Pathophysiology of disease – an introduction to clinical medicine (VI)
As I’ve now finished the book this will be the last post in the series.
The way I read this book has been different from the way I usually read books; most books I read I’ll read in one go over a relatively brief amount of time. As for this one, I certainly didn’t read it in one go and I had breaks from it lasting a quite significant amount of time. I’m not really sure why I read it that way, but one obvious factor which certainly contributed is that this book is hard to read and takes a lot of mental firepower to handle.
I gave the book five stars on goodreads and added it to my list of favourites. Here’s the review I wrote on that site:
“This review got to be rather longer than usual, but I guess I don’t have a hard time justifying that on account of the nature of the book.
To get this over with from the beginning: If you have never read a medical textbook before, don’t bother with this one. You’ll learn nothing and you’ll never finish it. Unless you speak more or less fluent medical textbook you’ll have to either look up a lot of new words, or you’ll read a lot of words you’ll not understand. The fact that the book is somewhat inaccessible was the most important factor pulling me towards 4 stars. I decided to let it have 5 stars anyway in the end – given how many hours I was willing to spend on this stuff I really couldn’t justify giving it any other rating, although there are also a few other small problems which I might have punished in other contexts.
If you know enough to benefit from reading this book it’s a great book, even though I’d prefer if future doctors – which would presumably make up most of the potential readers who ‘know enough to benefit from reading it’ – read a newer version of it. But in order to read it and get something out of it, you need some basic knowledge about stuff like microbiology, histology, immunology, endocrinology, oncology, (/bio-)chemistry, genetics, pharmacology, etc. And I don’t mean basic knowledge like what you’d get from a couple of wikipedia articles – having read textbooks and/or watched medical lectures on some of these topics is a must.
On top of relevant background knowledge you need to be willing to commit at the very least something like 50 hours of spare time to reading this thing. I spent significantly more time than that, and most people probably need to do that as well if they want to actually understand most of this stuff – you certainly do if you want some of it to actually stick.
There probably exist quite a few similar medical textbooks which are more up to date and which may provide slightly better coverage. But I’m not going to read those books. I read this one. And I’m glad I did. Don’t interpret the 5 stars to mean that this is the best book on this topic – I have no way of knowing whether or not it is, though I assume it isn’t. But it is a highly informative and well-written book which covers a lot of ground and from which I learned a lot.”
The ‘covers a lot of ground’ thing can’t be overemphasized – this book has 23 chapters mainly organized in terms of organ systems. It gives you an overview of how things work in general and some of the ‘classical’ ways which they may go wrong. It does this very well, and despite being the kind of book where one chapter will cover heart disease and another chapter will cover pulmonary disease they’re very good at ‘connecting the dots’ – that disorders are often interrelated and e.g. that a failing heart will cause problems with your lungs is not something they’re neglecting to deal with. Indeed the ‘big-picture view’ the book provides made me aware of multiple connections between ‘human subsystems’ which I’d been completely unaware of, and learning about these kinds of relationships was quite fascinating.
Another fascinating aspect was how much stuff there is to know about these things. It’s quite common for me to read books where the coverage overlap to some extent with what I’ve read in other books – I’ll often prefer to read such books (though I also take steps to avoid limiting my exposure to new stuff I don’t know about too much) because the information they cover will be easier to relate to and connect to other stuff up there in my head. One chapter (or a few pages) in one book may cover material which another book spent hundreds of pages dealing with. While reading this book I very often realized that I’d covered a specific topic somewhere else, which gave me a different perspective; ‘this topic is covered in more detail in Hall‘, ‘see Sperling for much more on this topic’, ‘see also Kolonin et al.’, ‘see also Eckel‘, ‘see Holmes et al.‘, and so on and so forth – I’ve added a lot of those kinds of comments along the way. While reading this book you sort of read the big-picture version, and at various points you’re likely to come across places where you can sort of ‘zoom in’, on account of knowing a lot about that topic. What was most amazing to me in this context was how many places I couldn’t zoom in. There’s such a lot of stuff to know and learn.
I won’t cover the last chapters in much detail. The chapters I’ve read over the last few days covered disorders of the hypothalamus and pituitary gland (chapter 19), thyroid disease (chapter 20), disorders of the adrenal cortex (chapter 21), and disorders of the female (chapter 22) and male (chapter 23) reproductive tracts. A few of these chapters I think I probably paid a bit more attention to than I would have done if I had not read Sperling (see link above) in one of my ‘breaks’ from this book. One reason for this is that Sperling, or rather ‘Tuomi and Perheentupa’ as they were the ones who wrote that specific chapter in the book, spent some time and effort in the book dealing with various forms of combinations of autoimmune conditions involving type 1 diabetes as one of the components, which suddenly makes in particular the chapter on thyroid disease more relevant than it otherwise would have been. Tuomi and Perheentupa covered this stuff because: “Two fundamentally different autoimmune polyendocrine syndromes (APSs) are generally recognized, and type 1 diabetes mellitus is common in both.” The risk of me developing another autoimmune condition on top of my diabetes one should think would be low, and it sort of is (it would incidentally most likely be significantly higher if I were a female); but a key observation here is that other autoimmune conditions usually show up later in life than does the diabetes, so the higher risk I face of developing e.g. Graves’ disease and Hashimoto’s disease (both are covered in chapter 20 of the Pathophysiology text) is not yet really accounted for, and the fact that I haven’t developed any of them yet is not very relevant to my risk of developing these conditions later in life (what is relevant is that I developed diabetes very early in my life – this actually makes it less likely that other organ systems will get hit as well, though it does not make the risk go away). I’ll include a quote from the relevant chapter from Sperling below as I’m aware this was some of the stuff I did not cover when I read that book and so people may be completely in the dark about what I’m talking about:
“All combinations of adrenocortical insufficiency, thyroid disease (Graves’ disease, goitrous or atrophic thyroiditis), type 1 diabetes, celiac disease, hypogonadism, pernicious anemia (vitamin B12 malabsorption), vitiligo, alopecia, myasthenia gravis, and the collagen vascular diseases, which include at least one of the said endocrine diseases but exclude hypoparathyroidism and mucocutaneous candidiasis, are collectively called APS type 2. The co-occurrence of these diseases is presumably the result of a common genetic background. No exact incidence or prevalence figures are available, and they would probably vary with the population concerned. APS-2 is more common than APS- 1, with a general prevalence of at least 1 per 10,000. Females are affected two to four times more often than men. The highest incidence of the components is in the third to the fifth decade of life, but a substantial number of patients develop the first component disease, usually type 1 diabetes, already in the first and second decade”
Note that the uncertain, yet seemingly low, prevalence estimate is easy to misunderstand. I haven’t looked at these numbers recently and I’m not going to go look for them now, but say type 1 diabetes (-T1DM) affects 1 out of 300 people. Now combine the ‘at least 1 in 10.000′ estimate with that one and observe that roughly 2 out of 3 patients with APS-2 have T1DM and the risk a type 1 diabetic will develop another autoimmune condition is already measured in percent. These numbers incidentally downplay the actual risk – I decided to include a few examples from Sperling to illustrate. It makes sense to start with Graves’ disease as I already mentioned that one: “Graves’ disease has been reported in 9.3% of patients with type 1 diabetes (76).” Also, “Hypothyroid or hyperthyroid AITD [AutoImmune Thyroid Disease] has been observed in 10–24% of patients with type 1 diabetes” – uncertain figures with big error bars, but not exactly low risks of no import. Especially not when considering that: “In addition, between 5% and 25% of type 1 diabetic patients without clinical thyroid disease have antibodies to thyroid microsomal antigens (TMAb) or thyroid peroxidase (TPOAb)”. Although combination forms with multiple autoimmune disorders are quite rare, they’re not actually that rare (‘not rare enough…’) when you take into account that T1DM is also, well, rare.
The stuff above was mostly just an aside explaining why I perhaps cared a bit more about the stuff covered in these last chapters than I otherwise would have, but hopefully it was an informative aside. I should note that the ‘more interesting’ stuff was not all of it more interesting on account of dealing with some elevated risk of ugly things happening to me; other parts of the last chapters were ‘particularly relevant’ because of other stuff, like the role cortisol plays in circadian variation in insulin resistance and the role ACTH-excretion plays in hypoglycemia. But I think it would take too much time and effort to go into the details of these things in this post so I’ll cut it short here.
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