About this blog: information for everyone else

Hi there! I’m a GP and this blog consists of the notes I take on journal articles, as part of my continuing professional development. It is intended purely for my own use in recording and remembering the things I learn so that I can refer back to them in the medical setting. While anyone is welcome to read it, please do not take it as any kind of substitute for seeing your own doctor for any medical-related queries or problems.

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About this blog: information for appraisers

This blog consists of notes made on any learning points I come across in the course of CPD and want to remember/look up later. The two main sources for this are on-line learning modules, and articles which I identify in the course of journal reading as meeting a learning need. Credits for the former are obviously counted elsewhere, so I’ve grouped the latter in a separate category in order to estimate the learning credits I’ve obtained from structured reading. You can find all posts in that category for the 2013 – 14 appraisal year here.

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Does Vitamin D deficiency cause fatigue?

This question came up regarding a patient. The National Osteoporosis Guidelines on Vitamin D weren’t helpful, so I went onto PubMed. I found the following:

  • This study found that vitamin D levels were negatively associated with fatigue in young Iranian nurses.
  • This study found that the presence of Vitamin D deficiency was associated with a greater likelihood of reporting fatigue (although the degree of deficiency didn’t correlate with the degree of fatigue. At least I think this is what it was saying; I only have the abstract, which is slightly unclear.)
  • This case report is of a case of hypersomnia without other apparent cause that was found to be associated with Vitamin D deficiency and improved rapidly when the deficiency was treated. Obviously only one case report so of limited use, but still interesting.

And, when it comes to treatment:

  • This double-blind RCT showed a significantly greater likelihood of improvement in fatigue symptoms in deficient patients with Vitamin D as compared to placebo, with an NNT of approximately 5. In this study, the initial levels were <20 mcg/l.
  • This RCT did not show any benefit of Vitamin D on fatigue in patients with CFS. However, as far as I can tell from the abstract, initial Vitamin D levels weren’t tested so we don’t know whether the patients were deficient or not.
  • This randomised trial showed Vitamin D supplementation to be of help in deficient patients with fatigue following renal transplantation, but as far as I can see it’s not clear whether the patients were blinded, or what the regime was.
  • Finally, although it’s about depression rather than fatigue, I thought it worth noting that this small RCT showed that Vitamin D supplementation also improved mood.

In conclusion, there seems to be at least some evidence that Vitamin D deficiency can manifest as fatigue and that supplementation can help.

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Stable angina – NICE guidelines

New official guidelines for assessing possibly cardiac chest pain; check for the following three features of the pain.

  1. Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest (or by sublingual GTN) within approximately 5 minutes.

The presence of all three features can be diagnosed as ‘typical’ anginal chest pain. Two out of three is classified as ‘atypical’. One or zero is ‘non-anginal’ and does not require further investigation unlses there are other factors of concern in the history or risk factor profile.

Ask about resting chest pain or rapidly progressive symptoms, which would indicate unstable angina or possibly ACS.

Investigation is now by CT coronary angiogram, with positive or inconclusive tests being followed up by functional testing with either stress echocardiography, stress perfusion cardiovascular magnetic resonance, or nuclear perfusion imaging. Angiography should now only be used in cases where other tests are inconclusive or show proximal or extensive coronary disease. CT coronary angiogram has very high sensitivity and thus is excellent for a rule-out test.

Medical therapy is still the first-line treatment.

(BJGP, April 2018)

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Itchy rashes

(from BMJ Learning module)

Lichen planus

Cause unknown, but does have an association with Hep C virus, so consider checking.

The rash, like acute leg ischaemia, is described by 6 Ps:

  • Planar (flat-topped)
  • Polygonal
  • Purple
  • Pruritic
  • Papules
  • Plaques

I knew about Wickham’s striae in the mouth (though I’m not sure I would have remembered the name) but didn’t remember that it can also affect theĀ lower back, genitals, scalp and nails.

Discoid eczema

This can be mistaken for psoriasis (red scaly plaques on extensor surfaces). However:

  • The plaques are not usually as well-defined or as thick.
  • Discoid eczema doesn’t have the silvery-white scale
  • It’s extremely itchy

Note that the steroid cream for discoid eczema has to be potent or very potent.

Guttate psoriasis

Is usually very itchy. The lesions are drop-shaped (hence ‘guttate’) and are initially flat before becoming raised. Scale may or may not be visible. There may be no history of psoriasis. Ask about history of sore throat about 7 – 10 days prior; this may be the most helpful diagnostic feature.

Pityriasis rosea can be differentiated from guttate psoriasis by the herald patch and collarette of scale.


Very itchy rash which is worse at night and after a shower.

Papules and nodules on the penile shaft of an adult male or around the areola of an adult female are very likely to be scabies.

Babies and small children may have papules on their palms and soles.

The burrows may show up as scaling. They’re easier to see with dermoscopy, which can show up the mite (‘delta-wing’ head and translucent body) and eggs as well as typical S-shaped burrows. As well as finger and webs, they may show up on the sides of the feet, the waist, and the axillae. Use gloves for examination.

Scabies normally needs about 15 minutes of close bodily contact to be transmitted, though crusted scabies can be transmitted after brief contact. It is rarely transmitted via bedding/furniture. It takes about six weeks from transmission before the generalised itch develops.

Correct diagnosis is important; empirical treatment can worsen other types of itchy rash, due to the irritation.

Tinea incognito

This can be caused not just by inappropriate steroid treatment of a dermal rash, but also by other causes of immunosuppression such as HIV, diabetes, and immunosuppressant medication. When steroids are used, the rash initially seems to clear before coming back worse (which can lead to a vicious circle).

Asymmetrical rashes should be strongly suspected as being fungal. Tinea incognito may also have pustules around the edge.

Diagnose with skin scrapings.

Topical antifungals aren’t usually enough and oral antifungal drugs will be needed for tinea incognito.

Allergic rashes

A first-time allergy will normally show up 7 to 14 days after the rash; if a rash shows up within 48 hours of starting a drug that the patient has previously tolerated with no problems (or hasn’t previously had before) then this is not likely to be an allergy.

A good general tip…

When examining for a generalised itchy rash, check the centre of the back. This is probably not going to have been scratched, as it’s the hardest part to reach, so if there are no lesions there then this suggests that the lesions on the other parts of the skin may have been caused by the scratching and may, for example, have an underlying metabolic cause.

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Degenerative cervical myelopathy

This is the new name for the conditon formerly known as cervical spondylotic myelopathy, and is spinal cord dysfunction from compression in the neck due to degenerative change (disc herniation, ligament hypertrophy/ossification, osteophyte formation).


Gradual onset and worsening of symptoms, which vary and may include:

  • Neck pain and/or stiffness
  • Limb or body pain; unilateral or bilateral
  • Upper limb weakness, numbness, or loss of dexterity; may be unilateral or bilateral.
  • Lower limb weakness, sensory loss, or stiffness; may be unilateral or bilateral.
  • Paraesthesia
  • Autonomic symptoms; bowel or bladder incontinence, erectile dysfunction, or difficulty PUing
  • Unsteadiness/poor balance, sometimes leading to falls.
  • Atypical symptoms; headaches, muscle cramps.

Symptoms can be insidious and the course, although generally downhill, is variable; patients may have mild stable symptoms for long periods of time, or a more rapid decline. Patients will typically have increasing loss of dexterity (difficulty with tasks such as doing up buttons, writing, using mobile phones) and/or mobility (may need walking aids/have frequent falls).



  • Pyramidal weakness (UL worse in extensors, LL worse in flexors)
  • Limb hyperreflexia
  • Spasticity (claspknife sign)
  • Clonus – esp Achilles tendon
  • Babinski’s (upgoing plantars)
  • Hoffman’s sign (flick the nail of the middle finger to flex it sharply, see whether there is any reflex contraction of the thumb and/or index on that hand)
  • Segmental weakness at the level of compression
  • Sensory loss (limb and/or trunk)
  • Lhermitte’s sign (neck flexion or extension causes electric shock sensation down the spine/into the limbs – this is an indication that the problem is quite severe)
  • Gait disturbance



Requires MRI of the cervical spine, not surprisingly. This may be routine in patients with mild stable symptoms, but needs to be urgent in patients with progressive symptoms and/or symptoms substantially affecting quality of life. If MRI can’t be ordered directly, refer to neurology first if needed.

Note that scan findings do not correlate well with disease severity; mild compression can cause severe disease.



Spinal decompression (although a wait-and-see approach may be appropriate for patients with mild, stable DCM).

Maximal recovery has usually taken place by around 6 – 12 months post-op; residual symptoms at this point are likely to be permanent.


DCM as an incidental finding

This is quite common, and does not need any treatment if asymptomatic; however, patients should be reviewed for symptoms and made aware of symptoms that need prompt reporting in the future.


BMJ: Degenerative cervical myelopathy

Posted in Credits 2018, Don't miss, Neurology, Orthopaedics | Leave a comment

Cutaneous horns

I’ve just spent a bit of time refreshing my memory on these, after seeing a lesion I wasn’t sure about. After looking at several photos I do believe the patient I saw does have a small cutaneous horn, and the Dermnetnz article confirmed that these need excision to exclude premalignant or even malignant cells at the base, which occur in about 50% of cases (which is a higher percentage than I thought). The article also had a list of features associated with a higher risk of malignancy in these lesions:

  • Pain
  • Large size
  • Wide base, or wide base compared to the length
  • Induration at the base
  • Redness at the base
  • Site: lesions on the nose, ears, scalp, face, forearms, or backs of hands are more likely to be malignant, which is not surprising given that these will be the high-risk areas for sun exposure. Lesions on the penis are also more likely to be malignant, which is more surprising; I don’t know the explanation for this.
  • Lack of terrace formation. ‘Terrace formation’ apparently refers to a pattern of horizontal ridges on the side of the horn – lack of this can be a sign of rapid unorganised growth.

This is reassuring as my patient’s lesion was small and not painful with a narrow base and no inflammation. However, it’s important to note that there is no single sign that can reliably confirm or exclude malignancy; only excision and histology will do that. This confirms that, as I suspected, I need to refer this patient as a two week wait.

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Slow initiation of warfarin protocol.

We’re all familiar with the usual 5mg warfarin initiation protocol (and many of us have distant memories of the 10-10-5 regimes started in hospital, or at least that’s what was being done when I was a junior doctor, back in the Dark Ages second half of the ’90s). I had, however, heard that it’s possible to initiate warfarin even more slowly, and that has obvious benefits in elderly people being started on it for AF, who don’t need the anticoagulation urgently and are at more risk if they’re overanticoagulated. So, when I had a patient fitting that description, I went looking for a protocol.

I found what I was looking for on the site GP Notebook, which directed me to two studies, of which this one looked like the best bet. The protocol here is to start patients on a 3 mg loading dose daily, and check on Day 8 and Day 15. I’ll try the 3 mg and checking on Day 8, and take it from there.

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Ulipristal warning

There’s a new warning out about ulipristal acetate 5 mg tabs (Esmya); it has been found to cause serious liver injury in some cases. The advice from the MHRA is that no new courses should be started, even in patients who have had previous courses without problems. Current courses do not need to be stopped, but precautions should be taken as below:

  • Warn patients on ulipristal of the symptoms of liver injury (N&V, loss of appetite, fatigue, RUQ pain, jaundice, etc. and advise them ‘about specific actions to take’ if they develop such signs (which I assume means ‘see your GP pronto’, although that seems to be left vague for some reason).
  • Monitor LFTs at least monthly, as well as one further time 2 to 4 weeks after stopping treatment, and immediately if a patient presents with symptoms of liver injury as above. (It would be useful to know whether, for patients presenting to their GP on Friday afternoon, ‘immediately’ in this context means ‘Monday morning’ or ‘send into hospital’, but, alas, that isn’t the kind of detail that people in medication regulatory agencies think of. I suppose it’s a judgement call based on the patient’s condition at the time.)
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