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.

Posted in About this blog | Leave a comment

About this blog: information for appraisers

I use this blog to record my learning points/reflections arising from my CPD. It’s a very handy way of doing it, as it lets me refer back to it easily and use the search function and category menu to find the notes I’ve made on a topic when needed.

My CPD typically consists of a mixture of online modules, articles which I come across in the course of routine journal reading and find useful, answers to DENs that I’ve looked up, and the usual regular courses in CPR and (on a three-yearly basis) child safeguarding. Of the online modules, some are compulsory; the rest I pick based on DENs I identify, either specific (“I wonder what the answer is to this question that arose with this patient?”) or general (“I really need to brush up on my knowledge of skin cancers”).

To read my overall notes for this year, just click on the picture at the top to get to the home page; you can then read the posts in reverse date order (newest first). If you want to check the list of posts on CPD that isn’t from learning modules (as CPD credits for those are recorded separately), those are under the category ‘Credits ____’ with the current year. You can find this by scrolling down the category menu on the right (under the archive menu). I will normally also put in a direct link to this category in my appraisal record.

Hope that’s clear, but happy to discuss any questions at appraisal.

Posted in About this blog, Credits 2016, Credits 2018 | 2 Comments

Multiple sclerosis

(Notes on the BMJ module regarding NICE guidelines)


There wasn’t much on this, but common presentations include:

  • Optic neuritis (loss of/reduction of vision in one eye, associated with aching)
  • Double vision
  • Ascending sensory disturbance (e.g. from feet to abdomen), with or without associated weakness.

Initial investigations

The point of investigating before neuro referral is to rule out other causes for the symptoms (MS diagnosis is complicated and can only be done by a consultant neurologist, which is fine by me). Most of these were the usual line-up: renal/liver/thyroid function, calcium, glucose, B12. However, the guidelines also advise doing:

  • Inflammatory profile (ESR, or PV in our case/CRP)
  • HIV serology


People with MS should be given a clear point of contact for concerns and should have yearly specialist follow-up. They should also be given a lot of information, which is obviously going to be hard to take in at the time, so it’s worth the GP checking that they have:

  • Information on how to contact the MS team with questions
  • Information on charities
  • Instruction to contact the DVLA
  • Advice on their rights involving employment/benefits.



…is an even worse idea than usual, since studies clearly show it to be linked to increased risk of relapses and progression. Ex-smokers seem to have the same risk as never-smokers, so stopping really can improve risk profile here.


Is beneficial, even for people with mobility problems/fatigue problems. If fatigue problems, consider referral for a supervised exercise programme. If mobility problems, refer to a rehabilitation team or physio with expertise in MS.

Don’t use something called fampridine; it’s not cost-effective. Fine by me, I’d never heard of it.

Some other things not to bother trying

  • Vitamin B12 unless diagnosed deficiency
  • Vitamin D unless in an at-risk group for other reasons as per usual Vitamin D guidelines
  • Omega 3 or Omega 6 fatty acids

According to the guidelines, there is no evidence for any of these.


Flu vaccination might sometimes trigger relapse, so consider carefully whether to use it or not and make an individualised decision weighing up the risks and benefits.

Remember that live vaccines might be contraindicated in DMTs.


Can present as intense stiffness, muscle jerking, or muscle spasms. Note that underlying conditions such as infection or constipation can make spasticity worse, so these should be identified and treated.

  1. 1st-line treatments: gabapentin, baclofen
  2. 2nd-line treatments: tizanidine, dantrolene
  3. 3rd-line: benzodiazepines such as clonazepam (which can also help with nocturnal spasticity).

Start at a low dose and titrate up gradually over weeks until either symptoms ease or the maximum tolerated dose is reached. Encourage patients to do their own auto-titration if possible. If there is partial relief at maximum tolerated dose, add another drug; if no relief, change to another drug. Note that too high a dose of the drugs can cause (reversible) muscle weakness.

If all that fails, refer to specialist services.

Sativex is not currently considered cost-effective for spasticity related to MS.


Treat SOS; exclude infection (especially UTI), start high-dose steroids (with bone protection if needed), and let the team know. Steroids might be oral or IV. Note that they can precipitate depression.

Urinary symptoms

Check a post-void scan for residual volume. If <100 ml, use anticholinergics. If >100 ml, try intermittent self-catheterisation.

Posted in Neurology | Leave a comment

Glucose control in Type II diabetes

(As per BMJ module ‘Clinical pointers: Blood glucose control in Type 2 diabetes’)

I’ve used sulfonylureas as second-line diabetic drugs for years on a ‘devil you know’ basis, but it now seems that’s out of date; one meta-analysis showed them to be associated with a higher risk of cardiovascular events (Diabet Med 2017; 24(12): 1412 – 18). (Another meta-analysis, in JAMA 2016; 316: 313 – 24, found all meds came out about the same in this aspect, so the jury’s out, but it does make me think perhaps I’m better getting with the programme and giving DPP-4s, at least until something dire inevitably comes out about those as well.)

NICE recommends a stepwise approach:

  1. HbA1c >48 on lifestyle measures: start metformin and aim for 48.
  2. HbA1c >58 on metformin + lifestyle measures: start a second drug and aim for 53. (I’m not sure how this is supposed to fit with aiming for 48 in people on non-hypoglycaemic drugs.)
  3. HbA1c >58 on two oral drugs + lifestyle measures: start a third drug, which can be insulin. Aim for 53.

Quick recap of the possible options for dual or triple therapy:

Second-line therapy with metformin:

  • Sulfonylurea
  • DPP-4 inhibitor
  • Pioglitazone
  • SLGT-2 inhibitor

Third-line therapy combos with metformin:

  • SU with any of the other three above
  • SLGT-2 with either SU (which obviously follows from the line just above) or pioglitazone
  • Insulin with metformin; review the need for other antihyperglycaemics when insulin is started.

To put that another way, the only two combos of the list of second-line drugs that can’t currently be given as part of oral therapy are DPP-4s with either pioglitazone or SLGT-2. That narrows things down; since I’ve now decided to give DPP-4s as my second-line drug with metformin unless there’s some good reason not to, my third-line, if not referring for insulin, will normally be a sulfonylurea. OK, I… I think I’ve got it.

But where do GLP-1 inhibitors fit in?

As combination therapy with metformin plus sulfonylurea in patients who fit anyof the following criteria:

  • BMI >35 (can be less in some ethnic minority groups) and this is causing specific medical or psychological problems
  • Weight loss would benefit other co-morbidities
  • Insulin therapy would have significant occupational implications

And what about people who can’t take metformin?

Firstly, if the problem is side-effects then consider trying a modified-release preparation before giving up completely. If that doesn’t work/isn’t an option:

Alternative first-line:

  • DPP-4i (target 48)
  • Pioglitazone (target 48)
  • Sulfonylurea (target 53)

Second-line: Any two of the above combined. (So, in other words, alternative first and second-line treatments are similar to the with-metformin second and oral third-line treatments except that SLGT-2 inhibs are off the table and DPP-4is apparently can be used with pioglitazone if metformin isn’t around, all of which is sounding more complicated than figuring out who can and can’t sit with whom at extended feuding family Christmas dinner.)

Third-line: Insulin.


Posted in Diabetes, Medication | Leave a comment

Assessment of purpuric/petechial rashes

This was a BMJ module, based on this article.

Steps in assessing purpuric/petechial rashes:

  1. Assess for acute illness and consider the possibility of meningococcal sepsis. If suspected, administer parenteral antibiotics and admit urgently.
  2. If meningococcus is not the suspected diagnosis, and if the patient is a child or young person (‘young person’ is left undefined here; from what I could find from the source, it seems to mean someone under 24), then send them for same-day specialist assessment. If patient is an adult, arrange FBC within 48 hrs, or sooner if indicated, ensure you have emergency contact details, and advise them to avoid aspirin/NSAIDs while awaiting results.
  3. The above should exclude anything serious, so if the FBC is normal then manage according to the most likely cause.

Causes of petechiae/purpura in adults

(Note that there are slightly different lists of causes in neonates or children. I haven’t bothered transcribing those, on the basis that, as per above, any children with petechial rashes are going to be referred directly to paediatrics anyway, and thus if I get a diagnostic problem in this area it’ll be with an adult.)

  • ITP
  • Primary bone marrow failure (leukaemia, myelodysplasia)
  • Secondary bone marrow failure (metastases)
  • Drug-induced
  • Nutritional deficiency (didn’t list causes; B12 deficiency is the one I could think of)
  • Degenerative causes such as senile purpura
  • Mild coagulopathies (which can show up only in adulthood; if very mild, they might only show up in the elderly)
  • Acquired haemophilia (which I’d never heard of, but it’s on the list so I guess it’s a thing).
Posted in Dermatology, Don't miss, Haematology | Leave a comment

Indications for urgent referral of childhood eczema

Same day:

  • Eczema herpeticum (widespread HHV infection of eczema). Will need same-day dermatology opinion and, if it affects periorbital skin, same-day ophthalmology opinion as well. Give systemic aciclovir in the meantime (not sure of practicalities of this).

Within two weeks:

  • Severe eczema not responding to a week of optimum topical treatment.
  • Bacterially-infected eczema not responding to treatment.

(from module on children’s acute skin rashes)

Posted in Dermatology, Paediatrics | Leave a comment

Managing menopause

(Notes from BMJ module)

From 45 yrs onwards, menopause/perimenopause can be diagnosed on history only. FSH or other blood tests are not actually helpful in diagnosis in the >40s because of the wide fluctuation in levels in the perimenopause. FSH can, however, be helpful in showing when women >50 can stop progestagen-only contraception; if FSH is >30 in a woman >50, she can stop one year after that. Don’t use it for this purpose in women on combined hormonal contraceptive (or on high-dose progestagen, but the doses used for progestagen-only contraception don’t count).

Note that women over 55 can stop contraception anyway even if still getting periods, as conception so rare at this point. CHC can be used in >50s, and is considered a UKMEC 2, but it’s also considered worth advising against it (note that it can mask the date at which menopause arrives). Women using HRT and requiring contraception can use CHC instead if age-appropriate; can use an IUS as the progestagen component; or can use any type of progestagenic contraception alongside HRT (note that the progestagen part of HRT has to  be used in that case, as only the Mirena is licenced to provide uterine protection in HRT).

When discussing menopause, discuss lifestyle factors for bone health, and also take the time for other health promotion (smoking cessation, exercise promotion, review alcohol consumption). Note that regular aerobic exercise seems to reduce menopausal symptoms (occasional high-impact exercise, on the other hand, can worsen them). Reducing/eliminating alcohol and caffeine can also help.

First-line treatment for vasomotor symptoms should be HRT if no contraindications; other methods are less effective and have a high rate of side-effects, so don’t offer them as first-line.

Women with a history of breast cancer obviously can’t be offered HRT as first-line; when offering SSRIs, be aware that fluoxetine and paroxetine might interact with tamoxifen, reducing its effectiveness, and thus those combinations are contraindicated. Citalopram or Venlafaxine are OK to use.

In terms of VTE risk, note the following:

  • Inform women of the small extra risk with HRT. This, however, only appears to apply to oral HRT; I can’t help feeling this creates some ethical problems.
  • If women are at increased baseline risk – e.g., BMI >30 – offer transdermal instead of oral. I guess women who have a normal starting risk just have to (literally) suck up the extra risk with oral HRT.
  • If the risk is on the ‘strong family history’ or ‘known hereditary thrombophilia’ level, consider referral to a haematologist for advice prior to starting HRT.
  • Women with a past history of unprovoked VTE should avoid HRT altogether.

In terms of cardiovascular risk, note that it only appears to exist in women starting HRT over the age of 60 years. (Also, it only appears to be for non-fatal cardiovascular disease; the risk of dying of an MI doesn’t appear to be increased.) In women under 60 who have no previous history of cardiovascular problems, it might even be cardioprotective. Any existing risk seems to be with the combined types, not the oestrogen-only. Cardiovascular risk factors aren’t a contraindication to HRT if well managed.

There’s a small increase in stroke risk with oral HRT, but not with transdermal.

After starting HRT, review in 3/12 and then annually.

Non-prescription therapies with some evidence of effectiveness include CBT, relaxation, acupuncture and St John’s Wort. However, with regard to the latter, bear in mind that it does have clinically significant interactions; also, the dosage isn’t clear, and potency of preparations can vary.

Remember that topical oestrogen can be helpful for urogenital symptoms, and can be needed to supplement systemic HRT.

Cognitive symptoms don’t seem to be caused directly by the menopause, although they can be caused by sleep deprivation from hot flushes.

Mood changes sometimes respond well to HRT, and can also respond to CBT. SSRIs might not be helpful for mood changes that don’t fit the clinical criteria for depression.

Premature ovarian failure refers to menopause prior to 40 yrs, and is diagnosed by taking two FSH levels 4 – 6 weeks apart in a woman with the typical symptoms and signs. Note that FSH cut-off in this case should be >40 iu/L, not >30 as in checking contraceptive need in the 50 – 55 yr age group. POI can, in occasional cases, reverse spontaneously, so specialist advice should be obtained on contraception. (It is reasonable to use the COC for bone protection, though HRT can also be used.)

Note that if women go through POI secondary to medical/surgical treatment, they’re getting a triple whammy; not only are they going through menopause early, they’re also likely to get very severe symptoms, and to have all this to deal with on top of whatever they were having treatment for in the first place. They might well come in with the menopausal symptoms only some months later when things have settled down regarding whatever the initial problem was. Specialist referral is likely to be indicated.

Note also that women with POI are at increased risk of cardiovascular disease unless on HRT.

Bleeding in the first three to six months of continuous combined HRT is common; if happening or persisting after that, treat as a PMB. If gynaecological pathology and non-compliance have both been excluded and bleeding is persisting, try changing to a different progestagen.

Posted in Gynaecology, HRT | Leave a comment

Antidepressants/NOACs and bleeding risk

A DEN came up while I was sorting out repeat prescriptions: While it’s well known that patients taking an SSRI with NSAIDs or antiplatelet agents should strongly consider GI prophylaxis, does that apply to people taking SSRIs with NOACs?

I asked for advice on Doctors.net.uk and was directed to a useful summary, downloadable here. The upshot is that:

  1. The SSRI/NOAC combination does seem to lead to increased bleeding risk (this is probably related to serotonin depletion in platelets). However, this is a general risk, not a risk to gastric mucosa in particular, so it’s dubious whether benefits of taking a PPI as prophylaxis would outweigh the risks of so doing.
  2. This only applies to SSRIs and SNRIs, not to other antidepressants. As it happens, the particular situation I was looking at involved mirtazapine plus a NOAC, and, although I had misremembered mirtazapine as being an SNRI, it is in actual fact a tetracyclic.

I was therefore able to stop an unnecessary omeprazole prescription, for which I am glad.


Posted in Medication | Leave a comment

Aspirin + clopidogrel short-term after TIA/ischaemic stroke

I belatedly got round to reading a January BMJ that contained this article, an analysis of previous work on DAPT (dual antiplatelet therapy) after TIA/stroke. The recommendations are:

  • After either a high-risk TIA or a minor ischaemic stroke, use both aspirin and clopidogrel together for between 10 and 21 days to reduce rethrombosis risk in the high-risk period.
  • Don’t do this after major stroke, as there’s an increased risk of intracranial bleeding.
  • Optimum doses are uncertain. Based on current evidence, the authors advise going for 300 mg loading dose followed by 75 mg daily dose of clopidogrel, and anything between 75 and 345 mg od of aspirin, which in practice I would interpret as 75 mg for the lower bleeding risk.
Posted in Cardiovascular, Credits 2019, Medication | Leave a comment