Primary Care Guidelines

The video version of this podcast can be found here:

·      https://youtu.be/pkP0aqNGqGI

This channel may make reference to guidelines produced by a number of NHS organisations. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the initial assessment and diagnosis of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS Health website, North East London ICB and Health Improvement Scotland. The links to this guidance can be found below.

In the next episode, I will go through the primary care management of PCOS.

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 link to the PCOS information on the NHS Health website can be found here:

·      https://www.nhs.uk/conditions/polycystic-ovary-syndrome-pcos/

The link to the PCOS guideline by Primary Care North East London ICB can be found here:

·      https://primarycare.northeastlondon.icb.nhs.uk/wp-content/uploads/2025/01/Pathway-Polycystic-Ovary-Syndrome-10_2024.pdf

The link to the PCOS information by Right Decisions for Health and Care - Healthcare improvement Scotland can be found here:

·      https://rightdecisions.scot.nhs.uk/ggc-clinical-guidelines/gynaecology/gynaecology-guidelines/guidelines-a-z-all-gynaecology-guidelines/polycystic-ovarian-syndrome-622/

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.

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 will go through the initial assessment and diagnosis of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS website, North East London ICB and Health Improvement Scotland. The links to them are in the episode description.

In the next episode, I will go through the primary care management, so stay tuned for that.

Right, let’s jump into it.

Polycystic Ovary Syndrome is a common endocrine disorder affecting approximately 6 to 10 percent of the female population in the UK. It is a heterogeneous condition, presenting with a spectrum of clinical features and long-term health implications.

The main clinical features are:

·      Hyperandrogenism (including hirsutism, acne, and male-pattern hair loss)

·      Menstrual irregularity with associated anovulatory infertility.

·      overweight in 40-50% of cases and

·      Insulin resistance in 10-15% of slim and 20-40% of obese women but all women with PCOS are at an increased risk of developing type 2 diabetes.

What causes polycystic ovary syndrome (PCOS)?

The exact cause of PCOS is unknown, but it often runs in families.

We know that it's related to abnormal hormone levels in the body, including high levels of insulin secondary to insulin resistance and an increased production and activity of hormones like testosterone.

But what is the exact pathophysiology of PCOS?

Well, it’s a complex condition with several interconnected mechanisms.

First, there’s disruption in the hypothalamic-pituitary-ovarian axis. The brain increases the frequency of gonadotropin pulses, which leads to more stimulation of LH than FSH. This imbalance, often with a higher LH to FSH ratio, stimulates the ovaries’ theca cells to produce excess androgens. These androgens are responsible for many of the clinical features, like hirsutism, acne, and male-pattern hair loss.

Low FSH also means the follicles in the ovary don’t develop properly. They tend to grow to around six or seven millimetres, but they don’t ovulate. These small, underdeveloped follicles build up around the edge of the ovaries, creating a classic appearance on ultrasound.

To make matters worse, those high androgen levels further disrupt follicle development, reinforcing the cycle of anovulation. And when ovulation doesn’t happen, periods become irregular or stop altogether, which increases the risk of endometrial hyperplasia due to unopposed oestrogen.

Another major part of the pathophysiology is insulin resistance. Many women with PCOS, even those who aren’t overweight, have insulin resistance. The exact reason isn’t fully understood, but it’s thought to involve a defect in insulin signalling inside muscle and fat cells.

This hyperinsulinemia together with LH stimulate even more androgen production by the ovaries and it also lowers the liver’s production of sex hormone-binding globulin, which raises the amount of free testosterone.

And to add to all this, those excess androgens go on to worsen insulin resistance at the tissue level, creating a vicious cycle of more insulin, more androgens, more resistance, and more insulin again.

How is it diagnosed?

PCOS can be diagnosed when two out of the following three Rotterdam criteria are met. These are:

1. Oligo- or anovulation.
2. Clinical or biochemical signs of hyperandrogenism and
3. Polycystic ovarian morphology on ultrasound.

But this is always after excluding other causes such as thyroid dysfunction, Cushing’s syndrome, hyperprolactinaemia, late-onset congenital adrenal hyperplasia, and androgen-secreting tumours.

There is no consensus on the criteria needed to diagnose PCOS in adolescents. This is because diagnosing PCOS in adolescents is harder as the diagnostic features used in adults e.g. oligomenorrhoea, acne and PCO morphology on USS can be normal pubertal physiological events that are transient. We should not diagnose it in under 18 unless both clinical hyperandrogenism and irregular cycles persist for more than two years post-menarche. Some like the American Academy of Family Physicians argue that, for this age group, all three Rotterdam criteria be met before the diagnosis is made.

As we can see, the clinical features of PCOS are varied. So let’s have a look at some definitions in the Rotterdam criteria:

Firstly, we have oligo or anovulation. Oligomenorrhea is defined as cycles more than 35 days apart but less than 6 months apart and amenorrhea as the absence of menstruation for 6 to 12 months after a previously established cyclic pattern.

Secondly, we have hyperandrogenism. This could be diagnosed either clinically, by the presence of excessive acne, androgenic alopecia, or hirsutism, or chemically, by high serum levels of total, or free testosterone 

And finally, we have Polycystic Ovary features on Ultrasound. A single ovary showing these features is sufficient for the diagnosis of polycystic ovaries. However, we need to be aware that USS is not necessary if the first two criteria are present. USS is only necessary if we need it to rule out a tumour or the patient has met only one of the other Rotterdam criteria. This is because Polycystic ovaries features can be found in as many as 62% of patients with normal ovulation, with prevalence declining with age.

A thorough history and examination are essential. We should ask about cycle regularity, acne, hirsutism, and family history. We should also record BMI and blood pressure, given that these patients are at higher cardiometabolic risk.

Baseline investigations should include:

• Thyroid function tests
• Prolactin
• LH, FSH, and oestradiol to exclude other causes of oligo- or amenorrhoea
• Total testosterone and SHBG
• Androstenedione and DHEA-S or dehydroepiandrosterone if testosterone is raised
• If clinically suspected, 17-hydroxyprogesterone to rule out congenital adrenal hyperplasia
• And finally, we should consider a transvaginal or transabdominal ultrasound to assess ovarian morphology and endometrial thickness

How should we interpret these results?

Well, SHBG is usually normal or low in PCOS and provides a measurement of the degree of hyperinsulinaemia."

This is because Insulin suppresses the production of SHBG (sex hormone-binding globulin) in the liver, so in PCOS where insulin resistance is common, SHBG levels are often low or at the lower end of the normal range; as a result, low SHBG can serve as a useful surrogate marker for insulin resistance. Low SHBG means more free active testosterone, contributing to symptoms like acne and hirsutism.

We also have that LH, oestradiol and free androgen index, are usually normal or elevated in PCOS.

The reason for the high free androgen index is that SHBG is used to estimate it. So, if SHBG is low then the free androgen index may still be high even when total testosterone is normal, suggesting true biochemical hyperandrogenism.

LH is often elevated, especially in slim women with PCOS, due to increased gonadotrophin pulsatility. A raised LH:FSH ratio (e.g., >2:1) is typical, but not required for diagnosis.

And then, oestradiol is usually normal or mildly elevated in PCOS due to continuous oestrogen production from the ovaries and peripheral conversion in adipose tissue, despite anovulation.

FSH, prolactin and TSH are usually normal and these tests are done to rule out other causes of oligo/amenorrhoea.

FSH is usually normal in PCOS. If elevated, we should consider premature ovarian insufficiency.

Equally, prolactin is usually normal. If elevated, we should consider prolactinoma or drug-induced hyperprolactinaemia.

TSH is done to exclude hypothyroidism, which can also cause menstrual irregularity.

So, these are exclusion tests. They are checked to avoid misdiagnosing PCOS when another endocrine disorder is responsible.

And finally, we have that total testosterone is normal or high in PCOS. However, if it is significantly elevated, generally > than 5 nmol/l or more than 2 x upper limit of normal range, we will need to check DHEA, or dehydroepiandrosterone, androstenedione and 17-hydroxyprogesterone to rule out congenital adrenal hyperplasia, Cushing’s syndrome, and androgen-secreting tumours."

The reason for this is that in PCOS, total testosterone is often normal to mildly elevated, but significant elevations raise red flags and need further investigations.

DHEA-S or dehydroepiandrosterone increases in adrenal disorders. Androstenedione is produced also by the ovary and adrenal glands and finally, 17-hydroxyprogesterone which is elevated in non-classic congenital adrenal hyperplasia

Additionally, we should also consider Cushing’s syndrome or androgen-secreting tumours if the clinical picture is severe (e.g., when there is rapid virilisation) even if the total number is not very high.

And let’s end with some referral recommendations.

When should we refer women with PCOS to endocrinology?

We should consider endocrinology referral if:

• There are severe symptoms such as signs of virilisation or rapidly progressing hirsutism
• When testosterone is significantly elevated, defined as greater than 5 nanomoles per litre or more than twice the upper limit of normal or
• Abnormal levels of DHEA or dehydroepiandrosterone, androstenedione, or 17-hydroxyprogesterone, which could indicate the possibility of alternative diagnoses

So that is it, a review of the assessment and diagnosis of polycystic ovary syndrome.

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.

The video version of this podcast can be found here:

·      https://youtu.be/58WdoYFUUjU

This channel may make reference to guidelines produced by a number of NHS organisations. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the assessment and management of hypomagnasemia, focusing on what is relevant in Primary Care only. For this advice I have looked at the published guidance by NHS Dorset, NHS Kent and Medway, NHS Lanarkshire, Gloucestershire Hospitals NHS Trust, and Royal Cornwall Hospitals NHS Trust. The links to this guidance can be found below.

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 link to the guideline by NHS Dorset can be found here:

·      https://nhsdorset.nhs.uk/Downloads/aboutus/medicines-management/Other%20Guidelines/Management%20of%20hypomagnesaemia%20in%20primary%20care%20Jan%2023%20-%20Copy.pdf?boxtype=pdf&g=false&s=true&s2=false&r=wide

The link to the guideline by NHS Kent and Medway can be found here:

·      https://www.dgsdvhformulary.nhs.uk/media/1168/hypomagnesaemia-in-adults-primary-care-guide.pdf

The link to the guideline by NHS Lanarkshire can be found here:

·      https://rightdecisions.scot.nhs.uk/media/1539/hypomagnesaemia-in-primary-or-secondary-care.pdf

The link to the guideline by Gloucestershire Hospitals NHS Trust can be found here:

·      https://www.gloshospitals.nhs.uk/media/documents/Hypomagnesaemia_jcPg0oV.pdf

The link to the guideline by Royal Cornwall Hospitals NHS Trust can be found here:

·      https://doclibrary-rcht.cornwall.nhs.uk/DocumentsLibrary/RoyalCornwallHospitalsTrust/Clinical/Pharmacy/TreatmentOfHypomagnesaemiaInAdultsClinicalGuideline.pdf

The link to the guideline by Worcestershire Acute Hospitals NHS Trust can be found here:

·      https://apps.worcsacute.nhs.uk/KeyDocumentPortal/Home/DownloadFile/1559

The link to the MHRA advice on hypomagnesaemia associated to long term PPI use can be found here:

·      https://www.gov.uk/drug-safety-update/proton-pump-inhibitors-in-long-term-use-reports-of-hypomagnesaemia

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.

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 will go through the assessment and management of hypomagnesemia, focusing on what is relevant in Primary Care only. For this advice I have looked at the published guidance by a number of NHS organisations in the UK including Dorset, Lanarkshire, Gloucestershire, Cornwall and Kent and Medway. The links to them are in the episode description.

Right, let’s jump into it.

Hypomagnesaemia is defined as a serum magnesium concentration below 0.7 mmol/L. The normal reference range for serum magnesium is between 0.7 and 1.0 or 1.05 mmol/L, depending on the guideline used.

Magnesium is the second most abundant intracellular electrolyte after potassium, and is an essential cofactor in numerous enzyme systems. It also regulates the transport of calcium and potassium across cell membranes, contributing to neuromuscular conduction, muscle contraction, and cardiac rhythm.

The majority of total body magnesium is stored in bone and soft tissue and only around 1% is in extracellular fluid. Therefore, serum levels may not accurately reflect total body stores. It is possible to see a normal serum level when there is a total body magnesium deficit like in a chronic magnesium deficiency secondary to inadequate dietary magnesium. The reverse, that is, a low serum level and normal total body magnesium, is also possible and is usually seen with drugs which increase excretion of magnesium. Additionally, approximately 25% of plasma magnesium is bound to albumin, so high or low albumin states can also affect the magnesium levels.

Changes in magnesium levels usually occur gradually over months or years and symptoms are often absent, particularly when serum levels are only mildly reduced. They become more common when concentrations fall below 0.5 mmol/L, but there are times when they may also occur in the 0.5–0.7 mmol/L range.

The most common symptoms are:

Muscular and mobility symptoms, including muscle weakness, tremors, ataxia, spasms, fasciculations.

Neurological symptoms, including dizziness, paraesthesia, hallucinations, delirium, seizures, depression, confusion, and coma.

Cardiovascular symptoms, including ECG abnormalities, arrhythmias, and increased sensitivity to digoxin.

Metabolic effects including altered glucose homeostasis, and associations with hypocalcaemia and hypokalaemia.

And finally, other symptoms such as anorexia, nausea, vomiting, and fatigue,

But let’s go back for a moment and ask, why is low magnesium associated with hypocalcaemia and hypokalaemia?

Low magnesium can lead to hypocalcaemia because magnesium is required for the release of PTH. When magnesium is very low, PTH secretion decreases, which leads to reduced calcium reabsorption in the kidneys and reduced calcium release from bone, resulting in low calcium levels.

And what about hypokalaemia? Here the mechanism is connected cellular pumps that regulate intra and extracellular potassium homeostasis which leads to increased renal potassium loss, causing potassium levels to decrease.

Both the hypocalcaemia and hypokalaemia may be refractory to treatment until magnesium is corrected

Let’s now look at the causes and risk factors of hypomagnesemia.

The first cause is Reduced Intake, reduced Absorption or increased gut losses like in:

• Malabsorption (including coeliac disease, Crohn’s disease, and short bowel syndrome)
• Malnutrition and anorexia nervosa
• Chronic diarrhoea
• And excess alcohol intake

Increased Renal Loss like in:

• Renal tubular disorders
• Diabetes and diabetic ketoacidosis
• Hyperaldosteronism
• Hyperthyroidism
• And vitamin D deficiency

Drug-Induced like for example with the use of:

• Proton pump inhibitors (PPIs)
• Both loop and thiazide Diuretics
• Theophylline
• Some chemotherapy agents
• And Digoxin, also bearing in mind that low magnesium may increase digoxin toxicity

And finally Miscellaneous causes such as

·      Acute pancreatitis

·      and excessive lactation

We should prioritise the monitoring of magnesium in patients taking multiple risk drugs or with two or more risk factors.

But let’s pause for a moment. Did we just say that vit D deficiency also causes hypomagnesaemia? And why is that?

Well, in fact, the relationship between magnesium and vitamin D is bidirectional, that is, each influences the metabolism and availability of the other. For example, vitamin D deficiency can cause or worsen hypomagnesaemia by reducing magnesium intestinal absorption and indirectly increasing its renal loss. Conversely, magnesium is a cofactor in the enzymatic steps that convert vitamin D to its active form and, as a result, magnesium deficiency can impair vitamin D activation and function.

Therefore, both deficiencies often coexist, especially in patients with malabsorption, chronic disease, or poor nutrition, and they may exacerbate each other.

Also, of all the drugs mentioned before, PPIs are probably the most commonly and widely prescribed. Because of reported cases of severe hypomagnesaemia associated with prolonged PPI use, normally after 1 year but sometimes as early as 3 months, the MHRA has published a drug safety alert advising healthcare professionals to:

• Consider baseline magnesium measurement before starting PPIs and to
• Monitor magnesium periodically during prolonged treatment, particularly in patients on diuretics or digoxin

We also need to reiterate that for patients on PPIs, symptoms may develop insidiously and be overlooked. PPI related hypomagnesaemia generally resolves upon magnesium replacement and discontinuation of the PPI.

PPIs can also be obtained over-the-counter but patients are advised not to take them for more than 4 weeks without consulting a doctor.

Hypomagnesemia can be graded as:

• Mild: when the levels are below 0.7 but above 0.50 (i.e. 0.51–0.69 mmol/L)
• Moderate: when the levels are 0.50 or below but above 0.40 (i.e. 0.41–0.50 mmol/L)
• And Severe: when the levels are 0.40 mmol/L or below. Here, urgent referral is advised, especially if symptomatic or with concurrent low potassium or calcium.

Let’s now look at the General Principles of management. We will:

• Treat underlying causes
• Discontinue offending drugs where possible (seeking advice if not feasible)
• Consider switching PPIs to H2 antagonists (e.g. famotidine, or nizatidine)
• And we will bear in mind that oral replacement is preferred for asymptomatic mild or moderate deficiencies whereas IV magnesium is required for severe deficiency, symptomatic moderate deficiency or if oral supplements are not tolerated

For Oral Replacement, we will look at the BNF, being aware that magnesium preparations may not be interchangeable due to differences in bioavailability, therefore we should exercise caution when switching between them.

Usually the first-line treatment is with:

• Magnesium aspartate (or Magnaspartate®) which comes in sachets and is preferred for all ages above 2 years

Second-line options include:

• Magnesium glycerophosphate tablets and
• Magnesium citrate

Another oral option includes:

• Magnesium glycerophosphate in liquid form, which is unlicensed but is sometimes used when there are tolerability issues.

Additionally,

• Magnesium sulphate can be administered in secondary care by intravenous infusion, or by intramuscular injection

And let’s remember that IV Replacement is required:

• In severe hypomagnesemia, when Serum magnesium is 0.4 mmol/L o r below
• In symptomatic Moderate hypomagnesaemia, that is, when magnesium is between 0.4 and 0.5 and there are symptoms and also
• Any low level in a patient on digoxin with symptoms

Possible Adverse Effects of oral magnesium include diarrhoea, so we should recommend having it with meals to reduce gastrointestinal irritation.

We should also bear in mind that oral magnesium reduces the absorption of:

• Bisphosphonates
• Tetracyclines and
• Quinolone antibiotics

In terms of monitoring and Follow-Up we should obviously:

• Monitor serum magnesium during and after replacement
• Then continue rechecking at regular intervals in patients with ongoing risk factors
• But also monitor for symptoms of hypermagnesaemia, particularly in renal impairment. Possible symptoms of hypermagnesaemia or high magnesium levels include Respiratory depression, loss of reflexes, confusion, vomiting, cardiac arrhythmias, and coma. Cardiac arrest may occur at levels above 6 mmol/L.

And let’s finish with a quick overview of recommended Patient Education. Patients who are at risk of hypomagnesemia, particularly those on long term PPIs, should be advised to

• Report symptoms such as tremor, vomiting, tiredness, muscle cramps, loss of appetite and fatigue
• They should also increase magnesium-rich foods including green vegetables, wholemeal grains, nuts, pulses, and seafood
• We should also advise them that “Hard” water also contains magnesium salts
• And advise OTC magnesium supplements if there are no clinical concerns such as, for example, severe renal impairment, heart block, bradycardia, or myasthenia gravis.

So that is it, a review of the guidance on the assessment and management of hypomagnesaemia.

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.

The video version of this podcast can be found here:

·      https://youtu.be/Y3POCL-rh_Y

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 May 2025 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 May 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-05-01&to=2025-05-31&ndt=Guidance&ndt=Quality+standard

The update on Suspected cancer: recognition and referral [NG12] can be found here:

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

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#upper-gastrointestinal-tract-cancers

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. In today’s episode, we’ll be looking at the NICE updates published in May 2025, focusing on what is relevant to Primary Care only.

We’ve got another short episode today, as there is only one clinical area to discuss: new advice on the cancer recognition guideline.

Right, let’s jump into it.

And this update refers to the early detection of upper gastrointestinal cancers. It only touches on the recommendations for oesophageal and stomach cancers, and it will not really change our practice very much, given that it affects the referral process only. The difference is that before, when someone developed red flag symptoms, we were advised refer them for an urgent direct access upper GI endoscopy (to be performed within 2 weeks), whereas now, the advice is to refer them using a suspected cancer pathway referral.

Is there a real difference? Well, in fact, there is. Let’s have a look at it:

The main difference between lies in who triages the referral, the urgency and coordination of care.

For example, in an urgent Direct Access Upper GI Endoscopy (done within 2 weeks)

• The GP directly refers the patient to the endoscopy service, who triages the referral without specialist review.
• Also, although urgent direct access endoscopy is expected within 2 weeks, it's not formally tracked like a cancer pathway.
• And finally, there is no coordinated follow-up if something is found. The GP will receive the report and must then arrange further care.

On the other hand, a Suspected Cancer Pathway Referral means that

• The hospital’s cancer referral team triages the referral and coordinates and tracks the process. This often means that the patient is seen or tested within 2 weeks, but the formal definition of a Suspected Cancer Pathway Referral is that the patient has the diagnosis of cancer either confirmed or ruled out within 28 days of the original referral.
• The advantage of this model is that if a cancer is found, follow-up is already embedded in the system.

So that is really the only change. Since today’s episode is so short, let’s take the opportunity to review re recommendation on upper GI cancers.

For Oesophageal and stomach cancers, we will refer them on a suspected cancer pathway if they:

• have dysphagia or
• are aged 55 and over, with weight loss, and they have any of the following:
• upper abdominal pain
• reflux or
• dyspepsia

We will consider non-urgent, direct access upper gastrointestinal endoscopy in people with haematemesis and in people aged 55 or over with:

• treatment‑resistant dyspepsia or
• upper abdominal pain with low haemoglobin levels or
• raised platelet count with any of the following:
• nausea
• vomiting
• weight loss
• reflux
• dyspepsia and
• upper abdominal pain or
• nausea or vomiting with any of the following:
• weight loss
• reflux
• dyspepsia and
• upper abdominal pain.

In terms of pancreatic cancer, we will refer if they are aged 40 and over and have jaundice. And we will also consider an urgent, direct access CT scan (to be done within 2 weeks), or an urgent ultrasound scan if CT is not available, in people aged 60 and over with weight loss and any of the following:

• diarrhoea
• back or abdominal pain
• nausea or vomiting
• constipation or
• new‑onset diabetes.

And finally, in terms of Gall bladder cancer or liver cancer

We will consider an urgent, direct access ultrasound scan (to be done within 2 weeks) in people with an upper abdominal mass consistent with either an enlarged gall bladder or an enlarged liver.

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.

The video version of this podcast can be found here:

·      https://youtu.be/mq658X-teEc

This channel may make reference to guidelines produced by the British Society for Haematology. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on thrombophilia testing, 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.  

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 link to the guideline by the British Society for Haematology on thrombophilia testing can be found here:

·      https://onlinelibrary.wiley.com/doi/10.1111/bjh.18239

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

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.

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 will go through the guideline by the British Society for Haematology on thrombophilia testing, focusing on what is relevant in Primary Care only. A link to it is in the episode description. We’ll go through the main tests included in a thrombophilia screen, explain why they matter, and go over when screening is recommended in specific clinical situations.

Right, let’s jump into it.

Thrombophilia is a condition where the blood has an increased tendency to clot. This increases the risk thrombosis and may be inherited, acquired, or a mix of both.

However, thrombophilia screening focuses only on factors identifiable through laboratory testing. Broader contributors like cancer, inflammation, and obesity, although linked to thrombosis, cannot be assessed with this panel and we are not going to address them today.

A thrombophilia screen includes a number of tests which we are going to group by their pathophysiological mechanism:

First, we assess for deficiency of natural anticoagulants like Antithrombin, Protein C and Protein S. Deficiencies in any of these increase the clotting risk. A simple way to remember them is with the mnemonic: C, S, A — Coagulation Suppressors Absent.

Second, we look for genetic mutations that make clotting factors resistant to natural anticoagulants. These include, Factor V Leiden and Prothrombin Gene Mutation. These mutations lead to excess clotting either by preventing anticoagulation or by increasing clotting factor levels.

Third, we consider acquired autoantibodies that interfere with the body's anticoagulant mechanisms or activate endothelial cells. These include Lupus anticoagulant, Anti-cardiolipin antibodies and Anti-β2-glycoprotein I antibodies. These markers are typically associated with antiphospholipid syndrome.

I hope that grouping the thrombophilia screen this way will make it easier to understand and remember.

We can classify thrombophilias between hereditary and acquired thrombophilias. The most clearly defined genetic thrombophilias are the factor V Leiden variant, the prothrombin gene mutation, protein C deficiency, protein S deficiency, and antithrombin deficiency. 

On the other hand, important acquired thrombophilias include antiphospholipid syndrome, paroxysmal nocturnal haemoglobinuria, myeloproliferative neoplasms and the presence of a JAK2 mutation. Pregnancy is a hypercoagulable state due partly to physiological changes.

Both heritable and acquired thrombophilias can interact to further increase the risk of thrombosis, for example during pregnancy and the postpartum period.

So now, let’s consider the actual laboratory testing. And the first issue to look at is, should we screen the general population for thrombophilia?

And although Elevated levels of procoagulant factors may increase the risk of thrombosis, the relationship is not straightforward. Why is this?

1. Firstly, there is a Multifactorial Risk. Thrombosis isn’t caused by one factor alone. Other conditions like obesity, inflammation, or immobility may coexist with elevated procoagulant factors, confounding the interpretation.
2. Then there is the Dual Roles of Coagulation Proteins. That is, some factors have both procoagulant and anticoagulant roles, which makes the overall effect more difficult to assess.
3. And then there is the issue of Limited Predictive Value. Measuring elevated levels of these factors (like Factor VIII, fibrinogen, etc.) may show associations with thrombosis risk in population studies, but it doesn’t consistently predict individual risk.

So, in summary, the guideline does not recommend routine screening of procoagulant factors because it would not change the management for the majority of people. Instead, it supports individualised decision-making.

Now, let’s look and the significance of testing in each category of test.

The first category refers to natural anticoagulants. What about testing for their Deficiency?

The associations of Protein C, Protein S and Antithrombin deficiencies with increased risks of VTE are well-established. The degree of deficiency is variable but in general thrombosis risk rises as soon the levels of protein C, S or Antithrombin fall below the normal range.

These deficiencies also interact with acquired risks. It has been found that a transient provoking factor is present in approximately 50% of episodes of thrombosis in genetically predisposed people. 

Another consideration is that, when testing for deficiencies of physiological anticoagulants, this should be performed only after 3 months of anticoagulation for acute thrombosis, given that the result would not change the initial acute management and there is uncertainty over the validity of earlier results.

The next category of tests includes Factor V Leiden and prothrombin gene mutation.

These two cases are the most common genetic variants predisposing to thrombosis. Their prevalence varies in populations of different ethnicity, being more common in people of European descent and being rare or absent in other ethnicities.

There are a large number of other genetic variants but the only ones that are included in thrombophilia panels at present are these two, factor V Leiden and prothrombin gene mutation because the clinical relevance of other genetic types is not well established.

The last two categories of tests make reference to cases acquired thrombophilia. They can be genetic and non-genetic.

Let’s look at the non- genetic causes first and the main one is Antiphospholipid syndrome

The diagnosis of antiphospholipid syndrome is dependent on the presence of at least one clinical feature (either thrombosis or pregnancy morbidity) and at least one laboratory feature of antiphospholipid antibodies which include lupus anticoagulant , anticardiolipin antibodies or anti-β2-glycoprotein-I (anti-β2GPI) antibodies. The antiphospholipid antibodies need to be persistent, that is, present on two or more occasions at least 12 weeks apart.

There is uncertainty in the thrombotic risks of these patients depending on whether the thrombosis was provoked or unprovoked.

Therefore, the advice is that:

• Screening for antiphospholipid antibodies is recommended following thromboembolic disease which is either unprovoked or provoked by a minor risk factor.
• And, as antiphospholipid syndrome is an acquired thrombophilia, screening for antiphospholipid antibodies is not recommended in family members.

I will just mention that catastrophic antiphospholipid syndrome is a rare, but a potentially fatal variant characterised by extensive microvascular thrombosis leading to multiorgan failure.

And finally, the last category of tests refers to the genetic causes of acquired thrombophilia.

Here, I will just mention that Paroxysmal nocturnal haemoglobinuria (PNH) and myeloproliferative neoplasms (MPN) are acquired genetic traits that have clonal stem cell abnormalities. Myeloproliferative neoplasms include polycythaemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The JAK2 mutation is strongly associated with an increased thrombophilia risk too.

Here the advice is that we should test for these conditions in patients with thrombosis at unusual sites and FBC abnormalities.

Now let’s look at the General advice on the role of thrombophilia testing in certain clinical scenarios

We have said that general screening is not recommended but, for patients with a strong personal and/or family history of unprovoked thrombosis, further genetic analysis is recommended.

The major hereditary thrombophilic traits follow Mendelian inheritance although with variable penetrance. Overall, the recurrence risk is determined by the clinical situation (e.g., whether the thrombosis was provoked or unprovoked) along with non-Mendelian risk factors (e.g., body mass index and age) rather than the inherited thrombophilia itself. Therefore, selective testing of first-degree relatives may be advisable only when this will alter their management choices, for example, in women of childbearing age.

What about Ischaemic stroke?

Well, excluding cerebral venous sinus thrombosis, this area remains controversial and the Recommendations after a stroke are that

• In general, testing for thrombophilia is not recommended.
• But testing for antiphospholipid antibodies should be considered in patients <50 years of age in the absence of identifiable risk factors for cardiovascular disease
• Additionally, in patients with stroke, an abnormal full blood count should prompt consideration for testing Paroxysmal nocturnal haemoglobinuria and myeloproliferative neoplasms

And to end, let’s look at the recommendations for Thrombophilia testing in relation to pregnancy

Pregnancy is an acquired hypercoagulable state. The incidence of thrombosis in pregnancy is a 5- to 10-fold increase in relation to non-pregnant females, rising further in the first 6 weeks postpartum to a 20- to 80-fold increase in risk.

Additionally, women who have had previous adverse outcomes—such as recurrent first-trimester pregnancy loss or stillbirth—should be screened but this screening should be limited to testing for antiphospholipid antibodies.

So the guideline recommends that:

• Testing for antithrombin deficiency may be considered in pregnant women with a known family history of this deficiency.
• In women with a history of unprovoked thrombosis or with recurrent or late pregnancy loss, testing for antiphospholipid antibodies should be performed
• And that Antiphospholipid antibody testing should be done outside pregnancy as the results may not be reliable during pregnancy.

So that is it, a review of the guideline on thrombophilia testing.

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.

The video version of this podcast can be found here:

·      https://youtu.be/qNboajtlrrs

This channel may make reference to guidelines produced by the British Society for Haematology. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin, focusing on what is relevant in Primary Care only.

In the last two episodes I covered the guideline on iron deficiency and functional iron deficiency.

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 link to the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin can be found here:

·      https://doi.org/10.1111/bjh.15166

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

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.

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 will go through the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin, focusing on what is relevant in Primary Care only. A link to it is in the episode description.

If you haven’t already, I recommend that you check out the last two episodes where we covered the laboratory diagnosis of both iron deficiency and functional iron deficiency

Right, let’s jump into it.

Serum ferritin level is one of the most commonly requested investigations in both primary and secondary care. Whilst low serum ferritin levels invariably indicate reduced iron stores, raised serum ferritin levels can be due to multiple different causes, including iron overload, inflammation, liver or renal disease, malignancy, and metabolic syndrome.

Reduced ferritin levels are only found in patients with reduced body iron stores. However, in some circumstances, for example in patients with co-existent inflammatory disorders, ferritin may be within the normal or elevated range even when iron stores are reduced and anaemia is due to iron deficiency.

On the other hand, the clinical and laboratory management of patients with raised ferritin values is not that well recognised and this is why we are covering it here.

Levels in serum can be raised because of inflammation, tissue damage as well as by any condition or treatment that leads to a genuine increase in iron stores (e.g. blood transfusion or iron infusion).

Most UK path labs simply report 300–400 μg/l as the upper limit of normal for ferritin in adult males and 150–200 μg/l as the upper limit of normal for adult females. There is however considerable variation in response to age, ethnic origin and sex. Mean ferritin values in neonates are high (around 200 μg/l) and remain so for about 2 months.

Mean ferritin values are higher at all ages in adult black males. In black females, higher ferritin values are only seen after the menopause. In multi-ethnic population studies in the USA it was found that elevated ferritin values are found more frequently in Afro-Caribbean and Asian subjects than in the white or Hispanic population. Indeed, very high ferritin levels >1000 μg/l are 2–3 times more common in black and Asian volunteers despite not having a true iron overload problem so it is argued that the normal ranges should take into account the variation due to age, gender and possibly ethnic origin

Serum ferritin is the most frequently requested haematinic assay in the UK and some 50% of ferritin requests are made from primary care.

The commonest causes of a high ferritin without iron overload relate to inflammatory disorders, malignancy, chronic alcohol consumption, liver disease or metabolic abnormalities.

For the majority of persons with a raised ferritin, chronic inflammatory or infective causes as well as liver disease, alcohol and malignancies will be the more likely conditions seen in practice, and if clinically apparent, further investigations of the causes of the high ferritin may not be necessary. Let’s look at the different causes individually:

In the Liver: Elevated ferritin is seen in almost any cause of liver injury, including alcoholic and non-alcoholic steatohepatitis (NASH), and viral hepatitis

In the Kidneys: Ferritin is not a useful marker of iron stores in patients with chronic kidney disease (CKD), and is elevated in almost half of all patients on maintenance haemodialysis but the raised ferritin does not represent iron that is available for erythropoiesis. For CKD patients on treatment with erythropoietic stimulating agents (ESA), iron supplementation should routinely be offered unless their ferritin is >800 μg/l.

In Malignancy: ferritin  is frequently elevated, and cancer has been the most frequent association in some studies of the causes of a high ferritin.

In Inflammatory and infective disorders: ferritin levels may correlate with disease activity, for example in systemic lupus erythematosus (SLE) and rheumatoid arthritis. Other inflammatory conditions and acute or chronic infections will also produce elevations in ferritin, usually with elevated CRP, but normal Tsat.

Mention should be made of anaemia of chronic disease (ACD), also termed anaemia of inflammation, the pathogenesis of which includes a state of functional iron deficiency, which we discussed in the last episode

A more recently described cause of raised ferritin is the metabolic syndrome, sometimes referred to as dysmetabolic hyperferritinaemia: patients typically demonstrate elevated ferritin levels with normal Tsat

Then we have Haematological causes and: A variety of red cell disorders, characterised by ineffective erythropoiesis or haemolysis, are associated with increased ferritin; these include thalassaemic disorders, hereditary spherocytosis and inherited or acquired sideroblastic anaemias. Prolonged or chronic transfusion therapy, for example in patients with major haemoglobinopathies, myelodysplastic syndromes, or during treatment for haematological malignancies, will also cause transfusional iron overload.

So in summary, reactive causes of raised serum ferritin levels, including malignancy, inflammatory disorders, renal failure, liver disease and metabolic syndrome, are all considerably more common than true iron overload.

There are other genetic causes of an elevated serum ferritin including hemochromatosis, Still disease, and other rare disorders

How do we investigate raised serum ferritin?

When ferritin is raised, the most crucial questions to ask are

(i)            is it secondary to a known clinical condition, and

(ii)          (ii) is it associated with iron overload?.

A clinical history and examination, together with a few simple investigations, will often reveal the probable underlying cause. In particular, patients should be questioned about alcohol intake and other risk factors for liver disease, transfusion history or oral iron supplementation, family history of iron overload and the presence or absence of diabetes mellitus, obesity and hypertension, history of early cataracts, as well as for symptoms and signs that may point to an underlying inflammatory or malignant disorder. Initial investigations should include a full blood count, repeat ferritin, Tsat, renal function tests and LFTs (with viral hepatitis serology if LFTs are abnormal) and inflammatory markers, such as CRP and ESR. Glycosylated haemoglobin levels may indicate impaired glucose tolerance, and raised serum lipids, body mass index and hypertension may point to underlying metabolic syndrome. Abdominal ultrasonography may demonstrate an echogenic liver suggesting alcohol- or non-alcohol-related fatty liver disease.

Iron overload is more likely to be present if the ferritin has risen progressively or the ferritin is >1000 μg/l.

It is worth noting that acute infections, menstrual bleeding and recent blood donation can temporarily reduce Tsat to within the normal range in patients with iron overload indicating that normal Tsat does not completely exclude iron overload. In the setting of persistent borderline results, genotyping for haemochromatosis should be performed.

Males with ferritin > 300 μg/l and Tsat >50% and females with ferritin > 200 μg/l and Tsat > 40% will usually have iron overload. We will leave this here as we are not looking into the diagnosis or management of haemochromatosis here today.

How do we manage a raised ferritin without elevated transferrin saturation?

In otherwise well patients with unexplained elevated ferritin and Tsat <40% (female) or <50% (male), a period of observation may be informative: stable, moderately increased levels may not require further investigation, whereas fluctuating levels are typically seen in hepatic steatosis or alcohol excess. Persistent unexplained high levels, especially at levels >1000 μg/l, merits consideration of onward referral to a specialist, usually a hepatologist.

In most cases of a high ferritin secondary to inflammatory or other conditions, management of the underlying condition will lead to reduction in ferritin levels. For example, alcohol abstinence will usually lead to improvement in ferritin within weeks to months; and weight loss and improved control of diabetes and blood pressure will usually lead to lowering of levels in patients with metabolic syndrome.

There is no evidence to support venesection therapy in patients with increased ferritin associated with liver disease other than heamochromatosis

In Conclusion

The finding of a raised serum ferritin is a common conundrum in modern day clinical practice, both in primary and secondary care. Iron overload is a relatively uncommon cause of this picture and can be excluded by the finding of a normal transferrin saturation, so consideration of the many reactive causes like hepatic, malignant, renal, haematological and metabolic causes is important: many cases will not require further investigation if a few simple investigations are performed. Rarer causes will require specialist molecular genetics for diagnosis.

So that is it, a review of the laboratory investigations of a raised serum ferritin.

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.

The video version of this podcast can be found here:

·      https://youtu.be/Ugo6U9QI2xY

This channel may make reference to guidelines produced by the British Society for Haematology. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency, focusing on what is relevant in Primary Care only.

In the last episode I covered:

·      The guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency

In the next episode, I will cover:

·      The assessment of raised ferritin

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 link to the new guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency can be found here:

·      https://onlinelibrary.wiley.com/doi/10.1111/bjh.12311

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

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.

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 will go through the guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency, focusing on what is relevant in Primary Care only. A link to it is in the episode description.

If you haven’t already, I recommend that you check out the last episode where I covered the laboratory diagnosis of iron deficiency

And in the next episode, I will cover the assessment of raised ferritin. So, stay tuned for that!

Right, let’s jump into it.

Whilst the concept of functional iron deficiency—or FID—is both important and very relevant to us in Primary Care, reading the full guideline can be overwhelming. It’s full of detailed considerations more relevant to specialists and secondary care. So, instead of summarising that in its entirety, I’m just going to give you a general overview. I’ll take you through the relevant investigations, explaining each one in plain terms, and linking it back to what we need to know and do in general practice.

And first of all, what is Functional Iron Deficiency (FID)?

Functional Iron Deficiency happens when the body has enough iron stored, but can’t get it to where it’s needed — particularly, the bone marrow where red blood cells are made. This is different from true iron deficiency, but the effect is similar: not enough haemoglobin is made, leading to anaemia.

Why Does This Happen?

FID is common in long-term illnesses, like:

• Chronic inflammation (e.g. rheumatoid arthritis)
• Infections
• Cancer and
• Chronic kidney disease (CKD)

In these situations:

• The liver produces hepcidin, a hormone that blocks iron release from stores and reduces absorption from the gut.
• So, even if ferritin looks normal or high, the bone marrow can’t access the iron, so red cell production is reduced.

What Should GPs Know about functional iron deficiency?

Let’s look at a very simplified version of the Pathophysiology. And that is that

• Chronic Inflammation leads to→ ↑a rise in Hepcidin → ↓which reduces Iron transport → which in turn leads iron not reaching the Bone.
• This results in anaemia of chronic disease.
• FID can also happen when bone marrow is overstimulated (e.g., from treatment with ESA in CKD), using iron faster than it can be delivered.

When should we Suspect FID? We should suspect it clinically if there is anaemia in chronic disease (especially if it is not improving with oral iron). We should also suspect it depending on test results. And let’s now look at the list of possible tests that can be requested for functional iron deficiency, starting with the ones that we can order in Primary Care:

·      Firstly, we have MCV or Mean cell Volume and MCH or Mean Cell Haemoglobin. They tell us the average size of red blood cells and the average amount of haemoglobin in each red cell respectively.

They are useful at the time of diagnosis and for tracking trends over weeks or months. However, they don’t change quickly, so they not suitable for identifying rapid changes.

·      Then we have serum Ferritin. This one we all know well. It reflects the amount of stored iron in the body. If it’s under 15 micrograms per litre, that strongly indicates true iron deficiency. Ferritin is an acute phase reactant—it rises in inflammation and chronic disease. So, a high ferritin doesn’t exclude FID. In CKD patients, a ferritin under 100, or sometimes even 200 increases the likelihood of requiring further iron treatment. In CKD, values as high as 1200 may still be consistent with iron-restricted anaemia. But we should not use ferritin alone to guide treatment but consider it in the context of other tests too.

·      Then we have Transferrin Saturation – or TSAT which shows the percentage of transferrin that is actually carrying iron. Alone, it’s not a reliable guide for iron therapy in CKD patients but combined with ferritin and other tests it can help diagnose FID or monitor treatment. Transferrin saturation can also be influenced by inflammation, so it’s not a standalone tool.

·      Now let’s move onto more specialist markers of iron status, especially for functional iron deficiency, like %HRC – Percentage of Hypochromic Red Cells, which measures the proportion of red cells that contain less haemoglobin than they should. It’s actually the best-established lab test for detecting FID.

·      Then we have CHr – Reticulocyte Haemoglobin Content, which measures how much haemoglobin is in reticulocytes. It’s the second most established marker for FID and a value of less than 29 picograms suggests functional iron deficiency.

·      There are other truly specialist tests, which are:

o  Zinc Protoporphyrin

o  Bone Marrow Examination

o  sTfR – Soluble Transferrin Receptor

o  Serum Erythropoietin and

o  Hepcidin, which we mentioned earlier and which plays a role in the pathophysiology of functional iron deficiency

What is the typical picture of anaemia in FID?

Well, haemoglobin is usually low or normal, often showing a normocytic normochromic picture.

Ferritin will be normal or high Because being an acute-phase reactant, it’s falsely elevated in inflammation

Transferrin saturation is usually low <20% despite the high ferritin. Transferrin saturation is reduced because of iron being unavailable.

Serum iron is low, both in true iron deficiency and functional iron deficiency. However, TIBC is normal or low, whereas it would be high in true iron deficiency

ESR or CRP tend to be high in functional iron deficiency reflecting underlying inflammation and finally functional iron deficiency also show that

Reticulocyte Hb content is low and percentage of hypochromic cells are high

When should we refer to Secondary Care?

We should consider referral if:

·      There is persistent or unexplained anaemia, and we suspect FID and when oral iron hasn’t worked.

·      If The patient is on (or might need) IV iron or erythropoiesis-stimulating agents (ESAs) which are managed in secondary care.

·      If There is diagnostic uncertainty like for example mixed deficiencies, or a high ferritin but the picture still points to iron deficiency anaemia or

·      If there is anaemia in CKD stages 4–5, active cancer, or complex comorbidities

And to end, let’s remember that our role in Primary Care is:

• To Recognise the FID pattern: that is, chronic disease + anaemia + and a ferritin which is not low
• To exclude other causes, for example bleeding, B12/folate deficiency, chronic kidney disease etc.
• To manage oral iron therapy and initial assessment remembering that
• We should not overlook anaemia in patients with chronic disease. FID is treatable but IV iron and ESA are specialist decisions.

So that is it, a review of the laboratory investigations of functional iron deficiency.

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.

The video version of this podcast can be found here:

·      https://youtu.be/ZdHSs-QBtac

This channel may make reference to guidelines produced by the British Society for Haematology. 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 them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency in adults (excluding pregnancy) and children, focusing on what is relevant in Primary Care only.

In the coming episodes, I will also cover the recommendations by the British Society for haematology on:

·      The assessment of raised ferritin

·      The concept of functional iron deficiency

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 link to the new guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency can be found here:

·      https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.17900

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

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.

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 will go through the guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency, focusing on what is relevant in Primary Care only.

In the coming episodes, I will also cover their recommendations on:

·      The assessment of raised ferritin

·      The concept of functional iron deficiency

So, stay tuned for those!

Right, let’s jump into it.

The British Society for Haematology produces Good Practice Papers to recommend good practice in areas where there is limited evidence but where a degree of consensus is likely to be beneficial to patient care.

The laboratory diagnosis of iron deficiency is difficult, because iron homeostasis is dynamic and no single test can provide an accurate assessment of iron absorption, transport, storage, and utilisation.

Iron metabolism in adults and children can be considered equivalent, and these recommendations are applicable to both paediatric and adult practice, but it does not include pregnancy.

Let’s start by saying that iron deficiency is the most common cause of anaemia worldwide. In the UK, the prevalence of iron deficiency anaemia can go up to 6% depending on age and sex, with higher rates in certain groups like menstruating women and those aged over 85 years.

The prevalence of iron deficiency without anaemia, however, is not well documented.

In this episode we are just focusing on the laboratory assessment of iron status and not the full guidance on iron deficiency anaemia which requires a detailed history, clinical examination and the review of, for example, national gastrointestinal and gynaecology guidelines as well as other local pathways.

The British Society for Haematology has suggested an algorithm for the laboratory investigation of iron deficiency anaemia which we will review at the end. But first, let’s look at the different laboratory parameters that we will need to consider.

As you may already be aware, the main diagnostic tests in iron deficiency anaemia are a full blood count and ferritin.

So let’s now start with the red cell parameters in a full blood count. Anaemia will be confirmed if haemoglobin or Hb is below the reference range. But Hb alone does not indicate iron status and at population level, there’s considerable overlap in Hb levels between iron-replete and iron-deficient people.

Iron deficiency is typically associated with microcytic hypochromic anaemia.

But low MCV, MCH, or MCHC can also appear in other conditions, especially the thalassaemias.

Interestingly, MCV can be normal in up to 40% of iron-deficient patients, and also in cases of mixed haematinic deficiency.

There are other advanced parameters like percentage of hypochromic cells (%HRC) and reticulocyte mean Hb content which can help evaluate iron availability further.

Given that Erythrocytes contain about half of the body’s iron at any one time,

a high percentage of hypochromic cells or low reticulocyte Hb content — without thalassaemia — suggests that iron is not adequately reaching newly formed red cells, which could be due to iron deficiency or iron restriction.

Morphological changes appear in iron deficiency and generally, anisocytosis precedes hypochromia and microcytosis but blood cell morphology is not diagnostic

So, in summary, in respect of full blood counts, it is recommended that:

• If thalassaemia is not present, any of MCV, MCH, or MCHC result which is below normal could suggest iron deficiency,
• On the other hand, normal red cell indices do not exclude iron deficiency as a cause of anaemia. Further investigation may still be required if there is high clinical suspicion.
• Mean reticulocyte Hb content of <29 pg can support the diagnosis of iron deficiency if initial tests are inconclusive and finally, although not diagnostic,
• Inspection of a peripheral blood film should be performed when the diagnosis is unclear.

Let’s now move onto ferritin.

Ferritin reflects iron stores and levels <15 µg/L strongly suggest iron deficiency.

Levels up to 30 µg/L can still be consistent with deficiency but are less specific.

Ferritin acts as an acute phase protein, meaning it rises with inflammation, kidney disease, liver disease, and malignancy and, because of this, interpreting ferritin in inflammatory states can be challenging.

Formulas to correct ferritin with CRP or ESR have been proposed, but the evidence isn’t robust enough for clinical use.

So, in summary, the recommendations are that:

• In children over 5 and adults a ferritin <15 µg/L is indicative of iron deficiency.
• For children under 5 the threshold is a ferritin <12 µg/L. However,
• A ferritin level within the normal range does not exclude iron deficiency if there’s inflammation or chronic disease and further investigation is often needed.

And this is where iron studies come into play. They should not be done routinely but they should be considered when:

• FBC shows microcytic or hypochromic anaemia
• Ferritin is borderline or normal but there's suspicion of iron deficiency e.g., in chronic inflammation or
• There's a need to differentiate iron deficiency from other causes of anaemia (like thalassaemia)

Iron studies include primarily: serum iron, total iron binding capacity (TIBC) and transferrin saturation (TSAT).

Let’s break this down.

Serum Iron only measures ferric iron bound to transferrin, not the iron in haemoglobin. Someone with iron deficiency will usually exhibit a low concentration of serum iron, but it is a dynamic parameter with well-established day-to-day variability. Consequently, measuring serum iron in isolation is not helpful but its measurement is required to allow calculation of percentage TSAT.

ON the other hand, TIBC and Transferrin rise in iron deficiency. Transferrin is a negative acute phase protein so its concentration may be reduced in inflammation. Although TIBC and transferrin have less variability than serum iron, their specificity remains poor so they are not really that useful for diagnostic purposes.

Finally, transferrin Saturation (TSAT) is calculated as the ratio of serum iron to TIBC or transferrin.

It reflects how much transferrin is carrying iron, but like serum iron, it’s variable and diurnal fluctuations can be up to 70%. Also conditions like malnutrition and chronic illness affect its accuracy.

A diagnostic threshold for TSAT has not been well established, but it has been suggested a target of <16% as a screening threshold.

So, in summary,

• Serum iron, TIBC and transferrin should not be used alone in diagnosing iron deficiency but a
• TSAT <16% can support the diagnosis if other tests are inconclusive.

As promised, let’s look at the algorithm proposed in this paper by the British Society for Haematology.

The first line tests for the investigation of iron deficiency anaemia are a FBC, ferritin and CRP. Based on the results, we have three main scenarios.

The simplest one is when haemoglobin is normal and no anaemia is identified.

In these cases, if ferritin is below 15, we should still suspect iron deficiency and investigations into the cause of the iron deficiency may still be required.

The other two scenarios is when there is anaemia.

And according to WHO criteria, anaemia is when Haemoglobin is:

Below 130 in adult males

Below 120 in non-pregnant females or

Below their age and gender specific reference range in children

So, if there is anaemia but no signs of inflammation, that is, CRP is normal,

But ferritin is below 15

Then this is a case of iron deficiency anaemia

However, if ferritin is 15 or higher,

Then iron deficiency is unlikely and we should consider other causes of anaemia

If there is anaemia but also signs of acute or chronic inflammation, that is, when the CRP is high

If ferritin is below 15

We should also regard this as iron deficiency anaemia.

If ferritin is higher than 150,

Then iron deficiency is also unlikely and we should consider other causes of anaemia

But if ferritin is between 15 and 150 in the context of a high CRP

Then further tests will be required, including a blood film and iron studies.

Blood film morphology will help us exclude alternative diagnoses and

We are likely to consider a diagnosis or iron deficiency anaemia if TSAT is <16% or mean reticulocyte haemoglobin content is less than 29 pg

In summary, we have summarised the current investigations for iron deficiency but this should be used alongside clinical guidelines, for example like in suspected gastrointestinal bleeding.

So that is it, a review of the laboratory investigations of iron deficiency.

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.

The video version of this podcast can be found here:

·      https://youtu.be/aB6Z7tASKrc

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 April  2025 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 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 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-04-01&to=2025-04-30&ndt=Guidance&ndt=Quality+standard

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

The NICE guideline on Falls: assessment and prevention in older people and in people 50 and over at higher risk [NG249] can be found here:

·      https://www.nice.org.uk/guidance/ng249

The update on Suspected cancer: recognition and referral [NG12] can be found here:

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

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#myeloma

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. In today’s episode, we’ll be looking at the NICE updates published in April 2025, focusing on what is relevant to Primary Care only.

We’ve got another short and snappy episode today, as there are only two clinical areas to discuss: the brand-new national guideline on fall prevention and new advice on cancer recognition and early detection.

Right, let’s jump into it.

And let us start with the update on the cancer recognition guideline, which affects the recommendations on blood tests for myeloma. These recommendations have been amended in response to a series of reviews to improve earlier diagnosis. So now those with an unexplained fracture or persistent bone pain, particularly back pain, and especially if they are aged 60 or over, should be investigated for myeloma, although we can consider it for people under 60 too. For this assessment we will request the following blood tests:

• a full blood count 
• serum calcium
• either plasma viscosity or ESR
• paraprotein, using serum protein electrophoresis and
• Serum free light chains. If the serum test is not available, we can use a Bence–Jones test to check for free light chains in the urine. 

The change means that we should now include serum protein electrophoresis and serum free light chain testing in the initial diagnostic blood tests and this testing should be offered instead of the traditional urine test for Bence–Jones protein. 

The second section refers to a brand-new guideline on falls assessment and prevention. These recommendations are for people who are:

• aged 65 or over or
• aged 50 to 64 with 1 or more factors that could increase their risk of falls. These factors include long-term conditions such as arthritis, dementia, diabetes or Parkinson's disease, having had a stroke and having a learning disability.

The guideline recommends a comprehensive assessment and management plan for these patients. But, who should we prioritise?

Well, we should offer comprehensive falls assessment and management to people who have fallen in the last year and who:

• Are frail.
• Were injured in a fall.
• Have experienced a loss of consciousness related to a fall.
• Have been unable to get up independently after a fall or that
• Have had 2 or more falls in the last year.

For people who have fallen in the last year and who do not have any of these criteria we should assess their gait and balance

And if they have a gait or balance impairment:

• We will simply offer a falls prevention exercise programme and
• a home hazard assessment.

But let’s go back to the people in the first group, those at highest risk and the ones that need a Comprehensive falls assessment. What should this assessment include? Well, we should check for:

• Alcohol misuse.
• Perform a Neurological and Cardiovascular examination including a lying and standing BP.
• We will do an Osteoporosis risk assessment including the risk of fragility fractures.
• A review of medication and long-term medical conditions and also include
• An overall review of the patient looking at things like:
• Cognition and mood.
• Diet, and weight loss.
• Hearing and visual impairments.
• Dizziness.
• Functional ability.
• Urinary continence
• Gait, balance, mobility, etc 

And once we have done this assessment, what does the comprehensive falls management entail? Well, apart from addressing obvious issues identified in the assessment, this management plan should include: 

1- A structured medication review and, for those on psychotropic drugs, we will discuss their increased risk of falls, considering stopping these medications, liaising with specialist services if necessary. Psychotropic medicines include antipsychotics, antidepressants, anxiolytics, mood stabilising agents, and antiepileptic drugs

2- we will refer to occupational therapy and any other appropriate service for a home hazard assessment and a fall prevention exercise programme

3- We will consider the need for surgical interventions, such as cataract surgery or a pacemaker, if these problems have played a role in their falls, and finally, 

2- Although there is insufficient evidence to support taking vitamin D supplements specifically to lower the risk of falls, we will encourage people to follow NHS advice on taking vitamin D to maintain bone and muscle health. For adults and children over 4 years old this advice is that they should consider taking a daily supplement containing 10 micrograms or 400 IU of vitamin D during the autumn and winter months, generally from early October to the end of March, and this includes pregnant and breastfeeding women. Between early April to the end of September, most people can make all the vitamin D they need through sunlight and from a balanced diet, so they may choose not to take a vitamin D supplement during these months. However, people at risk of vitamin D deficiency, including the frail and the housebound and also those with darker skin, for example those of African, African-Caribbean or south Asian background should take 10 micrograms or 400 IU of vitamin D throughout the year. The advice for infants and children under 4 is slightly different and it is not covered here.

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.

The video version of this podcast can be found here:

·      https://youtu.be/474v7gUrz38

This channel may make 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 (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the new NICE guideline on coeliac disease: assessment and management, NG20, 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.  

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 link to the NICE guideline on coeliac disease can be found here:

·      https://www.nice.org.uk/guidance/ng20/chapter/recommendations

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.

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 will go through the new NICE guideline on coeliac disease: assessment and management, or NG20, focusing on what is relevant in Primary Care only.

Right, let’s jump into it.

And before we start on the guideline itself, what is coeliac disease exactly?

Coeliac disease is a genetic, immune-mediated enteropathy triggered by gluten in some people. It primarily affects the small intestine, leading to villous atrophy, crypt hyperplasia, and malabsorption.

Why does it happen? Well, the pathophysiology is as follows:

Gluten (specifically gliadin) is found in wheat, barley, and rye. An enzyme called tissue transglutaminase (tTG) modifies gluten peptides. In genetically predisposed people, these modified peptides are presented to T-cells, triggering an inappropriate immune response. This leads to inflammation and damage to the small intestinal mucosa, particularly in the proximal small bowel.

We should suspect coeliac disease and offer serological testing if there is:

• persistent unexplained abdominal or gastrointestinal symptoms
• fatigue or weight loss
• mouth ulcers
• unexplained iron, vitamin B12 or folate deficiency
• first‑degree relatives affected.
• conditions such as type 1 diabetes, autoimmune thyroid disease, and irritable bowel syndrome (in adults) and we should also consider testing in a number of other conditions, for example:

·      reduced bone mineral density,

·      unexplained neurological symptoms (like peripheral neuropathy or ataxia)

·      persistently raised liver enzymes and

·      Down's and Turner syndromes

However, before arranging any investigations we will need to explain that any test is accurate only if a gluten‑containing diet is eaten during the entire diagnostic process. This also means that they should not start a gluten‑free diet until diagnosis is confirmed by a specialist, even if the results of a serological test are positive.

Additionally, people following a normal diet should be advised to eat some gluten in more than 1 meal every day for at least 6 weeks before testing.

If they have already restricted their gluten intake and they are unable to re‑introduce it, we will refer them to gastroenterology explaining that it may be difficult to confirm their diagnosis even by intestinal biopsy.

People who have tested negative for coeliac disease should be retested if new suggestive symptoms arise or persist, particularly if they have type 1 diabetes or a family history.

What serological testing should we do for coeliac disease?

NICE recommends that the first choice of test should be IgA tissue transglutaminase antibodies (tTG) together with total immunoglobulin A (IgA) to exclude deficiency. But why is this?

Let’s remember that everyone has the tissue transglutaminase enzyme (tTG). However, in people with coeliac disease, the immune system produces autoantibodies against this enzyme — particularly IgA autoantibodies.

This autoantibody response is:

• Highly specific to coeliac disease
• Triggered by gluten exposure in genetically susceptible people and
• Correlate with intestinal damage (i.e. the higher the autoantibodies, the more likely there is villous atrophy)

This is why serum IgA tissue transglutaminase antibodies are the first-line screening test — it’s convenient, non-invasive, and has high sensitivity and specificity, especially in untreated people.

Additionally in adults the lab should test for IgA endomysial antibodies (EMA) if IgA tissue transglutaminase antibodies are weakly positive and consider additional tests if IgA levels are low. Then the Lab should clearly communicate the interpretation of the results as well as the recommended action.

We should then refer anybody with positive serological test results to a gastrointestinal specialist for further assessment, which for adults will most likely include endoscopic intestinal biopsy.

We should also refer those with negative serological test results if coeliac disease is still clinically suspected.

People diagnosed with coeliac disease should have an annual review in order to:

• measure weight and height
• review symptoms and diet
• and consider the need for specialist dietetic advice.

For those who have persistent symptoms despite gluten exclusion we should:

• review the certainty of the original diagnosis
• refer them to a specialist dietitian to investigate continued exposure to gluten
• and investigate potential complications or coexisting conditions such as irritable bowel syndrome, lactose intolerance, bacterial overgrowth, or colitis.

If no other cause is found we would call it refractory coeliac disease and we will need to refer them and consider prednisolone while waiting for specialist advice.

We should give people with coeliac disease sources of information on the disease, including, for example:

·      Specialist groups and dietitians

• how to manage social situations, like eating out and travelling
• avoiding cross contamination at home and
• immunisation against pneumococcus, all of this
• Being aware that people with coeliac disease may experience anxiety and depression.

In terms of dietary management, they should seek advice before taking over‑the‑counter vitamin or mineral supplements, explaining that they may need to take specific supplements such as calcium or vitamin D if their dietary intake is insufficient.

We can also explain that:

• they can choose to include gluten‑free oats in their diet at any stage and
• continuing them will depend on their response.

So that is it, a review of the NICE guideline on coeliac disease.

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.

The video version of this podcast can be found here:

·      https://youtu.be/JP5EvxGd8g4

This channel may make 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 (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the new NICE guideline on acute asthma, NG244, focusing on what is relevant in Primary Care only. Given how extensive the guidance is, in this episode I will just focus on lessons from asthma deaths and near-fatal asthma as well as reviewing the concept of difficult asthma.

In the last four episodes I covered the initial assessment and treatment in both adults and children.

Just like the NICE guideline on the management of chronic asthma, which was updated in November 2024, the NICE guideline on acute asthma is also a collaborative initiative developed by NICE, the British Thoracic Society (BTS), and the Scottish Intercollegiate Guidelines Network (SIGN). It replaces previous guidance, and you can find a link to it in the episode description.

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 link to the new NICE guideline on acute asthma can be found here:

·      https://www.nice.org.uk/guidance/ng244/chapter/Managing-acute-asthma

Based on recommendations on managing acute asthma in the BTS/SIGN British guideline on the management of asthma:

·      https://rightdecisions.scot.nhs.uk/bts-nice-and-sign-asthma-pathway/managing-acute-asthma/

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.

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 will go through the new NICE guideline on acute asthma, or NG244, focusing on what is relevant in Primary Care only. Just like in chronic asthma, the NICE guideline on acute asthma is a joint effort by NICE, BTS and SIGN and a link to it is in the episode description.

In this episode I will just focus on lessons from asthma deaths and the concept of difficult asthma.

In the last four episodes I covered the initial assessment and treatment in both adults and children and, if you have not already, I recommend that you check them out.

Right, let’s jump into it.

Confidential inquiries into over 200 asthma deaths in the UK have identified that most asthma deaths occurred before the patient reached hospital and that there are three main contributing factors: the disease itself, medical management, and patient behaviour or psychosocial issues..

And let’s start by looking at Disease Factors:

Although, In a minority the fatal attack occurred suddenly in a patient with mild or moderately severe asthma, the majority of patients who died from asthma had chronically severe disease.

In terms of Medical Management:

Many deaths were linked to inadequate treatment with inhaled corticosteroids (ICS) or oral steroids, as well as poor monitoring of asthma severity. Follow-up care was often insufficient, and some patients should have been referred to specialists sooner. The use of written management plans was notably underutilised.

A key finding from the National Review of Asthma Deaths report, published in 2014 by the Royal College of Physicians, highlighted the link between heavy or increasing use of short-acting beta agonists (or SABAs) and asthma deaths. Prescribing more than 12 SABA inhalers per year should prompt a thorough review of the patient’s management.

Asthma deaths have also been reported after inappropriate prescriptions of beta blockers and non-steroidal anti-inflammatory drugs, so All asthma patients should be asked about any previous reactions to these medications.

Sedation should be avoided during acute asthma attacks unless it is necessary for anaesthetic or intensive care procedures.

The National Review of Asthma Deaths report also revealed an increased risk of death within one month of hospital discharge following an acute attack, underscoring the need for close follow-up in primary care.

Let’s now look at Adverse Psychosocial and Behavioural Factors:

And These factors are important because they were present in most patients who died of asthma. Key risk factors include poor adherence to treatment, failure to attend appointments, and psychiatric conditions. So we, as Healthcare professionals, must recognise that patients with severe asthma combined with psychosocial vulnerabilities are at greater risk of death.

So, who are these patients? Patients at Risk of Near-Fatal or Fatal Asthma are usually those who have severe asthma along with one or more of the following:

• A history of near-fatal asthma, including previous ventilation or respiratory acidosis.
• Previous hospital admission for asthma, especially within the past year.
• The need for three or more classes of asthma medication.
• Frequent or heavy use of β2 agonists. and
• Multiple emergency department visits, particularly in the last year.

AND additionally, adverse Psychosocial and behavioural factors, including:

• Non-adherence to treatment or monitoring.
• Missing appointments
• fewer GP contacts.
• Frequent home visits
• self-discharge from hospital.
• Mental health conditions such as psychosis, depression, or self-harm.
• Current or recent use of major tranquillisers.
• Denial of the severity of their condition.
• Substance or alcohol misuse.
• Obesity.
• Learning difficulties.
• Financial or employment problems.
• Social isolation.
• Childhood abuse. As well as
• Severe domestic, marital, or legal stress.

Patients admitted with a severe asthma attack should be followed by a respiratory specialist for at least a year post-admission.

For patients who have experienced near-fatal asthma, it’s advisable to involve a close relative when discussing future management plans and They should remain under specialist supervision indefinitely.

Let’s now touch on the concept of Difficult Asthma:

Difficult asthma refers to cases where asthma-like symptoms and attacks persist despite high-dose asthma therapy. There is no universally agreed definition, but it typically applies to patients with ongoing symptoms or frequent attacks despite maximum treatment.

In this context, difficult asthma is defined by:

·      persistent symptoms and/or frequent asthma attacks despite the following treatments:

o  in adults:

§ the use of high-dose ICS plus one other agent such as a LABA or LTRA or

§ The use of medium-dose ICS plus two other asthma agents such as a LABA and LTRA or any other appropriate additional therapy

o   However, in children this concept applies to those on:

§ medium-dose ICS plus one other agent such as a LABA or LTRA; or

§ low-dose ICS plus two other asthma agents such as a LABA and LTRA or any other appropriate additional therapy or

• those taking oral steroids Frequently or continuously.

Patients with difficult asthma require a thorough evaluation, including:

• Confirming the asthma diagnosis.
• Identifying the cause of persistent symptoms. and
• Assessing adherence to treatment.

This should be done by a multidisciplinary asthma service with expertise in managing complex cases.

The Factors Contributing to Difficult Asthma are:

• Poor Adherence and managing it is beneficial improve asthma control and there is some evidence that it can improve lung function and quality of life. Objective monitoring of adherence is more reliable than self-assessment.
• Then Given that difficult asthma is frequently linked to adverse psychosocial factors. We should routinely assess for coexisting psychological co-morbidity and, In children, this should include a psychosocial family assessment.
• Then Patients with difficult asthma have been found to have high rates of dysfunctional breathing, which can mimic asthma or coexist with asthma,
• Also, Given that Acute asthma can be associated with IgE-dependent sensitisation to indoor allergens, patients with difficult asthma and recurrent hospital admissions, should be tested for mould allergies.
• And finally patients with difficult asthma, could have induced sputum eosinophil counts to guide steroid treatment.

And what is this induced sputum eosinophil count?

Although this isn’t done routinely in primary care, let’s quickly explain what it involves.

Before starting, we will check spirometry or peak flow to get a baseline.

Then, in order to prevent bronchospasms, we will give the patient a short-acting β2-agonist (like salbutamol) before starting the test.

Then, For Sputum Induction, the patient inhales a mist of hypertonic saline (usually 3% to 5%) using a nebuliser. If their FEV₁ drops by 20% or more, we will stop the procedure immediately.

After Sputum Collection, the lab will provide the percentage of eosinophils seen. A result of >3% suggests eosinophilic inflammation, which can help guide asthma treatment decisions, such as oral steroids.

So that is it, a review of lessons from asthma deaths and the concept of difficult asthma.

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.