaemia and

·      Overweight with a BMI of 27.8

His only medication is atorvastatin 20 mg daily for hyperlipidaemia.

He denies alcohol excess. In fact, he is teetotal and does not drink alcohol at all. He has otherwise no symptoms.

In the previous consultation he had been told that raised liver transaminase were not uncommon during the prescribing of statins but that statins need not be stopped for raised liver transaminase levels as long as they are less than 3 times the upper limit of normal.

However, as a result of that consultation, the patient decided to stop the statin of his own accord so he has not been taking it for the last 3 months.

So, in summary, we have a patient with a background of overweight, prediabetes and dyslipidaemia with a slightly elevated ALT for 3 months without an obvious cause.

What should we do?

When we face this situation, we should consider all the possible causes and investigate them fully. But we must primarily consider the most common reason for abnormal liver blood tests in the UK, which is non-alcoholic fatty liver disease, or NAFLD.

This condition happens when excess fat builds up in the liver. But for the diagnosis to be made, we must also exclude other secondary causes.

Let’s quickly remind ourselves that NAFLD has a spectrum that goes from simple hepatic steatosis, meaning that there's fat in the liver, but it's not causing any significant inflammation or damage, to something more serious called non-alcoholic steatohepatitis, or NASH which involves inflammation and injury to liver cells which can lead to liver fibrosis and cirrhosis.

Most people don't have any specific symptoms. However, some might experience fatigue, or mild abdominal discomfort.

In our patient's case, we know that he is overweight, which is typical. However, NAFLD can affect even non-obese individuals. Surprisingly, about 40% of all NAFLD cases worldwide are found in non-obese people, and around 20% in those who are lean.

We also know that NAFLD is closely tied to the metabolic syndrome, involving insulin resistance, obesity, impaired glucose regulation, and hypertension and our patient does have some of these factors. While the exact cause of NAFLD isn't fully clear, it is thought that both environment and genetics play a role.

The outlook for NAFLD depends on the stage of the disease:

• For those with simple steatosis, the outlook is generally positive.
• However, if someone has non-alcoholic steatohepatitis (NASH), they're at higher risk for cirrhosis, liver failure, and even liver cancer.

Complications of NAFLD can be serious. They include:

• Hepatic and metabolic complications and
• Above all, cardiovascular disease, which is the leading cause of death for people with NAFLD.

We should suspect that someone has NAFLD if:

• There are risk factors linked to the metabolic syndrome.
• There are high levels of alanine aminotransferase (ALT) for more than 3 months, and it's usually higher than another enzyme called aspartate aminotransferase (AST).
• They're not consuming excess alcohol, in which case it would be alcoholic fatty liver disease.
• An ultrasound scan reveals a fatty liver.
• They are nor on medication that can cause a fatty liver, e.g. tamoxifen or amiodarone.

So based on all this, we will suspect that our patient could have NAFLD.

How should we confirm the diagnosis?

Next, we'll arrange some more blood tests to get a clearer picture and exclude secondary causes. We will do:

• Liver function tests, to include AST as well as ALT.
• A full blood count, which can help detect low platelets, which is a sign of advanced fibrosis.
• A clotting screen, as it might be off in advanced fibrosis.
• Screening for viral hepatitis B and C, and test for auto-antibodies that could suggest autoimmune hepatitis.
• Ferritin and transferrin saturation to screen for haemochromatosis,
• Serum caeruloplasmin for Wilson's disease,
• Alpha-1-antitrypsin levels to screen for deficiency
• Immunoglobulin (IgA) tissue transglutaminase antibody (tTGA) as coeliac disease can present with cryptogenic liver disease.
• HbA1c, Lipid profile, ESR, CRP, Renal and thyroid function tests as general screening.

Additionally, we could request a liver USS to exclude any other structural issue that we could be missing.

Right, so we organise these tests and we see the patient a few weeks later to discuss the following:

An USS of the abdomen confirms that he has steatosis of the liver.

His blood tests showed that:

ALT has improved but it is still high at 59 (NR 0-55) and AST is also high at 49 (NR 5-34). The rest of his liver function tests were normal.

His FBC was normal with a platelet count of 219 (NR 150-400 10*9/L)

His HbA1c is in the prediabetes range at 43 or 6.1%.

He has normal clotting screen, ESR, CRP, renal and thyroid function tests.

And all other investigations for secondary causes were also normal: viral hepatitis serology, autoantibody screen, ferritin, transferrin saturation, caeruloplasmin, Alpha-1-antitrypsin levels and Immunoglobulin (IgA) tissue transglutaminase antibody (tTGA) as coeliac screen.

His cholesterol was slightly high at 5.1 with an HDL of 1, an LDL of 3.9 and TG of 1.5.

His BP was 147/82 and his CVD risk score using QRISK3 is 8%.

I summary, we have confirmed steatosis of the liver on USS and, given that we have not found secondary causes for the liver function test abnormality, we can conclude that this is indeed NAFLD.

As part of our consultation, we also do a thorough examination looking out for signs of advanced liver disease, of which he has none.

As the next step, we should estimate the level of fibrosis, or scarring of the liver, by using non-invasive tools. There are two simple tests that we can use in Primary care:

·      One, the Fibrosis-4 score or FIB-4, which uses the person's age, AST, ALT, and platelet count.

·      And two, the NAFLD Fibrosis Score (NFS) which measures age, body mass index, blood glucose, platelet count, albumin, and the AST to ALT ratio.

·      The Enhanced Liver Fibrosis (ELF) test is another option but this is really only available in secondary care because of the complexity of the parameters required.

The links to the websites that can calculate these scores are in the episode description:

·      The NAFLD Fibrosis Score (NFS) is available at https://www.thecalculator.co/health/NAFLD-Fibrosis-Score-Calculator-969.html 

·      The Fibrosis 4 (FIB-4) Score available at https://www.mdcalc.com/calc/2200/fibrosis-4-fib-4-index-liver-fibrosis

If the fibrosis score is low, we may be able to manage this patient in Primary Care.

We calculate the FIB4 score for this patient and it is 1.92. which means that further investigations are needed. The interpretation of the scores is as follows:

·      If FIB-4 is < 1.45: we can be reasonably confident that there is absence of cirrhosis

·      If FIB-4 is between 1.45 - 3.25:  the test is inconclusive and

·      If FIB-4 is > 3.25: we can be reasonably confident that there is cirrhosis

So let's move on to the management.

The Primary Care approach would be as follows:

• We will advise lifestyle changes including weight loss, if the person is overweight.
• We will recommend a Mediterranean diet, which can actually reduce liver fat even without weight loss.
• We will encourage moderate-intensity exercise.
• We will offer alcohol advice.
• We will optimise management of co-morbidities such as hypertension, hyperlipidaemia, or type 2 diabetes. In this case, we may revisit his statin therapy because he has two independent risk factors for CVD, prediabetes and NAFLD.
• We need to be aware that statins, if prescribed, don't pose additional liver risks for people with NAFLD. In fact, they can help improve various aspects of the condition.

So, in summary, the primary care approach to NAFLD involves empowering patients to make lifestyle changes, ensuring associated conditions are managed, and offering support and information along the way.

If a person has a working diagnosis of NAFLD and other liver disease causes have been ruled out, and if non-invasive tests indicate a low risk of advanced liver fibrosis (using NFS, FIB-4, or ELF), then primary care management is in order.

However, because his FIB4 score is inconclusive in this case, we will refer him to secondary care for a second opinion.

Other reasons to refer to a Specialist are:

• If there's a high risk of advanced liver fibrosis.
• If there are clear signs of advanced liver disease during examination.
• In cases where there's uncertainty about the diagnosis.

We also need to be aware that specialist management may involve amongst other things:

• Transient elastography, also known as fibroscan, which measures liver stiffness non-invasively, which correlates with the degree of liver fibrosis.
• Liver biopsy.
• In cases of non-alcoholic steato-hepatitis (NASH), pioglitazone, and Vitamin E supplementation might be considered.
• Bariatric surgery, has led to the resolution of steatosis in 66% and fibrosis in 40% of patients.
• Considering liver transplantation. However, NASH recurrence after transplantation is possible.

Finally, this patient should be reviewed regularly in Primary Care. Patients with NAFLD should have an annual review, more frequently if necessary, as per our clinical judgement:

During the review, we will:

• Identify any signs that might indicate liver disease.
• Measure blood pressure and BMI.
• Check liver and renal function, HbA1c and a lipid profile.
• Reassess the CVD risk
• And, every three years, reassess the risk of advanced liver fibrosis and refer if the person has a high risk of advanced liver fibrosis

But remember that this is only a summary and my interpretation of the guidelines.

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye 

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I do a quick review of a mind map that I have created based on the NICE Guideline: Hypertension in adults: diagnosis and management (NG136 guideline), updated on 18^th March 2022. I have summarised the guidance from a Primary Care perspective, and I have created an e-book on this too. You are welcome to download both the mind map and both versions of the e-book here:

·      Mind map: https://1drv.ms/b/s!AiVFJ_Uoigq0l2boZjh4biBJ5WGv?e=7YqdBn

·      Condensed and easy to print e-book: https://1drv.ms/b/s!AiVFJ_Uoigq0l2cepU4PPQoY_0NQ?e=xymSS3

·      Digital and fully “clickable” e-book: https://1drv.ms/b/s!AiVFJ_Uoigq0l2iI6yHrZAU0VsWg?e=VtaO9N

By way of disclaimer, nothing that I say either in the video or the downloads is medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement. 

There is a YouTube version of this and other videos that you can access here: 

• The NICE GP YouTube Channel: NICE GP - YouTube 

NICE Guideline NG136 can be found here:

https://www.nice.org.uk/guidance/NG136

Other links relevant to this episode:

·     guideline on hypertension in pregnancy

·     NICE's guideline on cardiovascular disease

·     patient decision aid on treatment options for hypertension

·     NICE's guideline on multimorbidity

·     NICE guidelines on chronic kidney disease

·     type 1 diabetes 

·     MHRA safety advice on ACE inhibitors and angiotensin II receptor antagonists: not for use in pregnancy, recommendations on how to use for breastfeeding and the related clarification on breastfeeding

·      drug therapy for secondary prevention in the NICE guideline on acute coronary syndromes

·      treatment after stabilisation in the NICE guideline on acute heart failure

·      treating heart failure with reduced ejection fraction in the NICE guideline on chronic heart failure

·      drugs for secondary prevention of cardiovascular disease in the NICE guideline on stable angina

·      blood pressure management in the NICE guideline on type 1 diabetes in adults.

·     NICE's guideline on chronic heart failure

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Music provided by Audio Library Plus

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Script

Hello everyone and welcome. My name is Fernando, a GP in the United Kingdom.

Today, we'll be doing a quick revision on hypertension and we will do it by reviewing a mind map that I have made based on the NICE Guideline on hypertension. Therefore, this episode will be fairly short but make sure that you stay for its entirety because, at the end, I am going to tell you how you can download the mind map and I will also tell you about a mini e-book that I have created that summarises the guidance, as always, from a Primary Care perspective.

Please note that this is my interpretation of the guidelines, not medical advice. Always use your clinical judgement when treating your patients.

There is also a YouTube version which you can find in the episode description.

So, with that said, let's dive in! I hope that you enjoy this episode.

So let me introduce the mind map, and here it is. We are going to quickly navigate through it.

So we’re going to start in the centre of the mind map where it tells us about the guideline NG136. And here we see that it applies to people aged 18 and over, including those with type two diabetes. It also tells us that the updated guideline in March 2022, gives us new targets and new advice on drug treatment for cardiovascular disease. It also reminds us that when measuring the blood pressure we need to consider pulse irregularity when using automated devices, and also we should consider postural hypotension as well as the need to measure the blood pressure in both arms and to repeat the measurement if the difference is greater than 15 mmHg. 

When it comes to diagnosis if the clinic blood pressure is over 140/90 then we will need to arrange ambulatory blood pressure monitoring or alternatively home Blood pressure monitoring and if the average is above 135/85, then we will confirm the diagnosis.

In terms of lifestyle interventions, we will recommend a healthy diet, regular exercise, reduced alcohol, avoid excessive caffeine, as well as low dietary sodium and smoking cessation.

With monitoring we will remember that we need to use the clinic Blood pressure for monitoring purposes although in specific situations ambulatory home blood pressure monitoring may be used and we will base the blood pressure targets on age and comorbidities as well as remembering the need for an annual review of these patients.

When it comes to investigations we will assess for secondary causes, we will estimate the cardiovascular risk and we will assess for target organ damage. This assessment will comprise of at least a urine sample for albumin creatinine ratio, a number of blood tests, fundoscopy and an ECG

For urgent, same day referral we will consider patients with a clinic blood pressure of 180/120 or more with one of the following, either life-threatening symptoms, retinal, haemorrhage, or papilloedema as well as if we suspect pheochromocytoma (pause)

We are now going to focus on the antihypertensive drug treatment and we need to remember that we need to review the treatment when type two diabetes is diagnosed, as well as considering individual factors and medication safety when treating patients and this treatment will follow a stepwise approach. Step one is when we give one drug and this can be an ace inhibitor or ARB if the patient has diabetes, regardless of age and ethnicity. Or if the patient is less than 55 and not of Afro Caribbean family origin or, alternatively we can give a calcium channel blocker is the patient is of Afro-Caribbean family origin and has no diabetes or if the patient is over 55 and has no diabetes

Step two is one we give two drugs and it could be anyone of these combinations, an ace inhibitor or ARB and a calcium channel blocker; an ace inhibitor or arb and a thiazide like diuretic, or a calcium channel blocker, and a thiazide diuretic. Step three is when we give three drugs, and this would be an ace inhibitor, a calcium channel blocker, and a thiazide like diuretic. And step 4 is when we give four drugs. If this happens, we will say that the patient has resistant hypertension and we will consider specialist referral. But if we decide to treat ourselves, we will give triple therapy with an ace inhibitor or arb, a calcium channel blocker, a thiazide like diuretic, and we will check the potassium if the potassium is less than 4.5 we will give. Spironolactone and if potassium is more than 4.5 we will give an alpha blocker or a beta blocker.

And finally, we have a section giving definitions and terms used such as accelerated hypertension, which is when the blood pressure is over 180/120 with retinal involvement, masked hypertension, as well as the three stages of hypertension. 

Right, so this is it, this is the end of the mind map tour. As promised, let me tell you about the downloads. Just click in the episode description and there you will be find a link to download the mind map for free, without the need to provide your email address or any other information. You will also find two other links to download the two versions of the mini e-book that I have created. The first one is a printer friendly e-book, for those of you that would want to have a physical copy in your hands. It is more condensed and has therefore fewer pages. It is in black and white text so you will not be wasting ink unnecessarily on pictures or background colours. The second version is a fully digital “clickable” e-book. It has a few more pages as well as photographs and links to further information. Furthermore, under each section of the mind map there is a button that says “more” and if you click on it, you will be taken directly to the section of the summary that refers to it, followed by a button to take you back to the mind map.

Over the next few episodes, I will be producing more material similar to this so make sure to stay tuned.

But please, let me reiterate again that this is only a summary and my interpretation of the guideline.

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye  

The video version of this episode can be found here:

·      https://youtu.be/r0h6m-Hxoa0

The original video that this episode is based on can be found here:

·      https://youtu.be/VFiwyS1c3yk?si=Y-iz5dqx1KUKDXF8

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I use AI voices to discuss the issue of raised alkaline phosphatase levels. There are 3 parts and this is part 3.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

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There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

You can download a summary of my summary / interpretation of the guidance here:

·      My Summary: https://1drv.ms/b/s!AiVFJ_Uoigq0mC4pm_bYELFa9wEx?e=07p2dJ

The video version of this podcast can be found here:

• https://youtu.be/MxR8AMtBkDY

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in November 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for October 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-11-01&to=2024-11-30&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here:

Asthma: diagnosis, monitoring and chronic asthma management (BTS, NICE, SIGN) can be found here:

·      https://www.nice.org.uk/guidance/ng245

Asthma pathway (BTS, NICE, SIGN) can be found here:

·      https://www.nice.org.uk/guidance/ng244

Endometriosis: diagnosis and management can be found here:

·      https://www.nice.org.uk/guidance/ng73

Menopause: identification and management can be found here:

·      https://www.nice.org.uk/guidance/ng23

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in November 2024, focusing on what is relevant in Primary Care only.

In today’s episode we’re covering 3 really important clinical areas. We’ll look at the updates on endometriosis, the all-important menopause, and, of course, the wow factor, the one guideline that we’ve all been waiting for: the new collaborative guideline on asthma! Yes, it’s finally here!

Right, let’s jump into it

And, of course, we have to start with the star of the show, the new guideline on the diagnosis, monitoring and management of chronic asthma.

This is a new collaborative guideline developed jointly by NICE, the British Thoracic Society (or BTS), and the Scottish Intercollegiate Guidelines Network (or SIGN).

It updates and replaces parts of the BTS/SIGN guideline as well as previous NICE guidance. There’s also an updated asthma pathway, which presents the same recommendations in a different format.

This is a major development, so today I’ll just focus on the highlights. But I will dedicate the next episodes to cover this guideline in detail, so stay tuned.

When someone presents with a history suggestive of asthma, we need to confirm the diagnosis with objective tests.

And from a diagnosis perspective, there are 3 groups of patients:

·      Those aged over 16

·      Those aged 5 to 16 and

·      Those aged under 5

So, to confirm the diagnosis in anyone over the age of 16 with suggestive asthma symptoms we will start by measuring the blood eosinophil count or FeNO level.

And we will diagnose asthma if:

• The Eosinophil count is high, or
• FeNO level is 50 ppb or more.

Then, if these tests are negative and we still suspect asthma, we will do a spirometry with reversibility and diagnose asthma:

·      if FEV1 increases by ≥ 12% from baseline and by ≥ 200 ml or, and this is new,

• if the FEV1 increase is 10% or more of the predicted normal FEV1(that is, not the baseline)

If spirometry is unavailable or it is delayed, we will use peak flow (PEF) variability checking readings twice daily over 2 weeks and diagnose asthma if variability ≥ 20%.

If all tests are negative and there are still diagnostic doubts, we will refer for a bronchial challenge test.

The process is slightly different in children aged 5 to 16, because, as the initial test we will just:

• measure FeNO levels and diagnose asthma if level ≥ 35 ppb.
• This is also new because before FeNO testing was not recommended as an initial test in this age group. And please also note that we will not use eosinophil count as an initial test here, although it can play a part at a later stage. But we will come to that a little later.

If FeNO is not raised or is unavailable and asthma is still suspected in this group of children:

• We will check spirometry with reversibility and diagnose asthma if FEV1 increases ≥ 12%. But it does not need to be more than 200ml

If spirometry with reversibility is not raised or is unavailable:

• We will check peak flow readings twice daily for two weeks and diagnose asthma if variability ≥ 20%.

And finally, if asthma is not diagnosed with any of the above tests, we will move to Sensitisation Tests by:

·      Doing skin prick testing for house dust mite or measuring total IgE and eosinophil count.

And then we will diagnose asthma if:

• Sensitisation is present on skin prick testing, or
• Total IgE is raised and eosinophil count > 0.5 × 10⁹/L.

If all tests are negative and there are still diagnostic doubts, we will refer to paediatrics.

Diagnosing asthma in the under 5s is more complex and requires clinical judgement, so we will not cover this today.

Now that we have looked at the diagnosis, let’s look at what monitoring is recommended.

And a significant change is that we are now advised to avoid regular peak flow monitoring unless it's part of a personalised asthma action plan. Instead, we are advised to monitor symptoms and use validated symptom questionnaires for both adults and children. Additionally, for adults, we can also consider monitoring FeNO levels at regular reviews and before or after treatment changes.

And finally, let’s touch on a few new treatment recommendations.

And the main development is the end of step 1 treatment, where intermittent short-acting bronchodilators were used alone. From now on, the golden rule is clear: no prescribing short-acting beta2 agonists (or SABAs) for asthma at any age without an inhaled corticosteroid (ICS).

Let’s look at the management in a little more detail. And from a treatment perspective, there are three groups:

·      Those aged 12 and over

·      Those aged 5 to 11 and

·      Those aged under 5

For those aged 12 and over, the first step is to offer on-demand AIR therapy. So, what is AIR therapy? It stands for Anti-inflammatory Reliever therapy, where formoterol is used as a reliever in an inhaler that also contains an anti-inflammatory corticosteroid. While many of us are familiar with the MART regimen (that is, Maintenance and Reliever Therapy), AIR therapy is different: it involves using a formoterol/corticosteroid inhaler only in response to symptoms, without regular maintenance dosing. Currently, only specific budesonide/formoterol inhalers are licensed for this, with a low-dose budesonide/formoterol combination recommended as on-demand AIR therapy. So, anyone in this age group who is currently on PRN salbutamol only should now be switched to AIR therapy instead.

However, whilst this is really the death of the salbutamol inhaler for anyone aged 12 and over, there is still a role for it in children under 12, for whom a SABA may be prescribed, although always alongside an inhaled corticosteroid.

There are a few more changes but, as a taster, we will stop it here today, as we will be covering the full guideline more extensively in future episodes.

But, in summary, for me, the highlights are that:

·      New diagnostic criteria for adults include a high eosinophil count and a post bronchodilator increase in FEV1 of the predicted normal FEV1by 10% or more.

·      FeNO testing is the main initial test for children aged 5 to 16.

·      Skin prick testing, serum IgE, and eosinophil count now have a role in diagnosing asthma.

·      Peak flow readings are no longer recommended for routine monitoring.

·      And in a notable shift, SABAs have vanished from the management of patients aged 12 and over but remain in use for those under 12.

Let’s now move to the updates of endometriosis:

And now we are advised to ask if there are any first-degree relatives with a history of endometriosis, as this increases the likelihood of developing it.

We should offer an abdominal and an internal vaginal examination as part of the initial assessment, but only an abdominal examination if a vaginal examination is declined, or not suitable.

We will offer a transvaginal ultrasound scan even if the examination is normal. If it is declined or not suitable, we will organise a transabdominal pelvic ultrasound instead.

But we should not exclude the possibility of endometriosis if the examination and ultrasound scans are normal, so referral may still be necessary for consideration of pelvic MRI scan and laparoscopy.

And finally, we will not offer hormonal treatment if they are trying to conceive, because this management does not improve spontaneous pregnancy rates. 

And now, let’s look at the updated Menopause guideline

There are new recommendations on CBT to manage menopausal symptoms and we are advised to consider menopause-specific CBT as a treatment option.

There are also new recommendations on managing genitourinary symptoms.

If there is no history of breast cancer, we will offer vaginal oestrogen (including to those using systemic HRT), explaining that vaginal oestrogen is absorbed locally and only a minimal amount is absorbed into the bloodstream which is unlikely to have a significant systemic effect.

We should also give advice on the use of non-hormonal moisturisers or lubricants, which can be used either alone or in combination with vaginal oestrogens.

In resistant or difficult to treat cases, we can consider vaginal prasterone and oral ospemifene.

However, if there is a personal history of breast cancer, we will offer non-hormonal moisturisers or lubricants instead. Vaginal oestrogens can still be considered in certain circumstances by a menopause specialist, although this would be an off-label use and the individual safety should be assessed carefully.

For example, in oestrogen receptor negative breast cancer, vaginal oestrogen is unlikely to increase the risk, and so it is likely to be safe. 

On the other hand, in oestrogen receptor positive breast cancer, the risk of vaginal oestrogens is unknown but there is a potential risk. 

And finally, there are also new recommendations on the effects of HRT on specific health outcomes. There are tables in the guideline that you can use to explain the risks and benefits to patients, so I will only touch briefly on some key aspects.

For example, if there is a history of coronary heart disease or stroke, HRT should be discussed with a menopause specialist. This also applies to anyone with a history of breast cancer or at high risk of breast cancer.

The Breast cancer risk increases with combined HRT but there is little or no increase in the risk of breast cancer mortality with oestrogen-only HRT.

And Stroke risk is unlikely to increase with transdermal combined HRT but it increases with oral combined HRT.

And finally, we should not offer HRT for primary or secondary prevention of cardiovascular disease or for the purpose of dementia prevention.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In this episode I go through the NICE guidelines “Chronic heart failure in adults: diagnosis and management” or NG106, Published on 12 September 2018 

There is a YouTube version of this and other episodes that you can access here: 

·      https://www.youtube.com/@nicegp 

The NICE guideline on chronic heart failure can be found here:  

·      Website: https://www.nice.org.uk/guidance/ng106/chapter/Recommendations or as PDF: https://www.nice.org.uk/guidance/ng106/resources/chronic-heart-failure-in-adults-diagnosis-and-management-pdf-66141541311685

·      Or download here: https://1drv.ms/b/s!AiVFJ_Uoigq0lgl6iwROprZsSZ2u?e=G7Lte2 

The NICE recommendations on dapaglifozin and empaglifozin in HF can be found:

·      On website here:

o  Dapaglifozin in HF: https://www.nice.org.uk/guidance/ta679 or https://www.nice.org.uk/guidance/ta679/resources/dapagliflozin-for-treating-chronic-heart-failure-with-reduced-ejection-fraction-pdf-82609327985605

o  Empaglifozin in HF: https://www.nice.org.uk/guidance/ta773 or https://www.nice.org.uk/guidance/ta773/resources/empagliflozin-for-treating-chronic-heart-failure-with-reduced-ejection-fraction-pdf-82611494690245 

·      Or downloaded here:

o  Dapaglifozin: https://1drv.ms/b/s!AiVFJ_Uoigq0lgfx8IoyYutMx9rh?e=1Fc3uc

o  Empaglifozin: https://1drv.ms/b/s!AiVFJ_Uoigq0lggUBPl4p_XX1XzF?e=aMVtBp 

The Visual summaries on diagnosis and management of heart failure can be found here:

• Website:

1-Diagnosis: https://www.nice.org.uk/guidance/ng106/resources/chronic-heart-failure-diagnosis-visual-summary-pdf-6663137726

2-Management:  https://www.nice.org.uk/guidance/ng106/resources/chronic-heart-failure-management-visual-summary-pdf-6663137725

·      Or download here:  

1-Diagnosis: https://1drv.ms/b/s!AiVFJ_Uoigq0lgW9dPRAHiaT3Ueg?e=hfuU3x

2-Management:

https://1drv.ms/b/s!AiVFJ_Uoigq0lgZLGWycIkNN-Mcu?e=bTlnAN

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Transcript

Hello everyone and welcome.

Today we are going to look at the NICE guidelines on Chronic heart failure.

My name is Fernando Florido and I am a GP in the United Kingdom. Remember that there is also a YouTube version of these episodes so have a look in the podcast description. Let’s jump straight into it.

The first recommendation given by NICE is probably something that is often neglected. And this is to write a care plan for every patient with HF. This care plan must include:

·      diagnosis and cause

·      medication and monitoring

·      functional abilities and any social circumstances

·      details of clinical management including

• symptoms to look out for in case of deterioration

o  how to access the specialist team

o  contact details for a named healthcare coordinator or alternative specialist care providers, for urgent care or review.

When it comes to making the Diagnosis we will base it initially on the history, and clinical examination.

Some of the typical symptoms of HF may include:

·      Shortness of breath on exertion or when lying down

·      Fatigue and weakness

·      Bilateral leg, ankle or foot swelling

·      Rapid or irregular pulse

·      Reduced ability to exercise

·      Persistent cough or wheezing

·      Abdominal swelling and

·      Very rapid weight gain from fluid retention

Examples of examination findings in

left-sided heart failure include cool clammy skin, cyanosis, a laterally displaced point of maximum impulse consistent with an enlarged ventricle and on auscultation we can find lung crackles and a gallop rhythm. Signs in right sided heart failure include an elevated JVP, ankle of leg edema, ascites, hepatomegaly, a parasternal heave and hepatojugular reflux. Signs of both left and right sided heart failure can be present.

In order to confirm the diagnosis

We will measure the N-terminal pro-B-type natriuretic peptide (NT‑proBNP), which I will refer to now as simply BNP. 

And we will refer for a transthoracic echocardiography:

·      within 2 weeks if the NT-proBNP level is above 2,000 ng/litre (236 pmol / litre) and the urgency is because very high NT-PproNP levels carry a poor prognosis or refer

·      within 6 weeks if the NT-proBNP level is between 400 and 2,000 ng/litre (47 to 236 pmol/litre)

·      a NT-PROBNP level of less than 400 ng/litre (47 pmol/litre) in an untreated person makes a diagnosis of heart failure less likely. In these cases, we will look for alternative causes. 

But remember:

·      the NT-PROBNP level does not differentiate between heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. 

·      The NT-PROBNP level can be reduced by obesity, African or African–Caribbean family background, or treatment with HF drugs such as diuretics, ACE inhibitors, ARBs, beta‑blockers, or mineralocorticoid receptor antagonists (MRAs)

·      The NT-PROBNP level can be increased due to causes other than heart failure (for example, age over 70 years, left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia [including PE and COPD], eGFR less than 60, sepsis, diabetes, or liver cirrhosis). 

The purpose of transthoracic echocardiography is to exclude valve disease, assess the systolic and diastolic ventricular function, and detect intracardiac shunts. Heart failure caused by valve disease will need specialist referral. 

We will arrange alternative imaging (for example, radionuclide angiography, cardiac MRI or transoesophageal echocardiography) if the transthoracic echocardiography gives a poor image. 

We will also arrange other tests including:

·      ECG

·      chest X-ray

·      blood tests including full blood count, renal, liver and thyroid function as well as a lipid profile and HbA1c

·      urinalysis

·      peak flow or spirometry. 

In order to give the necessary information to the patient, NICE recommends an extended first consultation, followed by a second consultation 2 weeks later.

When it comes to treatment, there are specific recommendations for HFrEF but first we will look at the advice for all types of heart failure

Firstly, we will give Diuretics for the relief of congestive symptoms and fluid retention and titrate them up and down according to need. In particular, in heart failure with preserved ejection fraction we will normally give no more than a low to medium dose of loop diuretics (for example, less than 80 mg furosemide per day) and refer if this is not enouogh. 

By the way, I just wish to clarify that heart failure with preserved ejection fraction is usually associated with impaired left ventricular relaxation, rather than left ventricular contraction, and is characterised by normal left ventricular ejection fraction with evidence of diastolic dysfunction.

Amiodarone initiation will be by a specialist and we will review the need to continue at every 6‑monthly clinical review. Amiodarone monitoring must include 6 monthly liver and thyroid function tests. 

In sinus rhythm, anticoagulation should be considered for those with a history of thromboembolism, left ventricular aneurysm or intracardiac thrombus. 

We will now focus on the treatment of heart failure with reduced ejection fraction. By the way, I just want to clarify that Heart failure with reduced ejection fraction is when the ejection fraction is below 40%.

By way of introduction, we will say that some SGLT2 inhibotors such as dapaglifozin and empaglifozin have been shown to help in HFrEF even in the non-diabetic population. The guidance on their use in HF is covered outside this guideline, but in summary, NICE says that both Dapagliflozin and empaglifozin are recommended as an option for treating symptomatic chronic heart failure with reduced ejection fraction in adults, only if it is used as an add- on to optimised standard care with ACE inhibitors or ARBs, and beta blockers, mineralocorticoid receptor antagonists (MRAs) or sacubitril valsartan. I will put the link to the full SGLT2 guidance in the video description.

See NICE's technology appraisal guidance on dapagliflozin and empagliflozin for treating chronic heart failure with reduced ejection fraction

In terms of Calcium-channel blockers, we will avoid verapamil, diltiazem and short-acting dihydropyridine agents (like standard release nifedipine) in heart failure with reduced ejection fraction. 

The First-line treatment in heart failure with reduced ejection fraction is as follows:

1.     An ACE inhibitor and a beta‑blocker licensed for heart failure. The beta-blockers licensed in the UK for the treatment of heart failure are bisoprolol, carvedilol, and nebivolol. And we will use our clinical judgement when deciding which drug to start first. But we will not give an ACE inhibitor if there is haemodynamically significant valve disease until the valve disease has been assessed by a specialist.

a.     We will give an ARB licensed for heart failure if there are side effects with ACE inhibitors. ARB licensed for heart failure in the UK are Candesartan, losartan, and valsartan.

b.     If neither ACE inhibitors nor ARBs are tolerated, we will seek specialist advice, in order to consider hydralazine in combination with nitrate. 

c.      We will not withhold beta-blockers only because of age or the presence of peripheral vascular disease, erectile dysfunction, diabetes, interstitial pulmonary disease or chronic obstructive pulmonary disease.

d.     And, if stable, we will switch people already taking a beta-blocker for a comorbidity (for example, angina or hypertension), to a beta-blocker licensed for heart failure. That is again bisoprolol, carvedilol, and nebivolol in the UK.

2.     If there are persistent symptoms, we will then give an mineralocorticoid receptor antagonists (MRA), such as spironolactone or eplerenone, in addition to an ACE inhibitor (or ARB) and beta-blocker. 

Now, for all these drugs, that is ACEI, ARB, betablocker and MRA:

We will start at a low dose and titrate upwards at short intervals (for example, every 2 weeks) until the target or maximum tolerated dose is reached. 

We will measure BP and renal function, including sodium and potassium levels, before and 1 to 2 weeks after starting the drug, and after each dose increment. We will also assess heart rate if giving betablockers.

Once the target or maximum tolerated dose is reached, we will monitor treatment monthly for 3 months and then at least every 6 months, and at any time the person becomes acutely unwell. 

NICE recommends that the following drugs should be initiated by a Specialist

·      Ivabradine

·      Sacubitril valsartan

·      Hydralazine in combination with nitrate

·      Digoxin

Ivabradine is recommended if:

·      NYHA class II to IV stable chronic heart failure with systolic dysfunction and

·      sinus rhythm with a heart rate of 75 beats per minute (bpm) or more and

·      in combination with standard therapy including beta-blocker therapy, ACE inhibitors and aldosterone antagonists, or when beta‑blocker therapy is contraindicated or not tolerated and

·      with a left ventricular ejection fraction of 35% or less. 

Sacubitril valsartan is recommended if:

·      NYHA class II to IV symptoms and

·      with a left ventricular ejection fraction of 35% or less and

·      already taking a stable dose of ACE inhibitors or ARBs. 

By the way, if you want to learn a bit more about Sacubitril valsartan, stick around until the end, when I will give you a bit more information about it.

Hydralazine in combination with nitrate, is recommended especially if:

·      the person is of African or Caribbean family origin and

·      has moderate to severe heart failure NYHA class III/IV with reduced ejection fraction. 

Digoxin is recommended for worsening or severe symptoms despite first-line treatment. Routine monitoring of serum digoxin concentrations is not recommended. A digoxin concentration measured within 8 to 12 hours of the last dose may be useful to confirm a clinical impression of toxicity or non‑adherence. 

There are special considerations when treating heart failure with reduced ejection fraction in people with chronic kidney disease or CKD

If the eGFR is between 30 and 45 we will offer the same treatment but using lower doses and/or slower titration of ACEI, ARBs, MRAs and digoxin. 

If the eGFR is below 30 we will involve the renal team. 

And we will monitor closely the medication of CKD patients because of the increased risk of hyperkalaemia. 

Other general recommendations in terms of management are:

1.     an annual flu vaccination and a once only pneumococcal vaccination

2.     Contraception and pregnancy for women of childbearing potential

3.     Give appropriate advice on Smoking and alcohol

4.     Air travel will be possible for most, depending on their clinical condition. 

5.     In terms of driving, there may be restrictions for Large Goods and Passenger Carrying Vehicles and, in the UK, we will check the DVLA website for regular updates. 

6.     We will not routinely restrict sodium or fluid consumption. Instead, we will ask about salt and fluid consumption and:

o  advise fluid restriction if there is dilutional hyponatraemia

o  advise reducing intake if there are high levels of salt and/or fluid consumption. 

o  We will however advise to avoid salt substitutes that contain potassium. 

In terms of further monitoring for all types of heart failure

Apart from what has already been discussed, we will carry out full clinical assessment at every review.

If a person is taking digoxin or an MRA we will monitor potassium levels closely. 

And we will consider monitoring NT-PROBNP levels only if:

·      under 75

·      there is heart failure with reduced ejection fraction and

·      the eGFR is above 60 . 

In terms of Interventional procedures

1.     Coronary revascularisation should not be routinely offered but

2.     Cardiac transplantation, Implantable cardioverter defibrillators and cardiac resynchronisation therapy can be offered to the right patients.

Cardiac rehabilitation should normally be offered unless the HF is unstable.

And finally, in Palliative care

We will not offer long-term home oxygen therapy, although it may still be offered for comorbidities, such as for some people with COPD.

Now, this is the end of the actual NICE guideline on chronic heart failure. But if you are interested in learning how Sacubitril/valsartan works, here is some background information.

The first thing to understand is that the pathophysiology of heart failure involves an abnormal activation of the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, hypertension, increased aldosterone levels, increased sympathetic tone, and eventually, cardiac remodelling, all of which worsen the disease over time. ACEIs or ARBs play a major role in reducing HF morbidity and mortality by blocking this abnormal activation

At the same time that the renin-angiotensin-aldosterone system is activated, the natriuretic peptide system is also activated, hence the elevated BNP and NT-pro BNP seen in heart failure. This compensatory mechanism leads to vasodilation, natriuresis, and diuresis. As a result, the natriuretic peptide system decreases blood pressure, lowers the sympathetic tone, and reduces aldosterone levels. The natriuretic peptide system functions antagonistically to the renin-angiotensin-aldosterone system and has favourable impact on heart failure. Natriuretic peptides are broken down by an enzyme called neprilysin.

Sacubitril/valsartan is a combination product. Sacubitril is a pro-drug that, upon activation, acts as a neprilysin inhibitor. So it works by blocking the action of neprilysin, thus preventing the breakdown of natriuretic peptides, which leads to a prolonged duration of the favourable effects of these peptides.

However, because neprilysin also breaks down angiotensin II, inhibiting neprilysin will accumulate angiotensin II. For this reason, a neprilysin inhibitor cannot be used alone; it must always be combined with an ARB to block the effect of the excess angiotensin II. This is why Valsartan is used.

Another important substance broken down by neprilysin is bradykinin; neprilysin inhibition will also cause a build-up of bradykinin. Therefore, sacubitril cannot be used with an ACEI due to an increased risk of angioedema if both these drugs are combines or given in a short timeframe. And this is why when switching between ACEI and sacubitril/valsartan, the patient must undergo a 36-hour washout period to lower the risk of angioedema.

We have come to the end of this video. I hope that you have found it useful and, if so, please hit the like and subscribe buttons. Thank you for watching and good-bye

This podcast makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this video I will go through new and updated guidelines published in October 2023 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only. 

I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel:  

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulleting for October 2023 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2023-10-01&to=2023-10-31&ndt=Guidance&ndt=Quality+standard

The links to the update guidance covered can be found here:

Rimegepant for treating migraine:

·      https://www.nice.org.uk/guidance/ta919

Thyroid disease: assessment and management

·      https://www.nice.org.uk/guidance/ng145

Tirzepatide for treating type 2 diabetes

·      https://www.nice.org.uk/guidance/ta924

Suspected cancer: recognition and referral

·      https://www.nice.org.uk/guidance/ng12

Suspected neurological conditions: recognition and referral

·      https://www.nice.org.uk/guidance/ng127

Hearing loss in adults: assessment and management

·      https://www.nice.org.uk/guidance/ng98

Daridorexant for treating long-term insomnia

·      https://www.nice.org.uk/guidance/ta922

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  

• Music provided by Audio Library Plus  

• Watch: https://youtu.be/aBGk6aJM3IU 

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• Transcript

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in October 2023, focusing on what is relevant in Primary Care only. We will be covering: migraines, thyroid function tests, diabetes, suspected cancer and insomnia.

So let’s jump into it.

The first clinical area is an update on a new migraine medication, rimegepant.

And NICE says that Rimegepant is recommended, only if:

·      at least 2 triptans have been tried before but were ineffective or

·      if triptans cannot be used, and Paracetamol and NSAIDs are not effective.

What is Rimegepant?

Well, gepants are a new class of drugs that have been developed specifically for the treatment of migraines. Rimegepant is a calcitonin gene-related peptide receptor antagonist so it works by blocking this CGRP receptor. And although the mechanism of action is not fully understood, we know that this receptor is involved in the development of migraines. Gepants can be used as an acute treatment and, although rimegepant has a licence for migraine prophylaxis, NICE does not recommend it for this indication.

Unlike triptans, gepants do not cause vasoconstriction so they do not have the same cardiovascular contraindications and cautions as triptans. Rimegepant is an oral lyophilisate that should be placed on the tongue or under the tongue and it will disintegrate in the mouth and can therefore be taken without liquid.

The next update refers to thyroid disease and it says that when ordering thyroid function tests, patients should be routinely asked about biotin use. This is because the MHRA has reported that biotin may cause thyroid test results to be falsely increased or decreased, leading to inappropriate management. Biotin is increasingly found in dietary supplements which are typically taken for hair, skin and nail health so we should always check whether patients are taking such supplements over the counter.

The third area refers to a new diabetic agent, tirzepatide, and, like GLP1 receptor agonists, it is recommended if type 2 diabetes is not controlled:

·      on triple therapy with metformin and 2 other drugs, and

·      they have a BMI of 35 or more, with obesity related health problems, or

·      they have a BMI of less than 35, and:

o  insulin therapy would have significant occupational implications, or

o  weight loss would benefit other significant complications.

But we will use lower BMI thresholds (usually reduced by 2.5) for people from non-white family backgrounds.

We all know the supply issues that we have had with various GLP1 receptor agonists, so is tirzepatide a new GLP1 drug coming to the rescue? Well, not really. Because Tirzepatide is both a GIP and a GLP-1 receptor agonist, so it is a dual agent. It is a weekly injectable and clinical trials suggest that tirzepatide reduces HbA1c and BMI more than semaglutide. Weight reduction with tirzepatide is more pronounced with higher doses, whereas reductions in HbA1c seem less dose-dependent. 

No dose adjustment is required for patients with hepatic and renal impairment including end stage renal disease (ESRD) but experience with these patients is limited so we should exercise caution.

The Mechanism of action of tirzepatide is by increasing Insulin secretion and sensitivity, reducing Glucagon and delaying Gastric emptying

The next clinical area refers to suspected cancer: recognition and referral, and the guidance has been updated to reflect the new NHS standard on faster cancer diagnosis.

So, what this means is that, rather than focusing on these patients being seen within 2 weeks, the aim now is for them to have a diagnosis or have cancer ruled out within 28 days from referral.

This change applies when:

·      the referring GP suspects cancer

·      there are breast symptoms even where cancer is not initially suspected or when

·      there is an abnormal National Cancer Screening result.

So, this update will also appear in a number of other guidelines including, for example:

-         Neurological conditions

-         Ovarian cancer and

-         Urinary incontinence

Next there is also an update saying that we should use a suspected cancer pathway for adults of Chinese or south-east Asian family origin who develop hearing loss and a middle ear effusion not associated with an upper respiratory tract infection.

This is because of the higher incidence of nasopharyngeal carcinoma (NPC) in these populations. Nasopharyngeal carcinoma is rare in most parts of the world, but it’s much more common in East and Southeast Asia, which suggests that genetic and/or environmental factors can contribute substantially to its development.  

The final guidance is on Daridorexant for treating long-term insomnia. And NICE says that Daridorexant is recommended for insomnia lasting for 3 nights or more per week for at least 3 months, with affected daytime functioning but only if:

·      cognitive behavioural therapy for insomnia (CBTi) is ineffective or

·      it is not available or is unsuitable.

What is daridorexant? Well, unlike benzodiazepines and Z-drugs, which work by increasing sedation, daridorexant is a new type of drug, an orexin antagonist, which works in a different way. It inhibits arousal mechanisms. To understand this, we need to know that orexins are neuropeptides produced by the hypothalamus which promote a state of wakefulness. Therefore, daridorexant, by blocking the orexin receptors, reduces wakefulness and helps sleep

And the good news is that, in clinical studies, there has been no evidence of abuse or withdrawal symptoms indicative of physical dependence.

NICE recommends that the length of treatment should be as short as possible and the treatment should be reviewed within 3 months of starting and at regular intervals thereafter.

However, it is worth mentioning that, in October 2023, Daridorexant was still not available on the BNF.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

Episode: EASD ADA consensus guidelines on the overall approach in glucose lowering medication in type 2 diabetes

This podcast is intended for healthcare professionals. My name is Fernando Florido and I am a GP in the United Kingdom. In this episode I go through the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) consensus guidelines on the overall approach in glucose lowering medication in type 2 diabetes. I will firstly give you a list of the changes to the previous consensus recommendations followed by a description of the consensus recommendations flowchart on the subject. The original article was published on 19 December 2019 with a subsequent correction published on 15 May 2020.

There is a YouTube version of this episode in the NICE GP YouTube Channel that you can access here:

·      https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw

This episode also appears in the

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

Diabetes in Primary Care podcast:

·      Redcircle: https://redcircle.com/shows/diabetes-in-primary-care

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/us/podcast/diabetes-in-primary-care/id1562910252

The ADA-EASD consensus guidelines can be found here:

·      Website:

o  https://link.springer.com/article/10.1007/s00125-019-05039-w

·      Or download here:

o  https://1drv.ms/b/s!AiVFJ_Uoigq0lW-4rilnP_mruV41?e=FjPLGo

The Summary of the changes to the previous consensus recommendations can be

·      Viewed on website above:

o  https://link.springer.com/article/10.1007/s00125-019-05039-w

·      Or downloaded here:

o  https://1drv.ms/b/s!AiVFJ_Uoigq0lW72FZuzZZiv8bPr?e=7Fib8M

The Visual summary “glucose lowering medication in type 2 diabetes- overall approach” can be found here:

·      Website:

o  Figure 1 | 2019 update to: Management of hyperglycaemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) | SpringerLink

·      Or download here:

o  https://1drv.ms/u/s!AiVFJ_Uoigq0lXCNFscGYei60BiV?e=3n0Ern

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]

Music provided by Audio Library Plus

Watch: https://youtu.be/aBGk6aJM3IU

Free Download / Stream: https://alplus.io/halfway-through

Transcript:

This podcast is intended for healthcare professionals. Thank you for listening and welcome to a new episode, bringing you medical information and clinical guidance from a primary care perspective. My name is Fernando Florido and I am a GP in the United Kingdom.

In today’s episode I am going to go through the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) consensus guidelines on the overall approach in glucose lowering medication in type 2 diabetes.

I will firstly give you a list of the changes to the previous recommendations followed by a description of the consensus recommendations flow chart.

If you have been following previous episodes, you may be familiar with the updated NICE guidelines on the management of type 2 diabetes. However, the NICE recommendations, primarily followed in the UK, have some substantial differences when compared to other international recommendations and this is why I have decided to do this episode today. You will notice that the main difference with NICE refers to the use of GLP1 mimetics which NICE considers to be less cost effective. However, from a clinical perspective, there is now ample evidence in their favour, which justifies a wider use as described in the consensus guidelines.

I will put in the description below a link to download the full article as well as the summary of the changes and the flow chart. There is a YouTube version of this episode and other NICE guidance on the NICE GP YouTube Channel and a link to access it can be found in the podcast description. Because of the visual nature of the flow chart, I would highly recommend watching the YouTube video if you can.

Although describing visual aids as audio files can be challenging, I hope that you find the content clear and informative.

Right, let’s go right in. So, we are going to start looking at the European Association for the Study of Diabetes and the American Diabetes Association consensus guidelines on managing hyperglycemia in type 2 diabetes, published in December 2019, corrected in May 2020 and I have put links in to it in the episode description.

Now, before starting the treatment flow chart, we are going to go through the changes to the consensus recommendations and this is just a brief summary of what the changes are.

As a general consideration we will say that, in high-risk patients, the decision to treat with a GLP 1 receptor agonist or an SGLT 2 inhibitor should be considered independently of the HbA1c. This is because these agents have been proven to reduce major adverse cardiovascular events, hospitalisation for heart failure, cardiovascular deaths and CKD progression.

We will say that in patients with established atherosclerotic cardiovascular disease, the level of evidence for cardiovascular benefit is greatest for GLP 1 receptor agonist and this is in terms of reducing major adverse cardiovascular events.

And because of this, to reduce the risk of cardiovascular disease, the GLP 1 receptor agonists can also be considered in patients who have no cardiovascular disease but who are at high risk of cardiovascular disease.

For patients with heart failure, especially if their heart failure has a reduced ejection fraction, that is, an ejection fraction less than 45%, or if they have CKD with an eGFR between 30 and 60 and microalbuminuria, with urine albumin creatinine ratio greater than 30 particularly if it is greater than 300, the level of evidence is greatest for SGLT 2 inhibitors. So, SGLT 2 inhibitors are recommended with patients with heart failure and equally the SGLT 2 inhibitors are recommended for patients we CKD to prevent progression of CKD as well as the cardiovascular outcomes.

Obviously, because there is a link between SGLT 2 inhibitors and an increased risk of amputation, patients with foot ulcers or at high risk of amputation, should only be treated with SGLT 2 inhibitors after careful shared decision making around the risks and benefits and with comprehensive education and foot care and amputation prevention.

Well, that was the summary of the changes. Now we are going to dive in straight into the flow chart, which is titled: “glucose lowering medication in type 2 diabetes: overall approach”. And in the right top corner there is a note that tells us that, to avoid clinical inertia, we need to review the patients regularly, ideally every three or six months.

Now, the first thing that the flow chart tells us is that the first line therapy is always metformin and comprehensive lifestyle including weight management and physical activity. So, metformin first of all, and then, we are going to see if there are indicators of high risk or established atherosclerotic cardiovascular disease, CKD or heart failure. If the patient has any of these, then we will consider independently of the HbA1c the treatment.

This side of the flow chart then divides in two, one if cardiovascular disease predominates or, two, if heart failure or CKD predominate.

So, if atherosclerotic cardiovascular disease predominates, either because there is established cardiovascular disease or there are indicators of high risk for getting cardiovascular disease, then we will preferably give a GLP 1 receptor agonist with proven cardiovascular disease benefit and the chart tells us at the bottom in the notes that proven cardiovascular benefit means that it has a label indication for reducing cardiovascular events.

If you cannot give or do not want to give a GLP 1 receptor agonist then we will give an SGLT 2 inhibitor with proving cardiovascular benefit, as long as the eGFR is adequate. And again, it reminds us at the bottom of the chart that we have to be aware that SGLT 2 inhibitor labelling varies by region and individual agents with regard to the indicated level of eGFR for initiation and continued use.

Right, so we repeat again, independently of the HbA1c and if cardiovascular disease predominates, we will give either GLP 1 receptor agonist or an SGLT 2 inhibitor.

And then, we will look at the HbA1c and if the HbA1c remains above the target then we will consider further intensification of the treatment.

For patients who are on GLP 1 receptor agonists we will give an SGLT 2 inhibitor and, likewise, if they had initiated an SGLT 2 inhibitor then we will give them a GLP 1 receptor agonist. As an alternative, we can give a DPP 4 inhibitor if the patient is not on a GLP 1 receptor agonist, and this is because of their mode of action or we can also give basal insulin, pioglitazone or a sulphonylurea. So, we are just going to mix and match those agents, always preferably starting with GLP 1 receptor agonist, then SGLT 2 inhibitors and then we can give a DPP 4 inhibitor if the patient is not on a GLP 1 receptor agonist, or basal insulin, pioglitazone or a sulphonylurea.

And, also in the notes at the bottom, it tells us that degludec and U 100 glargine have demonstrated cardiovascular disease safety. It also tells us that a low dose of pioglitazone may be better tolerated though less well studied for cardiovascular effects and, in terms of sulphonylureas, it reminds us that we should choose later generations of sulphonylureas to lower the risk of hypoglycaemia and glimepiride has shown similar cardiovascular safety to the DPP 4 inhibitors.

So, that concludes the section where cardiovascular disease predominates. Now if heart failure or CKD predominate, particularly if it is reduced ejection fraction heart failure or if CKD has an eGFR between 30 and 60 and microalbuminuria at least 30mg per gram or more, we will use preferably an SGLT 2 inhibitor with evidence of reducing heart failure and / or CKD progression in cardiovascular outcome trials, as long as the EGFR is adequate.

So, it tells us in the notes at the bottom that both empaglifozin and canaglifozin have shown reduction in heart failure and also reduced CKD progression in cardiovascular outcome trials. Canaglifozin has primary renal outcome data from CREDENCE and dapaglifozin has primary heart failure outcome from the DAPA HF trial. But all these details may be becoming less and less relevant because it is now increasingly thought that the SGLT 2 inhibitors have a class effect.

Now if an SGLT 2 inhibitor is not tolerated or contraindicated or if the eGFR is less than adequate, we will give a GLP 1 receptor agonist with proven cardiovascular benefit.

So, it is more or the other way round from the cardiovascular disease branch. There we gave a GLP 1 receptor agonist first and then an SGLT 2 inhibitor. Here, in heart failure of CKD we are going to give an SGLT 2 inhibitor first and then GLP 1 receptor agonist second.

And, again, we need to remember that if a patient has heart failure or CKD, we will consider this treatment with an SGLT2 inhibitor or a GLP 1 receptor agonist independently of the HbA1c.

And then, we will look at the HbA1c, and if the HbA1c is above the target, we will consider further treatment.

The first thing that we have to consider is that we need to avoid pioglitazone in the setting of heart failure because it tends to worsen it because of fluid retention. We will try to stick to agents with cardiovascular safety. So, for patients on an SGLT 2 inhibitor, we will consider a GLP 1 receptor agonist. Or we can give a DPP 4 inhibitor but not saxagliptin in the setting of heart failure, as long as the patient is not on a GLP 1 receptor agonist. Alternatively, we can give basal insulin or a sulphonylurea.

So, in summary, after an SGLT 2 inhibitor and a GLP 1 receptor agonist, if we need to give anymore drugs, we will avoid pioglitazone and saxagliptin in in the setting of heart failure. We can consider a DPP 4 inhibitor, if not on a GLP 1 receptor agonist, or basal insulin or a sulphonylurea.

Right, this ends the branch of heart failure or CKD patients.  So, we have now covered both if a patient has got atherosclerotic cardiovascular disease, heart failure or CKD. However, if a patient has not got those conditions and they are not at high risk of those conditions, then we will give metformin and then will be guided by the HbA1c in order to decide whether to give more treatment.

And we will divide this treatment in three, depending on whether, one, we want to minimise hypoglycaemia, two, we want to minimise weight gain or promote weight loss and, three, when cost of treatment is a major issue. So again, we divide the treatment on whether we focus on hypoglycaemia, on weight or on cost.

Firstly, we will look at the branch where minimising hypoglycaemia is our priority. And for those patients, we will use any of the agents that are not associated with hypoglycaemia. That is, a DPP 4 inhibitor, a GLP 1 receptor agonist, an SGLT 2 inhibitor or pioglitazone. So, we give dual therapy with metformin and one of those drugs. If the HbA1c remains above target then we will give triple therapy with metformin and any combination of the drugs already mentioned, a DPP 4 inhibitor, a GLP 1 receptor agonist, an SGLT 2 inhibitor or pioglitazone bearing in mind that we must not combine a GLP 1 receptor agonist and a DPP 4 inhibitor. But all other combinations are allowed.

And then, if the HbA1c remains above target on triple therapy, we will continue with additions of other agents so we can go to quadruple therapy.

Finally, if the HbA1c remains above target. Then we will consider the addition of a sulphonylurea or basal insulin. And with sulphonylureas we will choose the later generations with lower risk of hypoglycaemia such as glimepiride or we will consider a basal insulin with lower risk of hypoglycaemia. And there is a small note at the bottom of the chart that tells us that the insulin with lowest risk of hypoglycaemia is degludec and glargine U300, followed by glargine U100 and detemir, followed by finally NPH insulin.

Now, the second branch is when we are going to focus on the weight because we need to minimise weight gain or promote weight loss. In these cases, we will give either at GLP 1 receptor agonist or an SGLT 2 inhibitor because both these agents are associated with weight loss. And a small note at the bottom of the chart tells us the GLP 1 receptor agonists with good efficacy for weight loss. The best one is semaglutide, followed by liraglutide, then dulaglutide, then exenatide and finally lixisenatide. So, if we can, we will give them always either semaglutide or liraglutide.

And then if the HbA1c remains above target then we will give the second of those two agents, so, if the patient is had a GLP 1 receptor agonist, we will give an SGLT 2 inhibitor and if they have had an SGLT 2 inhibitor then we will give in GLP 1 receptor agonist.

And if the HbA1c remains above target, then we will start quadruple therapy because the patient would already be on metformin, a GLP 1 receptor agonist and an SGLT 2 inhibitor. But if this combination is not tolerated or contraindicated, then the lowest risk of weight gain is with a DPP 4 inhibitor and this is because the DPP 4 inhibitors have got weight neutrality, but that can only be given if the patient is not already on a GLP 1 receptor agonist.

If the DPP 4 inhibitor is not tolerated or contraindicated or if the patient is already on a GLP 1 receptor agonist, we should use cautiously a sulphonylurea, pioglitazone or basal insulin, and this is because all these agents are associated with weight gain.

Finally, the last branch of the flowchart is when we are going to focus on the cost, because cost is a major issue. And there is a note at the bottom of the page that is going to tell us when we should consider cost to be a major issue. Therefore, cost should be our focus if there are no specific comorbidities, that is, no established cardiovascular disease, there is a low risk of hypoglycaemia and weight is not a real concern.

Also, there is a warning in terms of cost, saying that we need to consider country and region-specific cost of drugs because, in some countries for example, pioglitazone can be relatively more expensive and a DPP 4 inhibitor relatively cheaper.

So, looking at the flowchart, if cost is a concern, after metformin we will start with either a sulphonylurea or pioglitazone, which are generally the cheapest agents and if the HbA1c is above target, we will go into triple therapy with metformin, a sulphonylurea and pioglitazone. And if the HbA1c remains above target, then we will consider either insulin therapy, giving basal insulin with the lowest acquisition cost or we can consider a DPP 4 inhibitors or an SGLT 2 inhibitors with the lowest acquisition cost. Or, in other words, we go into quadruple therapy according to whatever is the most cost-effective combination.

Right, this is it, we have completed the review of the EASD ADA consensus guidelines flow chart. So, this is the end of this video and the summary of the consensus recommendations. There is also a YouTube version of this episode in the NICE GP YouTube Channel and I will leave a link in the episode description. Thank you for listening and I hope that you will join me in the next one.

THIS GUIDELINE IS NOW OBSOLETE. PLEASE CHECK THE UPDATED 2024 ASTHMA GUIDELINE AVAILABLE ON THIS CHANNEL. YOU CAN FIND IT IN THE VIDEO DESCRIPTION, BY CLICKING THE LINK IN THE TOP-RIGHT CORNER OF THIS VIDEO, OR ON THE END SCREEN.

The asthma playlist including the 2024 asthma guideline can be found here:

https://youtube.com/playlist?list=PLkDRVxR2chuhrU7IiPYiFYj7Wu_h3PURb&si=DmdpArNj9anQa5qx

My name is Fernando Florido and I am a GP in the United Kingdom. With today’s episode I continue with the series on asthma, focusing on the NICE guidelines on the diagnosis and management asthma. Firstly, I am going to go through the diagnosis flow charts and I am going to do them over 3 different episodes. In today's episode, the third one, I consider the diagnostic tests for adults. In the first one I go through the initial clinical assessment for all patients and in the second one I go through the objective tests for children and young people. There will be other videos on the pharmacological treatment of asthma so make sure you subscribe and stay tuned.

There is YouTube version of the podcast and other guidance that you can access here: 

·      https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw

The full NICE guideline on asthma can be found here:

·      Website:

https://www.nice.org.uk/guidance/ng80

·      Or download here:

https://1drv.ms/b/s!AiVFJ_Uoigq0lgCTpT8m-jvCCavu?e=z1Vs5z

The diagnostic flow chart “initial assessment” (Episode 1) can be

·      Viewed on website: https://www.nice.org.uk/guidance/ng80/resources/algorithm-a-initial-clinical-assessment-for-adults-young-people-and-children-with-suspected-asthma-pdf-4656176749

·      Or, if outside the UK, downloaded here:

o  Image: https://1drv.ms/u/s!AiVFJ_Uoigq0lXZgO7_Zad1zMIfX?e=cmzv91

o  PDF: https://1drv.ms/b/s!AiVFJ_Uoigq0lXWWt7TqIN0Cye1M?e=kL0i0p

The diagnostic flow chart “children and young people” (Episode 2) can be

·      Viewed on website: https://www.nice.org.uk/guidance/ng80/resources/algorithm-b-objective-tests-for-asthma-in-children-and-young-people-aged-5-to-16-pdf-4656176750

·      Or, if outside the UK, downloaded here:

o  Image: https://1drv.ms/u/s!AiVFJ_Uoigq0lXTL5o5XU2aOfChx?e=6qJk1M

o  PDF: 

https://1drv.ms/b/s!AiVFJ_Uoigq0lXlBBD1Wq7lak-mg?e=iLpgAX

The diagnostic flow chart “adults” (Episode 3) can be

·      Viewed on website: https://www.nice.org.uk/guidance/ng80/resources/algorithm-c-objective-tests-for-asthma-in-adults-aged-17-and-over-pdf-4656176751

·      Or, if outside the UK, downloaded here:

o  Image: https://1drv.ms/u/s!AiVFJ_Uoigq0lXgUR4QxwwxNNynL?e=OrBRwi

o  PDF: 

https://1drv.ms/b/s!AiVFJ_Uoigq0lXcaf4BUKI2k3TsR?e=tCn86P

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]

Music provided by Audio Library Plus

Watch: https://youtu.be/aBGk6aJM3IU

Free Download / Stream: https://alplus.io/halfway-through

My name is Fernando Florido and I am a GP in the United Kingdom. In this video I go through the NICE guidelines “Chronic kidney disease: assessment and management” or NG203, Published on 25 August 2021 

There is a Youtube version of this and other videos that you can access here: 

·      @nicegp : https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw 

The full NICE guideline on CKD can be found here: 

·      Website: https://www.nice.org.uk/guidance/ng203 or as 

·       PDF: https://www.nice.org.uk/guidance/ng203/resources/chronic-kidney-disease-assessment-and-management-pdf-66143713055173

·      Or download here: https://1drv.ms/b/s!AiVFJ_Uoigq0lgvjCLLzwi5sLeq7?e=JC2Z0g 

The Visual summaries on CKD can be found here:

• Websites:
• Identifying CKD: 

https://www.nice.org.uk/guidance/ng203/resources/visual-summary-identifying-chronic-kidney-disease-in-adults-pdf-9206256493

• Managing proteinuria: 

https://www.nice.org.uk/guidance/ng203/resources/visual-summary-chronic-kidney-disease-g15-a13-managing-proteinuria-pdf-9206256495

• Phosphate binders:

https://www.nice.org.uk/guidance/ng203/resources/visual-summary-chronic-kidney-disease-stages-4-and-5-phosphate-binders-pdf-9206256494

·      Or download here:

o  Identifying CKD: https://1drv.ms/b/s!AiVFJ_Uoigq0lgxMqWAve0P2Uqmw?e=r9Gaj2 

o  Managing proteinuria:

https://1drv.ms/b/s!AiVFJ_Uoigq0lg2n86ZBA-LtN8Sx?e=3iUfe7 

o  Phosphate binders:

https://1drv.ms/b/s!AiVFJ_Uoigq0lg62GGYNQmkebxqF?e=nG7cm6 

CKD tables- 1&2

·      Download: https://1drv.ms/u/s!AiVFJ_Uoigq0lhN1Hnk7TV08C5lC?e=FaLGZo

Abbreviations: ACR, albumin creatinine ratio; CKD, chronic kidney disease; GFR, glomerular filtration rate.

Note: ACR monitoring should be individualised based on a person's individual characteristics, risk of progression and whether a change in ACR is likely to lead to a change in management.

The episodes on the NICE guideline on hypertension are here: 

·      Full guideline: https://youtu.be/dELO3enIhsI

·      Flowchart: https://youtu.be/Ffa6IYrZWeo

·      Shorts: 

o  https://youtu.be/qmLJtwu677I 

o  https://youtu.be/Izo_eSuECEU 

o  https://youtu.be/BnbcUPriJ9g

For guidance on SGLT2 inhibitors for adults with CKD and type 2 diabetes, see chronic kidney disease in NICE's guideline on type 2 diabetes in adults.  

·      Summary of guidance: CKD section of diabetes guideline 1.8.17 

For adults with type 2 diabetes and CKD who are taking an ARB or an ACE inhibitor (titrated to the highest licensed dose that they can tolerate), offer an SGLT2 inhibitor (in addition to the ARB or ACE inhibitor) if:

·      ACR is over 30 mg/mmol and

·      they meet the criteria in the marketing authorisation (including relevant estimated glomerular filtration rate [eGFR] thresholds).

·      Website: Diabetes guideline: 

https://www.nice.org.uk/guidance/ng28/chapter/Recommendations#chronic-kidney-disease 

For guidance on dapagliflozin for adults with CKD, with or without type 2 diabetes, see NICE's technology appraisal guidance on dapagliflozin for treating chronic kidney disease.  

·      Website:

https://www.nice.org.uk/guidance/ta775

·      PDF:

https://www.nice.org.uk/guidance/ta775/resources/dapagliflozin-for-treating-chronic-kidney-disease-pdf-82611498049477

·      Or download here:

https://1drv.ms/b/s!AiVFJ_Uoigq0lg_O0S-awCfFqpI_?e=rrscuF 

For recommendations on hyperkalaemia treatment in adults with categories G3b to G5 chronic kidney disease, see NICE's technology appraisals on sodium zirconium cyclosilicate and patiromer. 

·      Website:

o  Zirconium: https://www.nice.org.uk/guidance/ta599

o  Patiromer: https://www.nice.org.uk/guidance/ta623 

·      PDF:

o  Zirconium:

https://www.nice.org.uk/guidance/ta599/resources/sodium-zirconium-cyclosilicate-for-treating-hyperkalaemia-pdf-82607272135621

o  Patiromer: https://www.nice.org.uk/guidance/ta623/resources/patiromer-for-treating-hyperkalaemia-pdf-82609015577029

·      Or download here:

o  Zirconium:

https://1drv.ms/b/s!AiVFJ_Uoigq0lhLUkpx5T4E0mrE_?e=XcfIQt

o  Patiromer: https://1drv.ms/b/s!AiVFJ_Uoigq0lhARwG8vfMNKvISz?e=VEsKLm 

Follow the recommendations in NICE's guideline on cardiovascular disease: risk assessment and reduction, including lipid modification for the use of statins in adults with CKD.  

·      Website: https://www.nice.org.uk/guidance/cg181

·      PDF:

https://www.nice.org.uk/guidance/cg181/resources/cardiovascular-disease-risk-assessment-and-reduction-including-lipid-modification-pdf-35109807660997 

·      Or download here:

https://1drv.ms/b/s!AiVFJ_Uoigq0lhEqiQX4EhaMN2A3?e=7u5KIK 

Follow the MHRA safety advice on recombinant human erythropoietins:

·      Website:

 https://www.gov.uk/drug-safety-update/recombinant-human-erythropoietins-new-advice-for-prescribing

·      Summary of advice: 

Recombinant human erythropoietins: new advice for prescribing

Over-correction of haemoglobin concentration may increase the risk of death and serious cardiovascular events in patients with chronic kidney disease; it may increase the risk of thrombosis and related complications in patients with cancer.

4-variable Kidney Failure Risk Equation

A person's 5-year risk of needing renal replacement therapy (defined as the need for dialysis or transplant) is estimated, as in Major 2019, as:

In the above, eGFR is reported in ml/min/1.73 m2 and ACR in mg/mmol. Where the term 'male' is used, this should be replaced by a 1 if the person being assessed is male, and a 0 if they are female. This equation and its coefficients are validated in a UK population, and it is important to use this version, and not a version validated in another country.

Transcript

Hello everyone and welcome to the channel.

Today we are going to look at the NICE guidelines on CKD.

My name is Fernando Florido and I am a GP in the United Kingdom. So, let’s get started.

The first thing that I want to say is that obviously this video is a summary of the guideline. I have removed anything that I thought was common-sense advice (e.g. involve patients in the decision making process, offer information, etc) but on this occasion I have removed all aspects about children and young people with CKD. Although their management is very similar to adults in many ways, most patients with CKD that we will see in general practice will be adults and this is why I have focused on them  

In terms of measuring kidney function, we will look at the eGFR. We need to remember that “e” in eGFR means “estimated” and that eGFRcreatinine may be less reliable in certain situations, for example, acute kidney injury, pregnancy, oedematous states, and has not been well validated in certain ethnic groups, for example, black, and Asian ethnic groups. Also, reduced muscle mass will lead to overestimation and increased muscle mass to underestimation of the GFR and therefore we will need to interpret eGFRcreatinine with caution in extremes of muscle mass, e.g., in bodybuilders, amputation or muscle wasting disorders.

And we shouuldn’t forget to advise patients not to eat any meat in the 12 hours before having a blood test for eGFRcreatinine. This is because meat contains creatinine so when you eat meat the serum creatinine naturally increases. Serum creatinine used in eGFR calculations. And so, eating less (or no meat) will cause the creatinine to fall and consequently, the eGFR to improve. 

The eGFR value is given as a whole number if it is 90 or less, or as 'greater than” 90 

If eGFR is greater than 90, we will use an increase in serum creatinine of more than 20% to infer significant reduction in kidney function. 

We need to interpret eGFR values of 60 or more with caution, as estimates of GFR become less accurate as the true GFR increases. 

And we will also confirm a first ever eGFR result of less than 60 by repeating it within 2 weeks. 

When it comes to proteinuria, we will not use reagent strips to detect it. We will:

·      use urine ACR rather than protein:creatinine ratio (PCR) because of the greater sensitivity for low levels of proteinuria. However, when ACR is 70 mg/mmol or more, PCR can be used as an alternative to ACR. 

• check an ACR between 3 mg/mmol and 70 mg/mmol in a subsequent early morning sample to confirm the result.
• A repeat sample is not needed if the initial ACR is 70 mg/mmol or more. 
• Regard an ACR of 3 mg/mmol or more as clinically important proteinuria. 

And we will routinely measure ACR in:

• diabetes (type 1 or type 2)
• people with an eGFR of less than 60 
• people with an eGFR of 60 or more if there is a strong suspicion of CKD

If unexplained proteinuria is found on a reagent strip, we need to offer testing for CKD using eGFRcreatinine and ACR.  

When it comes to haematuria, we will use reagent strips to test for it and:

• Evaluate further for results of 1+ or higher. 
• Do not use urine microscopy to confirm a positive result because red blood cells may not be seen in microscopy in haemolysed haematuria 

We will regard 2 out of 3 positive reagent strip tests as confirmation of persistent invisible haematuria. Otherwise, it may be transient haematuria

Persistent invisible haematuria, with or without proteinuria, should prompt investigation for urinary tract malignancy in appropriate age groups  

Persistent invisible haematuria in the absence of proteinuria should be followed up annually with repeat testing for haematuria, proteinuria or albuminuria, GFR and blood pressure monitoring as long as the haematuria persists.  

There are certain patients who should be regularly tested for CKD. 

We will monitor GFR at least annually if medicines that can adversely affect kidney function, such as calcineurin inhibitors (for example, ciclosporin or tacrolimus), lithium or non-steroidal anti-inflammatory drugs (long-term chronic use of NSAIDs) are given.  

We will also do eGFRcreatinine and ACR to people with any of the following risk factors:

• diabetes 
• hypertension
• previous episode of acute kidney injury
• cardiovascular disease (ischaemic heart disease, chronic heart failure, peripheral vascular disease, or cerebral vascular disease)
• structural renal tract disease, recurrent renal calculi, or prostatic hypertrophy
• multisystem diseases with potential kidney involvement, for example, systemic lupus erythematosus
• gout
• family history of end-stage renal disease (GFR category G5) or hereditary kidney disease
• incidental detection of haematuria or proteinuria. 

We will also monitor people for the development or progression of CKD for at least 3 years after acute kidney injury (longer for people with acute kidney injury stage 3) even if eGFR has returned to baseline.  

There is a classification of CKD depending on the ACR level (A1, A2 and A3) and the GFR level (G1 to G5).

§ A1: ACR less than 3 mg/mmol

§ A2: ACR 3 to 30 mg/mmol

§ A3: ACR over 30 mg/mmol

§ G1: GFR 90 or over

§ G2: GFR 60 to 89

§ G3a: GFR 45 to 59

§ G3b: GFR 30 to 44

§ G4: GFR 15 to 29

§ G5: GFR under 15  

We need to be aware that:

• increased ACR and decreased GFR is associated with increased risk of adverse outcomes 
• increased ACR and decreased GFR in combination multiply this risk.

The classification table (table 1) with the risk assessment of every category can be found in the video description. 

We will offer a renal ultrasound scan to all adults with CKD who:

• have accelerated progression of CKD (and we will look at the definition of this later)
• have visible or persistent invisible haematuria
• have symptoms of urinary tract obstruction
• have a family history of polycystic kidney disease and are older than 20
• have a GFR of less than 30 (that is GFR category G4 or G5) 
• are considered by a nephrologist to need a renal biopsy. 
•  

When it comes to the frequency of monitoring, we will bear in mind that CKD is not progressive in many people. 

There is also a table (table 2) to guide the minimum frequency of eGFRcreatinine monitoring depending of the CKD classification- you can see this table in the video description too. 

Generally, it would be:

1.    once a year for G1, G2 and G3a if the ACR is less than 30

2.    twice a year for G3a A3 (that is ACR more than 30) and also G3b and G4 if the ACR is less than 30

3.    three times a year for G4A3 (that is ACR more than 30)

4.    four times a year or more for G5 

Monitoring should be tailored according to:

• the underlying cause
• the rate of decline in eGFR or increase in ACR
• other risk factors, including heart failure, diabetes and hypertension
• changes to their treatment (such as renin–angiotensin–aldosterone system [RAAS] antagonists, NSAIDs and diuretics)
• intercurrent illness (for example acute kidney injury)

We will define accelerated progression of CKD as:

• a sustained decrease in GFR of 25% or more and a change in GFR category within 12 months or
• a sustained decrease in GFR of 15 per year. 
• These people are at high risk of progression to end stage renal disease 

If we are worried and we want to identify the rate of progression of CKD:

• We will obtain a minimum of 3 GFRs over no fewer than 90 days.
• If we see a low GFR for the first time, we will repeat the GFR within 2 weeks to exclude acute deterioration e.g. acute kidney injury or secondary to starting renin–angiotensin system antagonist therapy.  

Risk factors for CKD progression are:

• cardiovascular disease 
• proteinuria
• previous episode of acute kidney injury
• hypertension 
• diabetes 
• smoking
• African, African-Caribbean or Asian family origin
• chronic use of NSAIDs 
• untreated urinary outflow tract obstruction. 

When it comes to patient education, we will encourage exercise, a healthy weight and stop smoking. We will also offer dietary advice about potassium, phosphate, calorie, and salt intake appropriate to the severity of CKD. But we will not offer low-protein diets.  

There is a 4-variable Kidney Failure Risk Equation that can be used to give information about the 5-year risk of needing. Those who are interested in it can find more details in the video description.

We will refer for specialist assessment if they have:

• a 5-year risk of needing renal replacement therapy of greater than 5%
• an ACR of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated 
• an ACR of more than 30 mg/mmol (ACR category A3), together with haematuria
• accelerated progression of CKD , i.e., a sustained decrease in eGFR of 25% or more and a change in eGFR category within 12 months or a sustained decrease in eGFR of 15 ml/min/1.73 m2 or more per year
• poorly controlled hypertension despite 4 antihypertensive medicines
• known or suspected rare or genetic causes of CKD
• suspected renal artery stenosis. 

We will refer people with CKD and renal outflow obstruction to urological services 

When it comes to blood pressure control in adults with CKD and an ACR under 70, we will aim for a clinic BP below 140/90 mmHg 

However, in CKD and an ACR of 70 or more, aim for a clinic BP below 130/80. 

In order to treat hypertension, if the ACR is 30 or less (that is ACR categories A1 and A2), we will simply follow the NICE guideline on hypertension. And you can check out the corresponding episode on this channel. 

But for people with CKD who have hypertension and an ACR over 30 (that is an ACR category A3), we will definitely offer an ARB or an ACE inhibitor and we will titrate it to the highest licensed dose that the person can tolerate. If they also have diabetes, we will also give an ARB or ACEI if the ACR is 3 mg/mmol or more.  

SGLT2 inhibitors have been proven to help CKD in both people with and without diabetes. The guidance on their use is outside the scope of this guideline but I will put links to the guidance in the video description. 

Going back to the renin–angiotensin system antagonists, that is, ARBs and ACEIs, we will not offer a combination of both these agents. 

We will measure potassium and eGFR before starting an ARB or ACEI and between 1 and 2 weeks after starting treatment and after each dose increase. More frequent monitoring of serum potassium may be needed if medicines known to promote hyperkalaemia are prescribed alongside them 

We will not routinely offer an ARB or ACEI if their pre-treatment potassium is greater than 5.0 mmol/litre. In these cases, we will: 

• assess for and treat any other factors that promote hyperkalaemia and
• recheck serum potassium concentration.  

We will stop ARBs and ACEIs if the potassium level increases to 6.0 mmol/litre or more and other medicines known to promote hyperkalaemia have been discontinued.  

There is a separate guidance on hyperkalaemia treatment- see link in the video description. 

Because their mode of action, ARBs and ACEIs can reduce the GFR and increase the creatinine levels. However, after starting or increasing the dose of an ACEI or ARB, we will not modify the dose if either:

• the GFR decrease from pretreatment baseline is less than 25% or
• the serum creatinine increase from baseline is less than 30%. 
• In that case, we will repeat the test in 1 to 2 weeks and we will not change anything if the decrease in eGFR remains less than 25% or the increase in serum creatinine remains less than 30%. 

If the eGFR decrease is 25% or more, or the increase in creatinine is 30% or more:

• We will investigate other causes of a deterioration in kidney function, such as volume depletion or concurrent medication (for example, NSAIDs) 
• And if no other cause for the deterioration is found, we will stop the ARB or ACEI or reduce the dose to a previously tolerated lower dose, and add an alternative antihypertensive medication if needed. 

The advice on statins inn CKD is covered in a different NICE guideline. I will put it link to it in the video description.

We will offer antiplatelet medicines only for the secondary prevention of cardiovascular disease, but we need to be aware of the increased risk of bleeding. 

When it comes to anaemia, we will consider investigating and managing anaemia in CKD if:

• their Hb level falls to 110 g/litre or less or
• they develop symptoms attributable to anaemia (such as tiredness, shortness of breath, lethargy and palpitations). 

And in people with anaemia:

• If eGFR is above 60, investigate other causes as unlikely to be CKD.
• If eGFR is between 30 and 60 ml/min/1.73 m2:
• investigate other causes of anaemia, but
• use clinical judgement to decide how extensive this investigation should be, because the anaemia may be caused by CKD.
• If eGFR is below 30 ml/min/1.73 m2, think about other causes of anaemia but we will note that anaemia is often caused by CKD in these circumstances. 

We will need to determine the iron status in these cases and we will test for iron deficiency every 3 months, or every 1 to 3 months if haemodialysis. And to diagnose iron deficiency, we will:

• Use the percentage of hypochromic red blood cells (% HRC; more than 6%).
• If this is not possible, we will use the reticulocyte Hb content (CHr; less than 29 pg).
• And if these tests are not available or the person has thalassaemia or thalassaemia trait, we will use a combination of transferrin saturation (less than 20%) and serum ferritin measurement (less than 100 micrograms/litre). However, we will not routinely use transferrin saturation or serum ferritin measurement alone to assess iron deficiency status in people with anaemia of CKD. 

Equally we will not routinely measure erythropoietin levels for the diagnosis or management of anaemia of CKD. 

 In order to manage anaemia, there is separate guidance and I will put the link to it in the video description. But the management of anaemia in CKD is based on iron therapy, ESAs (erythropoietic stimulating agents) and blood transfusions.

 We will not start ESA therapy without managing possible iron deficiency. 

 In people treated with iron, serum ferritin levels should not rise above 800 micrograms/litre. In order to prevent this, we will review the dose of iron when serum ferritin levels reach 500 micrograms/litre. 

 We will not prescribe androgens, supplements of vitamin C, folic acid or carnitine as adjuvants specifically for the treatment of anaemia of CKD. But we will treat clinically relevant hyperparathyroidism to improve the management of the anaemia. 

 We will avoid blood transfusions in people in whom kidney transplant is an option. This is because exposure to multiple blood donations may cause alloimmunisation to human leucocyte antigen or HLA class I antigens on white blood cells. HLA antibodies can react with the transplanted kidney leading to higher rates of acute rejection and poorer long-term graft survival. However, the risk of alloimmunisation has reduced since the introduction of universal leucodepletion of blood components.

The dose and frequency of ESA should be:

• determined by the duration of action and route of administration of the ESA 
• adjusted to keep the rate of Hb increase between 10 -20 g/litre/ month. 

And we will not routinely correct Hb to normal levels with ESAs in people with anaemia of CKD.

• We will typically maintain the aspirational Hb range between 100 and 120 g/litre. 
• To keep the Hb level within the aspirational range, we will not wait until Hb levels are outside the aspirational range before adjusting treatment (for example, we will take action when Hb levels are within 5 g/litre of the range's limits, that is 105 and 115 g/litre).

There is MHRA advice on the prescribing of ESAs. I will put in the video description the link to these details. In particular, we will follow their advice to avoid Hb levels above 120 g/litre because of the increased risk of death and serious adverse cardiovascular events in people with CKD. We will use the lowest dose of ESA to provide adequate control of the anaemia symptoms and we will consider accepting Hb levels below the aspirational range if:

• high doses of ESAs are needed to achieve the aspirational range or
• the aspirational range is not achieved despite escalating ESA doses.

The use of ACEIs or ARBs is not precluded, but if they are used, we need to be aware that an increase in ESA therapy may be needed. 

 We will offer iron to people with anaemia of CKD who are receiving ESAs to achieve:

• percentage of hypochromic red blood cells less than 6% (unless ferritin is greater than 800 micrograms/litre)
• reticulocyte Hb count or equivalent tests above 29 pg (unless serum ferritin is greater than 800 micrograms/litre).
• If these tests are not available or the person has thalassaemia or thalassaemia trait, iron therapy should maintain transferrin saturation greater than 20% and serum ferritin level greater than 100 micrograms/litre (unless serum ferritin is greater than 800 micrograms/litre).

Most adults will need 500 to 1,000 mg of iron (equivalent doses for children) in a single or divided dose depending on the preparation. Intravenous iron should be administered in a setting with facilities for resuscitation.

• For people who are not having haemodialysis, we will consider a trial of oral iron before offering intravenous iron therapy. If they are intolerant of oral iron or target Hb levels are not reached within 3 months, we will offer intravenous iron therapy. 
• For people who are having haemodialysis, we will offer intravenous iron therapy. We will offer oral iron therapy to people who are having haemodialysis only if:
• intravenous iron therapy is contraindicated or
• the person chooses not to have intravenous iron therapy 

We will also offer intravenous iron therapy to adults with anaemia of CKD who are iron deficient and who are receiving ESA therapy. In these cases we will only offer oral iron if:

• intravenous iron therapy is contraindicated or
• the person chooses not to have intravenous iron therapy. 

When offering intravenous iron therapy to people not having haemodialysis, consider high‑dose low‑frequency intravenous iron as the treatment of choice.

High-dose and low-frequency iron is a maximum of 2 infusions, with a minimum of 500 mg of iron in each infusion for adults. Low dose and high frequency is more than 2 infusions with 100 mg to 200 mg of iron in each infusion for adults.

We will not check iron levels earlier than 1 week after intravenous iron and we will carry out routine ferritin every 1 to 3 months to prevent iron overload

 In anaemia of CKD, we will monitor Hb:

• every 2 to 4 weeks in the induction phase of ESA therapy
• every 1 to 3 months in the maintenance phase of ESA therapy
• more frequently after an ESA dose adjustment

After other causes of anaemia have been excluded, we will regard anaemia of CKD as resistant to ESAs when:

• an aspirational Hb range is not achieved despite high doses of ESAs or 
• there is a continued need for the administration of high doses of ESAs to maintain the aspirational Hb range. 

In people with CKD, pure red cell aplasia (PRCA) is indicated by a low reticulocyte count, together with anaemia and the presence of neutralising antibodies. In addition, aluminium toxicity should be considered as a potential cause of ESA resistance after other causes have been excluded. 

 If aluminium toxicity is suspected in a person with anaemia of CKD having haemodialysis, we will need to test for desferrioxamine and review the management

 We will consider specialist referral for people with ESA‑induced pure red cell aplasia or PRCA. 

 We will take into account symptoms, quality of life, underlying conditions and the chance of a future successful kidney transplant, in addition to Hb levels, when thinking about the need for red cell transfusion. 

Hyperphosphataemia in people with CKD stage 4 or 5 can be common and when it comes to managing hyperphosphataemia, a specialist renal dietitian should be involved. 

 And before starting phosphate binders we will optimise:

• diet
• dialysis, for people who are having this. 

 We will first offer adults with CKD stage 4 or 5 and hyperphosphataemia calcium acetate to control serum phosphate levels.

We will then offer sevelamer carbonate if calcium acetate is not indicated (for example, because of hypercalcaemia or low serum parathyroid hormone levels) or not tolerated.

 If calcium acetate and sevelamer carbonate cannot be used, we will consider:

• sucroferric oxyhydroxide, for adults on dialysis if a calcium-based phosphate binder is not needed or
• calcium carbonate, if a calcium-based phosphate binder is needed.

We will only consider lanthanum carbonate if other phosphate binders cannot be used.

If patients remain hyperphosphataemic after taking the maximum dose of a calcium-based phosphate binder:

• we will check that they are taking it as prescribed
• we will consider combining a calcium-based phosphate binder with a non-calcium-based phosphate binder, titrating the dosage to achieve the best possible control of serum phosphate while keeping serum calcium levels below the upper normal limit. 

At every routine clinical review, we will assess the person's phosphate, taking into account:

• diet
• whether they are taking the phosphate binders as prescribed
• other relevant factors, such as vitamin D levels, serum parathyroid hormone levels, alkaline phosphatase, serum calcium, medications that might affect serum phosphate, or dialysis.

There are other complications in CKD such as the effect on bone metabolism and osteoporosis.

 We will not routinely measure calcium, phosphate, parathyroid hormone and vitamin D levels in adults with a GFR of 30 ml/min/1.73 m2 or more (GFR category G1, G2 or G3). But we will measure serum calcium, phosphate and parathyroid hormone concentrations in adults with a GFR of less than 30 ml/min/1.73 m2 (GFR category G4 or G5).

 We will offer bisphosphonates if indicated for the prevention and treatment of osteoporosis in adults with a GFR of 30 ml/min/1.73 m2 or more (GFR category G1, G2 or G3). 

 We will not routinely offer vitamin D supplementation to manage or prevent CKD–mineral and bone disorders but we will offer colecalciferol or ergocalciferol to treat proven vitamin D deficiency. 

 If vitamin D deficiency has been corrected and symptoms of CKD–mineral and bone disorders persist, we will offer alfacalcidol or calcitriol to people with a GFR of less than 30 ml/min/1.73 m2 (GFR category G4 or G5) and we will monitor the calcium and phosphate levels. 

 Finally, we will consider oral sodium bicarbonate supplementation for if both:

• the GFR is less than 30 ml/min/1.73 m2 (GFR category G4 or G5) and
• a serum bicarbonate concentration of less than 20 mmol/litre. 

We have come to the end of this video. I hope that you have found it useful and, if so, please hit the like and subscribe buttons. Thank you for watching and good-bye

Podcast description 

The video version of this podcast can be found here:

https://youtu.be/IaId_nNbO-c?si=0FF7A5J7iPxocdBd

This episode refers to guidelines on the management of abnormal liver function tests by the British Society of Gastroenterology and a number of NHS organisations in the UK. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them. 

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the interpretation of an abnormal liver function tests, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the information consulted. You must always use your clinical judgement.   

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast: 

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk 

My summary guide can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ8MRxaNYnA1_pzh?e=H2U7rS 

The resources consulted can be found here:

BSG- British Society of Gastroenterology:

·      bsg.org.uk/clinical-resource/guidelines-on-abnormal-liver-blood-tests

·      Guidelines on the management of abnormal liver blood tests (bsg.org.uk)

o  First published on:

o  BMJ article:

o  Guidelines on the management of abnormal liver blood tests | Gut (bmj.com)

Southeast London pathway:

·      Microsoft Word - Abnormal liver function test pathway-explanatory.docx (selondonccg.nhs.uk)

North and East Devon pathway:

·      Management of Abnormal LFTs in Asymptomatic Adults - North & East (devonformularyguidance.nhs.uk)

North Bristol

·      https://www.nbt.nhs.uk/sites/default/files/Investigation%20of%20Adult%20Patients%20with%20Abnormal%20LFT%20in%20Primary%20Care.pdf

West Hampshire:

·      Liver Blood Test Pathway | GP Portal (westhampshireccg.nhs.uk)

Medscape:

·      Liver Blood Tests: How to Interpret Abnormal Results (medscape.co.uk)

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to go through the interpretation of abnormal liver function tests or LFTs, including initial follow up management, always focusing on what is relevant in Primary Care only.

And for that I will summarise the British Society of Gastroenterology guidelines on LFTs. They were first published in the BMJ and the relevant links are in the episode description. Although the full guideline covers both adults and children, in today’s episode I will be focusing only on adults. 

At the end, I will also tell you how to access my summary of the recommendations, which will be based not only on the BSG but also on a number of NHS bodies in the UK. The links to them are in the episode description and it’s worth having a look as they have flowcharts and other information that you may find useful. 

Right, there is a lot of information to cover, so let’s jump into it.

The three the most common causes of liver disease are alcohol-related liver disease, non-alcoholic fatty liver disease and viral hepatitis, although autoimmune liver disease is also a significant cause.

Liver disease develops silently and at earlier stages liver enzymes may be normal. If they are high, the degree of abnormality is not necessarily related to the severity of the underlying condition and this is why many patients are not diagnosed until they have developed significant liver fibrosis.

In many cases if used in isolation, LFTs are neither very specific or sensitive and they are better at assessing liver fibrosis if incorporated into algorithms or ratios.

What constitute LFTs? Well, the LFTs standard panel can vary from hospital to hospital. Although we call them LFTs, not all the tests assess liver function. For example, high liver enzymes point towards liver injury; bilirubin, albumin and INR give information on liver function, while platelets can give information on the level of liver fibrosis.

So, let’s have a look at a number of these tests.

Bilirubin is the by-product of the breakdown of haemoglobin. It exists in two forms, unconjugated and conjugated. Bilirubin is transported to the liver as unconjugated bilirubin, where it is converted into conjugated bilirubin. A high unconjugated level is usually due to haemolysis or impaired conjugation whereas a high conjugated level is typically due to liver disease or biliary obstruction.

Many path labs will routinely report just total bilirubin, but they will give a breakdown if the level is abnormal or if specifically requested.

In normal circumstances, the majority of bilirubin should be conjugated. So, if the majority of the bilirubin is unconjugated, then, in the absence of haemolysis, the cause is almost always Gilbert’s syndrome where the enzyme that conjugates bilirubin has a reduced activity with a consequent rise in unconjugated bilirubin. it is not associated with liver disease or ill health, so patients should be fully reassured.

Albumin is a protein that is produced only in the liver and because of this, it is often considered as a marker of liver function. However, albumin can also be reduced in for example, sepsis, inflammatory disorders, and malabsorption.

Prothrombin time (PT) and INR can also be used to measure liver function, as the underlying clotting factors are made in the liver. Therefore, a high PT and INR can indicate liver dysfunction but it can also be caused by vitamin K deficiency as seen in fat malabsorption and chronic cholestasis.

A reduction in platelets, or thrombocytopenia, is an indicator of advanced liver disease. A low platelet count is caused by decreased production due to bone marrow suppression, splenic sequestration due to portal hypertension and increased platelet destruction due to shear stress, and fibrinolysis in liver cirrhosis or due to antiplatelet antibodies in autoimmune liver disease.

Alkaline phosphatase (ALP) is produced mainly in the liver but is also found in bone, intestines, kidneys and placenta. Levels are physiologically higher in childhood, because of bone growth, and in pregnancy due to placental production. High levels cab be due to bone disease (e.g., bone metastases and fractures) and cholestatic liver disease (like for example, in biliary obstruction).

γ-Glutamyltransferase (or GGT) is present in the liver but not in bone and therefore when the ALP s high, the measurement of GGT can indicate whether the ALP is of hepatic or non-hepatic origin. The most likely cause of a non-hepatic high ALP in someone asymptomatic is vitamin D deficiency. A high GGT can als be due to obesity, excess alcohol or drugs.

AST and ALT are enzymes present in the liver cells and the levels increase in response to cell injury or death. ALT is considered more liver-specific while AST is also present in skeletal, cardiac and smooth muscle and so may be elevated in patients with an MI or myositis.

An AST:ALT ratio of >1 is a non-invasive marker of advanced fibrosis. Although AST and ALT can be normal even in liver disease, the high AST:ALT ratio generally persists even if both values are normal.

When should LFTs be checked? We should do so when there are:

·      Non-specific symptoms such as fatigue, nausea or anorexia.

·      Symptoms or signs of advanced liver disease, like ascites, peripheral oedema, spider naevi and hepatosplenomegaly. In these cases, checking the INR would also help assess the synthetic liver function.

·      Conditions which are associated with liver disease like autoimmune diseases, and inflammatory bowel disease.

·      Hepatotoxic drugs like for example carbamazepine, macrolide antibiotics, statins, terbinafine, and methotrexate. And although statins can lead to drug-induced liver injury, this is very rare, and they are generally safe in patients with raised liver transaminase levels if they are less than 3 times the upper limit of normal.

·      Family history of liver diseases such as haemochromatosis or Wilson’s disease.

·      Suspected alcohol-related liver disease. And

·      Suspected viral hepatitis.

So, what should we do when confronted by abnormal LFTs?

We often think that the extent of abnormality of the LFTs correlates with the severity, of the problem. However, this assumption is not supported by the evidence. Common conditions leading to chronic liver disease like NAFLD, and hepatitis C are frequently associated with only mild or moderate LFT abnormalities.

There is also the assumption that the duration of the abnormal LFTs is a reflection of clinical significance, so we often keep repeating the LFTs hoping that they will improve. And although LFTs can occasionally be high due to intercurrent illness, studies have shown that the vast majority still have abnormal LFTs after 2 years and therefore a strategy of simply repeating them can rarely be justified. Besides, in many chronic liver diseases such as hepatitis C and NAFLD, the LFTs returning to normal do not necessarily imply the resolution of the disease.

This has led to the BSG to recommend that patients with abnormal LFTs should have a full liver screen irrespective of level and duration of the abnormality.

And before moving on, let’s remember that there are three common patterns of abnormal LFTs:

1.     An Isolated raised bilirubin with otherwise normal liver tests

2.     A Cholestatic pattern: Normally showing a high ALP and GGT And

3.     A Hepatitic pattern: with a raised ALT and AST indicating hepatocellular injury, like, for example, viral hepatitis, NAFLD, and ARLD.

The BSG has produced a flowchart to guide us through the process. You can access it in the episode description.

But, in summary, if there are signs of synthetic liver failure like unexplained clinical jaundice, a low albumin or a high INR or if there is suspicion of malignancy, for example because of weight loss or marked cholestasis, we should urgently refer or admit the patient.

If there is an isolated raised bilirubin but no clinical concerns, then:

1.     We should request a FBC and repeat the LFTs on a fasting sample requesting the breakdown of conjugated and unconjugated bilirubin.

2.     Fasting causes the unconjugated bilirubin to rise further in Gilbert’s syndrome so this is the likely diagnosis when this happens and there is no evidence of haemolysis, like anaemia.

3.     If there is associated anaemia, we will have to consider haemolysis and we will request a reticulocyte count and LDH.

If the pattern is cholestatic or hepatitic we will do a liver screen. This should include an USS, hepatitis B and C screening, an autoantibody screen, serum immunoglobulins, both ferritin and transferrin saturation and, often, a coeliac screen, alpha-1-antitrypsin levels and caeruloplasmin.

If the patient has a cholestatic picture and the liver screen shows abnormalities or if the ALP and GGT remain high even in the context of normal investigations, we will refer the patient to secondary care.

If the patient has a hepatitic picture with a high ALT and AST, studies have shown that the majority will have NAFLD or ARLD and most will not need referral, but lifestyle advice and monitoring in primary care. The deciding factor is the level of liver fibrosis, which we can estimate using non-invasive fibrosis markers.

The BSG has also produced a specific flowchart for when NAFLD is suspected following a liver USS. You can also access it in the episode description.

In summary, it says that for patients with NAFLD or liver disease of unknown cause, the next step is to estimate the risk of fibrosis using the FIB4 or NAFLD fibrosis score.

Values <1.3 and ≤-1.455, respectively, represent a low risk of advanced fibrosis. Higher cut-off points, <2.0 and <0.12 respectively, should be used for patients over 65. In these cases, we will just manage the risk factors in Primary Care and reassess periodically, generally every 2 to 5 years.

FIB4 or NAFLD fibrosis score values >1.3 and >-1.455, respectively, should have second-line tests such as an enhanced liver fibrosis blood test, also known as an ELF tests or imaging such as a FibroScan or elastography.

However, patients with a very high FIB-4 score >3.25 or a NFS >0.675 should be referred without waiting to do an ELF test, Fibroscan or elastography.

Those with intermediate FIB-4 score (that is between 1.3 and 3.25) or NFS (that is, between -1.455 and 0.625), should have an ELF test or a Fibroscan. If the result is 9.5 or less or 7.8 or less respectively, we will manage them in primary care and we will refer if the result is above those limits

In primary care, the treatment for NAFLD is weight loss, alcohol advice, the reduction of cardiovascular risk and the management of co-morbidities.

Next, the BSG has also produced a specific flowchart to guide us if ARLD is suspected. I have also put a link to it in the episode description.

And in summary, those drinking ≥35 units/week for women and ≥50 units/week for men, will need referral to both alcohol services and hepatology for further assessment with a Fibroscan or elastography. For all other patients, the AUDIT C questionnaire alongside brief intervention is recommended initially. If the AUDIT C is 5 or more, we will need to give them the full AUDIT questionnaire.

For patients with an AUDIT score of >19, we will also need to refer them to both alcohol services and hepatology for further assessment with a Fibroscan or elastography. For those with an AUDIT score of between 8 and 19 we should check the GGT and if it is >100 we should refer them as for the higher-risk group. Otherwise, we could monitor them and refer to alcohol services if excessive drinking persists.

The treatment of ARLD is to stop drinking harmfully, and for many this usually means complete abstinence. Weight loss sometimes also helps because there is a synergy between alcohol and obesity. For example, when the BMI is >35, the risk of liver disease doubles for any given alcohol intake.

But, finally, what should we do if the patient has a hepatitic pattern with a high ALT and AST without an obvious cause, that is, when the liver screen is normal and there is no evidence of NAFLD on USS or excess alcohol?

In those cases, we will need to re-examine the history to exclude potential drug-induced causes. Also, ultrasound is only sensitive for steatosis when hepatocytes are more than 30% steatotic so patients with milder steatosis might have a normal USS. So, if these patients are obese or have metabolic risk factors and we suspect that they may still have NAFLD despite the normal USS, we should assess them in accordance with the NAFLD flowchart. As I mentioned earlier, we should follow it for patients with NAFLD or liver disease of unknown cause.

Well, this is the end of the BSG guideline itself. I have created a quick reference guide which contain the various BSG flowcharts as well as information found in the NHS pathways from Southeast London, North and East Devon, North Bristol, and West Hampshire. Links to their information and flowcharts are in the episode description. They all had similar advice to the BSG guideline but there were also some other elements which would be useful from a practical perspective. Where there was a discrepancy between their guidance, I have generally opted for the most conservative approach. If you are in any doubt, please consult the original guidance or seek local specialist advice. You will be able to find a link to download my summary in the episode description.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

https://youtu.be/o_q8TTra3Ys

This video makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the section on diagnosis and initial assessment of the NICE guideline [NG115] on COPD in adults, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

·      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

·      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

·      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

·      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

There is a YouTube version of this and other videos that you can access here: 

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

Chronic obstructive pulmonary disease in over 16s: diagnosis and management- NICE guideline [NG115]:

●      https://www.nice.org.uk/guidance/NG115

The visual summary for the treatment of COPD can be found here:

●      https://www.nice.org.uk/guidance/ng115/resources/visual-summary-treatment-algorithm-pdf-6604261741

The COPD Assessment Test score or CAT score can be found here:

●      https://www.catestonline.org/hcp-homepage/clinical-practice.html

The 6-minute walk test calculator can be found here:

●      https://www.omnicalculator.com/health/6-minute-walk-test

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to do an up-to-date review of the diagnosis and initial assessment of COPD in adults according to the NICE guideline [NG115], always focusing on what is relevant in Primary Care only. I will be creating further episodes on the management of stable COPD and COPD exacerbations so stay tuned.

Right, so let’s jump into it.

The diagnosis of COPD is suspected on the basis of symptoms and signs and is confirmed by spirometry.

So, we should suspect COPD in people over 35 who have a risk factor (generally smoking or a history of smoking) and who present with 1 or more of the following symptoms:

·      exertional SOB

·      chronic cough

·      regular sputum

·      wheezing and

·      frequent so-called winter 'bronchitis'

As part of our assessment, we will also check for signs such as:

·      weight loss

·      reduced exercise tolerance and fatigue

·      waking at night with breathlessness and

·      ankle swelling

Chest pain and haemoptysis, are uncommon symptoms in COPD and they should raise the possibility of alternative diagnoses. 

The Medical Research Council or MRC dyspnoea scale should be used to grade the breathlessness, so let’s have a look at it:

·      Grade 1 is when the patient is not troubled by breathlessness except on strenuous exercise

·      Grade 2 is when the patient develops shortness of breath when hurrying or walking up a slight hill

·      Grade 3 is when the patient walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace

·      Grade 4 is when the patient stops for breath after walking about 100 metres or after a few minutes on level ground and

·      Grade 5 is when the patient is too breathless to leave the house, or breathless when dressing or undressing

Once we have suspected COPD, we should confirm it with spirometry.

So, spirometry should definitely be done:

·      At diagnosis; but it can also be performed

·      To reconsider the diagnosis, for those who show an exceptionally good response to treatment and

·      To monitor disease progression. 

Let’s take a moment here to learn about spirometry interpretation.

The key measurements are:

·      Forced Expiratory Volume in 1 Second or FEV1 which is the volume exhaled in the first second after deep inspiration and forced expiration and it would be similar to the Peak flow rate.

·      Forced Vital Capacity or FVC, which is the total volume of air forcibly exhaled in one breath and the

·      FEV1/FVC Ratio which can be expressed as a figure or as a percentage.

Both FEV1 and FVC values are compared to predicted values based on sex, age, and height. So, taking this into account, the normal reference ranges are:

·      FEV1: >80% predicted

·      FVC: >80% predicted

·      FEV1/FVC ratio: >0.7 or 70%

A typical restrictive spirometry pattern would be

·      A Reduced FEV1of less than 80% of the predicted value.

·      A Reduced FVC of also less than 80% of the predicted value and

·      A normal FEV1/FVC Ratio, that is, a ratio greater than 0.7. This is because, although both FEV1 and FVC are reduced, the FVC value is reduced to a greater extent than the FEV1.

On the other hand, a typical Obstructive Spirometry Pattern would be:

·      A Reduced FEV1of less than 80% of the predicted value.

·      A Reduced FVC compared to the predicted value, although there are occasions when the FVC can be normal. However, because FEV1 is reduced to a greater extent than FVC, this means that the

·      FEV1/FVC ratio will be reduced below 0.7

So, in principle, could we diagnose COPD just with typical symptoms and a typical obstructive pattern on spirometry? What about doing reversibility testing.

And this is where NICE gives slightly ambiguous advice.

On one hand, first it says that we must:

“Measure post-bronchodilator spirometry to confirm COPD.” 

But later it says:

“For most people, routine reversibility testing is not necessary because it may be unhelpful or misleading”.

But, before we try to clarify this further, let’s look into reversibility testing itself a bit more.

If we are doing Reversibility testing because of wanting to rule out or confirm asthma, we should stop any inhaled short-acting beta-2-agonists or anticholinergics like ipratropium at least 6 hours before testing. LABAs should be stopped at least 12 hours before testing and LAMAs at least 24 hours. Reversibility is considered positive if:

·      The FEV1 Increases by at least 12% and at least 200 mL compared to the pre-bronchodilator test. However, some argue for an increase of at least 15% instead of 12%:

So, why does NICE say that reversibility testing may be unhelpful or misleading? This is because:

·      repeated FEV1 measurements can show small spontaneous fluctuations

·      the results of a reversibility test performed on different occasions can be inconsistent and not reproducible

·      over-reliance on a single reversibility test may be misleading unless the change in FEV1 is greater than 400 ml

·      the definition of a significant change is purely arbitrary and

·      response to long-term therapy is not predicted by acute reversibility testing. 

Consequently, if we want differentiate between COPD and asthma, we can frequently do so on the basis of history and examination rather than reversibility testing and, whenever possible, we will use clinical features to differentiate between them. Let’s have a look at these clinical features:

·      A positive smoking history is almost always present in COPD whereas it is only possible in asthma

·      Symptoms before the age of 35 is very rare in COPD whereas it is common in asthma

·      A chronic productive cough is common in COPD but uncommon in asthma

·      Breathlessness is persistent and progressive in COPD whereas it is variable in asthma

·      Night time waking due to breathlessness or wheeze is uncommon in COPD and common in asthma and finally

·      Significant diurnal or day-to-day variability of symptoms is uncommon in COPD but common in asthma.

When diagnostic uncertainty remains, or both COPD and asthma are present, we will use the following findings to help identify asthma:

·      a large response (that is, over 400 ml) to bronchodilators

·      a large response (that is, over 400 ml) to 30 mg oral prednisolone daily for 2 weeks or

·      serial peak flow measurements showing 20% or greater diurnal or day-to-day variability.

Also, we can’t talk about clinically significant COPD if the FEV1 and FEV1/FVC ratio return to normal with treatment and we should reconsider the diagnosis of COPD if there is a marked improvement with inhaled therapy.

So, in summary, according to NICE, although we should do reversibility testing to confirm the diagnosis of COPD, asthma and COPD can usually be distinguished on the basis of history and examination. If diagnostic doubt remains, or where the patient is thought to have both COPD and asthma, reversibility testing or serial peak flow rate measurements can assist in the diagnosis.

So, we have now made a diagnosis of COPD based on the clinical presentation and spirometry. Are there any other investigations that we should organise?

Well, at the time of diagnosis, in addition to spirometry, all patients should have the following:

·      a chest X-ray to exclude other pathologies

·      a full blood count to identify anaemia or polycythaemia and

·      we should also calculate the BMI. 

Additionally, we will perform additional investigations depending on the circumstances. For example:

●       Sputum culture if sputum is persistently present and purulent

●       Serial home peak flow measurements to exclude asthma if diagnostic doubt remains

●       ECG, serum natriuretic peptides and an echocardiogram if cardiac disease or pulmonary hypertension are suspected because of:

o  a history of cardiovascular disease, hypertension or hypoxia or

o  clinical signs such as tachycardia, oedema, cyanosis or features of cor pulmonale

●       CT scan of the thorax to:

o  Investigate symptoms that seem disproportionate to the spirometric impairment

o  Exclude another lung diagnosis (such as fibrosis or bronchiectasis) and

o  Investigate abnormalities seen on a chest X-ray

●       Serum alpha-1 antitrypsin to assess for deficiency if early onset, minimal smoking history or family history and

●       Transfer factor for carbon monoxide (TLCO) to investigate symptoms that seem disproportionate to the spirometric impairment

When discussing prognosis and treatment, we will look at the:

●       investigations

●       smoking status

●       frailty and multimorbidity

●       symptoms such as breathlessness using the MRC scale, symptom burden using assessment tests like the COPD Assessment Test score or CAT score, and exercise capacity using the 6-minute walk test. Links to these tests can be found in the episode description

●       chronic hypoxia, cor pulmonale and whether the person meets the criteria for long-term oxygen therapy and/or home non-invasive ventilation

●       low BMI and the

●       severity and frequency of exacerbations and hospital admissions

We will assess the severity of airflow obstruction according to the reduction in FEV1 post bronchodilator. There are 4 stages according to NICE:

●       Stage 1 or Mild obstruction is when the FEV1 is > 80% or predicted. However, we can only make a diagnosis here if they have COPD symptoms

●       Stage 2 or Moderate obstruction is when FEV1 is between 50-79%

●       Stage 3 or Severe obstruction is when FEV1 is between 30-49% and

●       Stage 4 or Very severe obstruction is when FEV1 is below 30% or below 50% with respiratory failure

We will refer people for specialist advice if they have severe disease or confounding factors such as cor pulmonale, need for long term oxygen, steroids or nebuliser therapy, dysfunctional breathing and for the assessment of pulmonary rehabilitation. In addition, we may also refer at an early stage. for example:

●       If there is diagnostic uncertainty

●       If the patient requests a second opinion

●       If there is a rapid decline in FEV1

●       If they are under 40 years or they have a family history of alpha-1 antitrypsin deficiency

●       If the symptoms are disproportionate to lung function deficit

●       If they have frequent infections in order to exclude bronchiectasis and

●       If they have haemoptysis to exclude cancer

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at the NICE guidelines: “Atrial fibrillation: diagnosis and management” (NG196), as well as the Clinical Knowledge Summaries (CKS) on diagnosis of AF and management of AF, both last updated in March 2023. I have summarised the guidance from a Primary Care perspective.

By way of disclaimer, I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here: 

• The NICE GP YouTube Channel: NICE GP - YouTube 
• 
  

The full NICE Guideline on “Atrial fibrillation: diagnosis and management” [NG196] can be found here:

·      Overview | Atrial fibrillation: diagnosis and management | Guidance | NICE

Also

The Clinical Knowledge Summary on “When should I suspect atrial fibrillation and how do I confirm the diagnosis? (Last revised in March 2023) can be found here:

·      Diagnosis of atrial fibrillation | Diagnosis | Atrial fibrillation | CKS | NICE

Also

The Clinical Knowledge Summary on “Management of AF” (Last revised in March 2023) can be found here:

·      Scenario: Management of AF | Management | Atrial fibrillation | CKS | NICE

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  

• Music provided by Audio Library Plus  

• Watch: https://youtu.be/aBGk6aJM3IU 

• Free Download / Stream: https://alplus.io/halfway-through 

Transcript  

Hello everyone and welcome. I am Fernando Florido, a GP in the United Kingdom.

Some of you have asked me to do more cardiovascular topics so, today, we'll be looking at the NICE guidelines on atrial fibrillation, also known as AF, specifically from a primary care perspective. Proper management of AF is very important, which is why I'm enthusiastic about sharing the most recent evidence-based recommendations from NICE, which were updated as recently as March 2023. However, please note that I'm here to provide information and interpretation of the guidelines, not medical advice. Always use your clinical judgement when treating your patients.

If you prefer a video format, there’s also a YouTube version of these episodes. The link is in the episode description.

By the way, please make sure to stay for the entire episode, as I'll be sharing fictitious clinical cases created by chat GPT that will illustrate how the guideline is applied in real-life situations.

By the way, I will be sharing fictitious clinical cases created by chat GPT in the next video, that will illustrate how the guideline is applied in real-life situations. I have not included them in this video to avoid making it too long. However, the next video will not take long so subscribe in order not to miss it!

Remember that my summary is a very simplified version of the guideline. I have put links to the full guidance in the episode description.

So, with that said, let's dive in!"

Let’s start by saying that we are going to address three clinical areas today: the diagnosis, management and annual review of a patient with AF.

One of the first steps in detecting AF is performing a manual pulse palpation. We should do this if a patient presents with symptoms such as breathlessness, palpitations, syncope or dizziness, chest discomfort, or a history of stroke or TIA.

If an irregular pulse is detected, the next step is to perform an ECG, which will help confirm the presence of AF. However, in cases where paroxysmal AF is suspected but is undetected by an ECG, it may be necessary to offer additional testing with ambulatory ECG monitors, event recorders, or other ECG technologies for an appropriate period of time to capture episodes of AF.

Assessing stroke and bleeding risks is crucial in managing AF. To assess stroke risk, we should use the CHA2DS2-VASc stroke risk score. Evaluating bleeding risk is equally important and we should use the ORBIT bleeding risk score. These two tools guide decisions regarding anticoagulation therapy.

The CHA2DS2VASc score tool gives the following points:

• Congestive heart failure/left ventricular dysfunction = 1
• Hypertension (BP>140/90 or on treatment) = 1
• Age 75 years or older = 2
• Diabetes mellitus = 1
• Stroke/TIA = 2
• Vascular disease (prior MI, PVD, or aortic plaque) = 1
• Age 65–74 years = 1
• Sex category (female) = 1

The ORBIT scoring tool gives

• 2 points for:
• Low Hb or HCT (Males Hb <130 g/L or HCT <40% and females <120 g/L or <36%)
• History of bleeding (e.g., GI bleeding, or haemorrhagic stroke) 
• 1 point for:
• Age 74 or more
• eGFR of less than 60
• On antiplatelet treatment
• A score of 2 or less is considered low, 3 medium and 4 or more high.
• 
  

We should see if modifying risk factors for bleeding is possible. This can include addressing uncontrolled hypertension, avoiding concurrent use of aspirin or nonsteroidal anti-inflammatory drugs, minimizing alcohol consumption, and treating reversible causes of anaemia. 

Now, let's talk about the management of AF.  

For all people with AF (including paroxysmal AF):

• We will admit urgently if:
• There are signs and symptoms of haemodynamic instability such as a rapid pulse (greater than 150 beats per minute) and/or low blood pressure (e.g. a systolic blood pressure less than 90 mmHg), as well as symptoms like severe dizziness or syncope, chest pain, or breathlessness. Also be aware that electrical cardioversion may be recommended if the onset of AF is within 48 hours.
• Or we should also consider admission if they are unwell due to another serious associated or underlying condition.
• In new onset AF (of less than 48 hours), we will seek urgent secondary care advice to manage both arrhythmia and anticoagulation (because the latter may involve heparin) and this may also involve sending the patient to the emergency department

It's also important to assess for underlying causes of AF.

These can include:

• Cardiac causes, such as hypertension, valvular heart disease, heart failure, and ischaemic heart disease —for this we will arrange an ECG and consider transthoracic echocardiogram if there is a high risk or suspicion of underlying structural heart disease (such as a heart murmur) or functional heart disease (such as heart failure).
• Respiratory causes, such as chest infection or lung cancer — we will arrange a chest X-ray if lung pathology is suspected.
• Systemic causes, such as excessive alcohol intake, hyperthyroidism, electrolyte depletion, infection, or diabetes mellitus — we will use our clinical judgement to determine the need for blood tests such as a full blood count, liver, renal and thyroid function tests, calcium, magnesium, and glucose
• In summary: We will normally do an ECG, a CXR, blood tests and possibly an echocardiogram depending on the circumstances.

Once an underlying cause is identified, it is essential to manage it whenever possible. Referral to a cardiologist may be necessary, especially in cases of valvular heart disease or suspected heart failure.

However, we will need to refer to a cardiologist for rhythm control (that is, either pharmacological or electrical cardioversion), if:

• The AF has a reversible cause (for example a chest infection).
• There is Heart failure that is caused, or worsened, by AF.
• There is atrial flutter suitable for ablation
• or any other patient for whom rhythm‑control would be more suitable using our clinical judgement. 

Looking at the management in Primary care, the first thing that we need to do is to assess their stroke and bleeding risks using the CHA2DS2VASc and the ORBIT bleeding risk tools, reviewing and managing any modifiable risk factors for bleeding

We will offer anticoagulation with a direct-acting oral anticoagulant (also known as a DOAC) if a CHA₂DS₂VASc score of 2 or above, and consider a DOAC for men with AF and a CHA₂DS₂VASc score of 1. 

• Apixaban, dabigatran, edoxaban and rivaroxaban are suitable options.
• We will not offer anticoagulation for lower scores, that is a CHA₂DS₂VASc score of 0 for men or 1 for women.
• And we will not withhold anticoagulation solely because of a person's age or their risk of falls.

In people with new‑onset AF, if there is uncertainty over the precise time since onset, we will offer oral anticoagulation.

• If DOACs cannot be given, we will offer a vitamin K antagonist, like warfarin.
• However, for those already taking warfarin we will discuss the option of switching treatment.

And we will definitely not offer aspirin solely for stroke prevention in atrial fibrillation. For guidance on antiplatelet therapy for people who have had a myocardial infarction and are having anticoagulation, there are separate guidelines. We will not cover it here because the decision should rest with their cardiologist in secondary care. 

In Primary care, we will also need to look at the arrhythmia management. For most individuals with AF, a rate-control treatment is offered as the first-line approach. This can involve using a standard beta-blocker (but not sotalol) or a rate-limiting calcium-channel blocker, such as diltiazem or verapamil. The choice of medication depends on the person's symptoms, heart rate, comorbidities, and personal preferences.

In some cases, digoxin may be considered as an alternative for those with non-paroxysmal AF who do little or no exercise or when other rate-limiting drug options are not suitable. However, we will not offer amiodarone for long-term rate control.

If there is concomitant heart failure, we will follow the guidelines for chronic heart failure in managing their condition.

We will need to arrange follow-up within 1 week of starting treatment to review symptoms, heart rate, and blood pressure. 

In terms of patient education, we will need to provide information to the patient on:

• AF and Stroke awareness 
• Flying — advising that there are no flying restrictions provided AF is stable.
• Driving — advising that they must inform the driving Licensing Agency and to check their driving insurance still covers them.

After having looked at the diagnosis and initiating treatment, we are now going to look at the regular follow-ups or reviews that are needed. It is recommended to review patients at least annually if the symptoms are controlled or more frequently if necessary, using our clinical judgement to determine the appropriate intervals.

During the reviews, we will do the following:

We will check for symptoms of AF at rest and during exercise, and assess the heart rate.

• Criteria for rate control vary with age, and it is suggested that ventricular rate should be controlled between 60 and 80 beats per minute at rest and between 90 and 115 beats per minute during moderate exercise
• Review the person's rate control drugs and if the person cannot tolerate it, we will prescribe an alternative.

For people taking a rate-control treatment who have persistent symptoms of AF or a fast heart rate, we will consider one of the following options:

• If they are not taking the maximum drug dose, we will consider increasing the dose
• If they are taking the maximum drug dose, we will consider combination treatment with any two of the following drugs: a beta-blocker, digoxin, or diltiazem. We will seek specialist advice before prescribing diltiazem with a beta-blocker because bradycardia, atrioventricular block, asystole, or sudden death can occur with concurrent use.
• If symptoms are not controlled by combination treatment, we will refer to a cardiologist promptly, that is, to be seen within 4 weeks.

For people who have received a rhythm-control treatment in secondary care who have recurrent or persistent symptoms, we will refer back to a cardiologist for further assessment. 

We will also reassess the person's stroke risk using the CHA2DS2VASc assessment tool and bleeding risk (using the ORBIT score tool) at least annually. Stroke risk should also be routinely reviewed when a person reaches 65 or years of age, or if at any age they develop diabetes, heart failure, peripheral arterial disease, coronary heart disease, stroke, transient ischaemic attack, or systemic thromboembolism.

• For people not already taking an anticoagulant, we will offer treatment if they have a CHA₂DS₂VASc score of 2 or more, and we will consider offering anticoagulation treatment to men with a CHA₂DS₂VASc score of 1.
• For people already taking an anticoagulant:
• we will not stop anticoagulation solely because atrial fibrillation is no longer detectable — we will base the decision on a reassessment of CHA₂DS₂-VASc and ORBIT.
• we will review and manage any modifiable risk factors for bleeding.
• we will review anticoagulant therapy, including possible new drug interactions and we will do a FBC, liver and renal function tests at least annually or more frequently if clinically indicated.
• For people with persistent poor anticoagulation control on warfarin, we will consider switching to a DOAC such as apixaban, edoxaban, dabigatran, or rivaroxaban).
•  

For people taking rhythm control drugs that were initiated in secondary care, we will carry out any required monitoring. For amiodarone for example, this includes 6 monthly blood tests and an annual ECG and eye examination. 

And we will assess and manage their CVD risk and any possible complications of AF, including stroke and thromboembolism, heart failure and reduced quality of life.

Right, this is the summary of the guideline. (pause)

 Now, let’s have a look at some fictitious clinical cases created by chat GPT:

Case 1

The first patient is Emily Thompson who is 62 years old.

And has a BP of 130/80 mmHg

Emily has a history of hypertension and hypercholesterolemia. Additionally, Emily was diagnosed with type 2 diabetes five years ago and is currently on the following medication:

·      Amlodipine 5mg once daily

·      Atorvastatin 20mg once daily

·      Metformin 1000mg twice daily

Emily consults you because she experiences occasional episodes of palpitations and breathlessness. She has also reported intermittent dizziness over the past few months. She has not experienced any stroke or TIA symptoms.

What should we do? 

We should suspect AF and therefore we should perform a manual pulse palpation. This detects an irregular pulse.

What diagnostic steps should we take?

1.    We should do an ECG to confirm the presence of AF. However,

2.    If paroxysmal AF is suspected but undetected by the initial ECG, an ambulatory ECG monitor, event recorder, or other ECG technology should be used. This will allow continuous monitoring over a specific period to capture intermittent or infrequent episodes of AF. We should also consider this if the manual pulse palpation was normal but we remain suspicious. 

Case 2

The second patient is John Anderson who is 65. His BP is 140/90 and his pulse rate is 96.

He has a Medical History of Hypertension, hypercholesterolaemia and Valvular Heart Disease

John is currently taking an ACE inhibitor (lisinopril 20 mg OD), a calcium channel-blocker (amlodipine 10 mg BD) and a statin (atorvastatin 20 mg OD).

John presents with symptoms of AF that have only just started in the last day or two and AF has been confirmed with an ECG.

How should we manage him?

1.    We should firstly assess for signs and symptoms of hemodynamic instability: for example, a rapid pulse of 150 beats per minute or more and low blood pressure, e.g. a systolic blood pressure 90 or less. If he exhibits these symptoms, he should be admitted urgently. Luckily, John’s pulse rate is 96 and his BP is 140/90.

2.    However, we should get urgent secondary care advice, given that John's AF seems to have been present for less than 48 hours. This is recommended to address the management of both the arrhythmia and anticoagulation. John may or not be suitable for electrical or pharmacological cardioversion and the initial anticoagulation may involve the use of heparin. This may still require sending him to the emergency department to be fully assessed.

3.    In addition, we should expect the cardiologist to carry out further assessment of possible underlying causes of AF. Since John has a history of valvular heart disease, it is likely that this is contributing to his AF. A transthoracic echocardiogram can be considered to assess any valvular heart disease progression in addition to a CXR and basic blood tests, including a full blood count, liver and renal function tests, thyroid function tests, calcium, magnesium, and glucose levels. 

In summary, the recommended management approach includes evaluating signs of hemodynamic instability, assessing for underlying causes (cardiac, respiratory, and systemic), conducting necessary tests (ECG, CXR, blood tests, and echocardiogram), and seeking urgent secondary care advice given that the onset of AF is within 48 hours.

Case 3

The third patient is Peter Richardson who is 76

His Blood Pressure is 135/85 mmHg and his pulse rate is 78

Peter has a Medical History of hypertension, hyperlipidaemia and an MI ten years ago.

Peter takes lisinopril (10 mg once daily), atorvastatin (80 mg once daily) and clopidogrel (75 mg once daily) as part of his post-MI regimen.

He has been found to have AF on incidental screening, confirmed by an ECG. He has no symptoms and initial assessment includes a normal CXR and blood tests. A non-urgent echocardiogram has been requested as a precaution but he does not have a heart murmur or symptoms of cardiac failure so there is a low suspicion of structural heart disease.

Because of his age and being asymptomatic, after discussion and agreement with the patient and, perhaps after discussion with secondary care, it was decided that he would be managed in primary care and that referral for rhythm control / cardioversion was not appropriate for him. 

How should we assess and manage him further?

• We should assess his Stroke Risk. Using CHA2DS2VASc, the score is 4 (because of age over 75, HTA on treatment and previous vascular disease), indicating a high risk of stroke.
• Using the ORBIT bleeding risk tool, his score is 2 (because of age >74 and taking antiplatelet therapy) so his risk of bleeding is low.
• Considering his CHA2DS2VASc score of 4 and low bleeding risk, Peter is a suitable candidate for anticoagulation. We should always consider modifiable risk factors for bleeding but given that clopidogrel was given for his previous MI, we would need to seek advice from his cardiologist about this.
• As Peter’s exact time of onset of AF is uncertain, oral anticoagulation is recommended.
• We have the options of apixaban, dabigatran, edoxaban, and rivaroxaban, and we decide to prescribe apixaban (5 mg twice daily). If there was a problem with a DOAC, a vitamin K antagonist such as warfarin could be an alternative.
• We should also start him on rate-control treatment, such as a beta-blocker or a rate-limiting calcium-channel blocker. Given his previous history of MI, he is started on a betablocker. Because he has no symptoms and his BP is normal, we could give him a small dose of bisoprolol 1.25 mg daily which can be increased as necessary.
• We should arrange a follow-up appointment within 1 week of starting treatment to assess his symptoms, heart rate, and blood pressure.
• We should also offer Patient Education, including information about AF and Stroke awareness, flying (saying that there are no restrictions if AF is stable), driving (advising him to inform the driving licensing agency and to check his insurance cover), and the need for annual review.

Case 4 

The fourth and final patient is Sarah Johnson, aged 62

Her Blood Pressure is 130/80 mmHg

And her Medical History includes known atrial fibrillation. Although the AF was diagnosed five years ago, recently she has been experiencing some AF symptoms in the form of intermittent palpitations, and occasional shortness of breath. She also has a history of hypertension and well-controlled type 2 diabetes. Sarah had a transient ischemic attack (TIA) two years ago but has not experienced any recurrent episodes since then.

Her medication includes a beta-blocker, atenolol 100 mg daily, to control her heart rate, which is the maximum recommended dose. She also takes an anticoagulant, rivaroxaban 20mg OD, to reduce her risk of stroke. In addition, Sarah takes metformin 500 mg BD for her diabetes management and amlodipine 5 mg OD for blood pressure control.

She comes to see you for her annual review.

What should we do during this review?  

1.    During the annual review, Sarah's symptoms of AF should be assessed, both at rest and during exercise. Her heart rate should be monitored to ensure rate control. It is recommended to maintain her ventricular rate between 60 and 80 beats per minute at rest and between 90 and 115 beats per minute during moderate exercise.

2.    The review should include an assessment of Sarah's current medications. Since she is experiencing persistent symptoms of AF, despite taking the maximum dose of atenolol, we should consider combination treatment with an additional rate-control drug, such as digoxin or diltiazem. Sarah is still active and does regular exercise and therefore digoxin is not felt to be appropriate. Therefore, before prescribing diltiazem with a beta-blocker, specialist advice should be sought due to potential complications.

3.    Sarah's stroke and bleeding risks should also be reassessed using CHA2DS2VASc and ORBIT. These assessments should be conducted annually, but particularly when she reaches the age of 65 or if she develops any new conditions related to cardiovascular health.

4.    As Sarah already has a high stroke risk with a CHA2DS2VASc score of 4 (because of a previous TIA, hypertension and being female), she should continue her anticoagulation treatment with rivaroxaban. We should monitor it, checking for possible new drug interactions and conducting blood tests including a FBC, liver and renal function tests. These assessments should occur at least annually or more frequently if clinically indicated.

5.    Sarah's modifiable risk factors for bleeding should also be reviewed and managed. Her BP is well controlled, she is not abusing alcohol and there are no other concerns in terms of anaemia or drug interactions.

6.    If Sarah were taking rhythm control drugs initiated in secondary care, for example amiodarone, we should arrange the required monitoring.  

In conclusion, the management of AF requires a comprehensive approach that addresses both the underlying causes and the patient's individual risk factors. We have discussed the importance of detection and diagnosis, the assessment of stroke and bleeding risks, management strategies, and regular reviews.

Please keep in mind that this is only a summary and my interpretation of the guideline.

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye  

The video version of this episode can be found here:

·      https://youtu.be/3KFod0_RiAI

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I use AI voices to discuss the NICE technology appraisal on Tirzepatide for managing overweight and obesity or TA1026, published in December 2024, focusing on what is relevant to Primary Care only. In particular, I also make reference to NHS implementation information and guidance.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The technology appraisal on Tirzepatide for managing overweight and obesity [TA1026] can be found here:

·      https://www.nice.org.uk/guidance/ta1026

The section on implementation of the technology appraisal on Tirzepatide for managing overweight and obesity [TA1026] can be found here:

·      https://www.nice.org.uk/guidance/ta1026/chapter/4-Implementation

The link to the NICE News- December 2024 discussing TA1026 can be accessed here:

·      https://youtu.be/Od1QDebGbBQ?si=EsJhm3IavpWu8ZC_

The video version of this episode can be found here:

·      https://youtu.be/OnnjnhsXu4A

The video on the NICE guideline on AF on this channel that this episode is based on can be found here:

·      https://youtu.be/AGdfwwzcKJs?si=G_TamzKCiQ-LW8WO

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I use AI voices to discuss CHA₂DS₂-VASc & ORBIT in AF.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]

Music provided by Audio Library Plus

Watch: https://youtu.be/aBGk6aJM3IU

Free Download / Stream: https://alplus.io/halfway-through

Information

CHA₂DS₂-VASc

NICE suggest to use the CHA₂DS₂-VASc stroke risk score to assess stroke risk in people with any of the following:

• symptomatic or asymptomatic paroxysmal, persistent or permanent atrial fibrillation
• atrial flutter
• a continuing risk of arrhythmia recurrence after cardioversion back to sinus rhythm

CHA₂DS₂-VASc score for stroke risk in atrial fibrillation

Feature

Score

Congestive Heart Failure

1

Hypertension

1

Age >75 years

2

Age between 65 and 74 years

1

Stroke/TIA/TE

2

Vascular disease (previous MI, peripheral arterial disease or aortic plaque)

1

Diabetes mellitus

1

Female

1

NICE recommends

• do not offer stroke prevention therapy to people aged under 65 years with atrial fibrillation and no risk factors other than their sex (that is, very low risk of stroke equating to a CHA₂DS₂-VASc score of 0 for men or 1 for women)
• anticoagulation based on CHA₂DS₂-VASc score
• anticoagulation may be with apixaban, dabigatran etexilate, rivaroxaban or a vitamin K antagonist
• consider anticoagulation for men with a CHA₂DS₂-VASc score of 1.
• offer anticoagulation to people with a CHA₂DS₂-VASc score of 2 or above.

ORBIT

NICE have suggested that the ORBIT bleeding risk score should be used in assessing the risk of bleeding when a patient commences, or is under review, regarding anticoagulation therapy in atrial fibrillation.

NICE state that "because evidence shows that it has a higher accuracy in predicting absolute bleeding risk than other bleeding risk tools. The ORBIT bleeding risk scoring system developed a five-factor numerical bleeding risk score from the five strongest predictors termed ORBIT:

Risk Factor For Bleeding

Points Attributed

(older (75 years or older)

1 point

reduced haemoglobin (<13 mg/dL in men and <12 mg/dL in women), haematocrit (<40% in men and <36% in women) or history of anaemia

2 points

bleeding history

2 points

insufficient kidney function (eGFR < 60 mg/dL/1.73 m2)

1 point

treatment with an antiplatelet agent

1 point

• Interpretation:

ORBIT Score

Risk group

Bleeds per 100 patient-years

0-2

Low

2.4

3

Medium

4.7

4-7

High

8.1

The ORBIT risk score can provide a simple, easily remembered tool to support clinical decision making

The video version of this podcast can be found here:

https://youtu.be/dVpfeUxt8K8

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through new and updated guidelines published in April 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for April 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-04-01&to=2024-04-30&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered can be found here:

Endometriosis: diagnosis and management- NICE guideline [NG743] can be found here:

·      https://www.nice.org.uk/guidance/ng73

Final draft guidance on Atogepant for preventing migraine [ID5090] | can be found here:

·      https://www.nice.org.uk/guidance/indevelopment/gid-ta10992/documents

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

Music provided by Audio Library Plus 

Watch: https://youtu.be/aBGk6aJM3IU 

Free Download / Stream: https://alplus.io/halfway-through 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in April 2024, focusing on what is relevant in Primary Care only.

And in April we have had very little new guidance relevant to primary care, in fact, there was only one guideline containing relevant information for us, the guideline on endometriosis. But, to make up for it, we also have the NICE final draft guidance on atogepant for migraine prophylaxis, which I will cover briefly after the endometriosis update.

Right, let’s jump into it.

So, let’s start with the guideline on Endometriosis. The management is normally guided by secondary care but this guideline also includes recommendations relevant to primary care such as the clinical presentation, diagnosis and referral recommendations.

And let’s start with the clinical presentation.

NICE says that we should suspect endometriosis in women (including those under 17) if they have at least 1 of the following:

·      chronic pelvic pain

·      dysmenorrhoea

·      deep pain during or after sexual intercourse and

·      either period-related or cyclical gastrointestinal and urinary symptoms, in particular, painful bowel movements, haematuria or dysuria

We will offer an abdominal examination to exclude masses and, if appropriate, a pelvic and vaginal examination too.

What investigations should we organise?

Well, we can do a transvaginal ultrasound, which can identify signs of endometriosis.

If a transvaginal scan is not appropriate, we will do a transabdominal pelvic ultrasound scan.

We will not use serum CA125 to diagnose endometriosis but if it is available we must be aware that:

·      a high level may be consistent with endometriosis but that

·      endometriosis may be present despite normal serum CA125 levels

Equally, pelvic MRI is not recommended as a primary investigation for endometriosis. However, this can be considered in secondary care to assess the extent of deep endometriosis involving the bowel, bladder or ureter.

But, and this is an important but, we must not exclude endometriosis just because the examination, ultrasound or MRI are normal. If there is a high clinical suspicion, we should refer for further assessment.

So, the question is, should we be initiating investigations in Primary Care if we know that we may end up referring to gynaecology anyway?

My view is that if there is a high clinical suspicion of endometriosis, then we are probably better off referring the patient straightaway, as this is likely to lead to an earlier diagnosis and management. However, if we are not certain or we wish to exclude other possible diagnoses, we could do some investigations first.

So, when do we need to refer?

And the answer is simple. We should refer if:

·      they have symptoms or signs of endometriosis or if

·      not responding to the initial management

There are updated management recommendations if fertility is a priority and these are obviously more relevant for secondary care. From a primary care perspective, we should know that, in general, surgical approaches are recommended because they are likely to improve the chance of spontaneous pregnancy.

However, the opposite is true for hormonal treatment, either alone or in combination with surgery, so it is not recommended because of its effect on fertility.

And that is it, this is the only published update for us.

But, as promised, let’s have a look at the NICE final draft on atogepant for migraine prophylaxis.

I will not say very much because we will be covering this fully when the final guidance is published, but I will give you just an overview.

Both Rimegepant and atogepant, are a new class of drugs, also known as gepants, that have been developed specifically for the treatment of migraines. They are a calcitonin gene-related peptide (or CGRP) receptor antagonist which works by blocking this CGRP receptor. And although the mechanism of action is not fully understood, we know that CGRP is a protein found in the sensory nerves of the head and neck and causes blood vessels to dilate, which can lead to inflammation and migraine pain. Unlike triptans, gepants do not cause vasoconstriction so they do not have the same cardiovascular contraindications and cautions as triptans. Gepants can be used as an acute treatment of migraine and, although rimegepant has a licence for migraine prophylaxis, NICE only recommends as prophylaxis of episodic migraines. However, NICE has recommended atogepant as an option for preventing both chronic and episodic migraines. But this is only if there have been at least 4 migraine days per month and where at least 3 previous preventive treatments have failed.

What’s the difference between episodic and chronic migraine?

The definition of Episodic migraine is when there are fewer than 15 headache days each month. On the other hand, chronic migraine is when there is at least 15 headache days a month, with at least 8 of those having features of migraine.

Currently, the most effective options for people with chronic migraines who have already tried 3 prophylactic treatments are drugs that need to be injected so an oral treatment such as Atogepant offers more choice for patients.

So, with that in mind, let’s quickly look at the preventative treatment pathway that NICE has produced in their new draft guidance.

First, for prophylaxis treatment to be considered, the patient needs to have 4 or more migraine days per month.

In that case, we will give 1^st, 2^nd and 3^rd line prophylaxis with propranolol, amitriptyline and topiramate.

If there is inadequate response, then we move to 4^th line treatment.

For episodic migraine we can give Rimegepant.

For both episodic and chronic migraines, we have a number of injectable medications and atogepant as the only oral medication.

Finally, if it is only chronic migraine, then the recommended treatment will be with botox.

Rimegepant is an oral lyophilisate that should be placed on the tongue or under the tongue and it will disintegrate in the mouth and can therefore be taken without liquid. However, atogepant is a tablet to be taken orally.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. With this episode I continue with the series on the monthly “NICE News” bulletin, which includes new guidance published in that month as well as any updates, also in that particular month, to already published guidelines. However, I will only address guidance which is relevant to Primary Care.

In today’s episode, I go through the NICE Guidance and advice published in February 2023.  

There is a YouTube version of this and other episodes that you can access here: 

NICEGP YouTube channel:  

·      NICE GP - YouTube

The Full NICE News bulleting for February 2023 can be found at:  

·      https://www.nice.org.uk/guidance/published?from=2023-02-01&to=2023-02-28

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Transcript

Hello everyone and welcome. My name is Fernando Florido and I am a GP in the United Kingdom.

With today’s episode I am continuing with the series on the monthly “NICE News” bulletin, which includes any new guidance published in that month as well as any updates, also in that particular month, to already published guidelines, also updated in that month. However, I will only address guidance which is relevant to Primary Care. In today’s episode, I go through the NICE Guidance and advice published in February 2023. 

Remember that there is also a Youtube version of these episodes so have a look in the episode description.

The first guideline update that we are looking at refers to Urinary tract infections in adults 

And the new quality statements are:

Statement 1 Women aged under 65 years are diagnosed with a urinary tract infection (UTI) if they have 2 or more key urinary symptoms and no other excluding causes or warning signs.

This means that according to the updated quality standard on urinary tract infections (UTI) in adults, healthcare professionals should diagnose women under 65 with a UTI if they have 2 or more key urinary symptoms. Therefore, women who present with 2 or more key symptoms should not require a dipstick test. Professionals should however exclude any other causes of urinary symptoms and consider warning signs of other conditions such as sepsis and cancer when diagnosing a UTI. We also need to ensure that vaginal and urethral causes of urinary symptoms are excluded by asking about vaginal discharge and irritation, and other possible urethral causes of urinary symptoms.  

Statement 2 Adult patients with indwelling urinary catheters do not have dipstick testing to diagnose UTIs. Therefore, instead, we need to assess signs and symptoms to diagnose a UTI and use urine culture and sensitivity testing to support the diagnosis. 

Statement 3 Men and non-pregnant women are not prescribed antibiotics to treat asymptomatic bacteriuria. Instead, we need to assess symptoms to determine if a urine sample should be sent for culture and if antibiotics should be prescribed when a urine culture identifies bacteriuria. 

Statement 4 non-pregnant women with an uncomplicated lower UTI are prescribed a 3-day course of antibiotics, and men and pregnant women with an uncomplicated lower UTI are prescribed a 7-day course of antibiotics. We also need to reassess if a person's symptoms worsen or do not start to improve within 48 hours of taking the antibiotic.

Statement 5 Men with a recurrent UTI, and women with a recurrent lower UTI where the cause is unknown or a recurrent upper UTI are referred for specialist advice.

The next section refers to an update to the antenatal care guidelines.

The new quality statements are:

Statement 1 Pregnant women are seen by antenatal care by 10 weeks of pregnancy.

Statement 2 Pregnant women have a risk assessment at routine antenatal appointments.

Statement 3 Pregnant women have coordinated care from a small team of midwives.

Statement 4 Pregnant women are offered vaccinations at routine antenatal appointments, including flu, pertussis and COVID-19 vaccinations. 

Statement 5 Pregnant women and partners who smoke are referred for stop-smoking support and treatment at routine antenatal appointments.  

The next guideline update refers to cardiovascular disease: risk assessment and reduction, including lipid modification 

And in February 2023, a new recommendation on aspirin for primary prevention of CVD has been added. This is based on a 2023 surveillance decision. The results of this evidence strongly suggests that the benefit from aspirin for primary prevention is very closely balanced or outweighed by the increased risk of bleeds. So, the overall decision is that we should not routinely offer the use aspirin for primary prevention of CVD. 

And finally, there was a brand-new guideline published for the first time this month in respect of the monitoring and management of Barrett's oesophagus and stage 1 oesophageal adenocarcinoma.

The recommendations are that:  

1.   We will Follow the recommendations for gastro-oesophageal reflux disease to achieve symptom control 

2.   We will not offer aspirin to patients with Barrett's oesophagus to prevent progression to oesophageal dysplasia and cancer. 

3.   We will discuss the benefits and risks of endoscopic surveillance with the person diagnosed with Barrett's oesophagus. 

4.   We will offer endoscopic surveillance with Seattle protocol biopsies:

a.   every 2 to 3 years to people with long-segment (3 cm or longer) Barrett's oesophagus

b.   every 3 to 5 years to people with short-segment (less than 3 cm) Barrett's oesophagus with intestinal metaplasia.  

5.   We will assess a person's risk of cancer based on their age, sex, family history of oesophageal cancer and smoking history and tailor the frequency of endoscopic surveillance accordingly.

6.   We will not offer endoscopic surveillance to people with short-segment (less than 3 cm) Barrett's oesophagus without intestinal metaplasia provided the diagnosis has been confirmed at 2 endoscopies

7.   We will not offer anti-reflux surgery to people with Barrett's oesophagus to prevent progression to dysplasia or cancer.

The rest of the guideline refers to the management of Barrett's oesophagus with dysplasia and management of oesophageal adenocarcinoma, which I will not go into because it is a specialist area.

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye

The video version of this podcast can be found here:

·     https://youtu.be/Od1QDebGbBQ

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in December 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for December 2024 can be found here:

·     https://www.nice.org.uk/guidance/published?from=2024-12-01&to=2024-12-31&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here:

Tirzepatide for managing overweight and obesity:

·      https://www.nice.org.uk/guidance/ta1026

Urinary tract infection (recurrent): antimicrobial prescribing:

·      https://www.nice.org.uk/guidance/ng112

Meningitis (bacterial) and meningococcal disease:

·      https://www.nice.org.uk/guidance/qs19

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in December 2024, focusing on what is relevant in Primary Care only.

In today’s episode, we’re covering two important clinical topics:

• Tirzepatide for managing overweight and obesity, and
• Antimicrobial prescribing for recurrent UTIs.

But before we jump into the details, let’s take a moment to highlight a game-changing development: the new NICE technology appraisal on Tirzepatide.

For many GPs, the surge in patient requests for Ozempic (or semaglutide) to manage obesity has been a challenging situation, especially as NICE does not recommend its use in primary care for this purpose. Could Tirzepatide mark the end of the GP Ozempic nightmare?

Right, let’s find out!

In the technology appraisal assessing Tirzepatide for overweight and obesity NICE has recommended it as an option for adults, alongside diet and exercise only if they have:

• an initial BMI of at least 35 kg/m² reduced to 32.5 for people from Asian, Chinese, Middle Eastern, and Black African or African-Caribbean ethnic backgrounds. and
• at least 1 weight-related comorbidity. Examples would be, for example, hypertension, dyslipidaemia, obstructive sleep apnoea, cardiovascular disease, prediabetes, and type 2 diabetes.

If less than 5% of the initial weight has been lost after 6 months on the highest tolerated dose, we will need to decide whether to continue treatment, taking into account the benefits and risks of treatment.

The availability of obesity treatments in primary care has been limited, with semaglutide for obesity currently recommended for use in secondary care only. However, this is an exciting development: NICE has now approved the use of tirzepatide in primary care too. Furthermore, indirect comparisons suggest that tirzepatide may be more effective than semaglutide in managing obesity.

While the manufacturer initially proposed a BMI threshold of 30 kg/m² with at least one weight-related comorbidity, NICE has a stricter criterion. For NICE the acceptable threshold for NHS resource use is a BMI of at least 35 kg/m² and at least one weight-related comorbidity.

Let’s talk a bit more about tirzepatide.

Tirzepatide, marketed as Mounjaro, is available as pre-filled pen devices for subcutaneous injection, with doses ranging from 2.5 mg to 15 mg.

It is a once-weekly injection indicated for:

• Type 2 Diabetes and
• Weight Management

What type of drug is Tirzepatide? Well, it is a dual GIP and GLP-1 receptor agonist.

GIP stands for glucose-dependent insulinotropic polypeptide. By activating the GIP receptor, tirzepatide enhances glucose-dependent insulin secretion from pancreatic beta cells, which improves glycaemic control. And it also modulates lipid metabolism.

GLP-1 stands for glucagon-like peptide-1. By activating the GLP-1 receptors, tirzepatide also enhances insulin secretion, but it also inhibits glucagon release, and slows gastric emptying, leading to a more gradual absorption of glucose and reduced postprandial glucose spikes.

Both GIP and GLP-1 pathways work synergistically to influence the central nervous system, suppressing appetite and promoting satiety, leading to weight loss. This combined mechanism offers unique benefits for managing both glycaemic control and obesity.

Is tirzepatide better than semaglutide?

Tirzepatide is considered potentially better than semaglutide in certain contexts.

For example, the dual pathway of tirzepatide allows multiple metabolic pathways, leading to superior outcomes. Clinical trials have demonstrated that tirzepatide leads to greater weight loss compared to semaglutide. Some studies reported reductions of up to 20% of body weight with tirzepatide versus around 15% with semaglutide.

Tirzepatide has also shown superior glycaemic control, achieving greater reductions in HbA1c levels compared to semaglutide in head-to-head studies.

In addition, GIP receptor activation by tirzepatide may have additional benefits on lipid metabolism, such as reducing triglycerides and improving HDL cholesterol. These benefits are less pronounced with semaglutide.

So, bearing this in mind, would we ever choose semaglutide over tirzepatide? Well, although both drugs share common side effects like nausea and vomiting, tolerability varies and some patients may be intolerant to one drug but not the other, so this may have an effect on the choice of treatment too.

Uncommon side effects of tirzepatide include gallbladder disorders and acute pancreatitis. We will discontinue it if there is persistent, severe abdominal pain and, if pancreatitis is confirmed, we will not restart treatment.

In summary, this is indeed a game changer. With Tirzepatide now approved by NICE for use in primary care, we may finally have another clear, accessible option to treat the pressing issue of obesity and overweight in General Practice.

Let’s now briefly touch on the updates on the prevention and management of recurrent UTIs. The changes include new referral recommendations, advice on oestrogen use, new advice on methenamine Hippurate, and choice of medication. Now, let’s have a look at a summary of the main points:

We will refer to secondary care anyone with:

·      recurrent UTI of unknown cause

·      recurrent UTI and suspected cancer

·      recurrent upper UTI

·      recurrent lower UTI in anyone with a male genitourinary system

·      pregnant people

·      children and young people and

·      anyone who has had gender reassignment surgery that involved structural alteration of the urethra. 

We will consider vaginal oestrogen if:

·      the person is experiencing perimenopause or menopause, or they have already experienced menopause, and

·      behavioural or personal hygiene measures alone are not effective

·      At the moment, this is an off-label use of vaginal oestrogen products.

We will also check the NICE guideline on the menopause, which includes advice on the use of vaginal oestrogen if there is a history of breast cancer.

We will review treatment with vaginal oestrogen within 12 months, or earlier if appropriate. 

But we will not offer systemic HRT specifically to reduce the risk of recurrent UTI. 

We will consider methenamine hippurate as an alternative to daily antibiotic prophylaxis for recurrent UTI in anyone with a female urinary system, if:

• they are not pregnant and
• any current UTI has been adequately treated and
• the recurrent UTI has not improved with behavioural and personal hygiene measures, vaginal oestrogen or single-dose antibiotic prophylaxis if appropriate.

When discussing prophylaxis with methenamine hippurate we will explain that:

• over-the-counter sachets that make urine more alkaline (such as sachets used to relieve UTI symptoms that contain potassium citrate or sodium citrate) should not be used while taking methenamine hippurate because these can make it less effective and that
• medical help should be sought for acute UTI symptoms. 

We will review treatment with methenamine hippurate within 6 months, and then every 12 months, or earlier if appropriate. 

But, what is Methenamine Hippurate?

Methenamine hippurate is a prodrug of methenamine, which means it is inactive in its original form but becomes active after metabolism in the body.

How does Methenamine Hippurate Work?

Methenamine is stable in neutral or alkaline conditions, but in acidic urine it is hydrolyzed into formaldehyde and ammonia. Formaldehyde is toxic to bacteria and has therefore antibacterial properties. So, for Methenamine Hippurate to be effective, it is necessary to maintain an acidic urine. This may be achieved naturally, through dietary measures (for example, cranberry juice or vitamin C) or with urinary acidifiers.

Unlike antibiotics, methenamine hippurate does not target specific bacteria but acts broadly against a wide range, therefore reducing the risk of developing antibiotic resistance.

Methenamine hippurate is used as a prophylactic agent rather than as a treatment for acute UTIs. It is especially helpful in recurrent uncomplicated UTIs for those who may want to avoid regular antibiotics.

And finally, let’s now look at the choice of prophylactic options. We can choose between:

• Antiseptic prophylaxis and
• Antibiotic prophylaxis

For antiseptic prophylaxis:

• Methenamine hippurate is recommended for adults.
• And it may be considered for children over the age of 6, but only with specialist advice.

For antibiotic prophylaxis:

• As a first-line option, we will use trimethoprim or nitrofurantoin.
• As a second-line option, we will use amoxicillin or cefalexin.
• The choice of antibiotic should take into account recent culture results and adhere to local antimicrobial policies.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this video I will go summarise the pharmacological management of neuropathic pain reviewing the guidelines on Neuropathic Pain and, because of the overlap in the clinical areas, also the guideline on Low Back Pain and Sciatica, both by the National Institute for Health and Care Excellence (NICE).

I am not giving medical advice; this video is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.   

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the PDF summary can be downloaded here: 

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mEiBizIQiitY4as7?e=HS9lhY 

The Full NICE guidance can be found at:  

·      Neuropathic pain : https://www.nice.org.uk/guidance/cg173

·      Low back pain and sciatica: https://www.nice.org.uk/guidance/ng59

Pictures:

·      Image by kjpargeter on Freepik: a href="https://www.freepik.com/free-photo/3d-female-with-pain-head_1270692.htm#query=neuropathic%20pain&position=0&from_view=search&track=ais"Image by kjpargeter/a on Freepik

·      Image by kjpargeter on Freepik: a href="https://www.freepik.com/free-photo/3d-brain-with-lightening_6214247.htm#query=neuropathic%20pain&position=45&from_view=search&track=ais"Image by kjpargeter/a on Freepik 

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• Music provided by Audio Library Plus  
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•  

Transcript

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE guideline on neuropathic pain and, because of a slight clinical overlap, I will also touch on the management of sciatica. Please note that I will only be focusing on the pharmacological treatment from a primary care perspective.

So let’s jump into it.

And we will start with a very straightforward condition: trigeminal neuralgia.

And for this, we will offer carbamazepine initially 100mg once or twice a day, increasing gradually according to response. The usual dose is 200mg 3-4 times a day but it can be increased to a maximum of 1.6 gr daily in divided doses. Of course, we will bear in mind that there is a risk of major congenital malformations in pregnancy and advise contraception accordingly.

And we have nothing else to offer in primary care so, if carbamazepine is not effective, or suitable, we will need to refer.

For all other neuropathic pain

We will discuss with the patient whether to give oral or topical treatment.

And if the neuropathic pain is localised and they wish to avoid or cannot tolerate oral treatments, we will consider capsaicin cream. 

Otherwise, we will offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as the initial treatment. Gabapentin and pregabalin are controlled drugs so it would make sense to start with either amitriptyline or duloxetine first to minimise the risk of dependency.

If the initial treatment is not effective or tolerated, we will offer one of the remaining 3 drugs, and consider switching again if the second and third drugs are also not effective or not tolerated.

And, as a general rule, when withdrawing or switching treatment, we will taper the dose to minimise any withdrawal symptoms.

So, for me, considering the cost of drugs and risk of dependency, I would consider:

1.   Amitriptyline first

2.   Then duloxetine,

3.   Then gabapentin and

4.   Lastly pregabalin

We will refer if despite treatment the pain is severe, disabling or affecting their sleep or if their underlying condition has deteriorated.

As acute rescue therapy, we could consider tramadol, but only for short term use.

The rest of the guidelines is going to sound like this:

No, no, no, no, no

Because it is going to tell us what treatments should not be used. And we should not start:

·      cannabis extract

·      capsaicin patch

·      opiates like morphine and tramadol (this is referring to long-term use; because careful short-term use of tramadol is allowed)

·      venlafaxine

·      antiepileptics such as lacosamide, lamotrigine, levetiracetam, oxcarbazepine, topiramate or sodium valproate

For sciatica, there is a separate guideline.

And from a Pharmacological perspective, we are very limited because nothing really seems to work very well in sciatica.

We can give NSAIDs but we need to be aware of their risks and limited evidence that they are of much benefit.

If prescribing NSAIDs for sciatica:

·      We will take into account gastrointestinal, liver and cardio-renal toxicity, and the person's risk factors, including age

·      think about risk factors, and the use of gastroprotective treatment

·      use the lowest effective dose for the shortest possible time. 

Can we use anything else if NSAIDs do not work?

For acute low back pain, we can consider weak opioids (with or without paracetamol) but only when managing acute low back pain and only if an NSAID hasn’t worked or can’t be used. We should not offer paracetamol alone for low back pain. 

But we should not be giving opioids for on-going, non-acute sciatica

For chronic sciatica, if NSAIDs are not effective, we are going to encounter the same as before.

So, we should not offer:

·      Gabapentinoids

·      other antiepileptics

·      oral corticosteroids

·      benzodiazepines

·      opioids 

If a person is already taking any of these drugs, we will consider a safe and gradual withdrawal regime

Although we are focusing on the pharmacological treatment, I would like to say that we should also discuss non-pharmacological treatments, for example, physical and psychological therapies and surgery.

We will advise self-management and appropriate exercise, including return to work programmes if possible.

Psychological therapy or manual therapies like spinal manipulation or massage should be offered only as part of a treatment package including exercise and

Combined physical and psychological programmes should be offered for people with persistent and significant symptoms that have not responded to treatment.

We should not offer:

·      Orthotics such as belts, corsets or foot orthotics

·      Traction

·      Acupuncture

·      Ultrasound

·      Electrical nerve simulation, either percutaneous or transcutaneous (PENS or TENS)

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at the NICE guidance on same day referral for hypertension. By way of disclaimer, I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement. 

 There is a YouTube version of this and other videos that you can access here:

 ·      The NICE GP YouTube Channel: NICE GP - YouTube

 The NICE hypertension flowcharts can be found here:

 ·      Website: https://www.nice.org.uk/guidance/ng136/resources/visual-summary-pdf-6899919517

·      Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgKKs3AbARF_VLEI?e=KRIWrn

 The full NICE Guideline NG136 can be found here:

 ·      Website: https://www.nice.org.uk/guidance/NG136

·      Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgP6nFVHRypL9fdj?e=Jbtgus

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]

Music provided by Audio Library Plus

Watch: https://youtu.be/aBGk6aJM3IU

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Transcript

Hello everyone and welcome. My name is Fernando Florido, a GP in the United Kingdom. 

 In today’s episode we will discuss hypertensive emergencies, and the NICE guidance on same day referral for hypertension. Please note, this is my interpretation and not medical advice; it’s intended for health care professionals, and you must use your clinical judgement. 

Remember that there is also a YouTube version of these episodes so have a look in the episode description. 

 Dealing with hypertension can be challenging, but the good thing is that we often have time to decide on the right treatment. However, in some situations, we do not have the luxury of time due to hypertensive emergencies. Today, we will focus on how to identify and manage these emergencies.

 Before we start, I would like to share some tips I've learned from my 25 years of experience as a GP.

 Remember that we are treating the patient, not the blood pressure. The patient that we are going to be talking about today is not your typical happy antihypertensive patient. We are talking about patients who are not well; they are not happy. They will tell us and we will see it. They may have a headache, or chest pains, extreme fatigue, abdominal pain, shortness of breath, visual disturbances etc. And then, their BP is also very high. This situation is when we need to worry.

 So, if someone comes into our consulting room with a spring on their step, happy and smiling and saying: hello! how are you today? we are not going to be instantly very worried, even if their BP is very high. On the other hand, we may really worry about someone who looks unwell, even if their BP is lower.

 Also, when we finish the consultation, we like the patient leave happy but we should also feel happy about our management. So, following our instinct, our gut feeling is very important. We shouldn’t let a patient go if we are not entirely happy with their management.

 It would be better to tell them: I am sorry, I am a little concerned about your BP today and I would like to recheck it in a few minutes. Please sit quietly in the waiting room for 15-20 minutes and then we will recheck it. And then, we can use that time to seek advice. We will normally be working alongside someone else, so maybe we could ask a colleague, or an experienced doctor in the practice. If we happen to be alone or no one is available, then, and I know that this is not going to be popular with hospital doctors, we could just pick up the phone and ask to speak to the medical duty doctor. We will explain why we are worried and we will get their advice and guidance. And in the worst-case scenario, if there is no one around and nobody picks up the phone, it’s probably best just to send the patient to A&E or the emergency department. Feeling a little silly when the patient tells us: why did you send me there? It was a waste of time! Is better than having the patient, or even worse, a relative tell us: why didn’t you? Because something horrible has happened.

But don’t worry, all of that comes with experience and our clinical judgement improves all the time. Until then, it is also a good idea to rely on clear NICE guidance, which is what we are now going to look at.

 So, what do the guidelines actually say:

 In summary, that we should arrange an urgent or same-day referral in hypertension when we are worried about either the patient’s:

·      BP levels or

·      Symptoms

Let’s start with when are concerned about BP levels, that is, when the patient’s BP is very high and there are red flags. And this situation would be when the

·      BP is 180/120 mmHg or higher and they have either:

o  signs of retinal haemorrhage or papilloedema or

o  new onset of life-threatening symptoms

 Let’s look at the retinal haemorrhage and papilloedema first. They are often a sign of accelerated or malignant hypertension which is often when the BP is >220/120

And you are probably screaming at me now saying: I can’t do fundoscopy!

 And that is fine. Fundoscopy is quite a skill to master and many, if not most doctors will not be trained at a level that makes their examinations reliable. So, what would we do?

We should then be guided by the possible symptoms of retinal haemorrhage or papilloedema, which are all of these:

·      Blurred or distorted vision

·      Vision loss, (partial or complete)

·      Seeing spots or floaters

·      Reduced peripheral vision

·      Difficulty seeing in the dark

·      Eye pain or discomfort

·      Headaches

·      Nausea and vomiting

·      Flashing lights and

·      Double vision

But we also need to be aware that a retinal haemorrhage can have no symptoms at all!

 This would be the case, for example, when the bleeding is small or occurs in the periphery of the retina

But normally that would be spotted because we would:

·      Always do investigations for target organ damage on initial diagnosis and

·      These investigations always include fundoscopy, so there will always be opportunities to spot this problem.

But you will probably want to shout at me again saying: I told you I can’t do fundoscopy!

 And basically, what we need to do is refer the patient for fundoscopy to either:

·      A doctor skilled in fundoscopy or

·      An optician

If we are worried because the BP is 180/120 or higher and the patient has visual symptoms, we could play it safe and send the patient to A&E or the emergency department.

 However, if they have a BP of 180/120 or higher and they do not have any symptoms, a more sensible approach would be to arrange an

o  Urgent referral to an optician or a doctor skilled in fundoscopy

o  Which should ideally be the same or next day

 One top tip.

Even though you say that you can’t do fundoscopy, I would advise you to love your ophthalmoscope and to use it. Look at the fundi every time that an opportunity comes along. We will probably not see anything half of the times and the other half we will not know what we are seeing. It will not change our management and we will still refer the patient for a proper assessment. However, over many years of practice and experience, we may learn to spot something. And even small victories can be satisfying and good for our professional development

Right, now, if we go to the previous slide, we see that we have dealt with the issue of a high BP and retinal concerns. The next point is to address a high BP of 180/120 or higher with new onset life threatening symptoms.

And what are these life-threatening symptoms? They would be new onset:

§ confusion

§ chest pain

§ signs of heart failure, or

§ acute kidney injury or AKI

OK, new onset confusion and chest pain are very clear but, heart failure and AKI?

You may be saying now, how can we diagnose new onset heart failure the same day?

Organising Blood tests and echocardiograms take time!

So, we do what we always do, which is to be guided by the symptoms, which we can also confirm with the physical examination:

And we need to remember that we are talking about new onset heart failure, which is basically acute heart failure. So, we are not talking about those patients who have chronic heart failure and have a little bit of shortness of breath or a bit of leg oedema, etc. We are talking about acute (or acute on chronic) heart failure which is when:

o  The patient is unwell!

So, we are talking about sending to A&E or the emergency department any unwell patient with a BP of 180/120 or higher and with any of the following new symptoms:

·      Shortness of breath, coughing or wheezing, especially at night or when lying down

·      Tachycardia, arrhythmia

·      Leg/ankle/foot oedema

·      Fatigue and weakness

·      Nausea and loss of appetite

·      Confusion or disorientation and

·      Chest pain or pressure

And now you may also be saying, how can we diagnose new onset AKI the same day?

Renal function test results take time!

So, again, we do what we always do, which is to be guided by the symptoms:

And we need to remember that we are talking about acute kidney injury, which is an acute problem. So, we are not talking about those patients who have CKD and have a few symptoms here and there. We are talking about an acute injury to the kidneys, which is when:

o  The patient is unwell!

So, we are talking about sending to A&E or the emergency department any unwell patient with a BP of 180/120 or higher and with any of the following new symptoms:

·      Decreased urine output or no urine output

·      Leg/ankle/foot oedema

·      Fatigue and weakness

·      Shortness of breath

·      Nausea and vomiting

·      Confusion or disorientation and

·      Chest pain or pressure

 So, we now go back to our very first slide and we can see that we have dealt with concerns about patients’ BP levels. But there is still the question of symptoms, so…

 Do you ever refer the same day if BP<180/120?

 And the answer is Yes!

Because we would refer patients if they have phaeochromocytoma symptoms

Now we need to remember that a phaeochromocytoma is a rare tumour of the adrenal glands. The adrenal glands produce adrenaline and noradrenaline, which control heart rate, blood pressure and metabolism. A phaeochromocytoma can produce too much adrenaline and noradrenaline, which often results in problems such as palpitations and high blood pressure.

 So what are those symptoms?

The symptoms of a phaeochromocytoma tend to be unpredictable, often occurring in sudden attacks lasting from a few minutes to an hour, sometimes longer, and the patient will therefore be intermittently unwell

So, we are talking about sending to A&E or the emergency department any patient who has hypertension (without a specific BP threshold) and who is intermittently unwell with any of the following symptoms:

·      headache

·      palpitations

·      pallor

·      abdominal pain and

·      diaphoresis or excessive sweating

Right, will that be difficult to remember?

 Nah!

Because in real life we will have common sense, we will follow our instinct and we will do what we would normally do for any seriously unwell patient

For example:

Regardless of their BP!

Would we refer a patient to A&E or the emergency department if they are unwell with any of these symptoms?

·      Acute confusion:

·      Acute chest pain: 

·      Acute shortness of breath:

·      Acutely unwell with decreased urine output or no urine output:

·      So the answer is yes, and we would do this regardless of the BP. In fact, we would probably call the ambulance first and then check the BP later!

Then, would we refer a patient to A&E or the emergency department if they had a BP of 180/120 or higher and either

·      visual disturbances or

·      the patient is Unwell? : And the answer is Yes! Especially if:

o  Rapid or irregular heartbeat

o  Leg/ankle oedema

o  Fatigue and weakness

o  Coughing or wheezing, especially at night or when lying down and

o  Nausea and vomiting

And, after what we have learned today about pheochromocytoma, would we refer a hypertensive patient to A&E or the emergency department if they were intermittently unwell with any of these symptoms?

o  Palpitations:

o  Pallor

o  abdominal pain or

o  diaphoresis

o  And the answer is Yes! we would do that because we would be worried about pheochromocytoma and we would do it regardless of their BP at the time.

But remember that this is only my interpretation of the guideline, so it is not necessarily correct.

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye 

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. Welcome to the latest instalment in our monthly video series, "NICE News," where we discuss new and updated guidelines published by the National Institute for Health and Care Excellence (NICE), specifically as it relates to primary care.

In this video, I'll be focusing on the NICE guidance and advice published in July 2023. We'll be reviewing the latest recommendations that are relevant to primary care practitioners, with the goal of keeping you informed and up-to-date on the latest developments.  

Please note, I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement. 

There is a YouTube version of this and other videos that you can access here: 

• The NICE GP YouTube Channel: https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw

The link to the PDF version of this video can be downloaded here: 

·      Printable version: https://1drv.ms/b/s!AiVFJ_Uoigq0l2tnS9ulRaEBT8Af?e=TCk7ZO

·      Colour & photo version: https://1drv.ms/b/s!AiVFJ_Uoigq0l2w1zRoLSYM34HhO?e=avMoqf

The links to the update guidance covered can be found here:

Obesity in adults: identification, assessment and management

·      https://www.nice.org.uk/guidance/cg189

KardiaMobile for detecting atrial fibrillation

·      https://www.nice.org.uk/guidance/mtg64

Semaglutide for managing overweight and obesity in young people aged 12 to 17 years (terminated appraisal)

·      https://www.nice.org.uk/guidance/ta910

Alcohol-use disorders: diagnosis and management:

·      https://www.nice.org.uk/guidance/qs11

Draft consultation: Vitamin B12 deficiency in over 16s: diagnosis 6 and management

·      Document: https://www.nice.org.uk/guidance/GID-NG10176/documents/draft-guideline

·      Consultation on draft guideline is open until 5pm on Tuesday 22 August 2023: https://www.nice.org.uk/guidance/indevelopment/gid-ng10176/consultation/html-content

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• Music provided by Audio Library Plus  
• Watch: https://youtu.be/aBGk6aJM3IU 
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Transcript

Hello and welcome to another episode of NICE News. My name is Fernando Florido, a GP in the United Kingdom. Today, we'll be discussing the NICE Guidance and advice published in July 2023, specifically for Primary Care.

This month we are focusing on obesity, atrial fibrillation and alcohol misuse. If you want to download a PDF version of this episode, the link is in the episode description.

Before we begin, I want to remind you that this episode is not medical advice. It is only my interpretation, and you must use your clinical judgement.

I'd like to remind you that there is a YouTube version of this episode which can be found in the episode description.

Now, with that said, let’s get straight into it.

The first clinical area refers to the guideline on obesity.

We will refer for bariatric surgery if they:

·     have a BMI of 40 or more, or over 35 with a significant health condition that could be improved if they lost weight

·     The BMI threshold is reduced by 2.5 for South Asian, Chinese, other Asian, Middle Eastern, Black African or African-Caribbean family background to account for the fact that these groups are prone to central adiposity with cardiometabolic risks at a lower BMI.

And in terms of Pharmacological interventions, NICE has not recommended naltrexone–bupropion but there is a list of three approved medicines for obesity. Liraglutide and semaglutide can only be prescribed for obesity by secondary care and orlistat, which can also be prescribed in primary care. The prescribing criteria are:

·     Liraglutide: BMI of 35 or 32.5 for members of minority ethnic groups

and

Non-diabetic hyperglycaemia (HbA1c level of 42 - 47 mmol/mol [6.0% to 6.4%] or a fasting plasma glucose level of 5.5 - 6.9 mmol/litre)

and

High risk of CVD

·     Semaglutide: BMI of 35.0 or 30.0 if they meet certain referral criteria but reduce BMI thresholds by 2.5 for people from Asian, Chinese, Middle Eastern, Black African or African-Caribbean family backgrounds

and

At least 1 weight-related comorbidity

And we will consider stopping if less than 5% of the initial weight has been lost after 6 months. We will use it for a maximum of 2 years

·     Orlistat: BMI of 30 or more or 28 or more with associated risk factors. It should not be used with other drugs aimed at weight reduction and we should continue beyond 3 months only if the person has lost at least 5% of their initial body weight. However, rates of weight loss may be slower in people with type 2 diabetes, so less strict goals may apply to theml

As a separate guidance NICE is unable to make a recommendation on semaglutide for managing overweight and obesity in people aged 12 to 17 years because the manufacturer considers that, at this time, there is not enough evidence to support it for this population.

The next topic is KardiaMobile for detecting atrial fibrillation

This guidance had been withdrawn because of technical issues but it has now been re-introduced. Therefore KardiaMobile is recommended for detecting atrial fibrillation (AF) for people with suspected paroxysmal AF, who are referred for ambulatory electrocardiogram (ECG). KardiaMobile is a portable ECG recorder and Clinical evidence shows that significantly more people had AF detected using the KardiaMobile single-lead device compared with a Holter monitor. Furthermore, cost modelling shows that KardiaMobile is cost effective.

In terms of alcohol-use disorders there are 5 new quality statements focusing on key areas. The two areas relevant to primary care are that:

1.   Adults who are being asked about their alcohol use have a validated alcohol questionnaire completed to identify any need for a brief intervention or referral to specialist alcohol services. 

2.   Adults seeking help are given information on community support networks and self-help groups. 

I will also mention that there is a first-ever NICE guideline on vitamin B12 deficiency, which at the moment is only in draft form. It basically says that older people with unexplained fatigue or mental health problems should be offered a vitamin B12 test. The draft publication offers recommendations on how to diagnose it and treat it. I will not say much more because, being in draft, it is likely to change, but it is something that we can look forward to in the near future. If you want to see the draft document or take part in their consultation, I have put the link to it in the episode description. 

And lastly, we will end with the sad news that NICE is to stop supplying print copies of the BNF. The guidance will now only be in a digital format, either online or as a mobile app, so if you have one of the printed copies of the BNF lying around, look after it because, given enough time, it may eventually become an important historic item.  

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through a number of NICE products on insomnia, including guidance on the medical technology sleepio, and the prescribing of z-drugs, daridodexant and melatonin.

I will summarise the guidance from a Primary Care perspective only.

I am not giving medical advice; this video is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here:  

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Medical technologies guidance [MTG70] on “Sleepio to treat insomnia and insomnia symptoms” can be found here:

·      https://www.nice.org.uk/guidance/mtg70

The Technology appraisal guidance [TA77] “Guidance on the use of zaleplon, zolpidem and zopiclone for the short-term management of insomnia” can be found here:

·      https://www.nice.org.uk/guidance/ta77

The Technology appraisal guidance [TA922] “Daridorexant for treating long-term insomnia” can be found here:

·      https://www.nice.org.uk/guidance/ta922

The Evidence summary [ES38] “Melatonin for treating sleep disorders in adults who are blind” can be found here:

·      https://www.nice.org.uk/advice/es38/chapter/Product-overview

Thumbnail photo: from Freepik: https://www.freepik.com/

·      Image by Freepik

·      Image by a href="https://www.freepik.com/free-photo/flat-lay-woman-laying-bed_28694061.htm#query=insomnia&position=21&from_view=search&track=sph&uuid=65539da6-4c29-453b-9d22-c39df5176601"Freepik/a

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Music provided by Audio Library Plus   

Watch: https://youtu.be/aBGk6aJM3IU  

Free Download / Stream: https://alplus.io/halfway-through  

Transcript

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through a number of NICE publications on insomnia, including guidance on digital cognitive behavioural therapy for insomnia (CBT-I), and the prescribing of hypnotics, daridodexant and melatonin, all of them from a Primary Care perspective.

By the way, make sure that you stay for the entire episode because, at the end, I will go through some audit ideas backed by NICE which you could use as a Quality Improvement Project in your practice.

So, let’s jump into it.

Let’s talk a little about the condition first.

Insomnia is a disturbance of sleep characterised by difficulty in initiating and/or maintaining sleep. However, insomnia is highly subjective and although most healthy adults typically sleep between 7 and 9 hours per night, patterns vary between people, and in any given person there are also variations from night to night.

Estimates of the prevalence of insomnia vary and while up to 48% of people have reported sleeping issues, only 6% met the criteria for a diagnosis of insomnia. So, in general practice, differentiating between simple sleeping problems and significant insomnia is important before considering treatment.

The prevalence of insomnia is higher in women and increases with age and, although the majority do not seek medical advice, the treatment depends on the duration and nature of the symptoms. Appropriate management of co-morbidities may help and sleep hygiene advice is fundamental, for example, avoiding stimulants and maintaining regular sleeping hours with a suitable environment for sleep. Other non-pharmacological interventions, for example, cognitive behavioural therapies, are also effective.

Insomnia can have a number of different causes: primary insomnia can be differentiated from insomnia associated with factors such as personal circumstances, physical or psychiatric co-morbidities, concomitant drug treatments or substance abuse. Epidemiology surveys have shown that over half of people with sleep problems have either a mental or a physical health disorder.

And in this video, we will not be talking about specific issues caused by physical conditions such as sleep apnoea or narcolepsy or sleep disturbances associated to severe mental illness.

For the management, it is crucial to differentiate between short-term insomnia and long-term insomnia.

For short-term insomnia, sleep hygiene advice is offered. After this, medicines such as zopiclone, zolpidem and melatonin can be used for a short time, that is, less than 4 weeks or less than 13 weeks for melatonin. In addition, up to 40% of people with insomnia self-medicate with over-the-counter drugs, for example, sedative antihistamines.

However, long-term insomnia, also known as chronic insomnia, is different and it’s defined as dissatisfaction with quantity or quality of sleep for 3 nights or more per week for at least 3 months with an effect on daytime functioning. Therefore, long-term insomnia has both night-time and daytime symptoms. Furthermore, once insomnia has lasted for more than 6 months, it may last for years and be difficult to resolve.

For long term insomnia, sleep hygiene advice is given first and then, CBT-I is the recommended first-line treatment. But there are access difficulties to CBT-I across the country and in many areas access is poor. And this is a real pity because CBT-I has a 70% to 80% response rate and roughly 50% experience long-term remission.

NICE has published 17 products on insomnia but the majority are for sleep apnoea and narcolepsy. Only 4 would be relevant for this video and these are:

·      The Medical Technology Sleepio

·      Advice on hypnotics like benzodiazepines and Z-drugs such as zolpidem and zopiclone

·      Recommendations on Daridorexant

·      And finally, we will also briefly touch on melatonin

Sleepio is a digital self-help programme that includes CBT‑I and that reduces symptoms compared with sleep hygiene and sleeping tablets. The gold standard treatment for insomnia is face-to-face CBT-I, but its availability is very limited and therefore Sleepio is recommended as an alternative to sleeping tablets. Unfortunately, Sleepio is not available on the NHS in all regions of the UK either.

Let’s have a look at the recommendations on hypnotics like benzodiazepines and Z-drugs such as zolpidem and zopiclone. They can be considered after sleep hygiene but for a short time only and bearing in mind that they do not treat any underlying cause.

A number of hypnotic agents are licensed for the treatment of insomnia, including benzodiazepines and Z-drugs.

Benzodiazepines enhance the effects of GABA, which is the major inhibitory neurotransmitter in the central nervous system. Examples licensed for insomnia are, amongst others, nitrazepam, temazepam and lorazepam.

The effects of benzodiazepines are dependent upon the dose administered and the pharmacokinetic profile. The BNF refers to temazepam and lorazepam, as having a shorter duration of action. Benzodiazepines with a longer half-life like diazepam and nitrazepam tend to have prolonged effects the next day.

The main concern with benzodiazepines is that many people develop tolerance to their effects, gain little benefit from chronic use, become both physically and psychologically dependent on them, and suffer withdrawal symptoms when stopping them. 'Rebound insomnia' also occurs and is characterised by worsening insomnia symptoms.

The use of benzodiazepines for the treatment of insomnia should be restricted to severe insomnia and treatment should not be continued beyond 4 weeks.

Zolpidem and zopiclone (the Z-drugs) are non-benzodiazepine hypnotics. Although the Z-drugs differ structurally from the benzodiazepines, they are also agonists of the GABA receptor complex and therefore enhance GABA-mediated neuronal inhibition.

Zolpidem has a half-life of 2.5 hours and Zopiclone of between 3.5 and 6.5 hours. They are licensed for "the short-term treatment of insomnia in situations where the insomnia is debilitating or is causing severe distress for the patient". The duration of treatment is a maximum of 4 weeks, including tapering off where appropriate.

Although the Z-drugs were developed to overcome the disadvantages of benzodiazepines, the sedative effects of the Z-drugs may also persist into the next day and they can cause tolerance, dependence and withdrawal symptoms.

It may be worth mentioning that, a review of the trial evidence comparing the Z-drugs with benzodiazepines licensed for insomnia showed, in summary, that there were no clinically useful differences between the drugs.

Because of the lack of evidence to distinguish between zolpidem and zopiclone, the drug with the lowest purchase cost should be prescribed and switching from one to another should only occur if a patient experiences adverse effects considered to be directly related to a specific agent.

Patients who have not responded to one of these hypnotic drugs should not be prescribed any of the others.

So, we have now seen that short term insomnia can be treated with sleep hygiene and short-term use of hypnotics and long-term insomnia with sleep hygiene and either face to face CBT-I or digital CBT-I like Sleepio.

But what does NICE recommend for long term insomnia if CBT-I or Sleepio have not worked or are not available?

And here is where we find the latest NICE guidance on this issue, published in October 2023. It refers to a new type of drug, Daridorexant.

And NICE says that Daridorexant is both clinically and cost effective and it is recommended for insomnia lasting for 3 nights or more per week for at least 3 months, with affected daytime functioning but only if:

·      cognitive behavioural therapy for insomnia (CBT-I) is ineffective or

·      it is not available or is unsuitable.

What is daridorexant? Well, Daridorexant is now available on the BNF and unlike benzodiazepines and Z-drugs, which work by increasing sedation, daridorexant is a new type of drug, an orexin antagonist, which works in a different way. It inhibits arousal mechanisms. To understand this, we need to know that orexins are neuropeptides produced by the hypothalamus which promote a state of wakefulness. Therefore, daridorexant, by blocking the orexin receptors, reduces wakefulness and helps sleep.

Because of the different mechanism of action, if necessary, daridorexant could be used at the same time as other medicines or non-medicine treatments available for insomnia.

And the good news is that, in clinical studies, there has been no evidence of abuse or withdrawal symptoms indicative of physical dependence.

NICE recommends that the length of treatment should be as short as possible and the treatment should be reviewed within 3 months of starting and at regular intervals thereafter. But it can be used as maintenance treatment for managing longer-term symptoms if necessary.

Now let’s touch on the prescribing of Melatonin for insomnia.

Melatonin is a hormone that occurs naturally in the body. It is involved in regulating sleep and circadian rhythms and it can be given as an oral medication to treat sleeping problems.

There is little NICE guidance on the use of melatonin. There is only an evidence summary on the use of melatonin for treating sleep disorders in adults who are blind, and, because of insufficient evidence, NICE was unable to determine its clinical effectiveness and safety.

The BNF states that melatonin is indicated as:

·      Short-term treatment for Insomnia in adults over 55 for up to 13 weeks

·      Short-term treatment for Jet lag in adults for up to 5 days, and

·      Treatment for Insomnia in patients with learning disabilities and challenging behaviour, although this use is unlicensed and it needs to be initiated under specialist supervision

Cautions for melatonin include autoimmune disease, as exacerbations have been reported occasionally, and susceptibility to seizures, as there is a risk of increased seizure frequency

Reported side effects are, amongst others, arthralgia, increased risk of infection, drowsiness, headaches, and pain

Now, as promised let’s have a look at audit ideas on the use of hypnotics (including Z-drugs) suggested by NICE and that you could use for a Quality Improvement Project in your Practice.

The objectives for the audit would be to assess the appropriateness of use of zolpidem and zopiclone.

The patients to be included in the audit could be, for example, all those for whom zolpidem and zopiclone are prescribed for a suitable period of time, for example, 3–6 months.

Possible audit criteria could be the following four:

Criterion 1- Non-pharmacological measures are considered before prescribing:

·      The standard would be 100% of all patients without exception

Criterion 2- When prescribed, hypnotic drug therapy is prescribed for a short period of time only, in strict accordance with the licensed indications:

·      The standard would also be 100% of all patients without exception

Criterion 3- When prescribed, the hypnotic drug with the lowest cost is chosen:

·      The standard would be 100% of all patients with the exception of those who have developed side effects with a cheaper first line agent

Criterion 4- A patient is switched from one hypnotic drug to another:

·     As switching is not recommended, the standard would be 0% of all patients with the exception of those who have developed adverse effects considered to be directly related to a specific agent

Once compliance has been calculated, the Practice can identify whether clinical management can be improved, agree on a plan and repeat the measurement after a period of time to close the audit cycle and to confirm that the desired improvement has been achieved.

And there you have it, a simple project to fulfil your QIP requirements for appraisal.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guideline. You must always use your clinical judgement.

Thank you for listening and goodbye.

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through the NICE guideline on “Heavy menstrual bleeding: assessment and management”, or NICE guideline [NG88.

I will summarise the guidance from a Primary Care perspective only.

I am not giving medical advice; this video is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline NG88 “Heavy menstrual bleeding: assessment and management” can be found here:

·      https://www.nice.org.uk/guidance/ng88/chapter/Recommendations

The Menorrhagia mind map or flow chart can be downloaded here:

·      https://1drv.ms/i/s!AiVFJ_Uoigq0mFegr4-vdKdhitAI?e=BJRIDK

Thumbnail photo: from Freepik: https://www.freepik.com/

·      Image by benzoix on Freepik

·      a href="https://www.freepik.com/free-photo/young-woman-with-pain-stomach-holding-hands-belly-feeling-terrible-ache-menstrual-cramps-stand_34232826.htm#query=heavy%20periods&position=17&from_view=search&track=ais"Image by benzoix/a on Freepik

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  

• Music provided by Audio Library Plus  
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

Transcript

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the NICE guideline on menorrhagia or, to be precise, “Heavy menstrual bleeding: assessment and management” and I will summarise the guidance from a Primary Care perspective only.

So, let’s jump into it.

We will obviously start with the history including the nature and impact of the bleeding and we will particularly pay attention to what NICE refers to as “related symptoms”. These are symptoms such as:

·      Persistent intermenstrual bleeding

·      Pelvic pain and/or

·      Pressure symptoms, because

they might suggest a uterine abnormality.

What may come as a surprise is that NICE says that if none of these symptoms are present, that is, no IMB, no pain and no pressure symptoms, we will consider pharmacological treatment without necessarily carrying out a physical examination.

But the converse is true, a physical examination is recommended if such symptoms exist or if we are considering a levonorgestrel-releasing intrauterine system [LNG IUS], that is, a Mirena coil or similar. 

In terms of blood tests:

·      we will perform a FBC for all patients and

·      we will consider testing for coagulation disorders if they have had heavy periods since they started and there is a personal or family history suggestive of it

·      However, NICE says that there is no need for routine ferritin, hormone or thyroid testing

We will then consider investigations for the cause of the HMB but

We will also consider starting pharmacological treatment without investigating the cause if we feel that there is a low risk of uterine abnormality.

If we do investigate further, we will consider the need for:

·      Hysteroscopy

·      A pelvic USS or

·      A transvaginal USS

And we will choose each investigation depending on whether we suspect:

·      submucosal fibroids, polyps or endometrial pathology (in which case a hysteroscopy would be needed)

·      larger fibroids (in which case a pelvic USS would be needed) or

·      adenomyosis (when a transvaginal USS would be recommended)

And we will use our clinical judgement to decide which one of those we should consider as most likely. For example:

·      We will suspect submucosal fibroids, polyps or endometrial pathology (and therefore the need to refer for possible hysteroscopy plus / minus biopsy) if, for example:

o  They are taking tamoxifen

o  They have persistent intermenstrual or irregular bleeding,

o  They have infrequent heavy bleeding and are obese or have PCOS or if

o  They have not responded to treatment. 

·      We will think about larger fibroids (and therefore the need to request a pelvic USS) if:

o  there is a palpable uterus on abdominal examination,

o  a Pelvic mass is suspected and

o  we will also consider a pelvic USS if the examination is inconclusive or difficult, because, for example, obesity

·      And we will think about adenomyosis (and therefore the need for a transvaginal USS) if:

• There is a bulky, tender uterus on examination or
• There is significant dysmenorrhoea or period pain but we also need to be aware that pain may be caused by endometriosis rather than adenomyosis

If hysteroscopy is declined, we will consider a pelvic ultrasound, explaining its limitations

If a transvaginal ultrasound is declined or unsuitable, we will consider a transabdominal ultrasound or MRI, also explaining their limitations.

Let’s now look at the management of menorrhagia. As we have previously said, we will refer for hysteroscopy those patients in whom we suspect an endometrial pathology, so we will leave their management in the hands of secondary care. 

So, from a Primary Care perspective, and for the purpose of their management we need to group the remaining patients into two types:

·      Patients with no identified pathology, with fibroids less than 3 cm in diameter, or with adenomyosis and

·      Patients with fibroids of 3 cm or more in diameter

For the first group, that is, patients with no identified pathology, with small fibroids, or adenomyosis, we will consider an LNG-IUS first line, as long as, if there are small fibroids, they do not cause distortion of the uterine cavity 

On offering this treatment, we will explain to them:

·      about the anticipated changes in bleeding pattern, particularly in the first few cycles and maybe lasting longer than 6 months and

·      that it is advisable to wait for at least 6 cycles to see the benefits of the treatment. 

If LNG-IUS is declined or unsuitable, we will consider pharmacological treatments, either:

·      non-hormonal like:

o  tranexamic acid and

o  NSAIDs or

·      Hormonal like:

o  combined hormonal contraception and

o  cyclical oral progestogens, also bearing in mind that

o  Progestogen-only contraception may suppress menstruation, which could be beneficial for some patients too

If the symptoms are severe or do not respond to pharmacological treatment, or the patient declines pharmacological treatment, we will refer.

For the second group, that is, patients with fibroids of 3 cm or more in diameter

We will consider referral and, if pharmacological treatment is needed while waiting investigations, we will consider tranexamic acid and/or NSAIDs, but we need to be aware that the effectiveness of pharmacological treatments may be limited if fibroids are substantially greater than 3 cm in diameter. 

Depending on the size, location and number of fibroids, and the severity of the symptoms a number or other treatments may be considered by secondary care, including further pharmacological or surgical treatments.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guideline. You must always use your clinical judgement.

Thank you for listening and goodbye.

This episode makes reference to guidelines produced by the “National Institute for Health and Care Excellence” in the UK, also referred to as “NICE”. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through the NICE guidance on the management of lower urinary tract symptoms in men.

I will summarise the guidance from a Primary Care perspective only.

I am not giving medical advice; this video is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The full clinical guideline CG97 on lower urinary tract symptoms in men: management can be found here:

·      https://www.nice.org.uk/guidance/cg97

The International Prostatism Symptom Score calculator can be found here:

·       https://www.uptodate.com/contents/calculator-international-prostatism-symptom-score-ipss

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  

• Music provided by Audio Library Plus  

• Watch: https://youtu.be/aBGk6aJM3IU 

• Free Download / Stream: https://alplus.io/halfway-through 

Transcript

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the NICE guidance on the management of lower urinary tract symptoms in men, which I have summarised from a Primary Care perspective.

So, let’s jump into it.

And to appreciate fully the importance of this subject, let’s have a look at this anonymous poem:

“As man draws near the common goal

Can anything be sadder

Than he who, master of his soul

Is servant to his bladder‟

And, of course, we know that the prevalence and severity of male lower urinary tract symptoms, also known as LUTS, increase with age and although transurethral resection of the prostate is often effective, about a quarter of men have poor post-surgical outcomes and some failures can be attributed to an incorrect initial diagnosis.

So, let’s start by talking about the conditions that can cause LUTS in men.

And in order to get the correct diagnosis, we should remember the ancient Chinese proverb that says that the “bladder is the mirror of the soul‟ and therefore LUTS can result from not only bladder dysfunction or prostatic pathology but also from a number of other causes, e.g., metabolic, hormonal, cardiac, respiratory, etc. And therefore, effective therapy depends on the accurate diagnosis of the underlying problem.

Although, the most common cause is benign prostate enlargement (BPE), which obstructs the bladder outlet, the term LUTS is an umbrella term introduced to dispel the perception that male urinary symptoms are simply caused by prostate problems.

Because other conditions, for example, detrusor muscle problems, prostatitis, UTIs, prostate cancer and neurological disease, can also cause LUTS.

We also need to be aware of the 3 stages of the bladder cycle, which are:

·      Storage - during which filling of the bladder occurs

·      Voiding - during which the bladder actively expels its contents and

·      Post micturition - immediately after voiding when the bladder returns to storage function.

And as a result, LUTS comprise three different types of symptoms:

·      First, storage symptoms normally causing daytime urinary frequency, nocturia, urgency and urinary incontinence

·      voiding symptoms, causing slow stream, spraying, intermittency, hesitancy, straining, and terminal dribbling and

·      post micturition symptoms, for example, sensation of incomplete emptying, and post micturition dribbling

In the management of male LUTS we need to understand that we are dealing with a complex functional unit comprising the bladder, bladder neck/prostate and urethra. LUTS may result from a combination of factors and, to avoid confusion, we should use the correct clinical terms. So let’s have a look at them:

·      “Benign prostatic hyperplasia” or BPH should be reserved for histopathological prostate hyperplastic changes (i.e. abnormality at the cell level). The prevalence of BPH increases with age and whilst it is often associated with LUTS, only 25% to 50% of men with BPH have symptoms.

·      “Benign prostatic enlargement” or BPE refers to an increase in size of prostate gland due to BPH. But only about half of men with hyperplasia will develop clinical enalrgement.

·      “Bladder outlet obstruction” (BOO) is an urodynamically diagnosed condition characterised by increased detrusor pressure and reduced urine flow rate.

·      “Overactive bladder” presents with urinary urgency, with or without incontinence, usually with frequency and nocturia. OAB does not include stress incontinence due to a weak sphincter or overflow incontinence due to chronic retention.

·      And finally, Detrusor overactivity (DO) is urodynamically characterised by involuntary detrusor contractions during the bladder filling phase and occurs in about two thirds of OAB cases and 50% of those with BOO.

There is also a clear association between LUTS and sexual dysfunction, including erectile dysfunction, ejaculatory dysfunction, decreased sexual activity and decreased sexual desire. However, we will not cover this area in today’s episode.

At initial assessment in General Practice, we will review their current medication and take a history and examination including an examination of the abdomen, genitalia, a digital rectal examination as well as a urine dipstick. 

We will check creatinine and eGFR if concerned about renal impairment and we will give information about PSA testing if:

·      their LUTS are suggestive of bladder outlet obstruction secondary to benign prostate enlargement (BPE) or

·      their prostate feels abnormal on digital rectal examination or

·      they are concerned about prostate cancer

If there are bothersome LUTS we could ask the patient to complete a urinary frequency volume chart and we will refer if the patient has not responded to the initial management or have complications such as UTIs, retention, renal impairment or suspected urological cancer. 

For uncomplicated LUTS, we will not routinely offer:

·      Cystoscopy

·      Imaging of the upper urinary tract

·      Flow-rate measurement

·      a post-void residual volume measurement

Although these investigations as well as other ones may be carried out following specialist referral.

To assess response to treatment, we should use a validated symptom score (for example, the International Prostatism Symptom Score or IPSS) before and after the intervention. There are online calculators that can facilitate this and I have included a link in the episode description.

As conservative management, we should offer advice on fluid intake and lifestyle measures, for example:

• cut down on fizzy drinks, and/or drinks that contain alcohol or caffeine

• avoid excessive drinking, aiming for between 1.5 and 2 litres of fluid a day and

• avoid constipation

If there is post-micturition dribble, we will advise how to perform urethral milking. 

If LUTS are suggestive of overactive bladder, we should refer to local community continence services for supervised bladder training

We should refer to urology if there is stress urinary incontinence but

If stress urinary incontinence is caused by prostatectomy, we should offer supervised pelvic floor muscle training for at least 3 months, again via local community continence services.

For urinary incontinence:

·      We will give temporary products, for example, pads or collecting devices, while waiting for a definitive management.

·      External collecting devices, for example, sheath appliances, pubic pressure urinals should be used before indwelling catheterisation

·      Intermittent bladder catheterisation should be considered before indwelling catheterisation.

·      Long-term indwelling urethral catheterisation maybe suitable when:

• medical management has failed and surgery is not appropriate and
• the patient is unable to manage intermittent self-catheterisation or
• there are skin problems aggravated by contact with urine or
• the patient is distressed by bed and clothing changes and

We will refer patients with symptoms of urinary retention and ensure that:

·      Men with acute retention are catheterised urgently and that

·      An alpha blocker should be given before removal of the catheter

·      Checking creatinine and imaging of the upper urinary tract is recommended for chronic urinary retention and

·      Surgery or permanent catheterisation will be guided by urology services

Drug treatment will be offered only when conservative management has been unsuccessful, after taking into account comorbidities and current medication.

Drug treatment may be guided by Urology but, in summary, we should be aware of the following:

·      An alpha blocker (like alfuzosin, doxazosin, tamsulosin or terazosin) can be offered to men with moderate to severe LUTS

·      An anticholinergic can be given if there are symptoms of an overactive bladder

·      A 5‑alpha reductase inhibitor such as finasteride can be given if LUTS are present with a prostate estimated to be larger than 30 g or a PSA level greater than 1.4 ng/ml

·      A combination of an alpha blocker and a 5‑alpha reductase inhibitor can be given if they have both moderate to severe LUTS and a prostate estimated to be larger than 30 g or a PSA level greater than 1.4 ng/ml.

·      An anticholinergic as well as an alpha blocker can be given if there are storage symptoms such as daytime urinary frequency, nocturia, urgency and urinary incontinence after treatment with an alpha blocker alone. 

·      A late afternoon loop diuretic may be offered if there is nocturnal polyuria although this is an unlicensed indication

·      Oral desmopressin may be offered to men with nocturnal polyuria if other medical causes have been excluded and they have not benefited from other treatments. This is an unlicensed indication and sodium should be measured 3 days after the first dose and desmopressin should be stopped if sodium is below the normal range.

We need to be aware that medical conditions that can cause nocturnal polyuria symptoms include diabetes mellitus, diabetes insipidus, adrenal insufficiency, hypercalcaemia, liver failure, polyuric renal failure, chronic heart failure, obstructive apnoea, dependent oedema, pyelonephritis, chronic venous stasis, and sickle cell anaemia.

Equally, medications that can cause nocturnal polyuria symptoms include calcium channel blockers, diuretics, and SSRIs.

We will review patients regularly to monitor symptoms and medication:

·      We will review men taking alpha blockers at 4 to 6 weeks and then every 6 to 12 months. 

·      We will review men taking 5‑alpha reductase inhibitors at 3 to 6 months and then every 6 to 12 months. 

·      We will review men taking anticholinergics every 4 to 6 weeks until symptoms are stable, and then every 6 to 12 months. 

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guideline. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at the NICE guidelines: “Stable angina: management” (CG126), and summarise it from a Primary Care perspective.

By way of disclaimer, I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here: 

• The NICE GP YouTube Channel: NICE GP - YouTube 

The full NICE Guideline on “Stable angina: management” (CG126), can be found here: 

• Website: Overview | Stable angina: management | Guidance | NICE

 Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]   

• Music provided by Audio Library Plus  

• Watch: https://youtu.be/aBGk6aJM3IU 

Free Download / Stream: https://alplus.io/halfway-through 

Transcript  

Hello everyone and welcome. I am Fernando Florido, a GP in the United Kingdom.

Today, we'll be looking at the NICE guidelines on the management of stable angina, specifically from a primary care perspective. Proper management of angina can have a huge impact on patients' lives and that's why I'm excited to share the latest evidence-based recommendations from NICE. However, it's important to note that I'm here to provide information and interpretation of the guidelines, not medical advice. Always use your clinical judgement when treating your patients.

If you prefer a video format, there’s also a YouTube version of these episodes. The link is in the episode description.

By the way, I'll be sharing a fictitious clinical case created by chat GPT, together with their treatment management. This will give you the opportunity to see practical guidelines in action and understand how they can be applied in real-life situations

So, with that said, let's dive in!"

We will start by addressing the following:

1.    To diagnose stable angina, we follow different guidelines set out by NICE on recent-onset chest pain of suspected cardiac origin. There are also different guidelines for unstable angina and NSTEMI and acute coronary syndromes.

2.    We’ll explain to patients the factors that can provoke angina such as exertion, emotional stress, exposure to cold, and eating a heavy meal.

3.    We should also explore any misconceptions and implications for activities, cardiovascular risk, and life expectancy.

4.    We will need to advise the patient to seek medical help if there is a sudden worsening in the frequency or severity of their angina.

5.    We should give lifestyle advice and psychological support and address self-management skills such as pacing their activities and goal setting, concerns about the impact of stress, anxiety, or depression, and advice about physical exertion including sexual activity.

In terms of General principles of treatment, we will say that: 

·     Age alone should not exclude patients from treatment.

·     In terms of Preventing and Treating Episodes of Angina:

o  We will offer a short-acting nitrate to prevent and treat episodes of angina.

o  We will advise people that they should use it immediately before any planned exercise or exertion.

o  We will explain the possible side effects, such as flushing, headache and light-headedness and to sit down or find something to hold on to if feeling lightheaded and

o  We will advise them to repeat the dose after 5 minutes if necessary and call an emergency ambulance if the pain has not gone.

·     In respect of Drugs for Secondary Prevention of Cardiovascular Disease:

o  We will consider aspirin 75 mg daily, taking into account the risk of bleeding and comorbidities.

o  We will consider ACE inhibitors for people with stable angina and diabetes.

o  We will offer both antihypertensive treatment and statin therapy in line with the respective NICE guideline on the subject.

·     Regarding Dietary Supplements:

o  We will not offer vitamin or fish oil supplements and we will inform patients that there is no evidence that they help stable angina.

When it comes to general treatment recommendations:

·     Optimal drug treatment for the initial management of stable angina should consist of one or two anti-anginal drugs as necessary plus drugs for secondary prevention of cardiovascular disease.

·     The aim of anti-anginal drug treatment is to prevent episodes of angina, while the aim of secondary prevention treatment is to prevent cardiovascular events such as heart attacks and strokes.

·     We will review the response to treatment, including any side effects, 2 to 4 weeks after starting or changing drug treatment and

·     We will titrate the dose up to the maximum tolerated dose.

So let’s have a look at the Drugs for treating stable angina:

·     We should offer either a beta blocker or a calcium channel blocker as first-line treatment. The decision on which drug to use should be based on comorbidities, contraindications, and the person's preference.

·     If the patient cannot tolerate the beta blocker or calcium channel blocker, we will consider switching to the other option.

·     If the person's symptoms are not satisfactorily controlled on a single drug, we will consider either switching to the other option or using a combination of the two.

·     When combining a calcium channel blocker with a beta blocker, we will use a dihydropyridine calcium channel blocker, for example, slow release nifedipine, amlodipine, or felodipine.

·     It's essential to remember not to offer anti-anginal drugs other than beta blockers or calcium channel blockers as first-line treatment.

·     If the person cannot tolerate beta blockers and calcium channel blockers, or both are contraindicated, we will consider monotherapy with one of the following drugs:

o  a long-acting nitrate,

o  ivabradine,

o  nicorandil, or

o  ranolazine.

o  Deciding which drug to use should be based on comorbidities, contraindications, the person's preference, and drug costs.

·     Adding a third anti-anginal drug those whose angina is controlled with two anti-anginal drugs is not recommended.

·     However, it's worth considering adding a third anti-anginal drug only when the symptoms are not controlled with two anti-anginal drugs. Deciding which drug to use should be based on comorbidities, contraindications, the person's preference, and drug costs.

Now let’s discuss the recommendations on revascularisation procedures when symptoms are not satisfactorily controlled with optimal medical treatment. And these procedures would be either a coronary artery bypass graft [CABG] or a percutaneous coronary intervention [PCI])

In addition, we can offer coronary angiography to guide our treatment strategy.

The main purpose of revascularisation is to improve the symptoms of stable angina. However, it is important to explain to the patient that repeat revascularisation may be necessary after either CABG or PCI, and the rate is lower after CABG. Stroke is uncommon after either CABG or PCI, and the incidence is similar between the two procedures.

We will offer CABG in suitable patients if symptoms are not controlled with medical treatment, and PCI is not appropriate.

We will offer PCI to suitable patients if symptoms are not controlled with medical treatment, and CABG is not appropriate.

We will take into account that PCI may be more cost-effective than CABG.

However, in Multivessel Disease, we need to be aware of the potential survival advantage of CABG over PCI for those who have diabetes or are over 65 years or have anatomically complex three-vessel disease.

If symptoms are controlled with medical treatment, prognosis without further intervention should be discussed with their cardiologist.

In terms of Pain interventions, we should not offer transcutaneous electrical nerve stimulation (TENS), enhanced external counterpulsation (EECP), and acupuncture.

Now, let’s address Stable angina that has not responded to treatment:

In these cases, it's important to provide comprehensive re-evaluation and advice. This may include:

·     exploring the impact of symptoms on their quality of life, and reviewing the diagnosis while considering non-ischaemic causes of pain.

·     Additionally, it's essential to review drug treatment and consider future drug treatment and revascularisation options.

·     It's also important to acknowledge the limitations of treatment and explain the self-management of the pain. Specific attention should be given to the role of psychological factors in pain, and skills to modify cognitions and behaviours associated with pain.

Cardiac syndrome X

In people with angiographically normal coronary arteries and continuing anginal symptoms, we need to consider a diagnosis of cardiac syndrome X. This condition can be challenging to diagnose, and additional testing may be necessary.

If a patient is diagnosed with suspected cardiac syndrome X, we will continue drug treatment for stable angina only if it improves their symptoms.

We will not routinely offer secondary prevention drugs in suspected cardiac syndrome X. This is because the effectiveness of these drugs in this population is uncertain, and they may cause unnecessary side effects.

Right, so now, let’s have a look at our fictitious clinical case created by chat GPT:

The Patient is John Smith, a 55-year-old man who has just been diagnosed with stable angina.

John has a history of hypertension, high cholesterol, and type 2 diabetes, which is well-controlled with metformin 1000mg twice daily. He has been experiencing chest pain and shortness of breath during exertion for the past 6 months. He is a non-smoker and leads an active lifestyle, but his symptoms are affecting her ability to exercise.

Recent test results: John's most recent blood pressure reading was 148/86 mmHg. His cholesterol levels were 5.8 mmol/L (224 mg/dL), with LDL cholesterol of 3.9 mmol/L (151 mg/dL) and HDL cholesterol of 1.4 mmol/L (54 mg/dL). His HbA1c level was 6.5% (48 mmol/mol).

How should he be treated?

In terms of preventing and treating episodes of angina, we offered John short-acting nitrates to be used immediately before any planned exercise or exertion in the form of a sublingual GTN spray. We advised him to repeat the dose after 5 minutes if necessary and call an emergency ambulance if the pain had not gone. We explained the possible side effects of the medication, such as flushing, headache, and light-headedness, and advised him to sit down or find something to hold on to if feeling lightheaded.

In respect of drugs for secondary prevention of cardiovascular disease, we started John on aspirin 75mg daily, taking into account his risk of bleeding. We also considered ACE inhibitors for John, as he has stable angina and diabetes and he was started on a small dose of lisinopril 2.5 mg daily. In terms of statin therapy, he was started on atorvastatin 80 mg daily for secondary prevention in line with NICE guidance on the subject.

We advised him that there is no evidence to support the use of dietary supplements such as vitamin or fish oil supplements in treating stable angina, and therefore did not prescribe them. The patient was also lifestyle advice.

For treating John's stable angina, both a beta blocker and a calcium channel blocker were considered as first-line treatment. Because of the patient’s concerns on erectile dysfunction, we decided to use a small dose of a CCB, felodipine 2.5mg daily as he had no contraindications to using this medication. We will titrate it against his symptoms up to the maximum tolerated dose.

John's case will be reviewed 2 to 4 weeks after starting his new medication to assess his response to treatment, including any side effects. We will also monitor his blood pressure, cholesterol, and HbA1c levels to ensure they are within the recommended targets.

In conclusion, the management of stable angina requires a comprehensive approach that addresses both the underlying cardiovascular disease and the patient's individual risk factors. By following the general principles of treatment and tailoring the treatment plan to the patient's specific needs, we can help to reduce the risk of cardiovascular events and improve their quality of life.

Please keep in mind that this is only a summary and my interpretation of the guideline. 

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye  

The video version of this podcast can be found here:

·      https://youtu.be/pxOeszuHRsI

This episode makes reference to guidelines produced for NHS Greater Glasgow and Clyde and Liverpool University Hospitals NHS Trust. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the management of hypocalcaemia, in particular, we will look at the guidance on the management of hypocalcaemia in NHS Greater Glasgow and Clyde and in Liverpool University Hospitals NHS Trust, always focusing on what is relevant in Primary Care only.  

I am not giving medical advice; this episode is intended for health care professionals; it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

●      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

●      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

●      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

●      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

●      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

There is a YouTube version of this and other videos that you can access here: 

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk 

The resources consulted can be found here:

The guidance on the management of hypocalcaemia by Liverpool University Hospitals NHS Trust can be found here:

·      https://pathlabs.rlbuht.nhs.uk/Guideline%20for%20Treating%20and%20Monitoring%20Hypocalcaemia%20for%20non-critical%20areas%20of%20Trust.pdf

The guidance on the management of hypocalcaemia by the Adult Therapeutics Handbook for the NHS Greater Glasgow and Clyde can be found here:

·      https://handbook.ggcmedicines.org.uk/guidelines/electrolyte-disturbances/management-of-hypocalcaemia/

Calcium – The Lancet - Bushinksy DA, Monk RD. Calcium. Lancet 1998; 352 (9124): 306-311:

·      https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(97)12331-5/abstract 

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. 

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to go through the management of hypocalcaemia, in particular, we will look at the guidance on the management of hypocalcaemia in NHS Greater Glasgow and Clyde, and in Liverpool University Hospitals NHS Trust, always focusing on what is relevant in Primary Care only. The links to their guidelines and the other sources consulted are in the episode description. 

Right, without further ado, let’s jump into it. 

As a quick overview of calcium metabolism, I will simply say that it is tightly regulated by vitamin D and the parathyroid hormone or PTH. Active vitamin D or calcitriol enhances intestinal calcium absorption and PTH both enhances calcium reabsorption in the kidneys, and releases calcium from the bones by increasing osteoclast activity and bone resorption. 

Both phosphate and magnesium can also affect calcium levels. For example, a low magnesium can impair PTH secretion and action, resulting in hypocalcaemia.  

On the other hand, a high phosphate, like seen in CKD, can lead to the precipitation of calcium with phosphate and the consequent reduction in serum calcium and hypocalcaemia.

Right, now that we have done this review, let’s now look at hypocalcaemia itself.

The reference range for adjusted serum calcium is 2.2 - 2.6mmol/L.

Symptoms of hypocalcaemia, typically develop when serum adjusted calcium falls below 1.9mmol/L. However, this threshold varies and symptoms also depend on the rate of fall. 

So, we will talk of hypocalcaemia when we have an adjusted serum calcium less than 2.2 mmol/L, although you should always take into account your local path lab reference range.  

The cause of hypocalcaemia may be varied depending on whether we are talking about acute or chronic hypocalcaemia. And we must remember that hypocalcaemia is far less common than hypercalcaemia because of the role of the bones as a calcium reserve to maintain homeostasis. 

So, let’s look at causes of acute hypocalcaemia first. The most common cause is hyperventilation which induces transient hypocalcaemia with normal serum total calcium levels normal. Let’s quickly see why this is the case. 

• When a person hyperventilates, they breathe out excessive CO₂ which leads to a decrease of carbonic acid, and respiratory alkalosis.
• Alkalosis causes more calcium to bind to albumin, reducing the concentration of free (ionized) calcium. Given that the ionized form is the physiologically active form, this decrease leads to symptoms of hypocalcaemia.
• However, despite the decrease in ionized calcium, the total serum calcium remains normal because this value includes the calcium bound to albumin. 

Other less common causes are:

·      Other forms of alkalosis.

·      Medications, for example post IV bisphosphonate or denusomab treatment

·      A high phosphate. We have to remember that phosphate and calcium often behave like two parts of a seesaw, where changes in one can inversely affect the other. Therefore, hypocalcaemia can be seen in clinical situations where phosphate is high, like in:

• rapid tumour lysis – like e.g. during cytotoxic treatment of leukaemia or
• in excessive phosphate intake – like for example excessive phosphate containing enemas.
• And finally, another less common cause of hypocalcaemia is acute pancreatitis. 

Let’s now look at the causes of chronic hypocalcaemia. And the most common cause is a decrease in levels of active vitamin D. This could be because there is:

• An overall vitamin D deficiency, like in dietary causes, malabsorption, and lack of sunlight or
• A reduction in the active form of vitamin D or calcitriol, due to poor renal conversion as seen in CKD

Less common causes are:

• hypoparathyroidism which can be post-surgical, autoimmune, genetic, idiopathic etc.
• hypomagnesaemia, because low magnesium impair the secretion and function of PTH, giving rise to a functional hypoparathyroidism.
• Pseudohypoparathyroidism, which is a rare, genetic disorder characterized by the body’s resistance to PTH despite normal or elevated PTH levels and finally
• low plasma albumin caused by, for example, malnutrition, or liver disease. However, it is worth mentioning that a low plasma albumin can lead to low total calcium levels but it does not cause true hypocalcaemia (understood as a low ionized or free calcium). Instead, it leads to pseudohypocalcaemia, where only the bound calcium is reduced, so patients typically do not experience symptoms of low calcium unless their ionized calcium is also low.

It is also worth mentioning that dietary lack of calcium intake is a very rare cause of hypocalcaemia. 

What are the symptoms and signs of hypocalcaemia?

Well, the clinical features of hypocalcaemia are connected to its effects on the nerves and muscles. Typical features include: 

·      Effects on the nervous system like:

• Paraesthesia
• convulsions which may occur because hypocalcaemia lowers the seizure threshold, and
• psychiatric effects, from general malaise to overt psychosis in chronic hypocalcaemia
• Effects on the muscles like:
• painful cramps
• tetany, which may result in spontaneous muscular spasms largely precipitated by exercise
• laryngeal spasm causing stridor, and obstructive respiratory symptoms and
• latent tetany, which may be demonstrated by Trousseau's and Chvostek's signs. Let’s quickly have a look at them:

For Trousseau’s sign, a blood pressure cuff is inflated usually about 20 mm Hg above the systolic BP, and it is left inflated for about 3 minutes. A positive sign is indicated by involuntary contraction of the muscles in the hand and fingers, known as carpal spasm or "Trousseau’s phenomenon." 

On the other hand, Chvostek's sign is performed by tapping on the facial nerve just in front of the ear, at the angle of the jaw, which is the area where the facial nerve crosses the masseter muscle. A positive sign is indicated by twitching of the facial muscles on that same side.  

Both Trousseau's and Chvostek's signs are indicative of increased neuromuscular excitability, which is often associated with hypocalcemia, although not exclusively. 

Other features of chronic hypocalcaemia depend on the underlying cause. They can be very varied so I will mention only a few like:

• candidiasis
• nail dystrophy
• alopecia, and
• rickets or osteomalacia - from chronic vitamin D deficiency

What investigations should be carried out in primary care if we find hypocalcaemia? And we are obviously talking about mild asymptomatic hypocalcaemia because patients with severe or symptomatic hypocalcaemia should be referred to hospital. 

Initial investigations should include as a minimum: 

• A repeat serum adjusted calcium and phosphate
• Parathyroid hormone (PTH)
• Urea and electrolytes
• Magnesium
• Vitamin D and
• A 12-lead ECG as there is a significant likelihood of QT prolongation, in which case cardiac monitoring may be required.

We should monitor calcium concentrations regularly to judge response and review treatment. Serum bone profile should be checked regularly according to clinical judgement, perhaps weekly or fortnightly depending on the case until concentrations are stable. 

Let’s now have a look at the treatment of hypocalcaemia. 

The treatment depends on the severity of symptoms and underlying condition: 

• treatment generally invovles administration of calcium. How calcium is administered and the need for additional agents such as vitamin D depends on the acuity and severity of the hypocalcaemia as well as the underlying cause.
• Severe Hypocalcaemia, that it, a serum adjusted calcium <1.9mmol/L and/or symptomatic hypocalcaemia should be treated as a medical emergency because it can be life-threatening. So, these patients should be referred to hospital for the administration of IV calcium.
• Chronic, Asymptomatic Mild Hypocalcaemia, that is, serum adjusted calcium between 1.9 - 2.2mmol/L is treated with oral calcium and often vitamin D supplements.
• Because calcium binds with dietary phosphate and oxalate we should advise patients that calcium is better absorbed when taken between meals.
• oral calcium is given to increase its availability and, often, vitamin D to enhance absorption.
• calcium carbonate is widely available in tablet form and we should aim for a daily dose of 1-2.6 g and then adjust according to response.
• Examples of calcium carbonate supplements are adcal and calcichew.
• NHS Greater Glasgow and Clyde recommend starting Calcichew Forte Chewable, 2 tablets twice a day, which is an unlicensed dose, and adjust the dose according to the patient’s requirements. As soon as it is appropriate, we should prescribe the licensed dose of 1 tablet daily.
• Alternatively, Liverpool Hospitals recommend starting oral calcium and vitamin D supplements such as Adcal D3 (2 to 4 tab daily) with monitoring and adjustment.
• calcium citrate and calcium phosphate should be avoided because they may cause problems, especially in patients with renal failure.
• If the patient is vitamin D deficient, we will start oral vitamin D supplementation with loading doses of colecalciferol as per the NICE guideline on vitamin D deficiency.
• vitamin D2 or ergocalciferol and vitamin D3 or colecalciferol at doses of 400 units a day are adequate to avoid nutritional deficiency, although higher doses may be needed in malabsorption.
• However, they require conversion to the active form calcitriol and therefore they are not suitable if the alpha-hydroxylation process is impaired, like for example in renal failure. In these cases, we should be guided by the renal team.
• Other general principles that apply to the management of hypocalcaemia are:
• magnesium levels should be checked and corrected if low. If patient has hypomagnesaemia, we should stop any precipitating drug and admit the patient to hospital for the administration of IV magnesium.
• patients on digoxin should be monitored carefully because administration of calcium may lead to digoxin toxicity and death
• Patients with hypoparathyroidism have decreased renal calcium reabsorption and oral calcium supplementation, may lead to hypercalciuria with possible nephrocalcinosis or kidney stones. Therefore, in hypoparathyroidism, the treatment should be guided by endocrinology.
• If hypocalcaemia is secondary to post-thyroidectomy, we will also seek specialist advice.
• When calcium is given to patients with hyperphosphataemia, there is a risk of soft-tissue calcium phosphate precipitation, so we should get specialist advice on the use of phosphate binders. Calcium supplements may have to be delayed until phosphate levels come down.

Right, so that is it. We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.  

Thank you for listening and goodbye.

The video version of this episode can be found here:

·      https://youtu.be/myqMGzw4SUQ

The original video that this episode is based on can be found here:

·      https://youtu.be/VFiwyS1c3yk?si=Y-iz5dqx1KUKDXF8

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I use AI voices to discuss the issue of raised alkaline phosphatase levels. There are 3 parts and this is part 1.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

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There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

You can download a summary of my summary / interpretation of the guidance here:

·      My Summary: https://1drv.ms/b/s!AiVFJ_Uoigq0mC4pm_bYELFa9wEx?e=07p2dJ

My name is Fernando Florido and I am a GP in the United Kingdom. In this video I go through the Visual summary “choosing medicines for first-line and further treatment” corresponding to the 2022 updated NICE Guideline: Type 2 diabetes in adults: management (NG28 guideline), updated on 29^th June 2022. The video focuses on the drug treatment recommendations in blood glucose management in adults with Type 2 Diabetes.

This podcast will be saved on a website. 

There is also a YouTube video on this subject and other NICE guidance. You can access the channel here:

https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw

This podcast also appears in the Diabetes in Primary Care podcast which can be found here:

·      Redcircle: https://redcircle.com/shows/diabetes-in-primary-care

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/us/podcast/diabetes-in-primary-care/id1562910252

NICE Guideline NG28 can be found here:

https://www.nice.org.uk/guidance/ng28

The full NG28 full guideline PDF document can be found here:

·      Website:

https://www.nice.org.uk/guidance/ng28/resources/type-2-diabetes-in-adults-management-pdf-1837338615493

·      If outside the UK, you can download it here: https://1drv.ms/b/s!AiVFJ_Uoigq0lWqK_tYk1rnOolRO

The visual summary “choosing medicines for first-line and further treatment” can be found here:

·      Website:

https://www.nice.org.uk/guidance/ng28/resources/visual-summary-full-version-choosing-medicines-for-firstline-and-further-treatment-pdf-10956472093

·      If outside the UK, you can download it here: https://1drv.ms/b/s!AiVFJ_Uoigq0lWugUmhgaYv1PHyf

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Transcript

Thank you for listening and welcome to a new episode of this podcast bringing medical information and NICE guidance from a primary care perspective. My name is Fernando Florido and I am a GP in the United Kingdom.

Now, imagine that we have Mr. Johnson, who is 78 and has type 2 diabetes. His diabetes control is reasonable or metformin, 500mg BD. With an HbA1c of 7.1% or 54 mmol/mol, but he has just developed stable angina. How should his diabetic treatment change? We have covered the 2022 NICE diabetes management update in previous episodes, but perhaps we need a quick reminder?

And this is what we’re going to do today because in this video I am going to go through the flow charts produced by NICE in respect of the blood glucose management in type 2 diabetes. The full guideline has 59 pages in a PDF format and NICE has produced a 5-page summary on the blood glucose management. This video is going to focus on the two flow charts that will advise how to choose first line medicines and how to choose medicines for further treatment.

I will put in the description below a link to download the full NICE guideline as well as the five-page summary. There is a YouTube version of this episode and other NICE guidance on the NICE GP YouTube Channel and a link to access it can be found in the podcast description. Because of the visual nature of the flow chart, I would highly recommend watching the YouTube video if you can.

Although describing visual aids as audio files can be challenging, I hope that you find the content clear and informative.

Now the first flow chart that we are going to look at is the one about how to choose first line medicines. It is only one page and there is a combination of arrows that will guide us through the treatment pathways and a number of boxes with further information and clarification on the treatments described.

Right at the top of the chart, we find a box that tells us about rescue therapy and it reminds us that for patients with symptomatic hyperglycaemia, we will consider insulin or a sulphonylurea and then review the treatment when their blood glucose control has been achieved.

Then the next step is to assess the HbA1c, the cardiovascular risk and kidney function. Obviously, as you know, to calculate the cardio vascular risk with, for example, the QRISK2 tool, we will need to know the patient’s age, sex, smoking status, blood pressure and the total cholesterol/HDL ratio.

Now, having checked the renal function, before starting to follow the pathway, there is a little box on the left telling us that for information on using SGLT 2 inhibitors for people with type 2 diabetes and CKD, there is specific guidance that is not on this flow chart and we will have to refer to CKD section of the diabetic guideline.

So, after we have done our initial assessment with the HbA1c, cardiovascular risk and kidney function, the flow chart divides into three categories. One, it could be that the patient is not at high cardiovascular risk. Two, that the patient has chronic heart failure or established atherosclerotic cardio vascular disease. Or three, that the patient has a high risk of cardiovascular disease, which is defined as a QRISK 2 of 10% or higher over ten years, or an elevated lifetime risk.

Now, the first pathway would be when the patient is not at high risk of cardio vascular disease and for these patients, we will offer metformin, or, if there are gastrointestinal side effects, we will give Metformin slow release. Now if metformin is contraindicated, we will consider one of the other antidiabetic agents, either a DPP-4 inhibitor, pioglitazone or a sulphonylurea, although it does also tell us that SGLT 2 inhibitors can also be given as monotherapy for some patients. Basically, NICE recommends an SGLT 2 inhibitor as monotherapy in people who can’t take metformin and for whom the diabetic control is poor, and only if a DPP-4 inhibitor would otherwise be prescribed and a sulphonylurea or pioglitazone is not appropriate. So, it is fairly restrictive.

We also see a small note saying that using your ertugliflozin to reduce cardiovascular risk when the blood glucose is well controlled was an off-label use.

So, if no cardiovascular risk, we give metformin first and if contraindicated one of the other agents, sulphonylurea, pioglitazone, DPPG4 inhibitors of an SGLT2 inhibitor, although the latter with a few restrictions.

Now the second pathway would be when the patient has got chronic heart failure or established atherosclerotic cardiovascular disease. And the flow chart tells us in a box what they actually mean by established atherosclerotic cardiovascular disease, and this is fairly intuitive. It includes CHD, acute coronary syndrome, previous MI, stable angina, prior coronary or other revascularisation, cerebrovascular disease, which includes both ischemic stroke and TIAs and finally, peripheral arterial disease. So, for those patients, we will do very similar. We will start with metformin or if there are gastrointestinal side effects, we will give Metformin slow release and then, as soon as metformin tolerability is confirmed, we will offer an SGLT 2 inhibitor with proven cardiovascular benefit. And this is because SGLT 2 inhibitors have now been found to reduce cardio vascular events. However, if metformin is contraindicated, then we will give an SGLT 2 inhibitor alone. So, this is fairly straight forward.

Finally, the third option after the initial assessment is that the patient has not got cardiovascular disease but is at high risk of it. In this case, the flow chart is basically fairly similar. We will give metformin or, if there are side effects, metformin slow release and then as soon as metformin tolerability is confirmed we will consider an SGLT 2 inhibitor with proven cardiovascular benefit. And also, if metformin is contraindicated, we will consider an SGLT 2 inhibitor alone.

So, you may ask what is the difference between those two, having cardiovascular disease and being at high risk of CVD? And the difference is basically that, if the patient has got cardiovascular disease or heart failure, we will definitely offer an SGLT 2 inhibitor, whereas if a patient is only at high risk of cardiovascular disease, we will consider it. But in practice you will probably find that pathways are exactly the same, because you’re going to consider it seriously and you're going to give it unless a contraindication or other major consideration.

In the middle of the flow chart there’s a little box that reminds us that we always have to start metformin alone to assess tolerability before adding an SGLT 2 inhibitor. So, metformin is always the start.

So, this is really the flowchart on how to choose first line medicines. After this, if the person’s HbA1c is not controlled below the target or a person develops cardio vascular disease or a high risk of cardiovascular disease, then we will move to the second flow chart, which is the one about treatment options if further interventions are needed.

So, there we go. The second flow chart which is on how to choose medicines for further treatment.

Here, at the beginning, there’s another box telling us again about rescue therapy and using insulin, or a sulphonylurea for symptomatic hyperglycaemia until the levels are controlled.

Now, if further treatment options are needed, it will be because either at any point the HbA1c is not well controlled, or at any point, the cardio vascular risk or cardiovascular status change.

Right, we’re going to start with the cardiovascular risk of cardiovascular status change and we’ve got two options. The first one is that the person has or develops chronic heart failure or established atherosclerotic cardiovascular disease, and the second one is that the person develops a high risk of cardiovascular disease.

If the person has or develops chronic heart failure or established atherosclerotic cardiovascular disease, we will basically switch or add treatments to make sure that we offer an SGLT 2 inhibitor if this is not already prescribed. So, if the person develops the condition, we will either add an SGLT 2 inhibitor if the HbA1c could do with lowering further or, if the HBA 1C, is fairly low and we don’t want to lower it any more then we will switch one of the existing drugs for an SGLT 2 inhibitor.

On the other hand, if the person has or develops a high risk of cardio vascular disease, then we will consider an SGLT 2 inhibitor when switching or adding treatments. So, like before in the previous flow chart, giving an SGLT2 is slightly more imperative when the person has developed cardiovascular disease, whereas, if the person is just at a high risk, we will only consider it. But again, in practice it may not make much difference.

Now, if at any point the HbA1c is not well controlled, there is a box that  tells us that we will switch or add treatments from different drug classes up to triple therapy or dual therapy if metformin is contraindicated. So basically, we will consider any combination to dual or triple therapy of the antidiabetic agents, that is, either a DPP 4 inhibitor, pioglitazone or a sulphonylurea, although it also tells us that SGLT 2 inhibitors may also be an option both in dual therapy or triple therapy.

Now you may ask when should we start insulin? Well at the bottom left corner we find a box that tells us that, when dual therapy is not enough to control the HbA1c, we can consider insulin-based therapy, with or without other drugs and there is additional guidance on how to use insulin with SGLT 2 inhibitors. So basically, if a patient goes up to dual therapy and is not well controlled, you may consider triple therapy if the patient is on metformin or just consider insulin as the next step.

And finally, what is happening to GLP 1 mimetics? Well, this is where NICE has been quite restrictive in their approach because it tells us that if triple therapy with metformin and two other oral drugs is not enough, we will consider triple therapy by switching one drug for a GLP 1 mimetic, but only for people:

·      who have a BMI of 35 or higher and specific psychological or other medical problems associated with obesity, although it does say that you can adjust the BMI to lower for people from Black, Asian and other minority ethnic groups, because these groups are at higher risk of cardiovascular disease and GLP mimetics have also been shown to reduce cardiovascular events, or

·      we can give it to patients who have a BMI lower than 35 and for whom:

o   insulin therapy would have a significant occupational implication or

o  weight loss would benefit other significant obesity related comorbidities.

Right, so this is it, we have finished our second flow chart and therefore we have come to the end of this episode, I hope that you have found it useful. There is also a YouTube version in the NICE GP YouTube Channel and I will leave a link in the podcast description. Thank you for listening and I hope that you will join me in the next one. Goodbye.

Episode: Chronic obstructive pulmonary disease in over 16s: diagnosis and management

NICE guideline [NG115]Published: 05 December 2018 Last updated: 26 July 2019

My name is Fernando Florido and I am a GP in the United Kingdom. In this podcast I go through the NICE Guideline: Chronic obstructive pulmonary disease in over 16s: diagnosis and management (NG115 guideline), updated on 26^th July 2019.

This podcast will be saved on a website.

There is also a YouTube video on this subject and other NICE guidance. You can access the channel here:

https://www.youtube.com/channel/UClrwFDI15W5uH3uRGuzoovw

NICE Guideline NG115 can be found here:

https://www.nice.org.uk/guidance/NG115

Other links referred to in this episode: 

·      guideline on antimicrobial prescribing for acute exacerbations of COPD

·      visual summary covering non-pharmacological management and use of inhaled therapies

·      MRC breathlessness scale 1959

·      NICE guideline on asthma

·      visual summary covering non-pharmacological management and use of inhaled therapies

·      asthmatic features/features suggesting steroid responsiveness

·      MHRA safety advice on Respimat and Handihaler inhalers

·      NICE's technology appraisal guidance on roflumilast for treating chronic obstructive pulmonary disease

·      NICE technology appraisals on oseltamivir, amantadine (review) and zanamivir for the prophylaxis of influenza

·      amantadine, oseltamivir and zanamivir for the treatment of influenza

·      NICE interventional procedures guidance on lung volume reduction surgery, endobronchial valves

·      endobronchial coils

·      British Thoracic Society recommendations

·      NICE guideline on antimicrobial prescribing for acute exacerbations of COPD

·      recommendations on systemic corticosteroids 

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Transcript

Thank you for downloading and welcome. This podcast is intended for healthcare professionals and it brings you medical information about clinical guidelines by the National Institute for Clinical Excellence or NICE from a Primary Care perspective. My name is Fernando Florido and I am a GP in the United Kingdom.

In this episode I am going to tell you about the NICE guidelines on Chronic obstructive pulmonary disease in over 16s: diagnosis and management (this is the NG115 guideline). These guidelines were last updated in July 2019. NICE checked this guideline in January 2022 and it was decided that it did not need to be updated at that time.

In this episode I am going to summarise the main body of the guideline. You may be aware that many clinicians and formularies now rely on the management recommendations produced by the Global initiative for obstructive lung disease, also known as GOLD, which some say are more easily applied in practice than the NICE recommendations. The NICE recommendations do not contradict the GOLD report, but there are some who say that they are much more concise in their approach. Considering that the PDF document of this NICE guideline is 72 pages long, that is quite a statement. However, stay tuned because I intend to create another episode in future on the GOLD guidelines.

I have also uploaded YouTube videos on this subject and other NICE guidance. A link to access the YouTube channel can be found in the episode description.

As ever, all information is correct at the time of recording and all views and opinions are my own. I hope that you enjoy this episode.

Right, this guideline covers diagnosing and managing chronic obstructive pulmonary disease or COPD (which includes emphysema and chronic bronchitis) in people aged 16 and older. It aims to help people with COPD to receive a diagnosis earlier so that they can benefit from treatments to reduce symptoms, improve quality of life and keep them healthy for longer.

NICE has also produced a guideline on antimicrobial prescribing for acute exacerbations of COPD and a visual summary covering non-pharmacological management and use of inhaled therapies.  I will put the links to these two in the episode description.

The recommendations in terms of Diagnosing COPD are as follows:

The diagnosis of COPD is suspected on the basis of symptoms and signs and is supported by spirometry.

IN terms of Symptoms

We will suspect a diagnosis of COPD in people over 35 who have a risk factor (generally smoking or a history of smoking) and who present with 1 or more of the following symptoms:

·      exertional breathlessness

·      chronic cough

·      regular sputum production

·      frequent winter 'bronchitis'

·      or wheeze. 

One of the primary symptoms of COPD is breathlessness. The Medical Research Council (MRC) dyspnoea scale (see table 1) should be used to grade the breathlessness according to the level of exertion required to elicit it. I will put the link to this table in the episode description. The scale goes from 1 to 5 where 1 means minimal breathlessness and 5 disabling breathlessness.

So, In the MRC dyspnoea scale

Grade 1

Means that the person is not troubled by breathlessness except on strenuous exercise

Grade 2

Means that the person is short of breath when hurrying or walking up a slight hill

Grade 3

Is when the person walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace

Grade 4

Is when the person needs to stop for breath after walking about 100 metres or after a few minutes on level ground

And Grade 5

Is when the person is too breathless to leave the house, or is breathless when dressing or undressing

In respect of Spirometry

We need to perform spirometry:

·      at diagnosis

·      to reconsider the diagnosis, for people who show an exceptionally good response to treatment

·      to monitor disease progression. 

We will measure post-bronchodilator spirometry to confirm the diagnosis of COPD. An FEV1/FVC ratio below 0.7 is typical in COPD

We will also think about alternative diagnoses or investigations for older people who have an FEV1/FVC ratio below 0.7 but do not have typical symptoms of COPD. 

And we will think about a diagnosis of COPD in younger people who have typical symptoms of COPD, even when their FEV1/FVC ratio is above 0.7. 

If we encounter Incidental findings on chest X‑ray or CT scans

We will consider primary care respiratory review and spirometry for people with emphysema or signs of chronic airways disease on a chest X-ray or CT scan. 

If the person is a current smoker, their spirometry results are normal and they have no symptoms or signs of respiratory disease:

·      we will offer smoking cessation advice and treatment

·      we will warn them that they are at higher risk of lung disease

·      we will advise them to return if they develop respiratory symptoms

·      So all this is if the person is a smoker. However

If the person is not a current smoker, their spirometry is normal and they have no symptoms or signs of respiratory disease:

·      We will ask them if they have a personal or family history of lung or liver disease and consider alternative diagnoses, such as alpha‑1 antitrypsin deficiency

·      We will reassure them that their emphysema or chronic airways disease is unlikely to get worse but

·      We will advise them to return if they develop respiratory symptoms

For both situations, smokers and non-smokers, we need to be aware that the presence of emphysema on a CT scan is an independent risk factor for lung cancer. 

IN terms of Further investigations

in addition to spirometry all patients should have:

·      a chest X-ray to exclude other pathologies

·      a full blood count to identify anaemia or polycythaemia

·      their body mass index (BMI) calculated. 

·      So these three investigations should always be carried out but

We will perform additional investigations when needed, and these investigations will be

Sputum culture

if sputum is purulent

Serial home peak flow measurements

To exclude asthma if diagnostic doubt remains

ECG and serum natriuretic peptides

To assess cardiac status if cardiac disease or pulmonary hypertension are suspected because of:

·      a history of cardiovascular disease, hypertension or hypoxia or

·      clinical signs such as tachycardia, oedema, cyanosis or features of cor pulmonale

Echocardiogram

To assess cardiac status if cardiac disease or pulmonary hypertension are suspected

CT scan of the thorax

To investigate symptoms that seem disproportionate to the spirometric impairment

To investigate signs that may suggest another lung diagnosis (such as fibrosis or bronchiectasis)

To investigate abnormalities seen on a chest X-ray and

To assess suitability for lung volume reduction procedures

Serum alpha-1 antitrypsin

To assess for deficiency if there is early onset, minimal smoking history or family history

Transfer factor for carbon monoxide (TLCO)

To investigate symptoms that seem disproportionate to the spirometric impairment and

To assess suitability for lung volume reduction procedures

In terms of Reversibility testing we will say that

For most people, routine spirometric reversibility testing is not necessary as part of the diagnostic. It may be unhelpful or misleading because:

·      repeated FEV1 measurements can show small spontaneous fluctuations

·      the results of a reversibility test performed on different occasions can be inconsistent and not reproducible

·      over-reliance on a single reversibility test may be misleading unless the change in FEV1 is greater than 400 ml

·      response to long-term therapy is not predicted by acute reversibility testing. 

Untreated COPD and asthma are frequently distinguishable on the basis of history (and examination) in people presenting for the first time. Whenever possible, we will use features from the history and examination to differentiate COPD from asthma.

These six Clinical features differentiating COPD and asthma are as follows

For example

COPD

Asthma

1- being a smoker or ex-smoker

Is a feature in almost all COPD patients

Whereas it is only possible in asthma

2- Symptoms under age 35

are Rare in COPD

Whereas they appear often in asthma

3- Chronic productive cough

Is common in COPD

But uncommon in asthma

4- Breathlessness

Is persistent and progressive in COPD

Whereas it is variable in asthma

5- Night time waking with breathlessness and/or wheeze

Is uncommon in COPD

Whereas it is common in asthma

6- Significant diurnal or day-to-day variability of symptoms

Is uncommon in COPD

Whereas it is common in asthma

For more information on diagnosing asthma you can refer to the NICE guideline on asthma and I will put a link to this in the episode description.

In addition to these six features, we can use the regular observation of symptoms or spirometry or peak flow readings to help differentiate COPD from asthma. 

And when diagnostic uncertainty remains, or we suspect that both COPD and asthma are present, we will use the following findings to help identify asthma:

1.    a response to bronchodilators or to 30 mg oral prednisolone daily for 2 weeks of over 400 ml in the FEV1.

2.    Or serial peak flow measurements showing 20% or greater diurnal or day-to-day variability.

In addition, we will conclude that clinically significant COPD is not present if the FEV1 and FEV1/FVC ratio return to normal with drug therapy and we will reconsider the diagnosis of COPD for people who report a marked improvement in symptoms in response to inhaled therapy. 

If diagnostic uncertainty remains, we will think about referral for more detailed investigations, including imaging and measurement of transfer factor for carbon monoxide (TLCO). 

It is also important to assess and classify the severity of airflow obstruction

For people for whom the FEV1/FVC ratio is <0.7 we will classify the severity of airflow obstruction according to the reduction in FEV1, and this is

Gradation of severity of airflow obstruction

If

FEV1≥ 80% predicted

It will be Stage 1 – Mild

FEV1 50–79% predicted

It will be Stage 2 – Moderate

FEV1 30–49% predicted

It will be Stage 3 – Severe

FEV1 <30% predicted

It will be Stage 4 – Very severe (or FEV1 below 50% with respiratory failure)

In trying to Identify early disease

We should perform spirometry in people who are over 35, current or ex‑smokers, and have a chronic cough. 

We will consider spirometry in people with chronic bronchitis given that a significant proportion of these people will go on to develop airflow limitation. 

We will refer patients for the following reasons:

If There is diagnostic uncertainty or there is severe COPD or cor pulmonale

In order to Confirm the diagnosis and optimise the therapy

We will also refer For Assessment for oxygen therapy long term nebuliser therapy or corticosteroid therapy

In order to Optimise therapy and measure blood gases

If there is Bullous lung disease, For Assessment for a lung volume reduction procedure and For Assessment for lung transplantation

In order to Identify candidates for intervention

We will also refer If there is A rapid decline in FEV1 and for pulmonary rehabilitation and If the Symptoms are disproportionate to the lung function deficit or if there is Dysfunctional breathing

In order to Look for other explanations

Finally we will refer If there is Onset of symptoms under 40 years or a family history of alpha‑1 antitrypsin deficiency

In order to Identify alpha‑1 antitrypsin deficiency

If there are Frequent infections

In order to Exclude bronchiectasis

If there is Haemoptysis

In order to Exclude carcinoma of the bronchus

When it comes to Managing stable COPD

NICE has produced a visual summary covering non-pharmacological management and use of inhaled therapies and I will put a link to this in the episode description.

This management includes Smoking cessation and for this we need to

Document an up-to-date smoking history, including pack years smoked (which is the number of cigarettes smoked per day, divided by 20 cigarettes in a pack, multiplied by the number of years smoked)

At every opportunity, we will advise and encourage to stop, and offer them help to do so. 

So, unless contraindicated, we will offer nicotine replacement therapy, varenicline or bupropion as appropriate to people who want to stop smoking, combined with an appropriate support programme

In terms of Inhaled therapy

We will use short-acting bronchodilators, as necessary, as the initial empirical treatment to relieve breathlessness and exercise limitation. This can include Short-acting beta2 agonists (SABA) and short-acting muscarinic antagonists (SAMA)

If we are considering Inhaled corticosteroids (ICS)

We need to discuss with the person, the risk of side effects (including pneumonia) of inhaled corticosteroids for COPD and

We will not use oral corticosteroid reversibility tests to identify which people should be prescribed inhaled corticosteroids, because they do not predict response to inhaled corticosteroid therapy. 

If we are considering Inhaled combination therapy with long-acting muscarinic antagonists (LAMA), long-acting beta2 agonists (LABA), and inhaled corticosteroids (ICS)

We will not assess the effectiveness of bronchodilator therapy using lung function alone but we will also include a clinical improvement in symptoms. 

We will offer LAMA+LABA to COPD patients who are on a short-acting bronchodilator if

·      do not have asthmatic features/features suggesting steroid responsiveness such as previous diagnosis of asthma or of atopy, a higher blood eosinophil count, substantial variation in FEV1 over time ( and of at least 400 ml) or substantial diurnal variation in peak expiratory flow (at least 20%)and

·      remain breathless or have exacerbations despite existing management.

We need to be aware of the MHRA safety advice on Respimat and Handihaler inhalers which basically refers to taking into account the risk of cardiovascular side effects for patients with conditions that may be affected by the anticholinergic action of tiotropium, including MI, cardiac arrythmia and heart failure. I will put a link to this advice in the episode description.

We will consider LABA+ICS for COPD patients who are on a short-acting bronchodilator if

·      they have asthmatic features/features suggesting steroid responsiveness and

·      remain breathless or have exacerbations despite existing management.

For people with COPD who are taking LABA+ICS, we will offer triple therapy with LAMA+LABA+ICS if:

·      their day-to-day symptoms continue to adversely impact their quality of life or

·      they have a severe exacerbation (requiring hospitalisation) or

·      they have 2 moderate exacerbations within a year. 

·      This is because adding the LAMA has a beneficial effect on symptoms and exacerbations

For people with COPD who are taking LAMA+LABA, consider LAMA+LABA+ICS if:

·      they have a severe exacerbation (requiring hospitalisation) or

·      they have 2 moderate exacerbations within a year. 

·      And this is because ICS have a significant impact on exacerbations and not so much on symptoms.

For people with COPD who are taking LAMA+LABA and whose day-to-day symptoms adversely impact their quality of life:

·      we will consider a trial of LAMA+LABA+ICS, lasting for 3 months only

·      And then:

o  if symptoms have not improved, stop LAMA+LABA+ICS and switch back to LAMA+LABA

o  if symptoms have improved, continue with LAMA+LABA+ICS. 

· We will Minimise the number of inhalers and the number of different types of inhaler used by each person as far as possible, using combination inhalers if necessary

In terms of Delivery systems used to treat stable COPD

We will say that

Inhalers

In most cases bronchodilator therapy is best administered using a hand-held inhaler (including a spacer if appropriate). And we will only prescribe inhalers after people can demonstrate satisfactory inhaler technique

Spacers

We will provide a spacer that is compatible with the inhaler advising that

·      They should administer the drug by single actuations of the metered-dose inhaler into the spacer, inhaling after each actuation

·      And ensuring that there should be minimal delay between inhaler actuation and inhalation and being aware that

·      normal tidal breathing can be used as it is as effective as single breaths

In respect of spacer cleaning, we will advise:

·      not to clean the spacer more than monthly, because more frequent cleaning affects their performance (because of a build-up of static)

·      to hand wash using warm water and washing-up liquid, and allow the spacer to air dry. 

Nebulisers

We will think about nebuliser therapy for people with distressing or disabling breathlessness despite maximal therapy using inhalers. 

And we will not continue it unless there is an objective or subjective improvement.

We will offer people a choice between a facemask and a mouthpiece to administer their nebulised therapy, unless the drug specifically requires a mouthpiece (for example, anticholinergic drugs). 

In terms of Oral therapy

We will first address Oral corticosteroids and

We will say that the long-term use of oral corticosteroid therapy in COPD is not normally recommended. Some people with advanced COPD may need long-term oral corticosteroids when these cannot be withdrawn following an exacerbation. In these cases, the dose of oral corticosteroids should be kept as low as possible. 

And we will monitor people who are having long-term oral corticosteroid therapy for osteoporosis, and give them appropriate prophylaxis. Prophylaxis should be started without monitoring for people over 65. 

In respect of Oral theophylline

We will say that

slow-release Theophylline should only be used after a trial of short-acting bronchodilators and long-acting bronchodilators, or for people who are unable to use inhaled therapy, as plasma levels and interactions need to be monitored. 

We will take particular caution when using theophylline in older people, because of differences in pharmacokinetics, the increased likelihood of comorbidities and the use of other medications. 

And we will reduce the dose of theophylline for people who are having an exacerbation if they are prescribed macrolide or fluoroquinolone antibiotics (or other drugs known to interact). 

IN respect of Oral mucolytic therapy

We will consider it for people with a chronic cough productive of sputum. And we will only continue it if there is symptomatic improvement. However, we will not routinely use mucolytic drugs to prevent exacerbations in people with stable COPD. 

Oral anti-oxidant therapy such as treatment with alpha-tocopherol and beta-carotene supplements, and Oral anti-tussive therapy are not recommended.

In respect of Oral prophylactic antibiotic therapy

We will consider azithromycin (usually 250 mg 3 times a week) for people with COPD if they:

·      do not smoke and

·      have optimised management and

·      continue to have either:

o  frequent exacerbations with sputum production (typically 4 or more per year)

o  prolonged exacerbations with sputum production or

o  exacerbations resulting in hospitalisation. 

Before offering prophylactic antibiotics, we need to ensure that the person has had:

·      sputum culture and sensitivity (including tuberculosis culture), to identify other possible causes of persistent or recurrent infection that may need specific treatment (for example, antibiotic-resistant organisms, atypical mycobacteria or Pseudomonas aeruginosa)

·      also training in airway clearance techniques to optimise sputum clearance

·      and a CT scan of the thorax to rule out bronchiectasis and other lung pathologies. 

In addition, before starting azithromycin, we need to ensure the person has had:

·      an electrocardiogram (ECG) to rule out prolonged QT interval and

·      baseline liver function tests. 

When prescribing azithromycin, we will advise people about the small risk of hearing loss and tinnitus, and tell them to contact a healthcare professional if this occurs. 

We will review prophylactic azithromycin after the first 3 months, and then at least every 6 months and

We will only continue treatment if the continued benefits outweigh the risks. This is because there are no long-term studies on the use of prophylactic antibiotics in people with COPD. 

For people who are taking prophylactic azithromycin and are still at risk of exacerbations, we will provide a non-macrolide antibiotic to keep at home as part of their exacerbation action plan, telling the patient that it is not necessary to stop prophylactic azithromycin during an acute exacerbation of COPD. 

In terms of Oral phosphodiesterase-4 inhibitors

We will say that for treating severe COPD with roflumilast, there is separate NICE guidance which is really outside the scope of this podcast. However, if you are interested, I will put the link to this guidance in the episode description. 

Oxygen

In respect of Long-term oxygen therapy

We need to be aware that inappropriate oxygen therapy in people with COPD may cause respiratory depression. 

We need to assess the need for oxygen therapy in people with:

·      very severe airflow obstruction (FEV1 below 30% predicted)

·      cyanosis

·      polycythaemia

·      peripheral oedema

·      a raised jugular venous pressure

·      oxygen saturations of 92% or less on air.

And we will also consider it for people with severe airflow obstruction (FEV1 30–49% predicted). 

We will make the assessment by measuring arterial blood gases on 2 occasions at least 3 weeks apart and we will consider long-term oxygen therapy for people who do not smoke and who:

·      have a partial pressure of oxygen in arterial blood (PaO₂) below 7.3 kPa when stable or

·      have a partial pressure of oxygen in arterial blood (PaO₂₎ between 7.3 and 8 kPa when stable, if they also have 1 or more of the following:

o  secondary polycythaemia

o  peripheral oedema and / or

o  pulmonary hypertension.

We will also conduct and document a structured risk assessment for people being assessed for long-term oxygen therapy. As part of the risk assessment, we will consider:

·      the risks of falls from tripping over the equipment

· the risks of burns and fires, and the increased risk of these for people who live in homes where someone smokes (including e‑cigarettes).

For people who smoke or live with people who smoke, we will ensure the person who smokes is offered advice and support to stop. However, we will not offer long-term oxygen therapy to people who continue to smoke despite these efforts.

We should advise people who are having long-term oxygen therapy that they should use it for a minimum of 15 hours per day. 

We will not offer long-term oxygen therapy to treat isolated nocturnal hypoxaemia caused by COPD. 

Oxygen concentrators should be used to provide the fixed supply at home.

People on long-term oxygen therapy should be reviewed at least once per year

Now, in terms of Ambulatory oxygen therapy

We will consider ambulatory oxygen in COPD if there is exercise desaturation and are shown to improve with oxygen

We will prescribe ambulatory oxygen to people who are already on long-term oxygen therapy, who wish to continue oxygen therapy outside the home, but we will only prescribe it after an assessment by a specialist. The purpose of the assessment is to assess the extent of desaturation, the improvement in exercise capacity with supplemental oxygen, and the oxygen flow rate needed to correct desaturation. 

We will use small light-weight cylinders, oxygen-conserving devices and portable liquid oxygen systems depending on the hours of ambulatory oxygen use and oxygen flow rate needed. 

Finally, in respect ot Short-burst oxygen therapy

We will not offer Short-burst oxygen therapy to manage breathlessness in people with COPD who have mild or no hypoxaemia at rest. 

In terms of Managing pulmonary hypertension and cor pulmonale

We will say that In this guideline ‘cor pulmonale’ is defined as a clinical condition that is identified and managed on the basis of clinical features. It includes people who have right heart failure secondary to lung disease and people whose primary pathology is salt and water retention, leading to the development of peripheral oedema.

Diagnosing pulmonary hypertension and cor pulmonale

We will suspect a diagnosis of cor pulmonale for people with:

·      peripheral oedema

·      a raised venous pressure

·      a systolic parasternal heave and

·      a loud pulmonary second heart sound. 

And it is recommended that the diagnosis of cor pulmonale is made clinically.

In respect of the treatment of pulmonary hypertension

We will not offer solely to manage pulmonary hypertension caused by COPD, any the following treatments:

·      bosentan, losartan, nifedipine

·      nitric oxide, pentoxifylline

·      phosphodiesterase-5 inhibitors

·      statins. 

So in order to treat cor pulmonale

caused by COPD we will ensure that patients are offered optimal COPD treatment, including stop smoking and oxygen therapy if there is hypoxia

Oedema associated with cor pulmonale can usually be controlled symptomatically with diuretic therapy. 

We will not use any of the following to treat cor pulmonale caused by COPD:

·      alpha-blockers

·      angiotensin-converting enzyme inhibitors

·      calcium channel blockers or

·      digoxin (unless there is atrial fibrillation). 

In terms of Pulmonary rehabilitation

We will offer pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD (usually Medical Research Council [MRC] grade 3 and above), including people who have had a recent hospitalisation for an acute exacerbation. Pulmonary rehabilitation is not suitable for people who are unable to walk, who have unstable angina or who have had a recent myocardial infarction. 

The rehabilitation process should incorporate a programme of physical training, disease education, and nutritional, psychological and behavioural intervention. 

In respect of Vaccination and anti-viral therapy

We will offer pneumococcal vaccination and an annual flu vaccination to all people with COPD.

There is separate guidance on preventing and treating flu using antivirals, and I will put the links to this guidance in the podcast description. 

There is a whole section on Lung surgery and lung volume reduction procedures

But being such a specialised area, I will not say much about this. Only that it applies only to the most severe forms of COPD, that it can involve lung volume reduction surgery, bullectomy, endobronchial valves and coils and lung transplantation and that careful investigations including imaging of the lungs will be required for this. I will put links to this specific guidance in the episode description.

In terms of Alpha‑1 antitrypsin deficiency,

We will also say that Alpha‑1 antitrypsin replacement therapy is not recommended  in Alpha‑1 antitrypsin deficiency

In terms of Multidisciplinary management

We will say that COPD care should be delivered by a multidisciplinary team including:

Respiratory nurse specialists

Physiotherapy

People Identifying and managing anxiety and depression

Nutritionists

Palliative care for people with end-stage COPD

Assessment for occupational therapy

Social services especially if they have disabilities caused by COPD. 

In terms of Advice on travel for people on long-term oxygen therapy we will follow the recommendations by the British Thoracic Society and I will put a link to these recommendations in the episode description. 

Scuba diving is not generally recommended for people with COPD.

We must obviously offer patient Education about their condition and how COPD will affect other long-term conditions that are common in people with COPD (for example hypertension, heart disease, anxiety, depression and musculoskeletal problems). Programmes designed for asthma should not be used in COPD. 

IN terms of Self-management

We need to develop an individualised self-management plan in collaboration with each person with COPD and their family members or carers (as appropriate), including an individualised exacerbation action plan. We will also offer people a short course of oral corticosteroids and a short course of oral antibiotics to keep at home as part of their exacerbation action plan if:

·      they have had an exacerbation within the last year, and remain at risk of exacerbations

·      they understand and are confident about when and how to take these medicines, and the associated benefits and harms

·      they know to tell their healthcare professional when they have used the medicines, and to ask for replacements. 

There is separate NICE guidance on the choice of antibiotics and I will put the link to this in the episode description. In summary the choice of antibiotics will be:

·      as first line amoxicillin, doxycycline or clarithromycin.

·      As second line if the first line antibiotic has failed, we will use an alternative first choice, preferably from a different class

·      Finally an Alternative choice antibiotic if person at higher risk of treatment failure would be co-amoxiclav, cotrimoxazole and levofloxacine

For people who have used 3 or more courses of oral corticosteroids and/or oral antibiotics in the last year, we should investigate the possible reasons for this. 

There is also separate guidance on the recommendations on systemic corticosteroids for more guidance on oral corticosteroids and the link will also be in the podcast description.

We will encourage people with COPD to respond promptly to exacerbation symptoms by following their action plan, which may include:

·      adjusting their short-acting bronchodilator therapy to treat their symptoms

·      taking a short course of oral corticosteroids if their increased breathlessness interferes with activities of daily living

·      adding oral antibiotics if their sputum changes colour and increases in volume or thickness beyond their normal day-to-day variation

·      telling their healthcare professional. 

In terms of Telehealth monitoring we will simply say that we should not offer routine telehealth monitoring of physiological status as part of management for stable COPD. 

When it comes to Following-up of people with COPD

· apart from offering the usual advice and treatment we will record the opportunistic measurement of spirometric parameters and if there is a loss of 500 ml or more over 5 years, this will show rapidly progressing disease and may need referral to specialist treatment and investigation. 

· We will review people with mild to severe COPD (stages 1 to 3) at least once per year and those with very severe COPD (or stage 4) should be seen at least twice per year in primary care

· A review should include:

o  Smoking status and advice,

o  symptoms and complications including cor pulmonale

o  response to treatment, including inhaler technique, pulmonary rehabilitation and long-term oxygen therapy

o  and measure FEV1 and FVC, BMI and the MRC dyspnoea score. We should also check oxygen saturation in patients with very severe COPD

In terms of Managing exacerbations of COPD

We will define an exacerbation as a sustained worsening of the patient's symptoms which is beyond normal day-to-day variations. The change in these symptoms often necessitates a change in medication.

·      a mild exacerbation requires increasing their medication in their own normal environment

·      a moderate exacerbation, requires treatment with systemic corticosteroids and/or antibiotics

·      a severe exacerbation, requires hospitalisation.

We will assess the need for hospital treatment

According to the patient’s symptoms and social circumstances as well as objective measurements. In particular significant changes on a chest x-ray and an oxygen saturation of less than 90% is likely to indicate the need for hospital treatment, as well as arterial blood gases showing a PH less than 7.35 or the partial pressure of oxygen in arterial blood is less than 7 kilopascals

When it comes to Investigating an exacerbation

sending sputum samples for culture is not recommended routinely for people who have their exacerbation managed in primary care but pulse oximetry can be of value

However, People referred to hospital should have

·      a chest X-ray

·      arterial blood gases

·      an ECG

·      a full blood count and urea and electrolyte

·      a theophylline level for people taking theophylline

·      a sputum culture if the sputum is purulent

·      and blood cultures if there is a fever

Hospital-at-home and assisted-discharge schemes are safe and can also be used as an alternative

We are now going to review the Pharmacological management during exacerbations

We can use both nebulisers and inhalers but we will change people to inhalers as soon as their condition has stabilised, because this may allow them to be discharged from hospital earlier. 

If a person with COPD is hypercapnic or acidotic the nebuliser should be driven by compressed air rather than oxygen to avoid worsening hypercapnia. If oxygen therapy is needed, we should administer it simultaneously by nasal cannulae. 

In the absence of significant contraindications, we will use oral corticosteroids, to people having an exacerbation, offering 30 mg of oral prednisolone daily for 5 days and we will think about osteoporosis prophylaxis for people who need frequent courses of oral corticosteroids. 

For guidance on using antibiotics to treat COPD exacerbations, there is separate guidance and I will put the link in the episode description. It is basically:

·      amoxicillin, doxycycline or clarithromycin as first line.

·      As second line if the first line antibiotics has failed, we will use an alternative first choice, preferably from a different class

·      Alternative choice oral antibiotics (if person at higher risk of treatment failure would be co-amoxiclav, cotrimoxazole and levofloxacine

We will only use intravenous theophylline with careful monitoring as an adjunct to exacerbation management if there is an inadequate response to nebulised bronchodilators. 

Respiratory stimulants such as doxapram should be used only when non-invasive ventilation is either unavailable or inappropriate. 

We will measure oxygen saturation if there are no facilities to measure arterial blood gases and if necessary, prescribe oxygen to keep the oxygen saturation of arterial blood within the individualised target range. 

Pulse oximetry gives no information about the partial pressure of CO2 in arterial blood ₂ or pH so we will measure arterial blood gases in all people who arrive at hospital with an exacerbation of COPD.

We will use Non-Invasive Ventilation as the treatment of choice for persistent hypercapnic ventilatory failure during exacerbations despite optimal medical therapy. 

We will treat hospitalised exacerbations of COPD on intensive care units, including invasive ventilation when this is thought to be necessary. 

We will also consider physiotherapy using positive expiratory pressure devices for selected people with exacerbations of COPD, to help with clearing sputum. 

Finally in order to monitor the recovery from an exacerbation

We will do regular clinical assessments, use pulse oximetry and for people who are hypercapnic or acidotic , we will measure intermittent arterial blood gases until they are stable.

We will not, however, routinely perform daily monitoring of peak expiratory flow or FEV1 because the magnitude of changes is small compared with the variability of the measurement. 

We have come to the end of this episode. I hope that you have enjoyed it and I hope that you will join me in the next one. Thank you for listening and goodbye.

This episode makes reference to guidelines produced by the "National Institute for Health and Clinical Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at a fictitious clinical case of a patient created by Chat GPT to see how the NICE guidelines could apply to it. 

I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement.   

There is a YouTube version of this and other videos that you can access here: 

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 
• https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk 

The patient was created using the following Chat GPT prompt:

A)   Provide a fictitious patient. Details that you should include are:

1)   patient's medical information including:

·      name

·      age

·      sex

·      ethnicity

·      BMI

·      blood pressure

2)   medical history- you must include:

·      either one or two of the following poorly controlled conditions:

·      type 2 diabetes

·      hypertension

·      dyslipidaemia,

·      Asthma or COPD

·      Any number of other medical conditions of your choice, along with whether they are well controlled or not – the medication for these conditions should appear in the next section “medications”

1. Medications given:

·      indicate whether the patient is currently taking medication for each medical condition or not.

·      If medication is prescribed for a condition, indicate the specific drug(s) and their dosages. You may choose to prescribe one, two, or three drugs for each condition as appropriate.

3)   State whether the patient tolerates the medication well or not, and if not, describe the side effect(s) and their severity.

4)   blood test results (give a bulleted list but do not number them):

·      HbA1c expressed in % and mmol/mol

·      renal function tests to include creatinine (expressed first in µmol/L and then in mg/dL), eGFR, urea, sodium, and potassium (expressed in UK units first and then USA units)

·      lipid profile expressed both in mmol/L first and then in mg/dL.

·      If the patient has asthma, give the peak flow reading expressed as a percentage of their best or expected reading.

·      If the patient has COPD, give the FEV1 reading expressed as a percentage of the predicted reading

·      include any other relevant test results for the patient, expressing them in both UK and USA units. If the patient has hypothyroidism or takes levothyroxine medication, provide the results of their thyroid function tests, including both T4 and TSH levels, in both UK and USA units. Also, include the normal range for these investigations.

B)  Provide the patient's cardiovascular risk using the QRISK2 tool, calculated as a percentage of the likelihood of experiencing a cardiovascular event over the next 10 years.

C)   At the end of the patient information, ask: 'What treatment recommendations would you make?' – do not make recommendations yourself

D)  Do not include a disclaimer that the patient is fictitious.

The NICE hypertension flowcharts can be found here: 

• Website: https://www.nice.org.uk/guidance/ng136/resources/visual-summary-pdf-6899919517 
• Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgKKs3AbARF_VLEI?e=KRIWrn 

The full NICE Guideline on hypertension (NG136) can be found here: 

• Website: https://www.nice.org.uk/guidance/NG136 
• Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgP6nFVHRypL9fdj?e=Jbtgus 

The full NICE Guideline on Type 2 diabetes (NG28) can be found here: 

·      https://www.nice.org.uk/guidance/ng28 

The full NICE guidance on cardiovascular disease risk reduction (CG181) can be found here: 

·      https://www.nice.org.uk/guidance/cg181

The full NICE guidance on asthma (NG80) can be found here: 

·      https://www.nice.org.uk/guidance/ng80 

The full NICE guidance on depression in adults (NG222) can be found here:

·      https://www.nice.org.uk/guidance/ng222 

The full guidance on obesity (CG189) can be found here:

·      https://www.nice.org.uk/guidance/cg189

Thumbnail photos-

From: www.freepik.com

·      Image by Freepik: Image by a href="https://www.freepik.com/free-photo/excited-young-friends-running-beach_9057871.htm#page=2&query=45%20year%20old%20obese%20woman&position=10&from_view=search&track=ais"Freepik/a 

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]   

• Music provided by Audio Library Plus  

• Watch: https://youtu.be/aBGk6aJM3IU 

• Free Download / Stream: https://alplus.io/halfway-through 

Transcript  

Hello everyone. My name is Fernando and I am a GP in the United Kingdom. Today we are looking at a fictitious patient generated by Chat GPT with a view to looking at the NICE guidelines from a practical perspective.  

Right, so let’s jump into it.

Patient Information:

·      Name: Sarah Davis

·      Age: 45

·      Sex: Female

·      Ethnicity: Caucasian

Examination:

·      BMI: 32 (Obese)

·      Blood Pressure: 153/91 mm Hg

Medical History:

·      Type 2 Diabetes

·      Hypertension

·      Dyslipidemia

·      Asthma

·      Obesity

·      Depression

Medications:

·      Metformin 1000 mg twice daily

·      Gliclazide 80 mg once daily

·      Amlodipine 10 mg once daily

·      Indapamide MR 1.5 mg once daily

·      Atorvastatin 20 mg once daily

·      Salbutamol inhaler as needed

·      Sertraline 50 mg once daily

Medication Tolerance:

·      Sarah tolerates her medications well. She has not reported any significant side effects.

Blood Test Results:

·      HbA1c: 8.5% (69 mmol/mol)

·      Renal Function:

o  Creatinine: 90 µmol/L (1.02 mg/dL)

o  eGFR: 91 mL/min/1.73m²

·      Lipid Profile:

o  Total Cholesterol: 5.2 mmol/L (200 mg/dL)

o  LDL Cholesterol: 3.0 mmol/L (116 mg/dL)

o  HDL Cholesterol: 1.2 mmol/L (46 mg/dL)

o  Triglycerides: 2.5 mmol/L (220 mg/dL)

Cardiovascular Risk (QRISK3):

·      Sarah's 10-year cardiovascular risk is estimated at 18%.

So, what treatment recommendations would we make?

Although there is a lot that we can do from a lifestyle perspective, we will focus on the drug treatment only.

Right, let’s start with her diabetes, which is poorly controlled with an hba1c of 8.9% or 74 mmol/mol. Sarah is on metformin 1gr BD and gliclazide 80 mg OD and we know she is at high risk of cardiovascular disease with a QRISK3 of 18%.

NICE says that for step 2 treatment after metformin, if a patient is at high risk of CVD, we should choose an SGLT2 inhibitor. But this patient has been given gliclazide instead. We would like to see if there is a reason for this and whether an SGLT2 inhibitor was tried before but not tolerated.

So, assuming that there have been no issues, I would recommend starting an SGLT2 inhibitor.

SGLT2 inhibitors are also associated with a degree of weight loss, and given that Sarah is obese, this will be good for her.

Gliclazide on the other hand is associated with weight gain, which is the last thing that Sarah needs. The question now is whether we should stop gliclazide and, if so, when.

In my opinion, gliclazide should be definitely stopped and substituted by another diabetic agent which is weight neutral, for example, a DPP4 inhibitor.

A more difficult question would be when to make this switch. Doing it straightaway has got the disadvantage that, if a side effect develops, we may not know which drug is the culprit. Also, we do not know how much the HbA1c will drop with the SGLT2 inhibitor so there could be a risk of overtreatment.

Right, a balanced decision that you can make depending on your clinical judgement.

I think that I would start the SGLT2 inhibitor first, so, I would start her on something like dapagliflozin 5 mg OD initially and, if tolerated, I may increase it to 10 mg daily fairly quickly, possibly within 3 or 4 weeks to get the maximum effect as soon as possible.

Research studies have shown that the introduction of an SGLT2 inhibitor can lead to a drop in Hba1c of around 1%. Although this could vary depending on the individual patient, Sarah’s HbA1c is poor at 8.9% so even after the SGLT2 inhibitor, she is likely to require a third diabetic agent.

NICE says that if dual therapy with metformin and another oral drug is not enough, we should consider either triple therapy by adding a DPP‑4 inhibitor, pioglitazone or a sulfonylurea or starting insulin. Because of the risk of weight gain, I would try to avoid gliclazide and insulin.

Given that she is on gliclazide 80 mg daily, that is, a quarter of the maximum daily dose of gliclazide, I would probably switch Sarah to a DPP4 inhibitor as soon as she is tolerating the full dose of dapagliflozin. So, we could stop gliclazide and start her on, for example, sitagliptin 25mg daily, which is also a quarter of the maximum daily dose of 100mg.

But I do not think that there is a right or wrong approach in terms of the gliclazide switch. The decision about the timing is very dependent on the individual patient and your clinical judgement. Switching early has some more uncertainty about treatment response whereas switching later may mean that the patient remains on a potentially unsuitable drug for longer.

We have to make sure that we inform the patient that SGLT2 inhibitors have been associated with an increased risk of DKA, toe and lower limb amputations and Fournier’s gangrene.

So, on starting the SGLT2 inhibitor:

1.   We will educate her about DKA symptoms and when to seek advice.

2.   We will also advise against ketogenic diets to lose weight while on an SGLT2 inhibitor, as this also increases the risk of DKA.

3.   We will improve foot care and

4.   We will advise patients to seek urgent medical advice if they experience pain, erythema or swelling in the genital or perineal area, as this may precede Fournier’s gangrene or necrotising fasciitis. 

If we were managing her diabetes according to the European or American guidelines, we would be talking a lot more about GLP 1 receptor agonists, given that they are also recommended for patients with high CVD risk and they are much better in terms of weight loss. We are following the NICE guidelines, which are more restrictive with GLP1 receptor agonists, but we can always use our clinical judgement to deviate from the guideline if we think that it is appropriate for a particular patient. 

Now that we have dealt with her diabetes, let’s look at her hypertension. 

Unless we have specific concerns, we do not need to arrange an ABPM or HBPM because NICE says that we can use clinic blood pressure measurements to monitor drug treatment for people already diagnosed with hypertension. However, NICE also say that in diabetes, we should check both the sitting and standing BP because of their higher risk of postural hypotension, especially if there is autonomic neuropathy. 

Sarah’s BP is 153/91 and NICE says that the target BP for people under the age of 80 is below 140/90. So, her BP is high.

She is on amlodipine and indapamide, which is not in keeping with NICE guidance. NICE says that, for people with diabetes of any age and any ethnicity background, an ACEI or ARB should be used as first line treatment.

So, I would have a look to see if an ACE inhibitor or ARB has been tried before and then stopped because of side effects like a cough or angioedema. Both of these side effects can happen with ACEIs and they are normally managed by switching to an ARB. But, although much rarer, these symptoms can also be a side effect of ARBs 

Assuming that there is no previous problem, I would start her on an ACE inhibitor, for example lisinopril 2.5 mg daily monitoring her renal function and titrating up according to response. 

If the target BP is achieved at a lower dose than the maximal dose of the ACE inhibitor, then I would recommend stopping indapamide and continue titrating up the ACE inhibitor dose to compensate. Thiazide like diuretics can worsen diabetes so stopping indapamide and replacing it with a higher dose of lisinopril would be the right thing to do.   

Once indapamide has been stopped, if the target BP is achieved before the ACE inhibitor is at the maximal dose, we could consider reducing the dose of amlodipine while we increase the ACE inhibitor further, because of the benefits that ACE inhibitors have particularly in diabetes. 

Now, let’s look at her hyperlipidaemia. Sarah has no history of cardiovascular disease so she is on atorvastatin 20 mg daily for primary prevention.

NICE says that we should offer atorvastatin 20 mg for the primary prevention of CVD if they have a QRISK score of 10% or more.

After atorvastatin 20mg has been started, and unlike secondary prevention, there are no specific lipid targets in primary prevention but, if we judge the person to be at higher cardiovascular risk, we will consider increasing the dose of atorvastatin in order to achieve a greater than 40% reduction in non‑HDL cholesterol.

In Sarah’s case, both her cholesterol and QRISK3 score are still high on atorvastatin 20 mg, so we could consider her to be at higher risk and, if the 40% drop in non HDL cholesterol has not happened, we could increase atorvastatin to 40 mg and monitor her blood tests.

Let’s now move on to her asthma. Sarah is on step 1 treatment, that is, on-demand Salbutamol inhaler as needed. If Sarah has infrequent symptoms, this is fine, but we should check that she has no symptoms that could indicate the need for maintenance therapy, for example, asthma-related symptoms 3 times a week or more, or symptoms causing waking at night. In that case, we should offer a low dose of an ICS, for example standard beclomethasone 100mcg, one or two inhalations twice daily. 

The next issue is Sarah’s depression, for which she takes sertraline 50 mg daily. We don’t know how long she has been taking them for but NICE recommends that SSRIs are taken for at least 6 months (and for some time after symptoms remit). So we should assess how long she has been on it and if she wishes to continue treatment or whether the time has come to consider stopping after a gradual reduction of the dose. 

It is worthwhile mentioning that the BNF says that SSRIs should be prescribed with caution in diabetes because SSRIs can affect diabetic control. We are advised to monitor blood glucose when starting or stopping an SSRIs. 

Finally, let’s have a look at her obesity. Her BMI is 32. Apart from the obvious dietary and lifestyle changes, NICE recommends a number of pharmacological treatments for obesity such as orlistat, liraglutide and semaglutide. They all have different BMI thresholds and I would advise you to look at the different criteria before prescribing. 

Except orlistat, liraglutide and semaglutide can only be given for obesity by a secondary care service. However, as discussed earlier and based on our clinical judgement, we could deviate from the NICE guideline and give a GLP1 receptor agonist for her diabetes instead of an SGLT2 inhibitor. 

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this episode can be found here:

• https://youtu.be/t-wXLOAr8ik?si=TR3eNXpNPlBP3NCs

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

This episode refers to guidelines produced by a number of organisations. Please note that the content reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the interpretation of an abnormal full blood count, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the information consulted. You must always use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

·      Medscape / Kevin Fernando- management of abnormal blood tests: https://1drv.ms/b/s!AiVFJ_Uoigq0mQPPwvFNZtsUSpIr?e=xYthDn

·      Oxford hospital referral pathway: https://nssg.oxford-haematology.org.uk/general-haematology/documents/general-haematology/raised-haematocrit.pdf

·      GP notebook: https://gpnotebook.com/en-GB/pages/general-information/abnormal-fbc-in-adults

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Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to go through the interpretation of full blood counts, including follow up management, always focusing on what is relevant in Primary Care only.

I will be covering several areas:

1.   Review of haematological indices

2.   Polycythaemia

3.   Anaemia

4.   Thrombocytosis

5.   Thrombocytopenia

6.   Neutrophilia

7.   Neutropenia

8.   Lymphocytosis

9.   Lymphopenia

10. Eosinophilia

11. Monocytosis

I have put time stamps throughout the video so that you can skip to the section that you are interested in.

I have based this episode on a variety of sources, primarily Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners, although other sources like Medscape and GP notebook were also reviewed. I have put links to them in the episode description. They are worth having a look as they have flowcharts and other information that you may find useful.

Make sure to stay for the entire episode because at the end, I will tell you how to access my summary of the recommendations, which I hope that you will find helpful. 

Right, there is a lot of information to cover, so let’s jump into it.

I will now go through the blood indices on the full blood count and I will also touch on iron investigations such as ferritin and total iron binding capacity. So, let’s look at them one at a time:

·      The Platelet Count gives us the absolute number of platelets

·      The Mean Platelet Volume or MPV gives us the average size of platelets. New platelets are larger, and an increased MPV occurs when increased numbers of platelets are being produced, for example during infection or inflammation.

·      The White Blood Cell Count or WBC, gives the absolute number of white blood cells present. Leucocytosis is when the White Blood Cell Count is raised and leucopenia when it is low. In these situations, we need to look at the subtypes of the white blood cells, that is, we need to look at the:

·      WBC Differential, which looks at the number and proportion of the different types of WBC. We have five types: neutrophils, lymphocytes, monocytes, eosinophils, and basophils.

·      The Red Blood Cell Count or RBC is the absolute number of red cells. It is an important value but we often rely on other red blood cell indices to interpret the results correctly

·      Haemoglobin or Hb is crucial for the diagnosis of anaemia but, again, other indices are needed for the final interpretation.

·      The Haematocrit or HCT measures how much volume is taken up by red blood cells and it is expressed either as a percentage (that is from 0 to 100) or a proportion (that is, from 0 to 1). The haematocrit is therefore influenced not only by the number of red blood cells but also the amount of plasma present.

·      The Mean Corpuscular Volume or MCV refers to the average size of each RBC. An elevated MCV or macrocytosis is when the RBCs are larger than normal, for example in vitamin B12 or folic acid deficiency. A low MCV or microcytosis is when the RBCs are smaller than normal which may indicate, for example, iron deficiency anaemia.

·      The Mean Corpuscular Haemoglobin or MCH measures the average haemoglobin per red cell. Since macrocytic or larger RBCs tend to carry more haemoglobin that normal, they would normally have higher MCH values. 

·      The Mean Corpuscular Haemoglobin Concentration or MCHC is about concentration, that is, the amount of haemoglobin relative to the size of the cell. A decreased MCHC or hypochromia is seen in conditions such as in iron deficiency anaemia, chronic inflammation or thalassaemia. An increased MCHC or hyperchromia is seen when the haemoglobin is abnormally concentrated in the cells, such as in spherocytosis.

·      The Red Cell Distribution Width or RDW measures how uniform the red cells are in size. A high RDW indicates a mix of small and large cells, which can happen in some anaemias, such as iron deficiency or vitamin B12 deficiency. An increase in RDW happens when red blood cells have different sizes also called anisocytosis, or different shapes also called poikilocytosis.

·      Ferritin is the most useful indicator of iron deficiency, as it can drops before any decrease in levels of iron in the blood occurs. Ferritin is the main form of iron storage and is present mostly in the liver. Ferritin levels are low in long-term iron deficiency. Ferritin may also be decreased if protein levels are very low, like in malnutrition. Ferritin is high in states of iron overload, especially in haemochromatosis. However, ferritin can be high for a number of other reasons including inflammatory conditions, infection and liver disease. 

·      Total Iron Binding Capacity, or TIBC, measures the total capacity to bind iron in the blood. TIBC correlates with the amount of transferrin, and while both tests (TIBC and transferrin) are different, they measure essentially the same thing and most laboratories only measure one or the other. The amount of transferrin transporting iron is called transferrin saturation. Iron deficiency results in a low transferrin saturation, but an increased TIBC. In iron overload, such as in haemochromatosis, iron and transferrin saturation will be high and TIBC will be low or normal. Because transferrin is made in the liver, TIBC and transferrin will also be low in liver disease.

Now let’s start looking at the different haematological conditions. And the first section refers to polycythaemia.

Polycythaemia is judged on basis of HCT and it can be diagnosed if the HCT > 0.52 in men and > 0.48 in women.

Polycythaemia is also sometimes referred to as Erythrocytosis but this is not always correct. Why? Well, erythrocytosis indicates an excess number of erythrocytes or red blood cells and, as we have said, polycythaemia is judged on haematocrit, not red blood cells.

And this is because there are two types of polycythaemia, absolute polycythaemia, that is, when erythrocytosis is present, and relative or apparent polycythaemia, when this is not the case.  

For example, in apparent or relative polycythaemia, the HCT increases as a result of a reduced plasma volume rather than an increased red blood cell mass. It is common in obese men, and it is also associated with smoking, diuretics, alcohol, hypertension, stress, and dehydration. Despite the potentially reversible causes, these patients are also at risk of occlusive vascular episodes.

On the other hand, we have absolute polycythaemia, which can be primary or secondary. The primary cause is Polycythaemia Vera. Well over 90% of PV patients have an acquired mutation in a gene called JAK2 that regulates erythropoiesis. These patients do not need as much erythropoietin or EPO to drive red cell production. So, the features of PV are a positive test to the JAK2 mutation, and a low serum EPO level. It also has a low ferritin secondary to the excess production of red cells, which consumes a significant amount of iron. Being a myeloproliferative disorder, it can also sometimes be associated with raised WBC and / or platelets.

Secondary Polycythaemia is due to the physiological response to increased EPO levels. It can be an appropriate response to hypoxia like in COPD, heart disease and smoking or to an inappropriate response due to an EPO producing tumour like in some Renal & liver tumours or fibroids. Other possible causes are anabolic steroids and testosterone therapy, as androgens can also stimulate EPO production. In cases of secondary polycythaemia, the JAK2 mutation is negative, EPO levels are high and ferritin, WBC and platelets are normal.

Criteria for urgent referral are a HCT >0.60 in men or >0.56 in women or also if there is recent thrombosis, abnormal bleeding, or neurological or visual symptoms.

If the criteria for urgent referral are not met, we should confirm the results by repeating the blood test. In order to differentiate between apparent and absolute polycythaemia, the blood sample should be uncuffed and we should ensure that the patient has not fasted, is well hydrated, and has been advised about alcohol and smoking.  

In this blood test, we should request a:

·      Repeat FBC

·      A blood film and screen for diabetes, hyperlipidaemia and hypertension, checking

·      HbA1c

·      Lipids

·      Ferritin

·      Renal and liver function tests. Additionally, if we suspect absolute polycythaemia, we should also request

·      Genetic testing for the JAK2 mutation and do

·      EPO levels.

Criteria for routine referral are unexplained persistently elevated HCT >0.52 in men or >0.48 in women, taking into account that we should refer at lower limits if there is associated iron deficiency. “Persistently” means at least two readings above these levels 4 weeks apart.  

Alternatively, routine referral is also justified if the HCT >0.52 in men or >0.48 in women without waiting for a second test if there are associated symptoms of concern like pruritus, raised WBC and / or platelets or splenomegaly, or if there is a past (not recent) history of arterial or venous thrombosis. 

Right, let’s move on to the next chapter, which is a very important and common one, anaemia.  

Anaemia presents as a low haemoglobin and is not a disease in itself, but may reflect an underlying disease process. It may also result from an increase in plasma volume and a dilutional effect, like in pregnancy. There may be local variations in the thresholds for diagnosis but the WHO uses the following haemoglobin thresholds to define anaemia at sea level in adults:

·      women - 12 g/dl (reduced to 11 g/dl in pregnancy)

·      men - 13 g/dl 

So, I will be using these thresholds in this episode. 

Also, I will be focusing on what we normally see in Primary Care, that is, chronic anaemia rather than anaemia secondary to acute bleeding requiring admission. Hospital admission will also be required with very severe anaemias, for example when the Hb <50 or even at higher levels if the patient is very symptomatic 

The first thing to look after a low haemoglobin is the mean corpuscular volume or MCV. Depending on this value, the anaemia can be described as: 

·      Microcytic if the MCV is below 80

·      Macrocytic if it is over 100 and

·      Normocytic if it is between 80 and 100

·      Bearing in mind that there may be mixed deficiencies, so we should look at the whole picture. 

So, let’s look at the microcytic anaemias first. The most common cause of microcytosis is iron deficiency, so we will repeat the full blood count and check the patient’s iron status.  

As we said earlier, ferritin can be an acute phase reactant so it can be raised in cases like, for example, inflammation, malignancy, alcohol excess, liver or renal disease and infection. If we suspect any of this, we should check ferritin together with iron studies or transferrin saturation to get a clearer picture. If the ferritin is >50mcg/L and transferrin saturation is >20%, then iron deficiency can be excluded. In that situation, we will consider haemoglobinopathy screening in order to exclude thalassaemia or other haemoglobin variants and, if positive, we will refer to haematology as necessary. 

If the haemoglobinopathy screen is normal or if testing is not considered necessary , then we will think about the following conditions: 

·      One, Anaemia of chronic disease and we will look for causes of:

o  Chronic inflammation: for example, autoimmune diseases, malignancy or tuberculosis

o  Endocrine problems: for example, hypothyroidism, hypopituitarism or Addison’s and

o  Other conditions such as CKD, liver disease or malnutrition

·      Two, Myelodysplastic syndrome, usually presenting as lone unexplained and persistent anaemia and

·      Three, We will also consider haemochromatosis where ferritin is raised. 

And we will refer to the appropriate service if necessary. 

On the other hand, if ferritin is:

·      <30 mcg/L or

·      <100 mcg/L with transferrin saturation less than 20%  

We will regard it as iron deficiency anaemia. We will then enquire about upper and lower GI symptoms and we will consider an urgent cancer referral for upper and lower GI endoscopy after requesting a FIT test if:

·      There are red flag symptoms

·      There is an unexplained drop in Hb to below 110 in men and below 100 in non-menstruating women or if

·      There is a strong family history of colorectal cancer, that is, two first degree relatives with the diagnosis or one first degree relative with a diagnosis before the age of 50. 

If there are no criteria for urgent referral, and the cause of the iron deficiency is unknown, we will look for other possible causes, for example: 

·      Testing for coeliac serology and refer to gastroenterology if it is positive.

·      Enquire about Heavy menstrual bleeding

·      Consider Dietary causes

·      Do Urinalysis to test for haematuria (as 1% of IDA have a renal malignancy)

·      Do Stool testing for parasitology and we will also

·      Consider aspirin, NSAIDs and anticoagulants as an aggravating factor but we will still investigate these patients fully. 

When the cause of the iron deficiency anaemia is known, we will give iron therapy and treat the underlying cause accordingly and then recheck the Hb and ferritin within 3 months. If the deficiency has not resolved and it is not due to menstrual loss, we will refer to gastroenterology or other specialist services depending on the presentation and our clinical judgement.  

Let’s now look at macrocytic anaemias, that is, when the MCV is >100.

If there is macrocytosis, with or without anaemia we should consider some of the possible causes and: 

·      Check alcohol intake

·      Enquire about family history

·      Review medication that could cause it, for example methotrexate, metformin, and some anticonvulsants, amongst others and

·      remember that a high MCV can be a normal physiological finding in pregnancy. 

Initial investigations will include: 

·      A Repeat FBC

·      A Blood Film

·      Vitamin B12 and folate levels

·      Renal and liver function tests, including GGT

·      TFTs

·      Ferritin, iron studies

·      Myeloma screen, including bone profile, serum immunoglobulins, serum Free Light Chains and Urinary Bence Jones protein

·      And finally, we will also check the Reticulocyte count and LDH levels, looking for evidence of haemolysis, bearing in mind that markers of haemolysis include a raised reticulocyte count, a high bilirubin and a high LDH  

Criteria for urgent referral to haematology are: 

·      Leucoerythroblastic features or blasts seen on blood film

·      Unexplained symptomatic and progressive anaemia and if there is

·      Associated splenomegaly, lymphadenopathy or other significant cytopenias 

If the urgent criteria are not met, we will then act on the results and refer the patient accordingly. That is:

·      If the reticulocyte count is high: we will look for evidence of bleeding or haemolysis and refer to the appropriate department.

·      If there is CKD related anaemia: we will refer to the renal team

·      If the TFTs are abnormal, we will treat the dysfunction and repeat the FBC 4-6 weeks later

·      If vitamin B12 and / or folate levels are low: we treat the deficiencies and assess for the underlying cause. For example:

o  In vitamin B12 deficiency, we will check for intrinsic factor Antibodies and Parietal Cell Antibodies and treat as pernicious anaemia if positive and

o  In both vitamin B12 and folate deficiencies we will do a coeliac screen.  

Criteria for routine haematology referral are: 

·      If paraprotein is detected

·      If all results are normal, but there is persistent unexplained anaemia

·      If there is persistent unexplained macrocytosis with an MCV >100 as this can be a feature of myelodysplasia

·      If there is persistent unexplained vitamin B12 deficiency because persistent unexplained vitamin B12 deficiency can also occur in myelodysplastic syndromes

·      If there is anaemia with associated abnormalities in other blood cells

·      If the reticulocyte count is low or the picture is unclear and

·      If there is an abnormal blood film

Finally, let’s now look at normocytic anaemias, that is, when the MCV is between 80 and 100.  

Possible causes of normocytic anaemias are: 

·      A mixed haematinic deficiency

·      Myelodysplastic syndrome

·      Recent blood loss

·      Anaemia of chronic disease like in:

o  Chronic inflammation

o  Endocrine problems or

o  Other conditions such as CKD, liver disease or malnutrition

·      And haemochromatosis if ferritin is raised. 

In these cases, we will investigate similarly to macrocytic anaemias, that is, we will check the following: 

·      A repeat FBC with a Blood Film

·      Vitamin B12 and folate levels

·      Renal and liver function tests, including GGT

·      TFTs

·      Ferritin, iron studies

·      Myeloma screen

·      And finally, we will also check the Reticulocyte count and LDH levels, looking for evidence of haemolysis  

And we will act on the results and refer the patient accordingly.

The next section refers to thrombocytosis or a raised platelet count above 450 x 10⁹/L.

Possible causes of thrombocytosis are:

·      Iron Deficiency Anaemia

·      Malignancies especially the LEGO cancers, that is:

o  Lung

o  Endometrium

o  Gastric

o  Oesophageal

·      Inflammation

·      Infection

·      Post-Splenectony and Hyposplenism like in Coeliac Disease

·      Post-Operatively situations and finally a

·      primary Myeloproliferative Disorder

But before moving on, let’s clarify a concept: should we call it thrombocytosis or thrombocythemia? Well, in fact, there is a difference. In summary, thrombocytosis is more common and arises as a secondary response, and therefore it is also referred to as reactive thrombocytosis. On the other hand, thrombocythemia, also referred to as primary or essential thrombocythemia, is less common and is a form of myeloproliferative disorder. Another key difference if that people with reactive thrombocytosis have normal platelets and therefore, also have a lower risk of blood clots and bleeding whereas those with thrombocythemia have abnormal platelets and also a higher risk of clots and bleeding. Thrombocythemia often presents with splenomegaly and a platelet count >1000.

Therefore, criteria for urgent haematology referral are if:

·      The PLT count exceeds 1000 x 10⁹ / L

·      There is splenomegaly

·      There is a recent history of thromboembolism

·      The PLT count is >600 x10⁹/L and the patient is at high risk of thromboembolism or CVD

·      There are neurological symptoms

·      There is abnormal bleeding

·      There are any signs of malignancy or

·      There are any other significant abnormal FBC indices 

If the urgent referral criteria are not present, we will then look for causes by doing the following initial investigations: 

·      A repeat FBC

·      A blood film

·      Inflammatory markers like ESR and CRP

·      Ferritin and iron studies and we will also

·      consider doing a coeliac screen as it can be associated with thrombocytosis 

If the patient is asymptomatic and there is no obvious cause, we will repeat the FBC 4-6 weeks later. If the thrombocytosis persists >450, we will refer to haematology routinely. 

The next section is thrombocytopenia, which is defined as a low platelet count below 150 x 10⁹/L. We need to remember that thrombocytopenia can frequently be an artefact, stemming from platelet clumping, rather than reflecting an actual decrease in platelet count. We should always confirm it with a second FBC and a blood film report. 

We will enquire about travel, drugs and alcohol because possible causes of thrombocytopenia include:

·      Alcohol excess

·      Recreational drugs

·      Malaria

·      TB

·      Liver & Renal disease

·      Medications, for example, NSAIDs, Heparin, Digoxin, Quinine, anti-epileptics, antipsychotics, and PPIs

·      B12 and folate deficiency

·      Viral infection including:

o  EBV (it usually resolves within few weeks in this case)

o  HIV and

o  Hepatitis B and C

·      Malignancy

·      Bone marrow failure like in aplastic anaemias

·      Immune thrombocytopenic purpura or ITP and

·      Autoimmune diseases, like SLE 

Baseline investigations will include: 

·      Repeat FBC and blood film

·      Vit B12 and folate

·      Ferritin and iron studies

·      Inflammatory markers such as ESR and CRP

·      Autoimmune profile

·      Renal, liver and thyroid function tests

·      HIV, hepatitis B and C serology and

·      Any other test suggested by the clinical history or examination findings 

We should arrange a hospital urgent same day assessment if the platelet count is <20 with: 

·      Active Bleeding

·      An abnormal blood film like Blasts or Fragments on the blood film or an

·      Altered Conscious Level Or Confusion 

We should make an urgent referral to haematology if: 

·      The platelet count is 50-100 and there is splenomegaly, lymphadenopathy, other cytopenias, the patient is pregnant or there is upcoming surgery or if

·      The platelet count is <50. In this case, we will stop all antiplatelet agents and anticoagulants as it would be unsafe to continue. 

If the platelet count is over 50 and the urgent referral criteria are not present, we will repeat the FBC after 4-6 weeks and refer to haematology routinely if the thrombocytopenia persists and remains unexplained.

 Now, next, let’s have a look at neutrophilia, which is when the neutrophil count is raised, that is, over 7.5. 

Infection is the most common cause but other possible causes are: 

·      Infection

·      Inflammation

·      Steroids

·      Pregnancy

·      Smoking

·      Underlying Malignancy including Lymphoma and Leukaemia

·      Connective tissue disease like RA

·      Haemorrhage

·      Haemolysis

·      Hypoxia and

·      Tissue damage including infarction 

If the cause is unclear, we will investigate further by doing: 

·      A repeat FBC

·      A Blood Film

·      Inflammatory markers such as ESR and CRP

·      Renal and liver function tests

·      Autoimmune screen and

·      Any other tests led by history 

Criteria for urgent haematology referral will include a high suspicion of leukaemia because of: 

·      A leucoerythroblastic film or an

·      Absolute Neutrophil count, ANC > 50 x10⁹/L  

We will make an early routine haematology referral, that is, without waiting for a repeat FBC, if the neutrophil count is >15 and: 

·      There is splenomegaly or

·      There are other FBC abnormalities.

Otherwise, we will repeat the FBC 6 weeks later and we will refer to haematology routinely if: 

·      The neutrophilia persists and remains unexplained 

Let’s now look at neutropenia, which is when the neutrophil count is low. A normal neutrophil count in adults is from 2.0 to 7.5. However, an isolated low neutrophil count is very common and a neutrophil count of between 1-5 -2.0 x 10⁹/l, whilst below the normal range, is unlikely to be of any clinical significance. Also, people of Afro-Caribbean or Middle Eastern ethnicity have a lower normal range between 1 and 1.8 x 10⁹/l, which is also referred to as constitutional or ethnic neutropenia. This is of no clinical consequence and we should only refer them if their neutrophils are <1.0 x 10⁹/l on repeat testing. 

For everybody else and for the purpose of this episode, we will say that neutropenia is when the neutrophil count is below 1.5. 

Possible causes of neutropenia are: 

·      Drugs e.g. Phenytoin, Carbimazole, Antipsychotics and Clotrimoxazole

·      Malignancy, like myeloma, bone marrow infiltration and chemo or radiotherapy

·      Vitamin B12 and / or folate deficiency

·      Iron deficiency

·      Autoimmune diseases

·      Any viral infection including EBV, HIV and Hepatitis B and C

·      Excess alcohol

·      Liver disease and cirrhosis and, as already mentioned, the

·      Ethnic variation in people of Afro-Caribbean and Middle Eastern descent  

We should send the patient to hospital as an emergency if: 

·      There is any evidence of sepsis

·      The neutrophil count is <1 and:

o  The patient is on chemotherapy

o  There is lymphadenopathy

o  There is splenomegaly or

o  There is other cytopenia 

We should make an urgent haematological referral on a cancer pathway if: 

·      The neutrophil count is <0.5 and the patient is otherwise well

If the neutrophil count is >0.5 and the patient is well, we will repeat the blood test within 1 week and investigate the cause by doing:  

·      A repeat FBC

·      A blood film

·      Vitamin B12

·      Folate

·      Ferritin and iron studies

·      Autoimmune screen

·      HIV and

·      Hepatitis B and C serology 

If the patient is well and the cause remains unknown, we will:

·      Refer to haematology urgently if the neutrophil count remains <1 but

·      If the neutrophil count is between 1 and 1.5, we will monitor the FBC for 4-6 weeks and refer to haematology routinely if: 

o  The neutrophil count remains below 1.5 (or 1 in African-Caribbean patients)

o  There are other FBC abnormalities or

o  There is a history of infections or ulcers 

The next section refers to lymphocytosis, which is when the lymphocyte count is high that is, more than 3.5 x10⁹ / L. 

Possible causes of lymphocytosis are: 

·      Viral infections especially

o  Glandular fever but also others such as:

o  Measles, mumps, rubella

o  EBV and

o  CMV

·      Bacterial infections, e.g. pertussis infection or whooping cough

·      Lymphoproliferative disorders (such as Acute or Chronic Lymphatic Leukaemia or non-Hodgkins lymphoma)

·      Post-splenectomy

·      Rheumatoid arthritis

·      Smoking

·      Stress and

·      Vigorous exercise

If there are features of acute or recent viral illness and the patient is otherwise well, we will repeat the FBC once resolved after 4-6wks.

We will refer to haematology urgently if: 

·      The Lymphocytosis is >20x10⁹/L

·      There are other cytopenias

·      There is Lymphadenopathy

·      There is Splenomegaly or if

·      There are B symptoms, that is:

o  Unexplained fever >38

o  Drenching night sweats

o  Weight loss  

Otherwise, if the lymphocyte count is >5, we will repeat the blood in 4 to 6 weeks and investigate the cause by doing:

·      A repeat FBC

·      A Blood film

·      Inflammatory markers such as ESR and CRP

·      Glandular fever screen or other virology serology where indicated due to the clinical presentation and we will also request

·      Immunophenotyping screen 

And after this, we will refer to haematology routinely if the lymphocytosis persists and remains unexplained. 

The next section is lymphopenia, when the lymphocyte count is low, that is below 1 x 10⁹/L.

Possible causes of lymphopenia are:

·      Elderly patients

·      Excess alcohol

·      Malnutrition

·      Medication, for example steroids and chemotherapy

·      Infection including legionella, HIV and hepatitis B and C and post viral lymphopenia is common

·      Malignancy for example, lymphoma, bone marrow infiltration, and myeloma and we should consider a myeloma screen if there are suggestive symptoms.

·      Renal or hepatic impairment

·      Autoimmune conditions like RA and SLE

·      Sarcoidosis

·      Anorexia Nervosa and

·      Primary immune deficiency 

We will refer to haematology urgently if the lymphocyte count is <1 and there are any red flags. Red Flag signs in lymphopenia are: 

·      Recurrent infections or

·      B symptoms, that is :

o  Unexplained fever >38

o  Drenching night sweats

o  Weight loss 

If there are no red flags, we will do a new blood test in 6 weeks and look for causes. So, we will do: 

·      A repeat FBC

·      A blood film

·      Renal and liver function tests

·      Inflammatory markers such as ESR and CRP

·      Autoimmune profile

·      Viral serology as appropriate depending on the clinical presentation and a

·      Myeloma screen if symptoms justify it 

If the cause is found, we will refer to the appropriate specialist department. However, if it persists and remains unexplained, we will refer routinely to haematology. 

There may be times when, if the lymphocyte count is >0.5x10⁹/L and the patient is >70 years of age and otherwise well, we could consider just monitoring the FBC, but this will depend on our clinical judgement.

The next section refers to eosinophilia, when the eosinophil count is high. There may be local variations in the threshold but, in general, eosinophilia is defined as an eosinophil count over 0.5 x 10⁹/L.

Examples of possible causes of eosinophilia are: 

·      Asthma

·      Skin disease like eczema, atopic dermatitis, urticaria, and psoriasis

·      Infections: especially those due to parasites (like hookworm, schistosomiasis and giardiasis), fungal infections as well as TB and malaria.

·      Drugs such as penicillin, allopurinol, amitriptyline, and carbamazepine but in fact any drug is a possible cause

·      Connective tissue disease like rheumatoid arthritis, and polyarteritis nodosa,

·      Solid malignancies, for example breast, renal, stomach and lung cancer

·      Myeloproliferative disorders like leukaemia and lymphoma

·      Respiratory diseases such as bronchiectasis, and cystic fibrosis

·      Endocrine conditions like Addison’s and

·      Post-splenectomy 

If the eosinophil count is >2.5, we will look for signs of organ damage and consider urgent admission if there are red Flags like: 

·      Severe symptoms secondary to organ involvement like:

o  difficulty breathing

o  chest pain

o  abdominal pain, or

o  neurological symptoms or

·      other Complications such as tissue damage, venous thromboembolism, or end-organ damage like AKI or heart failure. 

Criteria for urgent referral to haematology are:  

·      Leucoerythroblastic film or an

·      Absolute Eosinophil Count > 5 x10⁹/L,  

If the eosinophil count is >0.5 and the patient is well, we will check the travel and drug history and check for any evidence of atopy. We will then repeat the blood test within 1 to 2 weeks and look for possible causes.

 Initial investigations will include: 

·      A repeat FBC

·      Blood film

·      Inflammatory markers like ESR and CRP

·      Immunoglobulin E

·      Autoimmune profile

·      Renal and liver function tests

·      Bone profile

·      LDH

·      Vitamin B12 and folate

·      Chest X-ray (e.g. if TB or pulmonary sarcoidosis are suspected)

·      Stool culture for ova, cysts and parasites

·      Serological antibodies for threadworm or other nematode infection and

·      Serological antibodies for Schistosomiasis depending on the travel history and after discussion with microbiology 

If the cause is found, we will treat it accordingly. However, we will refer to haematology routinely if the eosinophilia remains unexplained and 

·      It is more than 1.5 for 3 months or longer or

·      if it is rising without an obvious cause. 

The final section refers to monocytosis when the monocyte count is raised, that is over 0.8 x 10⁹/L. 

Possible causes of monocytosis include: 

·      CMML or Chronic Myelomonocytic Leukemia

·      Myelodysplasia

·      Hodgkins’s lymphoma and

·      Infections such as:

o  Malaria

o  Tuberculosis

o  Brucellosis

o  Infective endocarditis and

o  Rickettsial infections 

Criteria for urgent haematology referral would be: 

·      Evidence of CMML features on blood film

·      A persistently raised monocyte count >1.5 (which is typical of CMML)

·      Associated cytopenias, particularly if involving multiple blood cell lineages or of there is any

·      Clinical Suspicion of Hematologic Malignancy 

If the monocyte count is >0.8 and the patient is well, we will check the travel history and check for any evidence of malignancy. We will then repeat the blood test and look for possible causes.  

Initial investigations could include: 

·      A repeat FBC

·      A blood film

·      Inflammatory markers like ESR and CRP

·      Any investigation as appropriate based on clinical suspicion, for example:

o  A chest X-ray to screen for Tb

o  Malaria parasites, and

o  Serological tests for infectious diseases such as Brucella, Epstein-Barr virus, and cytomegalovirus 

If the monocytosis remains unexplained and over 0.8 we will refer to haematology. 

Well, this is the end of the clinical scenarios. I have created a quick reference guide based on the guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners which you are welcome to have a look at. Where there was a discrepancy between their guidance, I have generally opted for the most conservative approach, for example, if one neutropenia guideline recommends referral if the neutrophil count is <1 and another when it is <1.5, my summary will show <1.5. If you are in any doubt, please consult the original guidance or seek local specialist guidance. I have included links to sources consulted in the document itself, which you will be able to download in the episode description. 

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In this podcast I go through a section of the NICE guideline NG12 “Suspected cancer recognition and referral”, last updated in December 2021. This episode will summarise the section “recommendations by site of cancer” covering skin cancer, head and neck cancers, haematological cancers, nervous system cancers, sarcoma and childhood cancers as well as other non-site specific symptoms of concern..

This podcast will be saved on a website.

NICE guideline NG12 can be found here:

https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer

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Transcript

Welcome to a new episode of the Clinical Guidelines in Primary Care podcast. My name is Fernando Florido and I am a GP in the United Kingdom. This is the third episode of the cancer guidelines series and is the last one reviewing the section “recommendations by site of cancer” of the NICE guideline NG12 “Suspected cancer recognition and referral”. In this podcast, I will cover skin cancer, head and neck cancers, haematological cancers, nervous system cancers sarcoma and childhood cancers as well as other non-site specific symptoms of concern. I hope that you enjoy the episode.

We will start with Skin cancers and the first ones to consider will be

Malignant melanoma and squamous cell carcinoma of the skin. For this,

We need to consider a cancer referral for melanoma in people with a pigmented or non‑pigmented skin lesion that suggests clinically the possibility of nodular melanoma or squamous cell carcinoma. This includes the use of dermoscopy

We must also refer people using a suspected cancer pathway referral to exclude melanoma if they have a suspicious pigmented skin lesion with a weighted 7‑point checklist score of 3 

We will quickly go through the Weighted 7‑point checklist which lists

Major features of the lesions (scoring 2 points each): 

·      change in size

·      irregular shape

·      irregular colour.

And Minor features of the lesions (scoring 1 point each): 

·      largest diameter 7 mm or more

·      inflammation

·      oozing

·      change in sensation.

In respect of Basal cell carcinomas

We should only consider a suspected cancer pathway referral for a basal cell carcinoma if there is particular concern that a delay may have a significant impact, because of factors such as lesion site or size. 

Otherwise it should be a routine referral.

We are now going t move to Head and neck cancers and the first one to look at is

Laryngeal cancer

For this we need to consider a suspected cancer pathway referral in people aged 45 and over with:

·      persistent unexplained hoarseness or

·      an unexplained lump in the neck. 

For Oral cancers

We need to consider a suspected cancer pathway referral in people with either:

·      an unexplained ulceration in the oral cavity lasting for more than 3 weeks or

·      a persistent and unexplained lump in the neck. 

We also need to consider an urgent referral to a dentist (for an appointment within 2 weeks) for assessment for possible oral cancer in people who have either:

·      a lump on the lip or in the oral cavity or

·      a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia. 

Then the dentist will decide whether these patients get referred through a full

For Thyroid cancers

We need to consider a cancer referral in people with an unexplained thyroid lump. 

The next section is Brain and central nervous system cancers

And the recommendations are different depending if the suspicion refers to adults or children and young people.

In Adults

We need to consider an urgent, direct access, MRI scan of the brain (or CT scan if MRI is contraindicated; to be done within 2 weeks) in adults with progressive, sub‑acute loss of central neurological function. That is, to be done within 2 weeks if there is progressive, sub‑acute loss of central neurological function. 

However, in Children and young people

We need to consider a very urgent referral (which means an appointment within 48 hours) in children and young people with newly abnormal cerebellar or other central neurological function. This is straightforward and simple, to be seen within 48 hours if there is newly abnormal cerebellar or other central neurological function. 

We will nnow look at the Haematological cancers

And for Leukaemia in adults

We need to consider a very urgent full blood count (which is to be done within 48 hours) with any of the following:

·      pallor

·      persistent fatigue

·      unexplained fever

·      unexplained persistent or recurrent infection

·      generalised lymphadenopathy

·      unexplained bruising

·      unexplained bleeding

·      unexplained petechiae

·      hepatosplenomegaly. 

To say this again, do a FBC within 48 hours if there is:

·      pallor

·      persistent fatigue

·      unexplained fever

·      unexplained persistent or recurrent infection

·      generalised lymphadenopathy

·      unexplained bruising

·      unexplained bleeding

·      unexplained petechiae

·      hepatosplenomegaly. 

In terms of Leukaemia in children and young people

Firstly, We need to Refer children and young people for immediate specialist assessment for leukaemia if they have unexplained petechiae or hepatosplenomegaly. 

Also, similarly to adults, we must offer a very urgent full blood count (within 48 hours) in children and young people with any of the following:

·      pallor

·      persistent fatigue

·      unexplained fever

·      unexplained persistent infection

·      generalised lymphadenopathy

·      persistent or unexplained bone pain

·      unexplained bruising

·      unexplained bleeding. 

For Myeloma

We need to offer a full blood count and blood tests for calcium and plasma viscosity or erythrocyte sedimentation rate in people aged 60 and over with persistent bone pain, particularly back pain, or unexplained fracture. 

And then We need to offer very urgent protein electrophoresis and a Bence–Jones protein urine test (that is within 48 hours) in people aged 60 and over with hypercalcaemia or leukopenia or if the ESR or plasma viscosity are abnormal and the presentation is consistent with possible myeloma. Obviously we will refer people using a suspected cancer pathway referral if the results of protein electrophoresis or a Bence–Jones protein urine test suggest myeloma. 

Finally, the recommendations are the same for Hodgkin’s and Non-Hodgkin's lymphoma but Separate recommendations have been made for adults and for children and young people to reflect that there are different referral pathways.

For adults Adults

We need to consider a suspected cancer pathway referral in adults presenting with unexplained lymphadenopathy or splenomegaly. When considering the referral, we will take into account any associated symptoms, particularly fever, night sweats, shortness of breath, pruritus or weight loss or, in the case of Hodgkin’s lymphoma, if there is alcohol‑induced lymph node pain. [. 

For Children and young people

We need to consider a very urgent referral (, that is, for an appointment within 48 hours) for specialist assessment in children and young people presenting with unexplained lymphadenopathy or splenomegaly. Equally, when considering the referral, we will take into account any associated symptoms, particularly fever, night sweats, shortness of breath, pruritus or weight loss. 

In respect of Sarcomas

Separate recommendations have been made for adults and for children and young people to reflect that there are different referral pathways.

In terms of Bone sarcoma in adults 

We need to consider a suspected cancer pathway referral for adults if an X‑ray suggests the possibility of bone sarcoma. 

For Bone sarcoma in children and young people

We need to consider a very urgent direct access X‑ray (to be done within 48 hours) in children and young people with unexplained bone swelling or pain. 

And then we need to consider a very urgent referral (for an appointment within 48 hours) for specialist assessment if an X‑ray suggests the possibility of bone sarcoma. 

In respect of Soft tissue sarcoma in adults

We need to consider an urgent direct access ultrasound scan (to be done within 2 weeks) in adults with an unexplained lump that is increasing in size. 

And then we need to consider a suspected cancer pathway referral (also for an appointment within 2 weeks) for adults if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists. 

Now, for Soft tissue sarcoma in children and young people the recommendations are exactly the same a for adults with the exception of where we said to be done or seen within 2 weeks it is now 48 hours. So, for children

We need to consider a very urgent direct access ultrasound scan (to be done within 48 hours) to assess for soft tissue sarcoma in children and young people with an unexplained lump that is increasing in size. 

And then we need to consider a very urgent referral (for an appointment within 48 hours) for children and young people if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists. 

We are now going to look at three types of Childhood cancers

And the first one is Neuroblastoma. For this

We need to consider very urgent referral (for an appointment within 48 hours) for specialist assessment for neuroblastoma in children with a palpable abdominal mass or unexplained enlarged abdominal organ. 

For Retinoblastoma

We need to consider urgent referral (for an appointment within 2 weeks) for ophthalmological assessment for retinoblastoma in children with an absent red reflex.

For Wilms' tumour

We need to consider very urgent referral (for an appointment within 48 hours) for specialist assessment in children with any of the following:

·      a palpable abdominal mass

·      an unexplained enlarged abdominal organ

·      unexplained visible haematuria. 

Finally, for Non-site-specific cancer symptoms

We need to say that Some symptoms or symptom combinations may be features of several different cancers. For some of these symptoms, the risk for each individual cancer may be low but the total risk of cancer of any type may be higher. This section includes recommendations for these symptoms.

Firstly we will look at Symptoms of concern in children and young people

We need to consider referral for children if their parent or carer has persistent concern or anxiety about the child's symptoms, even if the symptoms are most likely to have a benign cause. 

Lastly, in respect of Symptoms of concern in adults we will say the following:

For people with either unexplained weight loss, unexplained appetite loss and deep vein thrombosis , all of which can be a symptom of several cancers:

·      we must carry out an assessment for additional symptoms, signs or findings that may help to clarify which cancer is most likely and

·      then offer urgent investigation or a suspected cancer pathway referral depending on our clinical judgement

This is the end of this episode of the Clinical Guidelines in Primary Care podcast. I hope that you have enjoyed this episode and I hope that you will join me in the next one. Thank you for listening

The video version of this podcast can be found here:

https://youtu.be/KjALe_M-tIw

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through new and updated guidelines published in May 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The YouTube video on the management of headaches can be found here:

·      https://youtu.be/6AZttMzfFr0?si=yxPcoC4legE8zS_p

The Full NICE News bulletin for May 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-05-01&to=2024-05-31&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered can be found here:

Atogepant for preventing migraine - Technology appraisal guidance [TA973] can be found here:

·      https://www.nice.org.uk/guidance/ta973

Headaches in over 12s: diagnosis and management - Clinical guideline [CG150] can be found here:

·      https://www.nice.org.uk/guidance/cg150

The educational poster on the diagnosis of diagnosis of tension-type headache, migraine and cluster headache can be found here:

·      https://www.nice.org.uk/guidance/cg150/resources/diagnosis-poster-pdf-188219341

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Music provided by Audio Library Plus 

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Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at the NICE updates published in May 2024, focusing on what is relevant in Primary Care only.

And again, in May we have had very little new guidance relevant to primary care, in fact, there was only one guideline containing relevant information for us, the published technology appraisal on atogepant for migraine prophylaxis. You may remember that we covered this to some degree last month, when we reviewed the final draft NICE guidance on the subject. To make up for the shortage of Primary Care updates, we will also go through the clinical signs and symptoms that differentiate between tension-type headache, migraine and cluster headache. We will do so by reviewing the NICE guideline on headaches. If you are interested in the full headache guideline, covering headaches other than migraine, please see the corresponding video on this channel. The link is in the episode description.

Right, we have a migraine heavy episode, so let’s jump into it.

And let’s start with an overview. Although we are covering atogepant, the guidance on Rimegepant is very similar. Both Rimegepant and atogepant, are a new class of drugs, also known as gepants, that have been developed specifically for the treatment of migraines. They are a calcitonin gene-related peptide (or CGRP) receptor antagonist which works by blocking this CGRP receptor. And although the mechanism of action is not fully understood, we know that CGRP is a protein found in the sensory nerves of the head and neck and causes blood vessels to dilate, which can lead to inflammation and migraine pain. 

Unlike triptans, gepants do not cause vasoconstriction so they do not have the same cardiovascular contraindications and cautions as triptans.

Gepants can be used as an acute treatment of migraine and also as prophylaxis, but only if there have been at least 4 migraine days per month and where at least 3 previous preventive treatments have failed. Rimegepant is only recommended as prophylaxis of episodic migraines, whereas NICE has recommended atogepant as prophylaxis for both chronic and episodic migraines.

What’s the difference between episodic and chronic migraine?

The definition of episodic migraine is when there are fewer than 15 headache days each month. On the other hand, chronic migraine is when for more than 3 months there are at least 15 headache days a month, with at least 8 of those having features of migraine.

And here it is a good time to look at the clinical features of migraine compared to other types of headaches such as tension-type headache and cluster headache.

NICE has produced a poster that classifies the signs and symptoms for all three types of headaches. Let’s have a look at it:

The first thing to look at are the features of the headache in terms of:

·      Location

·      Quality

·      Intensity and

·      Duration

So, the location of the pain is:

·      Bilateral in tension type headache,

·      Unilateral or bilateral in migraine and

·      Unilateral, generally around the eye, above the eye and along the side of the head/face in cluster headache.

The quality of the pain is:

·      Pressing or tightening and non-pulsating in tension headache,

·      Pulsating in migraine although it can be described as throbbing or banging in young people and

·      It can be variable in cluster headache, as it can be sharp, boring, burning, throbbing or tightening.

As for the intensity of the pain, it can be:

·      Mild or moderate in tension-type headache

·      Moderate or severe in migraine and

·      Severe or very severe in cluster headache.

And for the duration, we will say that it generallylasts:

·      From 30 minutes to continuous in tension-type headache,

·      4 to 72 hours in migraine in adults although it can be shorter in young people, from 1 to 72 hours and

·      From 15 minutes to 3 hours in cluster headaches, so usually a shorter headache but much more intense.

Other factors that can help us differentiate between them are the effects that the headaches have on daily activities and whether there are other associated symptoms.

When considering the effects of daily living, we will say that:

·      Tension-type headache is not usually aggravated by routine activities,

·      Migraines are aggravated by, or causes avoidance of, routine activities and

·      Cluster headache causes restlessness or agitation.

And when considering other symptoms, we must be aware that:

·      Tension headaches don’t normally have any 

·      Migraine can be associated to light and sound sensitivity or nausea and vomiting.

·      If there is migraine with aura, we need to remember that typical aura symptoms can occur with or without headache and include:

o  Visual symptoms such as flickering lights, spots or lines and partial loss of vision

o  Sensory symptoms such as numbness and pins and needles and

o  Speech disturbance.

o  But in order to diagnose migraine with aura the symptoms must be fully reversible, develop over at least 5 minutes and last generally between 5 minutes and 1 hour.

Finally, in cluster headache, we will find, usually on the same side as the headache, associated symptoms such as:

·      A red or watery eye

·      Nasal congestion or a runny nose

·      A swollen eyelid

·      Forehead and facial sweating and

·      A constricted pupil or drooping eyelid

This is the summary poster that NICE has produced in the headache guideline. The link to it is in the episode description. Now that we have had a look at the clinical features, let’s go back to the management.

Currently, the most effective prophylactic options for people with chronic migraines who have already tried 3 prophylactic treatments are drugs that need to be injected, such as for example:

·      Erenumab and galcanezumab and

·      botox

So, oral treatments such as atogepant or Rimegepant offer more choice for patients.

When should we stop atogepant? We should stop it after 12 weeks if the frequency of migraines does not reduce by:

·      at least 50% in episodic migraine (that is, fewer than 15 headache days per month)

·      at least 30% in chronic migraine (that is, 15 or more headache days per month, with at least 8 of those having features of migraine).

Clinical trial evidence shows that atogepant reduces monthly migraine days more than placebo, but there is no clinical trial evidence directly comparing it with other preventive medicines. The results from indirect comparisons are uncertain and it is unclear whether atogepant is better or worse than the other treatments. However, it has lower costs than injectables, so it is recommended for preventing episodic and chronic migraine after 3 or more preventive medicines have been tried.

So now, with that in mind, let’s quickly look at the preventative treatment pathway that NICE has produced.

First, for prophylaxis treatment to be considered, the patient needs to have 4 or more migraine days per month.

In that case, we will give 1^st, 2^nd and 3^rd line prophylaxis with propranolol, amitriptyline and topiramate.

If there is inadequate response, then we move to 4^th line treatment.

For episodic migraine we can give Rimegepant.

For both episodic and chronic migraines, we have a number of injectable medications and atogepant as the only oral medication.

Finally, if it is chronic migraine, then the recommended treatment will be with botox.

Rimegepant is an oral lyophilisate that should be placed on the tongue or under the tongue and it will disintegrate in the mouth and can therefore be taken without liquid. However, atogepant is a tablet to be taken orally.

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE" as well as other institutions such as the British Association of the Urological Surgeons, as well as the American and European Urology Associations. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this video I will go through clinical guidance and advice on erectile dysfunction provided by the following institutions:

·      BAUS- British Association of Urological Surgeons

·      AUA- American Urology Association

·      EAU- European Association of Urology

·      NICE- National Institute for Health and Care Excellence

I will summarise the guidance from a Primary Care perspective only.

I am not giving medical advice; this podcast is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement.  

There is a YouTube version of this and other videos that you can access here:  

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The guidelines can be found here: 

·      BAUS: https://www.baus.org.uk/patients/conditions/3/erectile_dysfunction_impotence

·      NICE : https://cks.nice.org.uk/topics/erectile-dysfunction/

·      EAU: https://www.europeanurology.com/article/S0302-2838(21)01813-3/fulltext

·      AUA : https://www.bing.com/ck/a?!&&p=c5356f703dad5a45JmltdHM9MTY5Njg5NjAwMCZpZ3VpZD0xM2M1MGRhYS1mMDZkLTZlM2EtMWIzYi0wMTRhZjQ2ZDZkYjcmaW5zaWQ9NTI1OQ&ptn=3&hsh=3&fclid=13c50daa-f06d-6e3a-1b3b-014af46d6db7&psq=erectile+dysfunction+american+guideline&u=a1aHR0cHM6Ly93d3cuYXVhbmV0Lm9yZy9kb2N1bWVudHMvR3VpZGVsaW5lcy9QREYvRUQtSlUucGRm&ntb=1 

The shortened Sexual Health Inventory for Men (SHIM/IIEF-5) can be found here:

·      https://www.baus.org.uk/_userfiles/pages/files/Patients/Leaflets/SHIM.pdf

Thumbnail photo:

·      Image by Drazen Zigic on Freepik

·      a href="https://www.freepik.com/free-photo/young-man-having-headache-holding-his-head-pain-home_26343730.htm#query=upset%20men&position=1&from_view=search&track=ais"Image by Drazen Zigic/a on Freepik 

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• Music provided by Audio Library Plus  

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Transcript 

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through clinical guidance and advice on erectile dysfunction. For this I have looked at guidance by the:

·      BAUS- British Association of Urological Surgeons

·      AUA- American Urology Association

·      EAU- European Association of Urology

·      NICE- National Institute for Health and Care Excellence

·      As well as other local NHS Hospital Trusts protocols available in the London area.

I will summarise the guidance from a Primary Care perspective only.

So let’s jump into it.

Erectile dysfunction is seen in 50 - 55% of men between 40 and 70 years old. It is often associated with obesity, high blood pressure, high cholesterol and diabetes and most treatable causes can be identified by a clinical history, physical examination and routine blood tests.

And we will start by taking a detailed sexual history. It is advisable to use validated patient questionnaires, such as the shortened Sexual Health Inventory for Men (SHIM/IIEF-5), to assess the presence, severity, and impact of erectile dysfunction. A link to this questionnaire can be found in the episode description. Otherwise, we will ask about:

·      onset, duration, and quality of erections;

·      whether night-time or early-morning erections are still present

·      whether there are problems with their sex drive or libido, arousal, and orgasm;

·      whether there are symptoms of premature ejaculation or symptoms of prostatic obstruction because they are often associated with erectile dysfunction and

·      whether the relationship with their partner is affected.

We will then ask about lifestyle factors such as their:

·      Job and work pressures

·      Ability to exercise

·      Smoking and alcohol and

·      Drug consumption

And we will then look at their past medical history for other medical conditions which may be contributing to it. We must remember that ED can be a marker for cardiovascular disease.

Then we will perform a general physical examination checking their:

·      BP, heart rate,

·      Height, weight and waist circumference,

·      peripheral pulses and the nerve reflexes in their legs.

·      We will also look for any abnormality of the penis or testicles and

·      We will check for gynecomastia or possible signs of hypogonadism.

·      Rectal examination may be performed to assess the anal tone and to examine the prostate.

After this we should do a few routine tests that will normally include:

·      HbA1c, lipid profile, and fasting morning testosterone level (that is, before 11AM) in all men.

·      Other blood tests such as a FBC, renal, liver and thyroid function tests, and PSA can be done depending on our clinical judgement.

·      We should also consider urinalysis to test for glycosuria and haematuria

If the free testosterone level is low or borderline, we will repeat it together with FSH, LH, sex hormone binding globulin, and prolactin levels. If on repeat testing, testosterone is still low and LH is high, then we are talking about primary hypogonadism, whereas if testosterone is low and LH is also low, then it would be secondary hypogonadism.

When considering the possible cause, we should bear in mind that a physical cause normally has a gradual onset of symptoms, lack of tumescence, and low-to-normal libido, whereas a psychogenic cause normally has a sudden onset, low libido, and good quality spontaneous or self-stimulated erections.

A psychological component, often called "performance anxiety", is common in men with ED, as well as relationship issues; stress; anxiety; and depression. However, a purely psychological problem is seen in only 10%.

Of the 90% of men who have an underlying physical cause, the main abnormalities found are:

·      Up to 40% of men may have cardiovascular disease, for example, heart disease, hypertension and peripheral artery disease

·      Up to 33% of men may have diabetes 

·      Up to 11% of men may have hormonal or drug problems. Examples of

o  Hormonal problems are hyperprolactinaemia and hypogonadism and

o  Drugs commonly associated with ED are:

§ Antihypertensives and diuretics,

§ Antipsychotics and antidepressants,

§ Antihistamines,

§ methadone and

§ recreational drugs such as heroin and cocaine.

§ If a drug cause is suspected, we will consider stopping or switching the medication, depending on our clinical judgement.

·      Around 10% of men may have neurological disorders, for example, MS, Parkinson's disease, stroke, or other diseases of the spinal cord or central nervous system

·      Up to 3-5% of men may have a history of pelvic surgery or trauma and

·      Between 1 to 3% of men will have anatomical abnormalities like phimosis, short penile frenulum, Peyronie’s disease, inflammation, penile curvature and prostate cancer

When it comes to treatment in Primary care, we should advise on sources of information and support as well as encouraging lifestyle improvements. In fact, losing weight and increasing exercise can dramatically improve erectile dysfunction. by up to 70%.

We should obviously optimise the management of any underlying conditions and, if clinically appropriate, we should consider drug treatment with a phosphodiesterase-5 (PDE-5) inhibitor.

However, before offering PDE-5 inhibitors we will need to do a cardiac risk stratification which will assess men into low-, intermediate-, or high-risk cardiovascular categories, depending on their risk factors and co-morbidities. Men at low risk would be asymptomatic doing moderate exercise, and may have controlled hypertension, mild stable angina, mild valvular heart disease and mild heart failure or may have had an uncomplicated MI or a successful revascularisation procedure

Men with a more significant cardiac history will be at intermediate or high risk and we would normally arrange a referral to a cardiologist for advice and recommend stopping all sexual activity until the specialist assessment.

The European Association of Urology estimates that sexual activity is equivalent to walking 1 mile on the flat in 20 min or briskly climbing two flights of stairs in 10 seconds. Men who can complete this level of exercise without symptoms are deemed to be low risk and those who would struggle would be referred to cardiology for further assessment, including an exercise ECG. Sexual activity is generally considered to be equivalent to 4 min of the Bruce treadmill protocol.

We should refer to secondary care:

·      As an emergency if there is priapism (that is, painful prolonged erection for more than 4 hours following ED treatment).

·      To Urology if there is anatomical abnormality; young age or not responding to maximum tolerated dose of at least two PDE-5 inhibitors.

·      To Endocrinology if we suspect testosterone deficiency or hypogonadism.

·      To Cardiology if at high or intermediate cardiac risk of sexual activity and

·      To Psychosexual and relationship counselling, or mental health services if there is a psychogenic cause or severe mental health condition.

Alternatively, if we decide to prescribe a PDE-5 inhibitor in Primary Care, we will:

·      Explain that these drugs will have no effect on their sex drive and that they require sexual stimulation to be effective

·      And that sildenafil 50 mg tablets (Viagra Connect®) can be purchased over-the-counter without a prescription.

·      We will warn, however, that ED medications are amongst the most commonly counterfeited medicines in Europe and that buying online should only be through legitimate sources like registered pharmacies 

·      and we will advise about the importance of dose timing.

o  Sildenafil should be taken about one hour before planned sexual intercourse and the effect can last about 4-5 hours. We also need to explain that food intake can reduce the absorption of sildenafil by an average of one hour.

o  On the other hand, tadalafil for example needs to be taken only 30 minutes before sexual intercourse, has a duration of up to 36 hours and food ingestion has not effect on it.

·      We will also explain that PDE-5 inhibitors, except generic sildenafil, are not automatically prescribable on the NHS. Therefore, before prescribing it, we need assess whether the man qualifies for an NHS prescription and, if not, we will offer a private prescription. NHS prescriptions should be endorsed SLS if the man qualifies for NHS treatment because of:

o  diabetes,

o  Neurological conditions such as multiple sclerosis, Parkinson's disease, spina bifida etc,

o  prostate cancer,

o  pelvic trauma like in pelvic injuries, radical pelvic surgery or prostatectomy,

o  renal failure treated with dialysis or by transplant or

o  Is experiencing 'severe distress' as assessed by a specialist

o  However, as already mentioned, generic sildenafil does not need to be endorsed with 'SLS' for NHS prescribing.

·      Phosphodiesterase-5 (PDE-5) inhibitors are usually taken intermittently as needed, normally as one treatment dose per week on the NHS. However, if clinically appropriate, NICE says that a higher frequency may also be prescribed on the NHS.

After the initial prescription:

·      we will follow-up the patient after 6–8 weeks, and, if there is a poor response,

·      we will consider increasing to the maximum dose, trying each PDE-5 inhibitor 4–8 times at the maximum tolerated dose before switching to an alternative.

·      We will suggest a trial of at least two different PDE-5 inhibitors taken sequentially before considering the patient as a 'non-responder'.

·      If taking tadalafil, we can consider increasing the dose frequency, such as switching to once daily (rather than 'on-demand') dosing depending on our clinical judgement.

o  The BNF states that tadalafil may be prescribed daily as a dose of 5 mg once daily, for patients who anticipate sexual activity at least twice a week, although the dose can be reduced to 2.5 mg once daily, depending on the response,

·      We also need to be aware that hypogonadism and a low testosterone level may result in a reduced response or non-response to phosphodiesterase-5 (PDE-5) inhibitors.

I will now give just an overview of some prescribing information and, in terms of contraindications, we will not prescribe a phosphodiesterase-5 (PDE-5) inhibitor if there is:

·      Unstable angina or angina occurring during sexual intercourse.

·      Regular or intermittent use of nitrates in any form

·      Hypotension (that it, a systolic blood pressure below 90 mmHg).

·      A Recent MI or stroke or

·      A history of non-arteritic anterior ischaemic optic neuropathy (NAION).

There are a number of other contraindications for specific PDE-5 inhibitors in renal or hepatic impairment and other cardiovascular conditions, so I would recommend looking at the specific recommendations for whichever drug you intend to prescribe. Equally, there is also a long list of cautions which we would need to check for each individual patient.

In terms of drug interactions, there is a severe interaction with nitrates and concurrent use of PDE-5 inhibitors and nitrates, including nicorandil, or amyl nitrate (also known as 'poppers') are absolutely contraindicated due to the risk of hypotension.

There is also an increased risk of hypotension with alpha-blockers and sacubitril/valsartan so caution is advised. 

Finally, just to mention that other treatments available for Erectile Dysfunction are:

·      Penile injections

·      Medicated urethral system for erection (MUSE)

·      Vacuum erection assistance devices (VEDs)

·      Vascular surgery/angioplasty and

·      Penile prostheses

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

The video version of this podcast can be found here:

https://youtu.be/W0LL-1BwV3w?si=OT-GNCXaHoA7dcbs

This podcast makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this video I will go through a National Patient Safety Alert released on 3.1.2024 by the Department of Health and NHS England on the shortage of GLP1 receptor agonists, touching on sections of the NICE guideline on type 2 diabetes as well as relevant pharmaceutical information, always focusing on what is relevant in Primary Care only. 

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.   

There is a podcast version of this and other videos that you can access here: 

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk 

The PDF document related to the safety alert on GLP- RA shortage can be found here:

·      https://www.cas.mhra.gov.uk/ViewandAcknowledgment/ViewAttachment.aspx?Attachment_id=104161

The safety alert on GLP- RA shortage can be found here:

·      https://www.cas.mhra.gov.uk/ViewandAcknowledgment/ViewAlert.aspx?AlertID=103245

The Central Alerting System Homepage can be found here:

·      https://www.cas.mhra.gov.uk/Home.aspx

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Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. In this episode I will go through a National Patient Safety Alert released on 3.1.2023 by the Department of Health and NHS England on the shortage of GLP1 receptor agonists, touching on sections of the NICE guideline on type 2 diabetes as well as relevant pharmaceutical information, always focusing on what is relevant in Primary Care only.

If you want to access the safety alert website or the associated PDF document, the link is in the episode description.

Right, let’s jump into it.

You are probably aware that the supply of GLP-1 receptor agonists continues to be limited, with supplies not expected to return to normal until at least the end of 2024. The supply issues have been caused by an increase in demand for these products for licensed and off-label indications.

The situation at the moment is that exenatide as Byetta® will be discontinued in March 2024. In addition, liraglutide as Victoza® continues to be out of stock and further stock is not expected until end of 2024. The supply of other agents such as injectable semaglutide as Ozempic® and Dulaglutide as Trulicity® may be unreliable and the shortages may cause significant issues.

So, what is the solution?

Well, oral semaglutide has come to the rescue. Semaglutide as Rybelsus® tablets are now available in sufficient quantities to support initiation of GLP-1 RA for type 2 diabetes in line with NICE guidance. 

So let’s remind ourselves of what NICE recommends for type 2 diabetes. 

NICE says that if triple therapy with metformin and 2 other oral drugs is not effective, not tolerated or contraindicated, we can consider triple therapy by switching one drug for a GLP‑1 receptor agonist if:

·      The BMI is 35 or higher and there are psychological or medical problems associated with obesity. We will adjust the BMI to 32.5 for people from Black, Asian and other minority ethnic groups or

·      For lower BMIs if:

o  insulin would have occupational implications or

o  weight loss would benefit other significant comorbidities.  

NICE also says that we should only continue GLP‑1 receptor agonists if there is a reduction in HbA1c of at least 1.0% or 11 mmol/mol and weight loss of at least 3% of the initial body weight in 6 months.  

And NICE also states that starting GLP1 RAs in combination with insulin should only happen following specialist advice and with ongoing support from a consultant-led service.  

So, what do we need to do until supply issues have resolved?

1. First, we must only prescribe GLP-1 RAs for licensed indications.

2. Second, we will prescribe Rybelsus® tablets for new initiations

3. Third, we should identify patients prescribed Byetta® and Victoza® and switch to Rybelsus® tablets, counselling patients accordingly and referring to structured education and weight management programmes where available

4. Fourth, we will discuss stopping GLP1-RA if patients have not achieved a beneficial metabolic response as per the NICE guideline, that is, again, a reduction in HbA1c of at least 1% or 11 mmol/mol and weight loss of at least 3% of initial body weight in 6 months. 

5. And finally, we should not double up a lower dose preparation or switch between strengths solely based on availability. 

So, if oral semaglutide is going to be prescribed a lot more, let’s familiarise ourselves with it and let’s have a look at the summary of product characteristics.

How do we initiate oral semaglutide or Rybelsus tablets?

The starting dose of oral semaglutide is 3 mg once daily for one month. After one month, the dose should be increased to a maintenance dose of 7 mg once daily. After at least one month on 7 mg, if necessary, the dose can be increased to a maintenance dose of 14 mg once daily to further improve glycaemic control.

The maximum recommended dose of oral semaglutide is 14 mg once daily but this should be achieved by prescribing one 14mg tablet, not two 7mg tablets.

What about if the patient is already on subcutaneous semaglutide? Well, switching between oral and subcutaneous semaglutide cannot be easily predicted because of the high pharmacokinetic variability of oral semaglutide. However, we can say that oral semaglutide 14 mg once daily is comparable to s.c. semaglutide 0.5 mg once weekly. An oral dose equivalent to 1.0 mg of s.c. semaglutide has not been established.

How should it be taken? It should be taken on an empty stomach, swallowed whole with a sip of water (up to a maximum of half a glass of water equivalent to 120 ml). Splitting, crushing or chewing the tablets may decrease the absorption.

Patients should wait at least 30 minutes before eating, drinking or taking other drugs. Waiting less than 30 minutes also decreases the absorption.

When oral semaglutide is used in combination with metformin, an SGLT2i or pioglitazone, the current dose of those drugs can be continued.

However, when used in combination with a sulfonylurea or with insulin, a reduction in the dose of sulfonylurea or insulin may be considered to reduce the risk of hypoglycaemia. Blood glucose self-monitoring is necessary for this reduction but otherwise, self-monitoring of blood glucose is not needed to adjust the dose of semaglutide.

No dose adjustment is required for patients with hepatic or renal impairment but semaglutide is not recommended in patients with end-stage renal disease.

When should we use it with caution?

Semaglutide should not be used in patients with bariatric surgery, severe congestive heart failure, type 1 diabetes mellitus or for the treatment of DKA. Diabetic ketoacidosis has been reported in insulin-dependent patients who had a rapid dose reduction of insulin following the start of oral semaglutide.

The use of GLP-1 receptor agonists may be associated with gastrointestinal adverse reactions that can cause dehydration, which in rare cases can lead to a deterioration of renal function. Nausea, diarrhoea, and vomiting tend to be mild to moderate in severity and of short duration normally during the first months on treatment.

Patients should be informed of the risk of acute pancreatitis and if it is suspected, semaglutide should be discontinued and, if confirmed, it should not be restarted. Caution should be exercised in patients with a history of pancreatitis.

In patients with diabetic retinopathy treated with insulin and s.c. semaglutide, an increased risk of developing diabetic retinopathy complications has been observed, and this risk cannot be excluded for oral semaglutide.

Because of a drug interaction, patient on levothyroxine should have their thyroid function tests monitored closely.

So, we have an oral medication that is simple to take and has few interactions. Why has it not been more widely recommended instead of the seemingly more problematic injections?

And the answer is because of its pharmacokinetic properties.

Oral semaglutide has a variable absorption and a low bioavailability, approximately 1% following oral administration. As we have mentioned, the absorption of semaglutide is decreased if taken with food or large volumes of water and a longer post-dose fasting period results in higher absorption.

The variability in absorption between patients is also high and if the treatment response is lower than expected, we need to be aware that it may be due to a low absorption and that 2-4% of patients will not have any exposure to it after oral administration.

On the other hand, with an elimination half-life of approximately 1 week, semaglutide will be present in the circulation for about 5 weeks after the last dose. The primary excretion routes are via the urine and faeces. 

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at Chat GPT generated case of heart failure with co-morbidities to see how the NICE guidelines could apply to it.

I am not giving medical advice; this video is intended for health care professionals; it is only my interpretation of the guidelines and you must use your clinical judgement. 

There is a YouTube version of this and other videos that you can access here: 

·      The NICE GP YouTube Channel: NICE GP - YouTube 

You can download my summary of the guideline with additional information here: 

·      https://1drv.ms/b/s!AiVFJ_Uoigq0l3uRYZ7-U3R808gA?e=2LT5XI

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Free Download / Stream: https://alplus.io/halfway-through 

Transcript

Hello everyone and welcome. My name is Fernando Florido and I am a GP in the United Kingdom.  

In today’s episode I look at the journey from diagnosis to treatment of a ChatGPT generated patient with heart failure and other co-morbidities to see how the NICE guidelines could be applied. Make sure that you stay for the whole episode because at the end, I am going to give you the pathophysiological reasons why ACEIs, ARBs, betablockers and MRA are so beneficial in heart failure, and I am sure that once you have understood it, you will never forget. 

By the way, I am not giving medical advice; this is for health care professionals and it is only my interpretation of the guidelines so you must use your own clinical judgement. 

If you want to download a copy of my summary of the NICE guidelines on Chronic heart failure, the link is in the episode description.

Remember that there is also a Youtube version of these episodes so have a look in the episode description.  

Right, so let’s have a look at our fictitious patient: 

- His Name is: John Smith

- His Age: 68

- Ethnicity: Caucasian

- Past Medical History includes: Obesity, Hypertension, Type 2 Diabetes, and Hyperlipidaemia 

His Current Symptoms are:

- Shortness of breath on exertion and lying down

- a Persistent cough

- Fatigue and weakness

- Bilateral ankle swelling

- And The symptoms have been developing gradually over the last 4-6 months but recently he has noticed more rapid weight gain which could be from fluid retention 

His usual medication is:

- Amlodipine 5 mg OD for hypertension

- Lisinopril 2.5 mg OD for hypertension

- Metformin 500 mg BD for type 2 diabetes and

- Atorvastatin 20 mg OD for hyperlipidaemia 

So, we have a 65-year-old Caucasian male who presents with shortness of breath, fatigue, ankle swelling, and a persistent cough. 

On examination we find the following:  

His BMI is 34, so he is obese.

His Weight is 97 and John says that this is 4Kg more than his usual weight

His BP is 151/92 mmHg and

On auscultation, he has lung crackles. His heart sounds are regular with no murmurs, and his heart rate is 96 bpm. Palpation of the chest reveals a laterally displaced point of maximum impulse consistent with an enlarged ventricle. 

His Oxygen saturation is 98%

And his Peak Flow is: 450 L/min (which is normal for his age and sex)

Abdomen showed no hepatomegaly and there is no raised JVP 

He has Slight bilateral pitting ankle oedema

His Urinalysis and His Temperature are normal  

Right, we have someone with lung crackles and a normal temperature and no other sings of infection, so it would be reasonable to suspect HF rather than bronchopneumonia. His main symptoms are suggestive of left sided heart failure although he also has some ankle oedema which is a possible symptom of right sided heart failure. However, he is also on amlodipine and at this stage we cannot be 100% sure of whether this is a side effect of his medication or secondary to heart failure.  

Let’s remember that typical symptoms of left-sided heart failure include cool clammy skin, cyanosis, a laterally displaced point of maximum impulse consistent with an enlarged ventricle, lung crackles and a gallop rhythm. On the other hand, signs in right sided heart failure include an elevated JVP, ankle of leg oedema, ascites, hepatomegaly, and hepatojugular reflux. Signs of both left and right sided heart failure can be present at the same time.  

In order to confirm the diagnosis of heart failure, we will need to measure the levels of the N-terminal pro-B-type natriuretic peptide, or BNP levels. In addition, and in order to exclude other diagnoses, NICE says that we should also arrange an ECG, a chest X-ray, especially as he has a persistent cough, other blood tests including full blood count, renal, liver, thyroid function, lipid profile, and HbA1c. Peak flow was normal for John but if we are in any doubt about a respiratory condition, we should also request spirometry testing. 

Right, so we are going to send him off to have some tests. Should we be doing anything else in the meantime? 

Well, if we feel that, clinically, he is having signs and symptoms of congestion and fluid retention, NICE says that we should offer diuretics for short term symptomatic relief. So, I would go for a loop diuretic, something like furosemide 20-80 mg daily depending on the severity of the symptoms and, obviously, the higher the dose, the closer that you will want to monitor him. But we should be seeing him again for a review within a day or two.  

I am going to say that his symptoms and signs are significant so I will start him on furosemide 80mg daily and see him in a couple of days or sooner if he does not feel better.  

Right, so, we organise the blood tests, to be done ideally the same day of next day and then we see him again to reassess and discuss the results. 

At the next appointment, John states that his symptoms are better, his breathing is easier and his ability to do physical activities has also improved. On examination 

His weight has gone down to 94.5 Kg but John says that his usual weight is around 93Kg 

His BP is slightly better but still high at 144/87 mmHg. Remember that NICE says that for patients under the age of 80 their target BP should be below 140/90.

On auscultation, there are now minimal crackles at the lung bases and heart sounds are normal and in sinus rhythm with no murmurs. His heart rate is also lower at 80 bpm. 

Oxygen saturation is 99% and

There is also less ankle swelling.  

His Blood tests show that:

• His creatinine is 130 and his eGFR is 75 , so reasonable renal function
• His HbA1c is 60 or 8%
• He has a Normal FBC, LFT and TFTs
• His TC is 4.8, LDL 3.4, HDL 1 and TG 0.9
• And his BNP Level: 800 ng/litre

So, what do we say here?

We know that, if there is no heart failure, we would expect the BNP to be below 400 and therefore, with a raised BNP we can fairly confidently say that this is likely heart failure.  

And because the symptoms have had an insidious onset over several months, we are going to say that he has chronic heart failure rather than anything acute that we should admit him to hospital for. 

It's important to note that the BNP level does not differentiate between heart failure with reduced ejection fraction (or HFrEF) and heart failure with preserved ejection fraction (or HFpEF). We will need to organise an echocardiogram for this.  

Also, we need to be aware that certain factors like obesity, African or African–Caribbean family background, and heart failure drugs can reduce BNP levels. Equally, they may be elevated for other reasons, for example, age over 70 years, ischaemia, tachycardia, hypoxaemia [including PE and COPD], renal failure, diabetes, or liver cirrhosis. John is both obese and has diabetes so he has factors that could be influencing his BNP in both directions.  

His HbA1c is also high so we will need to intensify his diabetes treatment. 

To know if his cholesterol levels on atorvastatin 20 mg are acceptable, we will need to look at his pre statin levels to be absolutely certain that he is on the right dose. 

His other test results show that

- his ECG is normal with no signs of arrhythmia or ischaemia:

- his Chest X-ray shows: Mild pulmonary congestion and

- his Spirometry is also normal ruling out respiratory obstruction or restriction:  

So, with these test results, we will discuss the diagnosis of heart failure with the patient and we will proceed with the referral for a echocardiogram. Because the BNP level is between 400 and 2000 ng/litre, he can have the echocardiogram withing 6 weeks. If it had been over 2000 ng/litre we would need to make urgent to be done within 2 weeks.  

NICE also says that the purpose of the echocardiogram is to exclude valve disease, assess the ventricular function, and detect intracardiac shunts.  

But now that we have a working diagnosis and that we are likely to be waiting for a few weeks for the echocardiogram, we need to start him on some further active treatment. And we have several issues with him:

1.   Hypertension

2.   Chronic heart failure

3.   Diabetes

4.   Lipids and prevention of CVD and

5.   Obesity 

So, let’s start with his hypertension. John is already on step 2 treatment, a combination of two drugs, amlodipine and lisinopril, none of which are at maximal doses. So, should we simply increase the doses of those drugs and then move to step 3 with 3 drugs if necessary? That would be the standard advice on the Hypertension guidelines. But not in his case. 

The NICE guideline on hypertension says that for people with hypertension and CHF we must first follow the guidelines on CHF. So, if the HTA guidelines says that betablockers and spironolactone are considered at step 4 and the CHF guidelines say differently, we need to put the HTA guidelines to one side and give priority to the CHF guideline.  

So, let’s have a look at the guidelines on CHF. What does it say about treatment? You may be familiar with the advice to give ACEIs, betablockers, mineralocorticoid receptor agonists or MRAs etc.  

But these drugs are recommended in HFrEF and the first problem is that we do not know what type of heart failure this patient has. Is it HFrEF or is it HFpEF? Because, when it comes to treatment, the advice for each one can be different. 

Could we assume that it is the most common type of heart failure? Unfortunately, that is not going to work because, at present, about 50% of patients with heart failure have HFpEF and the other 50% HFrEF. 

By the way, remember that heart failure with preserved ejection fraction is characterised by a left ventricular ejection fraction of 50% or more. Heart failure with reduced ejection fraction has an ejection fraction of <40%. And there is now a third type, which NICE refers to as HF with mildly reduced EF which is when the ejection fraction is between 40 and 50%. 

Right, so what do we do?

Well, we could look at the treatment of heart failure from 2 different perspectives:

·      One, Symptomatic treatment

·      And two, Preventative treatment 

Symptomatic treatment addresses the congestive symptoms. And NICE says that we can give Diuretics for the relief of congestive symptoms and fluid retention in both types of HF. We will titrate them up and down according to need but, in particular, NICE says that in heart failure with preserved ejection fraction we will normally give no more than a low to medium dose of loop diuretics (for example, less than 80 mg furosemide per day) and refer if this is not enough.  

The preventative treatment on the other hand is offered in order to reduce morbidity and mortality in the long run and it does not necessarily improve symptoms in the short term. These drugs are ACEIs or ARBs, betablockers, MRAs, ARNIs (which stands for Angiotensin Receptor-Neprilysin Inhibitors) and SGLT2 inhibitors. But all these drugs except the last one, SGLT2 inhibitors, confer these long-term benefits only to HFrEF, and we should not be pushing them if the patient has HFpEF.  

Up to very recently, the same applied to SGLT2 inhibitors but, NICE changed the advice in June 2023 and now recommends dapagliflozin for all types of heart failure. 

So, we conclude that not all drugs recommended for HF with reduced Ejection Fraction are recommended for HF with preserved Ejection Fraction. However, the opposite is true. General management for HFpEF can be applied to HFrEF.  

So, let’s see what drug treatment NICE recommends for HFpEF, which is basically the recommendations for all types of heart failure, and how they apply to our patient:

·      First, as we have already said, we can give low to medium doses of a loop diuretic, say furosemide 20-80 mg daily to relieve symptoms of fluid overload

o  Our patient is on furosemide 80 mg daily and this has had a significant improvement in his symptoms. There are still some fine crackles in both lung fields and I may not rush to reduce the dose too quickly, although a careful reduction could be tried, for example to 60 mg daily advising the patient to increase the dose again if there are worsening of symptoms.

• Second, Dapagliflozin is an option for treating symptomatic chronic heart failure on the advice of a heart failure specialist only
• John still has some symptoms and this drug may be beneficial, but in order to give it for heart failure, we would need to get specialist advice. But we will touch on this a little later.
• Third, We will review drugs which may cause or worsen heart failure and stop them if appropriate- examples of these drugs would be both recreational drugs such as alcohol and cocaine as well as medication such as nonsteroidal anti-inflammatory drugs, beta-blockers, and calcium-channel blockers
• Our patient does not abuse alcohol and on our advice, he will cut down or even stop. He does not use other recreational drugs and he is not taking NSAIDs or betablockers. However, he is taking a calcium channel blocker, amlodipine. Is this going to be a problem?
• NICE says that (Calcium-channel blockers | Treatment summaries | BNF | NICE) calcium channel blockers, with the exception of amlodipine, should be avoided in heart failure as they can further depress cardiac function and exacerbate symptoms and they can also increase mortality after an MI in patients with left ventricular dysfunction and pulmonary congestion.
• So, with that said, our patient does not have to stop amlodipine, which is fortunate because he still needs to for his hypertension. There was a question mark as to whether some of the ankle oedema is secondary to amlodipine but for now, I would leave it as it is and reconsider this prescription later when more information about the patient’s condition is known.
• Number 4, we will consider An antiplatelet drug if there is atherosclerotic CVD (which is not always the case in HF)
• And John does not have this so he does not need aspirin or clopidogrel
• Number 5, we should give A statin if the patient is at risk of atherosclerotic CVD as per the NICE guidelines on CVD prevention
• John has already been found to be at high risk of CV disease and he is already on atorvastatin 20 mg daily. But the guidelines on prevention of CVD state that after statin therapy we should aim for a reduction in non-HDL cholesterol of 40% or more. His current lipids show a TC of 4.8, and an HDL of 1 so his non-HDL cholesterol is 3.8 (TC-HDL). Looking at his previous records we find that before the statin his TC was 5.9 and his HDL was 0.9, therefore then his non-HDL cholesterol was 5. 40% of 5 is 2 so his target non-HDL cholesterol should be 3 and instead it is 3.8. he is not hitting the target of a 40% reduction and I would therefore advise him to increase the dose of atorvastatin to 40 mg daily and recheck his lipids and LFTs again in 3 months.

·     Number 6, part of the CHF management is the Management of other co-morbidities such as hypertension, diabetes, CHD, obesity, AF, COPD etc

o  John has hypertension, obesity and type 2 diabetes as co-morbidities.

o  Let’s look at the hypertension first. He is already on lisinopril and amlodipine and his BP is not down to target. We are worried that his amlodipine may be aggravating his ankle oedema, so I would probably elect not to increase the dose at this stage. However, It would make sense to increase the dose of lisinopril to, for example, 5mg OD, monitoring his BP and renal function. This way, if he has HFrEF, we are titrating one of the medicines that reduce mortality and morbidity in the long run. On the other hand, if he has HFpEF, we will still be managing it correctly by lowering his BP and improving one of his co-morbidities

o  Let’s now look at his diabetes, which is not well controlled with metformin 500 mg BD. NICE says that the first step is always metformin and if metformin is not enough or not tolerated, we will assess the patient’s cardiovascular risk and status. And if the patient has heart failure, atherosclerotic CVD or is at risk of it, we should start and SGLT2 inhibitor.

o  But you may be saying… did we not have to get a specialist opinion before giving an SGLT2 inhibitor for heart failure? And the answer is yes, if you are giving it for heart failure to someone without diabetes. But if the person has diabetes, it is the perfect opportunity to give it and treat both his diabetes and his heart failure, especially as it’s recommended for both HFrEF and HFpEF.

o  But wait a minute, this patient is not on maximal doses of metformin. His eGFR is >60 so his dose could go from 500 mg BD to the maximum, double that, 1000 mg BD. Should we do that first? And my answer would be perhaps at some point. But I would not do this at this stage. Although HF is not a contraindication to metformin, the BNF says amongst other things that “the Manufacturer advises caution in chronic stable heart failure (and to monitor cardiac function), and avoid in conditions that can cause tissue hypoxia.” John’s heart failure is far from stable at the moment so I would not risk increasing the dose of metformin at this stage. With heart failure there may be a degree of tissue hypoxia which could put him at risk of the most feared side effect of metformin, lactic acidosis. In fact, some of you may be thinking that we should have stopped his metformin at the first visit, And perhaps that would have been a good option too, although you would be then be dealing with a whole lot of other issues secondary to uncontrolled hyperglycaemia. Because his oxygen saturation on the first visit was 98% and his condition had developed over many months, I wouldn’t view stopping metformin as an urgent matter. Of course, if he had been truly unwell and hypoxic, that would have been the right thing to do.

o  Another co-morbidity to consider would be his obesity. So, lifestyle advice, maybe orlistat and further referral for support will be indicated at some point. But he has enough on his plate now, so I would park this for the time being and revisit it in future.

• Finally, in HFpEF NICE says that we need to refer if there is poor response to diuretic therapy or if valve disease is discovered.
• But John has responded well to furosemide and auscultation of his heart did not detect any murmurs, so hopefully there will not be anything significant there. But we will have to wait for the echocardiogram report to be completely sure. 

So, in summary:

·      We will continue furosemide either the same dose of 80 mg daily or more likely cautiously reducing it to 40-60 mg according to our clinical judgement, especially considering that

·      We are going to start an SGLT2 inhibitor, which also have a diuretic effect. Something like for example dapagliflozin 10 mg daily would be good.

·      We will also continue amlodipine 5 mg OD and

·      We will increase atorvastatin to 40 mg daily and

·      We will increase lisinopril to 5 mg, monitoring his renal function and

·      We will advise him to continue monitoring his weight and to let us know any concerns 

I would suggest that we see him possibly 7-10 days later to review his progress and medication but we will also give him very careful safety-netting advice to come sooner if anything does not go to plan 

Ok, so, When we see him next, John is feeling very much better, his breathing has improved as well as his tolerance to exercise. 

His weight is now 92.8 which is more like his usual weight.

BP is 138/82 mmHg

On auscultation, his chest is clear and his heart sounds are normal

Oxygen saturation is 99%

Ankle oedema has all but disappeared.

And His renal function has remained reasonably stable although since increasing lisinopril, his eGFR has decreased from 75 to 69 and his creatinine has risen from 130 to 143 

We have also received his Echocardiogram Result which shows:

- that There is evidence of left ventricular hypertrophy, possibly the effect of prolonged hypertension

-Right ventricular function and cardiac valves are normal and there are no cardiac shunts but

- he has a Left ventricular ejection fraction (LVEF) of 35%, so, being <40%, he has HFrEF 

So let’s have a look at the guideline for this. For the treatment of heart failure with reduced ejection fraction NICE says that: 

1. for First-line Treatment we need to give the maximal tolerated doses of:

1.   An ACE inhibitor and

2.   A beta-blocker licensed for heart failure

·      The beta-blockers licensed for heart failure in the UK are bisoprolol, carvedilol, and nebivolol.

·      And We will not withhold betablockers solely based on age or the presence of peripheral vascular disease, erectile dysfunction, diabetes, interstitial pulmonary disease, or COPD.

3.   NICE says that we should use our clinical judgement when deciding which drug to start first. 

4.   But we will not give an ACE inhibitor if there is haemodynamically significant valve disease until the valve disease has been assessed by a specialist.

5.   And We will give an ARB licensed for heart failure if there are side effects with ACE inhibitors. 

·      ARB licensed for heart failure in the UK are Candesartan, losartan, and valsartan.

6.   If there are persistent symptoms, we will then give a mineralocorticoid receptor antagonist (or MRA), such as spironolactone or eplerenone, in addition to an ACE inhibitor (or ARB) and beta-blocker 

OK, so John is already on lisinopril so we should start him on a betablocker next, for example bisoprolol starting at 1.25 mg daily increasing gradually according to the BNF. Also, we should also gradually increase his lisinopril and, as the blood pressure drops, it is likely that we will need to discontinue amlodipine. We will use our clinical judgement as to how quickly the titration of both lisinopril and bisoprolol is but NICE recommends doing so at short intervals (for example, every 2 weeks) until the target or maximum tolerated dose of both drugs is reached.   

But we have noticed that both John’s creatinine and eGFR have deteriorated since we increased the dose of lisinopril. Is that going to be a problem?

NICE says that we only need to worry and take further action if the creatinine level increases by more than 20% or the eGFR falls more than 15%.

John’s creatinine has increased by 10% and his eGFR has only decreased by about 8% so we should not be too concerned but we will keep monitoring it. 

In terms of monitoring, we will do a full clinical assessment at every review, measuring his BP and renal function, including sodium and potassium levels, before and 1 to 2 weeks after starting the drugs, and after each dose increment. We will also assess heart rate when giving betablockers. 

And we will not forget to monitor his HbA1c and his lipids after the management changes. 

NICE says that once the target or maximum tolerated dose is reached, we will monitor the treatment monthly for 3 months and then at least every 6 months, and at any time if he becomes acutely unwell.  

NICE says that we should monitor BNP levels only if:

·      The patient is under 75

·      there is heart failure with reduced ejection fraction and

·      the eGFR is above 60. 

So, we should monitor John’s BNP levels which will help track his response to treatment. 

A follow-up echocardiogram may be performed from time to time to assess if there have been changes in the left ventricular ejection fraction  

If his symptoms do not improve with the initial treatment with an ACEI or ARB and a betablocker, We will consider the addition of Mineralocorticoid Receptor Antagonists (MRA), for example, something like spironolactone 25mg daily increasing to 50 mg, according to response.

I am obviously describing the steps that we would have to follow according to the guidelines but, in practice, we would also refer him to see a cardiologist, early on, to ensure that he gets specialist advice and that his treatment is fully optimised 

For your information, NICE recommends that the following drugs should be initiated by a Specialist only

·      Ivabradine

·      Sacubitril valsartan

·      Hydralazine in combination with nitrate

·      Digoxin 

Other General Recommendations for John will include: 

1. an annual flu vaccination and a one-time pneumococcal vaccination

3. Advise to stop Smoking and reduce alcohol to recommended levels and

6. in terms of Sodium and Fluid Consumption:

   - we will not routinely restrict them but will enquire about his intake and.

   - If John experiences dilutional hyponatremia, fluid restriction may be advised and

   - If John has high levels of salt and/or fluid consumption, he will be encouraged to reduce.

   - And Finally, we will advise him to avoid salt substitutes containing potassium. 

Right, so we will make this the end of this patient’s journey with us.   

But, as promised, let’s talk pathophysiology and the reason why ACEIs, ARBs, MRAs and betablockers have long term benefits in heart failure.

And we will start by saying that Heart failure with reduced ejection fraction, even in its early subclinical stages, leads to reduced organ perfusion, precisely because of the reduced ejection fraction. To compensate for this, the body triggers a response that stimulates the sympathetic system and the RAAS. Stimulation of the sympathetic system produces vasoconstriction and faster and stronger myocardial contractions, whilst the stimulation of the RAAS causes vasoconstriction due to the angiotensin effect and increased fluid and sodium reabsorption due to the aldosterone effect, both of which lead to an elevated blood pressure. Although these mechanisms may initially improve tissue perfusion, they also have a remodelling effect on the heart, eventually inducing harmful structural changes which exacerbate heart failure over time.

The mentioned medications act through different pathways to reduce the heart's workload, enhance cardiac output, and counteract the detrimental effects of the neurohormonal activation. The betablockers do so by blocking the sympathetic system and the ACEIs, ARBs and MRAs by blocking different sections of the RAAS. They are all essential components of evidence-based heart failure management, reducing hospitalisations and mortality.

Given that one of the problems of the RAAS is fluid and sodium retention, you might wonder why patients aren't routinely advised to reduce their fluid and sodium intake. Well, in this world of evidence-based medicine the answer is easy. The reason is that there is currently no research evidence supporting this advice. While it might seem intuitively reasonable, we should refrain from recommending it unless there is concrete evidence indicating that the patient's salt consumption or fluid intake is excessive. 

But remember that this is only my interpretation of the guidelines. 

We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye 

The video version of this podcast can be found here: https://youtu.be/XZxllA7iSIk?si=2d9kxQLJOY6ER0iu

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through new and updated guidelines published during 2023 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

The Clinic BP targets flowchart can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mFp2iUfq8rimJSmo?e=BnJaCD

The Clinic BP targets tables can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mFtrsXeUGOB58DKE?e=J7filE

There is a podcast version of this and other videos that you can access here: 

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

Music provided by Audio Library Plus 

Watch: https://youtu.be/aBGk6aJM3IU 

Free Download / Stream: https://alplus.io/halfway-through 

The Full NICE News bulletin for January 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-02-01&to=2024-02-29&ndt=Guidance&ndt=Quality+standard

The links to the update guidance covered can be found here:

The guidance on chronic heart failure in adults can be found here:

·      https://www.nice.org.uk/guidance/qs9

The guidance on UTI in adults can be found here:

·      https://www.nice.org.uk/guidance/qs90

The guidance on Type 1 diabetes in adults can be found here:

·      https://www.nice.org.uk/guidance/qs208

The guidance on Type 2 diabetes in adults can be found here:

·      https://www.nice.org.uk/guidance/qs209

The full NICE guideline on “Hypertension in pregnancy: diagnosis and management” can be found here:

·      https://www.nice.org.uk/guidance/ng133

Dapagliflozin for treating chronic heart failure with preserved or mildly reduced ejection fraction:

·      https://www.nice.org.uk/guidance/ta902

Empagliflozin for treating chronic heart failure with preserved or mildly reduced ejection fraction:

·      https://www.nice.org.uk/guidance/ta929

Obesity in adults: identification, assessment and management

·      https://www.nice.org.uk/guidance/cg189

Quantitative faecal immunochemical testing to guide colorectal cancer pathway referral in primary care

·      https://www.nice.org.uk/guidance/dg56

Joint guidelines from ACPGBI and BSG can be found at: 

·      https://www.acpgbi.org.uk/resources/1075/fit_in_patients_with_signs_or_symptoms_of_suspected_crc_a_joint_guideline_from_acpgbi_and_bsg 

Chronic obstructive pulmonary disease in adults: quality standard

·      https://www.nice.org.uk/guidance/qs10

Rimegepant for treating migraine: 

·      https://www.nice.org.uk/guidance/ta919

Transient loss of consciousness ('blackouts') in over 16s:

·      https://www.nice.org.uk/guidance/cg109

Bipolar disorder: assessment and management:

·      https://www.nice.org.uk/guidance/cg185

Cardiovascular disease: risk assessment and reduction, including lipid modification:

·      https://www.nice.org.uk/guidance/ng238 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, as usual, I intended to do the usual monthly review of the NICE updates published in February 2024, focusing on what is relevant in Primary Care only. But, surprisingly and for the first time since I started doing these monthly updates, I have not found any new information relevant to General Practice. 

So, instead, we are going to do an overview of what I think were some of the most relevant updates published in the whole of 2023.  

Right, so let’s jump into it. 

In January 2023 

There were updated quality statements on chronic heart failure in adults. They say that: 

1.   If we suspect HF, we will check the BNP levels.

2.   If the result if high, we will organise an echocardiogram

3.   If the echo confirms heart failure with reduced ejection fraction, we will give optimal doses of an ACE inhibitor or ARBs and a beta-blocker. If clinically indicated, we will also give a mineralocorticoid receptor antagonist like spironolactone, an SGLT2 inhibitor, like dapagliflozin or empagliflozin, and refer for other specialist drugs if necessary.

4.   And We will review patients with heart failure within 2 weeks of any medication change and at least every 6 months thereafter.  

In February 2023

There were new quality statements on UTI saying that

1.   We can diagnose women under 65 with a UTI without having to do a urine dipstick as long as they have at least 2 key urinary symptoms.

2.   Equally, we can also diagnose catheterised patients with a UTI based on symptoms without needing a urine dipstick.

3.   Three, We will give a 3-day course of antibiotics to non-pregnant women with an uncomplicated lower UTIs, but a 7-day course to men and pregnant women with the same. And

4.   Four, We will refer patients with recurrent symptoms.

In March 2023

There were changes in the diabetes quality statements saying that:

·      We should offer continuous glucose monitoring to patients with type 1 diabetes and also to those with insulin-treated type 2 diabetes if they cannot self-monitor independently

·      Also that Adults with type 1 diabetes aged 40 and over should be offered a statin and