Year 3 of medschool is said to connect all the science of the body we learned in the first 2 years with all the clinical context where we will be using that information for the rest of our lives. I just started year 3, and while enjoying Histology and Physiology more than the average student, I was excited to break those pieces of information I gathered until now and finally put them to use in the real world of medicine.
The first book I got for this is the Oxford handbook for clinical diagnosis. This is a book of semiology, if we want to distil it down to medical disciplines. Semiology is specific to some European universities, originating from the French school of medicine, not from the Anglo-Saxon one. So my American readers might have not even heard of this subject before. It is basically the discipline that studies the clinical signs we can observe in the physical exam an in the patient’s history, and their association with diseases. (photo of the book for context)
When I finally finished with the good practices for history taking and physical examination (which is what I am still doing at uni 2 weeks in) it was finally time to start reading the clinical signs and the affections linked to them. And reading up on the clinical signs that show up on nails specifically has sent me down a rabbit hole that gave the title of this post.
I will first explain the terms I wrote in the title, because I don’t want this post to gatekeep medical information. But I will keep it brief because I don’t want it to be a course either.
An infection is the invasion of any body tissue with a microorganism or a parasite. Basically , if anything manages to get in the body (through the skin or through any mucosa, like through the gut or through the mouth) that is already considered an infection. The response of the organism to such a process is a local inflammation, in any place where a foreign agent managed to enter (foreign agent being the generic term for anything the body cannot recognise as being created by itself, be it a different life form, a dust particle, or even cells from other people).
Inflammation is a vast and interesting, but too long of a process to explain in detail here. What is important is that the inflammation process uses some cells, naturally present in the blood, called leucocytes (“leucos” is just the word for white in Greek, and “cyte” is the word for cell. Hence, their name comes from the fact that they are white when seen in microscopy, but old scientists had a thing for dead languages).
As for anemia, the other word in the title, it simply represents the fact that the blood lacks enough of the protein used to carry blood, a protein named hemoglobin (shortened to Hb and present on any blood test someone takes in their life). To capture the oxygen and deliver it, hemoglobin has, in the middle of its structure, an atom of iron. And that might seem odd at first sight, but think about rust. Iron rusts if it is left outside, and that happens because the oxygen in the air binds to it and destroys its purity. And that is a bad process back home in the countryside, where I want my axe shiny to cut the wood with, but it is very valuable for our bodies, in order to keep us alive.
The reasons why hemoglobin might be lacking can be due to many factors, but in general is due to either loss of red blood cells (the cells that carry hemoglobin around and let it take the oxygen from lungs and send it to the rest of the body) or due to problems in the process of production for red blood cells (shortened to RBC , another thing you surely saw on your blood work last time you went to the hospital).
But, here comes the question: how could an infection, let’s say, in your left foot, generate anemia? As you can imagine, the body has a lot of systems to make sure your blood does not lack this essential resource, so it is quite fascinating that such an event produces this pretty serious effect. And I need to mention, as it is always in medicine, that this process does not always happen, and that the infection has to be around for a few weeks before this takes effect. But for when it happens, I was curious as to how. So, after discussing the issue with a few friends and coming with some theories, I went and asked my pathophysiology teacher, and got a cool answer.
First, hepcidin. Hepcidin is an acute-phase protein, which is a fancy term for saying it is a protein that appears only when a person is infected by something. This protein is produced by the liver, but only when the liver gets the command to produce it, as a result of the infection. What this protein does is that it captures the iron in the leucocytes, as oxygen is also used as a weapon to kill bacteria (oxygen can do many things I know). But the fact of the matter is, that iron that was now taken by leucocytes, with hepcidin as some sort of arms dealer, has to be taken from someone. And, like a corrupt government that invests all their money in the military power, the poor workers of society, the Red Blood Cells, have less hemoglobin to work with.
The second mechanism is something I like to liken to a school. In our bodies, all cells age, be it leucocytes or RBC. When cells become old, they die (hopefully have a nice, programmed death and not a violent, spontaneous one) and their place is taken by new, eager young cells. And for every part of the body, there are places where new cells grow and get their education to be a good member of your body and keep you alive. And RBC and leucocytes have a common place to go to school to, situated in the deep parts of the bone, called the Bone Marrow. This is where they grow and learn to do their functions in society. And when an infection comes around, because there is need for more leucocytes, as to say the body needs a strong army, they invest into their development way more than in the development of the workers in society, the RBC.
Also, there is a process to accelerate the manifestation in this event. If the infection is affecting the body in a way that actually kills some RBC itself (in the example from my book the bacteria had the ability to produce weapons called streptolysins it used to kill RBC if they came into contact). So, the lower Hb level could appear quicker.
At the end of the day, why did I use my time to investigate this topic? And why did I use even more time to explain it on the blog? Well, except for the clinical applications which make it more than worth it for me to look out for the explanation, I think it speaks to a broader idea which everyone should know. That the value of a good doctor is not only in how they can solve the problem you came to the hospital with, but also in knowing what that treatment can do to other parts of the body and making sure you will not leave with more problems than you came. Hb is in no way involved in fending off infections, but it is still affected by the inflammation. And like such, there are hundreds of other implications a doctor should be aware off, and make a patient aware off. Thanks for reading.
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