Oxford Handbook of Clinical Medicine (II)
Here’s my first post about the book. I’ve read roughly 75% of the book at this point (~650 pages). The chapters I’ve read so far have dealt with the topics of: ‘thinking about medicine’ (an introductory chapter), ‘history and examination’, cardiovascular medicine, chest medicine, endocrinology, gastroenterology, renal medicine, haematology, infectious diseases, neurology, oncology and palliative care, rheumatology, and surgery (this last one is a long chapter – ~100 pages – which I have not yet finished). In my first post I (…mostly? I can’t recall if I included one or two observations made later in the coverage as well…) talked about observations included in the first 140 pages of the book, which relate only to the first three topics mentioned above; the chapter about chest medicine starts at page 154. In this post I’ll move on and discuss stuff covered in the chapters about cardiovascular medicine, chest medicine, and endocrinology.
In the previous post I talked a little bit about heart failure, acute coronary syndromes and a few related topics, but there’s a lot more stuff in the chapter about cardiovascular medicine and I figured I should add a few more observations – so let’s talk about aortic stenosis. The most common cause is ‘senile calcification’. The authors state that one should think of aortic stenosis in any elderly person with problems of chest pain, shortness of breath during exercise (exertional dyspnoea), and fainting episodes (syncope). Symptomatic aortic stenosis tends to be bad news; “If symptomatic, prognosis is poor without surgery: 2–3yr survival if angina/syncope; 1–2yr if cardiac failure. If moderate-to-severe and treated medically, mortality can be as high as 50% at 2yrs”. Surgery can improve the prognosis quite substantially; they note elsewhere in the coverage that a xenograft (e.g. from a pig) aortic valve replacement can last (“may require replacement at…”) 8-10 years, whereas a mechanical valve lasts even longer than that. Though it should also be noted in that context that the latter type requires life-long anticoagulation, whereas the former only requires this if there is atrial fibrilation.
Next: Infective endocarditis. Half of all cases of endocarditis occur on normal heart valves; the presentation in that case is one of acute heart failure. So this is one of those cases where your heart can be fine one day, and not many days later it’s toast and you’ll die unless you get treatment (often you’ll die even if you do get treatment as mortality is quite high: “Mortality: 5–50% (related to age and embolic events)”; mortality relates to which organism we’re dealing with: “30% with staphs [S. Aureus]; 14% if bowel organisms; 6% if sensitive streptococci.”). Multiple risk factors are known, but some of those are not easily preventable (renal failure, dermatitis, organ transplantation…); don’t be an IV drug (ab)user, and try to avoid getting (type 2) diabetes.. The authors note that: “There is no proven association between having an interventional procedure (dental or non-dental) and the development of IE”, and: “Antibiotic prophylaxis solely to prevent IE is not recommended”.
Speaking of terrible things that can go wrong with your heart for no good reason, hypertrophic cardiomyopathy (-HCM) is the leading cause of sudden cardiac death in young people, with an estimated prevalence of 1 in 500. “Sudden death may be the first manifestation of HCM in many patients”. Yeah…
The next chapter in the book as mentioned covers chest medicine. At the beginning of the chapter there’s some stuff about what the lungs look like and some stuff about how to figure out whether they’re working or not, or why they’re not working – I won’t talk about that here, but I would note that lung problems can relate to stuff besides ‘just’ lack of oxygen; they can also for example be related to retention of carbon dioxide and associated acidosis. In general I won’t talk much about this chapter’s coverage as I’m aware that I have covered many of the topics included in the book before here on the blog in other posts. It should perhaps be noted that whereas the chapter has two pages about lung tumours and two pages about COPD, it has 6 pages about pneumonia; this is still a very important disease and a major killer. Approximately one in five (the number 21% is included in the book) patients with pneumonia in a hospital setting die. Though it should perhaps also be observed that maybe one reason why more stuff is not included about lung cancer in that chapter is that this disease is just depressing and doctors can’t really do all that much. Carcinoma of the bronchus make up ~19% of all cancers and 27% of cancer deaths in the UK. In terms of prognosis, non-small cell lung cancer has a 50% 2-year mortality in cases where the cancer was not spread at presentation and a 90% 2-year mortality in cases with spread. That’s ‘the one you would prefer’: Small cell lung cancer is worse as small cell tumours “are nearly always disseminated at presentation” – here the untreated median survival is 3 months, increasing to 1-1,5 years if treated. The authors note that only 5% (of all cases, including both types) are ‘cured’ (they presumably use those citation marks for a reason). Malignant mesothelioma, a cancer strongly linked to asbestos exposure most often developing in the pleura, incidentally also has a terrible prognosis (”
5-8% of people in the UK have asthma; I was surprised the number was that high. Most people who get it during childhood either grow out of it or suffer much less as adults, but on the other hand there are also many people who develop chronic asthma late in life. In 2009 approximately 1000 people in the UK died of asthma – unless this number is a big underestimate, it would seem to me that asthma at least in terms of mortality is a relatively mild disease (if 5% of the UK population has asthma, that’s 3 million people – and 1000 deaths among 3 million people is not a lot, especially not considering that half of those deaths were in people above the age of 65). COPD is incidentally another respiratory disease which is more common than I had thought; they note that the estimated prevalence in people above the age of 40 in the UK is 10-20%.
The endocrinology chapter has 10 pages about diabetes, and I won’t talk much about that coverage here as I’ve talked about many of these things before on the blog – however a few observations are worth including and discussing here. The authors note that 4% of all pregnancies are complicated by diabetes, with the large majority of cases (3.5%) being new-onset gestational diabetes. In a way the 0,5% could be considered ‘good news’ because they reflect the fact that outcomes have improved so much that a female diabetic can actually carry a child to term without risking her own life or running a major risk that the fetus dies (“As late as 1980, physicians were still counseling diabetic women to avoid pregnancy” – link). But the 3,5%? That’s not good: “All forms [of diabetes] carry an increased risk to mother and foetus: miscarriage, pre-term labour, pre-eclampsia, congenital malformations, macrosomia, and a worsening of diabetic complications”. I’m not fully convinced this statement is actually completely correct, but there’s no doubt that diabetes during pregnancy is not particularly desirable. As to which part of the statement I’m uncertain about, I think gestational diabetes ‘ought to’ have somewhat different effects than type 1 especially in the context of congenial malformations. Based on my understanding of these things, gestational diabetes should be less likely to cause congenital malformations than type 1 diabetes in the mother; diabetes-related congenital malformations tend to happen/develop very early in pregnancy (for details, see the link above) and gestational pregnancy is closely related to hormonal changes and changing metabolic demands which happen over time during pregnancy. Hormonal changes which occur during pregnancy play a key role in the pathogenesis of gestational diabetes, as the hormonal changes in general increase insulin resistance significantly, which is what causes some non-diabetic women to become diabetic during pregnancy; these same processes incidentally also causes the insulin demands of diabetic pregnant women to increase a lot during pregnancy. You’d expect the inherently diabetogenic hormonal and metabolic processes which happen in pregnancy to play a much smaller role in the beginning of the pregnancy than they do later on, especially as women who develop gestational diabetes during their pregnancy would be likely to be able to compensate early in pregnancy, where the increased metabolic demands are much less severe than they are later on. So I’d expect the risk contribution from ‘classic gestational diabetes’ to be larger in the case of macrosomia than in the case of neural tube defects, where type 1s should probably be expected to dominate – a sort of ‘gestational diabetics don’t develop diabetes early enough in pregnancy for the diabetes to be very likely to have much impact on organogenesis’-argument. This is admittedly not a literature I’m intimately familiar with and maybe I’m wrong, but from my reading of their diabetes-related coverage I sort of feel like the authors shouldn’t be expected to be intimately familiar with the literature either, and I’m definitely not taking their views on these sorts of topics to be correct ‘by default’ at this point. This NHS site/page incidentally seems to support my take on this, as it’s clear that the first occasion for even testing for gestational diabetes is at week 8-12, which is actually after a substantial proportion of diabetes-related organ damage would already be expected to have occurred in the type 1 diabetes context (“There is an increased prevalence of congenital anomalies and spontaneous abortions in diabetic women who are in poor glycemic control during the period of fetal organogenesis, which is nearly complete by 7 wk postconception.” – Sperling et al., see again the link provided above. Note that that entire textbook is almost exclusively about type 1 diabetes, so ‘diabetes’ in the context of that quote equals T1DM), and a glucose tolerance test/screen does not in this setting take place until weeks 24-28.
The two main modifiable risk factors in the context of gestational diabetes are weight and age of pregnancy; the risk of developing gestational diabetes increases with weight and is higher in women above the age of 25. One other sex/gender-related observation to make in the context of diabetes is incidentally that female diabetics are at much higher risk of cardiovascular disease than are non-diabetic females: “DM [diabetes mellitus] removes the vascular advantage conferred by the female sex”. Relatedly, “MI is 4-fold commoner in DM and is more likely to be ‘silent’. Stroke is twice as common.” On a different topic in which I’ve been interested they provided an observation which did not help much: “The role of aspirin prophylaxis […] is uncertain in DM with hypertension.”
They argue in the section about thyroid function tests (p. 209) that people with diabetes mellitus should be screened for abnormalities in thyroid function on the annual review; I’m not actually sure this is done in Denmark and I think it’s not – the DDD annual reports I’ve read have not included this variable, and if it is done I know for a fact that doctors do not report the results to the patient. I’m almost certain they neglected to include a ‘type 1’ in that recommendation, because it makes close to zero sense to screen type 2 diabetics for comorbid autoimmune conditions, and I’d say I’m probably also a little skeptical, though much less skeptical, about annual screenings of all type 1s being potentially cost-effective. Given that autoimmune comorbidities (e.g. Graves’ disease and Hashimoto’s) are much more common in women than in men and that they often present in middle-aged individuals (and given that they’re more common in people who develop diabetes relatively late, unlike me – see Sperling) I would assume I’m relatively low risk and that it would probably not make sense to screen someone like me annually from a cost-benefit/cost-effectiveness perspective; but it might make sense to ask the endocrinologist at my next review about how this stuff is actually being done in Denmark, if only to satisfy my own curiosity. Annual screening of *female*, *type 1* diabetics *above (e.g.) the age of 30* might be a great idea and perhaps less restrictive criteria than that can also be justified relatively easily, but this is an altogether very different recommendation from the suggestion that you should screen all diabetics annually for thyroid problems, which is what they recommend in the book – I guess you can add this one to the list of problems I have with the authors’ coverage of diabetes-related topics (see also my comments in the previous post). The sex- and age-distinction is likely much less important than the ‘type’ restriction and maybe you can justify screening all type 1 diabetics (For example: “Hypothyroid or hyperthyroid AITD [autoimmune thyroid disease] has been observed in 10–24% of patients with type 1 diabetes” – Sperling. Base rates are important here: Type 1 diabetes is rare, and Graves’ disease is rare, but if the same HLA mutation causes both in many cases then the population prevalence is not informative about the risk an individual with diabetes and an HLA mutation has of developing Graves’) – but most diabetics are not type 1 diabetics, and it doesn’t make sense to screen a large number of people without autoimmune disease for autoimmune comorbidities they’re unlikely to have (autoimmunity in diabetes is complicated – see the last part of this comment for a few observations of interest on that topic – but it’s not that complicated; most type 2 diabetics are not sick because of autoimmunity-related disease processes, and type 2 diabetics make up the great majority of people with diabetes mellitus in all patient populations around the world). All this being said, it is worth keeping in mind that despite overt thyroid disease being relatively rare in general, subclinical hypothyroidism is common in middle-aged and elderly individuals (“~10% of those >55yrs”); and the authors recommend treating people in this category who also have DM because they are more likely to develop overt disease (…again it probably makes sense to add a ‘T1’ in front of that DM).
Smoking is sexy, right? (Or at least it used to be…). And alcohol makes other people look sexy, right? In a way I find it a little amusing that alcohol and smoking are nevertheless two of the three big organic causes of erectile dysfunction (the third is diabetes).
How much better does it feel to have sex, compared to how it feels to masturbate? No, they don’t ask that question in the book (leave that to me…) but they do provide part of the answer because actually there are ways to quantify this, sort of: “The prolactin increase (♂ and ♀) after coitus is ~400% greater than after masturbation; post-orgasmic prolactin is part of a feedback loop decreasing arousal by inhibiting central dopaminergic processes. The size of post-orgasmic prolactin increase is a neurohormonal index of sexual satisfaction.”
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