Happy Holidays from the Annals of Medical School! Here is a little song about the serology findings in many common rheumatic diseases, including rheumatic arthritis, lupus, and more, all set to a familiar holiday tune!
Serology Christmas Song
Deck the Halls with Serology It is quite simple, we do it in a jif Start it off with SLE ANA, DNA, anti-Smith!
DR 2 and 3 add to the score, SLE is RF positive If it's drug induced look a bit more Anti-histone we might very well see!
When your hands hurt think RA Look to HLA DR 4 RF positive and X-Ray, CCP, smokes hist'ry all the more!
Sjogren's Syndrome makes my eyes dry ANA and RF positive When my cheeks swell then I will sigh SS-A, SS-B or Ro and La!
Scleroderma has two subtypes Both are ANA and RF+ PSS is antitoposiomerase CREST think speck-led anti-centromeres!
Myositis, poly and dermato Anti synthetase gives lung disease SRP will cause heart problems M i 2 is classic dermato findings!
Ankylosing Spondylitis is the end B twenty seven, and RF minus Now you know what to the lab you must send Fa La La La La, La La La LA!
Annals of Medical School interviews former U.S. Surgeon General Dr. C. Everett Koop about the events of the summer of 2007 surrounding the office of Surgeon General. It looks at how the most recent Surgeon General, Dr. Richard Carmona, brought the office into the spotlight by accusing the Bush Administration of restricting his medical message, and discusses how medicine and politics intermingle.
The Recapitulation Theory. A debunked postulate first popularized in the middle of the nineteenth century, the recapitulation theory famously states that "ontogeny recapitulates phylogeny." Simply put, during development, the human embryo was thought to fully repeat its evolutionary development. A human embryo would climb out of the primordial ooze, so to speak, and pass through different phases of evolution on its way to becoming a grown fetus. This recapitulation of "lower" forms is commonly demonstrated by comparing embryos at various ages between species, from fish to reptile to mammal, and seeing the similar morphology of the embryos. Granted, this theory has long since been rejected. However, I think it has provides an interesting lens through which to view the development of the kidneys.
Over the course of development, we actually have three different pairs of kidneys, which all have parallels to a different evolutionary form. The most basic of these is the pronephros, which is the most rostral (closest to the head) of the kidneys and is a functioning kidney in immature fish and amphibians. In mammals, however, it doesn't seem to do much but serve as a transitory structure before the mesonephros, the second kidneys, develop during the 4th week. The mesonephros is similar to the functioning kidney in adult amphibians, and is functional in birds and reptiles until they hatch. The mesonephros in mammals is a rudimentary, functional kidney--it has glomeruli, which are the filtering units, and which drain into the mesonephric, or Wolffian, duct, running through the center of the mesonephric tissue. This duct is the great legacy of the mesonephros, because near the distal end it sprouts a little bud, called the ureteric bud, which stimulates the metanephrogenic blastema (the precursor to the kidney) during the 5th week to form the metanephros, the third and final kidney. This metanephros will become the bean shaped organ we have all grown fond of, and then rise upward out of the pelvis and to the costovertebral angle as the fetus grows.
It is easy to see how this process apparently recapitulates lower evolutionary forms, going from amphibian to avian to a final mammalian state, and yet further inquiry has shown that this is not exactly true and that while these are important developmental stages, a human fetus does not undergo all steps of evolution during its time in the womb. What I find fascinating is how two distinct parts of this system, the ureteric bud and the metanephrogenic blastema, interact so precisely to create a connection for the kidneys. The ureteric bud induces the metanephrogenic mesenchyme to form the nephric tubules, the DCT, loop of Henle, PCT, and Bowman's capsule. This mesenchyme reciprocally acts on the ureteric bud causing it to branch and form a tree-like system of collecting ducts. Many growth factors are involved in this nephrogenesis, but of interest is the role of angiotensin II, a vasoconstrictor that interacts with the kidney to help regulate blood pressure. Angiotensin II is often blocked with ACE inhibitor or angiotensin receptor blocker (ARB) medications in people who have hypertension, effectively lowering blood pressure. Recent studies suggest that angiotensin, by interacting with receptors on the ureteric bud, stimulates branching morphogenesis as well as collecting duct elongation and papillogenesis. Therefore, patients are taken off of ACE inhibitors and ARBs when pregnant, because there can be failure of the ureteric bud to stimulate correct nephrogenesis and a wide array of kidney defects may result.
Although the recapitulation theory is defunct, there is something to be said for thinking of the kidneys evolutionarily, since they allow us to concentrate our urine, and regulate body water, so that we can live on land in the first place. An impressive feat, given the extensive multistep process it takes for a single adult kidney to develop.
I am not usually one to brag, but I am pretty good at holding my breath. You may have heard that pearl divers can hold their breaths for minutes at a time; my all-time record makes that seem like a fleeting moment. Yes, at one point I did not take a single breath for over 9 months.
Of course, I am being a little gratuitous here. As you may have guessed, I am talking about the time I spent in the womb, when there was no air to fill my immature lungs anyway. The cardiovascular system is at times remarkable in its simple elegance of function, and one place I think that exemplifies this is in the fetal circulation at the heart and lungs. Normally, all of the blood in our bodies must first be pumped by the heart into the lungs to be oxygenated, and then pumped into the rest of our body to distribute that oxygen. In the fetus, as I alluded to a little bit ago, there is no oxygen in the lungs because you are living in the fluid of the amniotic sac. Oxygenated blood must instead come from the mother by way of the umbilical vein. The fetal body has a unique way of separating oxygenated blood from deoxygenated blood to make sure the most vital organs can grow during crucial stages of development.
There are basically two streams of blood inside the heart: blood from the mother enters through the eustacian valve of the inferior vena cava, and goes across the heart and through a temporary valve between the right and left atria, the foramen ovale. This well-oxygenated blood can then be pumped like in an adult, going from the left heart up into the aorta and primarily heading to the oxygen-hungry developing brain via the carotid arteries. This blood also bypasses the lungs, which would only serve to remove oxygen from the blood. The other stream is oxygen poor, comes from the rest of the body into the superior vena cava, and heads down into the right side of the heart. Normally this would then go to the lungs to become oxygenated, but remember that the lungs are don't function yet. Instead, the blood goes through the ductus arteriosus, a structure that closes after birth, and enters the aorta after the carotids to go to the brain. This steers oxygen-poor blood away from the head and into the unbilical artery, returning it to the mother to be reoxygenated.
A major factor in this shunting has to do with the very high resistance of the arteries of the lungs. In the fetus, the lungs provide a huge barrier to blood flow, which means that most of the blood entering the pulmonary trunk with be diverted through the ductus arteriosus, a good thing for reoxygenation. However, at birth, when taking the that first breath, the pulmonary vascular resistance plummets and all the circulating blood is diverted to the normal pattern of entering the lungs before the systemic circulation. This might seem a little paradoxical, because normally oxygen is a potent vasoconstrictor; vessels that have a high oxygen tension will constrict as if saying "I'm fine here, go oxygenate someone else." In the fetus, the lung vascular expansion is in part due to the mechanical strain of inhalation, but also due to vasodilation mediated by oxygen. It is thought that this is in fact due to oxygen-sensitive potassium channels: fetal pulmonary vasoconstriction may be mediated by inhibiting calcium-sensitive potassium channels. Likewise, the ductus arteriosus is kept open by circulating prostaglandin E2, generated due to the relatively hypoxic, or low oxygen, state. When the newborn begins breathing on its own, this effect will stop (as long as it isn't premature) and the ductus will close.
That shift of blood flow will normally mean the end of the fetal circulation: a large return of blood from the lungs will close the valve to the foramen ovale, and the ductus arteriosus will constrict into a ligament, the end result being that the right side of the heart pumps oxygen poor blood to the lungs and that reoxygenated blood is then returned to and pumped out from the left side of the heart to the body. So, given that I had an impressive bypass tract to leach oxygen from my mom, perhaps I was cheating a little when I held my breath all that time in the womb; nonetheless, with such an elegant fetal circulation, I remain impressed.
I started this blog with the hopes of sharing a bit of the more interesting things we learn here at medical school with anyone who might be interested. The scope is broad, ranging anywhere from curious facts on obscure disease, to the reasons behind common illnesses, to commentary on current news and discoveries in the medical community. Please feel free to join in on any discussion; as we have learned already, the best patient-physician relationship can only be found when both sides are talking. Enjoy!
