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

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

Diabetes management

The alphabet mnemonic is useful for remembering all the things that need to be discussed with patients:

  • Advice – smoking, diet, exercise, weight loss. See about referring to structured educational programmes.
  • Blood pressure
  • Cholesterol
  • Diabetes control
  • Eye checks
  • Foot checks
  • Guardian drugs (ACEi or ARB, statins, and to my surprise they also advised aspirin)


Remember that the exercise recommendation for adults 150 min/wk of moderate activity (i.e., harder for you to have a conversation but still possible) plus muscle exercises twice a week plus reducing amount of sedentary activity. If physical activity is vigorous rather than moderate, you can halve the amount of time needed per week (i.e. 75 min/wk for anyone whose arithmetic is as bad as mine); this doesn’t seem to be recommended for >65s, and advice on exercise for this age group should be individualised according to their capabilities; which seems like a good idea for anyone from any age group, but what do I know). Activity can be split into bouts of 10 mins or more.

Blood pressure

Target is <140/80 if no complications or <130/80 if end-organ damage is present. (As far as I can see from the algorithm, if the systolic is <140 and diastolic is 80 – 89, you can manage with lifestyle advice.)

Don’t start antihypertensives straight away for raised BP unless it’s over 180 systolic or 110 diastolic. Instead, give lifestyle advice and advise review in two months, unless the BP is >150/90 in which case make it one month.

  • 1st drug: ACEi
  • 2nd drg: CCB or diuretic
  • 3rd drug: whichever wasn’t picked for 2nd drug
  • 4th drug: alpha-blocker, beta-blocker or potassium-sparing diuretic
  • 5th drug: same as 4th but also consider specialist review.

When checking renal function after starting ACEi or ARB, the things to look for are a 30% rise in creatinine or a 25% drop in renal function. However, if this happens, look for other possible causes before stopping tablets. (Which is all very well, but in practice having a trial off the tablets is probably going to be easier than any other investigation.)


The goal is >40% reduction in non-HDL cholesterol. Things I would love to know at this point: How much extra benefit does that goal hold over a flat target or even just a fire-and-forget strategy? What evidence is there for this? And how does that work out in terms of effective use of time and resources?

The normal starting dose for primary prevention is 20 mg od. For secondary prevention, it’s 80 mg od, although still 20 mg in cases of CKD (it doesn’t say what level of CKD).

Diabetes control

Targets are 48 in people who are on either no medication or metformin only, and 53 in people who are on multiple diabetic meds or any hypoglycaemia-inducing medication.

Options after metformin are as I wrote in this post here, but now SGLT-2 inhibitors are also an option for a second or a third drug. In the third-line, the combos with SGLT-2 can be metformin + sulfonylurea or metformin + DPP-4-inhib. Remember insulin can also be used at this stage; in some circumstances so can GLP-1 agonists, but they’re only supposed to be used when under the advice of a specialist team, so I won’t really have a role there beyond referring people. Through all of this, keep reinforcing advice on lifestyle.

Note that SGLT-2 inhibitors can promote weight loss and help blood pressure and lipid profile. Interestingly, it seems the creatinine increase that can be seen is actually transient (which interested me as I had a patient whom I took off one of the flozins for this reason). However, they do cause polyuria and an increased risk of UTIs/genital infections, and they can cause volume depletion and dizziness (I assume due to the polyuria) so ideally I wouldn’t use them in the elderly. They can also increase LDL cholesterol, although that might well not be an issue as the EMPA-REG outcome study showed them to be associated with a significant drop in the risk of CV events (14% drop in events, 38% drop in mortality from CV events). They have been associated with an increase in lower limb amputations, especially toe amputations, and in rare cases with necrotising fasciitis of the perineum, so be very alert for any tenderness, redness, or swelling of the perineal area in patients taking these drugs.

DPP-4 inhibitors are weight-neutral, generally well tolerated, and useful in situations where hypoglycaemia needs to be avoided (e.g. in elderly patients). In renal failure the best one to use is linagliptin, which is mainly excreted via the liver, but any can be used with appropriate dose adjustment. They have been linked with an increased risk of acute pancreatitis, but the suspected increased risk of pancreatic cancer has probably been disproved, as a large study showed no risk increase compared to SUs; however, this possibility will need to be followed up for longer.

Interestingly, it now looks as though pioglitazone probably isn’t associated with bladder cancer. However, remember the side-effects of fluid retention, weight gain, and increased risk of distal long bone fracture.

(BMJ Learning module on management of diabetes)

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Cannabinoid hyperemesis syndrome

Interesting new one in the BMJ this week; Apparently a complication of regular cannabis use (where ‘regular’ apparently seems to mean ‘at least once weekly’) is the development of cyclic nausea/vomiting/abdominal painĀ  which, bizarrely, leads the sufferer to take compulsive hot showers or baths to relieve symptoms. (Which actually work, albeit briefly; it’s just very odd that everyone who suffers somehow seems to know they’ll work.)

The treatment, not surprisingly, is to stop using cannabis. This is the only known treatment with long-term effectiveness, but the good news is that it’s very effective; symptoms resolve completely and permanently within a fortnight.

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Depression management

Some interesting points in this BMJ article about depression management:

For mild depression (symptoms fairly manageable), appropriate routes for initial treatment include active monitoring (seeing them at intervals and discussing problems), exercise, and guided self-help. If this isn’t helping, other options include:

  • Group CBT
  • Counselling
  • Problem-solving therapy
  • Behavioural activation (which, as far as I can see from the description, seems in effect to be the BT part of CBT)

Antidepressants are only recommended where the depression is at least of moderate severity (i.e. impacting significantly on life). SSRIs are first-line; mirtazapine, venlafaxine or duloxetine are second-line.

The article also referenced this very large meta-analysis from the Lancet comparing the efficacy/tolerability of different antidepressants. I was concerned to see that my usual standby, citalopram, actually ranked among the least effective. On closer inspection this turned out to be possibly exaggerated due to that particular graph being based on the relative effectiveness in different RCTs; however, I checked out the graph of head-to-head comparisons and it seems that escitalopram does have a statistically significant advantage over citalopram in terms of effectiveness. It looks as though I might need to change my first-line treatment.

Finally, the article advised that ADs should be changed if no effect in the first three weeks, although if there’s a small effect then it might be worth continuing as some people are slow responders. And the reduction in chances of recurrence with six months of ADs after symptoms settle is greater than I thought.

Posted in Credits 2019, Psychiatry | Leave a comment

Diagnosing tremor

I wanted to brush up on my knowledge here, so I checked out the BMJ Learning module on Parkinson’s diagnosis, which led me to this BMJ article. I also had to look for more details on some of the points, which led me to this one.

There are, broadly speaking, three types of tremor; rest, postural, and intention. (It gets more complicated, but that seems to be good enough for my purposes.) Postural tremor is tremor which occurs when maintaining a position against gravity; carrying cups is a classic situation in which it gets noticed.

Rest and intention tremors are much as I remember from medical school:

Rest tremor: Parkinson’s disease. Typical pill-rolling rest tremor, normally asymmetrical for the first few years, possibly with associated bradykinesia and/or rigidity; in practice, those signs can show up as quiet voice, decreased facial expression, shuffling gait.

Intention tremor: Characterised by ‘overshooting movements of increasing amplitude when approaching a goal‘. Typically due to cerebellar disorders.

Other causes of tremor seem mostly to be postural, though this isn’t clear-cut as they can overlap with kinetic tremor, and drug-induced or thyroid-induced tremors don’t seem to have been categorised by type anyway. Basically, here are the other causes of tremor:

  • Essential tremor. Postural or kinetic. Usually symmetrical. Relieved by alcohol. No other associated features. Can affect the head or the voice (only rarely the legs). Can be genetic; a family history of tremor is strongly suggestive of essential tremor (though lack of a family history doesn’t rule it out).
  • Dystonic tremor; this is tremor affecting a dystonic body part. Look for dystonic posturing (e.g. hyperextension of the fingers when hands are outstretched).
  • Physiological/enhanced physiological tremor. (Physiological we all have, obviously. Enhanced physiological tremor can be due to stress
  • Drug induced – see below.
  • Thyroid-induced. Most articles on tremor advise doing routine TFTs to rule this out, but one letter in response to the BMJ article above pointed out that anyone with thyrotoxicosis bad enough to cause a tremor would also have other symptoms or signs, which strikes me as eminently sensible.

Medications that can cause tremor

  • Beta-agonists
  • SSRIs or tricyclics
  • Anticonvulsants (don’t know which types this applies to)
  • Lithium (note that a fine tremor is a common SE of therapeutic levels; a coarse tremor indicates toxic levels).
  • Caffeine/aminophylline
  • Withdrawal from alcohol, opiates, or benzos

Medications for essential tremor

This article had a batting order, which was useful. Propranolol or primidone are first-line, and if neither works separately then they can be used together. Gabapentin, topiramate, or lorazepam are second or third-line.

Botulinum injections can also be used in extreme cases. So, to my interest, can clozapine.

I recall once e-mailing a neurologist for advice on treating a tremor, and receiving the advice that there were a lot of things that could be tried, but most of them just weren’t going to be that effective.


Posted in Credits 2019, Neurology | Leave a comment

Back pain – NICE guidelines

This is the BMJ Learning module I started when I was trying to look up red flags for back pain; as promised, I’ve now gone back to finish the module.

Guidelines recommend using the STarTBack questionnaire for identifying risk of ongoing problems and targeting higher levels of physio towards them; this is supposed to be more cost-effective. However, when I checked out the study in question, I found that all participants still received a basic level of intervention (30-minute assessment, 15-minute video, and a copy of The Back Book produced by the RCGP) that’s beyond what we’d be able to manage as GPs, so it strikes me it would make far more sense for us to continue referring anyone whose pain isn’t settling in short order to the physiotherapists and for them to do the STartTBack assessment.

Prescription-wise, we’re limited. Paracetamol don’t help and have more long-term risks than we previously acknowledged. NSAIDs are first line; weak opioids are second-line where NSAIDs don’t work, aren’t tolerated, or are contraindicated. Opioids should be avoided in chronic low back pain (not helpful, risk of addiction), as should anything designed to work on neurological pain. This leaves us with the option of telling patients to go away because we’re not going to prescribe anything, which is a lot easier said than done.

According to a Cochrane review, there is evidence, not of brilliant quality, that exercise is of some help in chronic back pain.

Recommendations are for ‘manual therapy’, which can include physio, osteopathy and chiropractic and ideally includes a combination of therapies used holistically in combination with advice on getting back to work. Acupuncture is not now recommended as it only has a placebo effect. Though, of course, a placebo effect isn’t to be sneezed at.

In the case of sciatica, surgical treatment actually gives similar results to conservative treatment in the long term; the only difference is that it gives the results more quickly. For LBP, surgery is not recommended except as part of an RCT; there isn’t enough evidence of benefit to outweigh the significant potential harms.

Spinal injections aren’t recommended for LBP by NICE guidance; the evidence of benefit isn’t clear, and there are potential harms.

There is one useful treatment I hadn’t heard of; where the pain arises from the facet joints, radiofrequency denervation (in which the nerves leading to the facet joints are ablated) can be useful. The problem is that there is no clinical way of telling which back pains arise from the facet joints. Therefore, the best approach seems to be to try a local anaesthetic block of the facet joints in patients with LBP who haven’t responded to other approaches, and try RFD if that works.

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NNTs/ARRs for secondary prevention of cardiovascular events

The other day, I had one of those “Do I really need all these pills, Doctor?” questions that requires a grey-area conversation about risk reduction. Anyway, in medical terms the information needed is “What is the NNT for each of these drugs following stenting for unstable angina?” so I’m now going to look stuff up.

The first thing I found is a very useful-looking website actually called nnt.com, so my thanks to whomever set that up. So I went down the cardiology section:


From this 2009 meta-analysis: ARR for MI was 1% per year, and for CVA was just under 0.5% per year. Much less than I’d have expected, but maybe that’s because it’s done as ‘per year’ figures. This 2002 meta-analysis (BMJ): Post-MI it’s 3.6%/2 yrs, and post ‘other high risk patient’, which includes stable angina, AF and PAD, it’s 2.2%/2 yrs, for any serious vascular event. So a fair estimate would be about 2 or 3 per hundred over 2 years, for MI or CVA.


From this summary on the NNT site, NNT for adding clopidogrel to aspirin for a year in high-risk patients was 27. So, just under 4%.


From the NNT site: NNTs were 1 in 39 for MI prevention, 1 in 125 for stroke prevention, and 1 in 83 for life saved. However, some of their studies seem to be in primary prevention, which wasn’t much help. This meta-analysis found that, over 5 years, 48 major vascular events per 1000 were prevented as secondary prevention.


NNT site failed me at this point, so I looked elsewhere and found this article: apparently the key is to keep blood pressure down and it doesn’t matter what you use to do this, as long as you use something. Atenolol is less effective than other antihypertensives, but other beta-blockers are fine; but so is any other antihypertensive. (Of course, beta-blockers have the advantage of controlling symptoms.)

Having read this, I found that the AHA still recommends beta-blockers, so I checked out their guidelines. However, when I read their references, one didn’t seem relevant and the other was comparing beta-blockers to placebo, not to other antihypertensives, so I don’t feel either of them contradicts the above article. (Not that any of this is much help to someone who wants to reduce total pill numbers, but it’s still interesting.)

Anyway… time to put all this together. Given a hypothetical group of 1000 people with pre-existing cardiovascular disease, and the ability to look into a magical crystal ball and see how many would have different outcomes if given a tablet rather than not given one, the numbers, over 5 years, come to:

Statins: 25 – 26 MIs and 8 CVAs prevented. Of those 33 – 34, 12 people would have died of the MI or CVA.

Aspirin: 50 MIs and 25 strokes prevented.

Clopidogrel, given alongside aspirin for the first year only: A further 37 MIs/strokes combined (I don’t have the figures separately). None of those would have been fatal, however.



Posted in Cardiovascular, Credits 2019, DENs | Leave a comment

Temporal arteritis

Some notes:

Not everyone gets headache. 4% of sufferers have a normal ESR. Biopsy can show false negatives.

Constitutional symptoms (fever, sweats, weight loss/anorexia, fatigue) are common; but do consider other causes (infection, malignancy).

Visual symptoms can affect part of the visual field rather than all of it; check fields. It can cause scotomata or diplopia.

Ultrasound is often diagnostic, which can reduce the number of biopsies needed.

Aspirin has been shown to reduce risk of neurovascular complications.

(BMJ article)

Posted in Credits 2019, Don't miss, Rheumatology | Leave a comment