Interesting Medical Tidbits

[Sela]

So I've been thinking about this for a while and finally I've decided I'm gonna go ahead and actually do it. During classes in med school we learn a lot of stuff; most of it is details and can get quite technical or dull, but a lot of it is just *really* cool. Unfortunately the really cool stuff often is either potentially fatal or very crippling, but yeah anyway.

So this topic is aimed not at the doctors or medical professionals (for whom a lot of this will likely either be old news and too "low level" to bother with). Rather its for anyone out there who doesn't have much grounding in medicine but still finds it fascinating what cool stuff crops up in the human body. I'll do my best to keep adding interesting posts with new stuff when I can.

I know most people here will be smart enough to figure this out but let me put an upfront disclaimer anyway: nothing I say here should be taken as solid or fact, nor should you use ANY of this to diagnose, treat, or influence your medical decisions. If in doubt *SEE A DOCTOR*. Often the level of information here will barely surpass wikipedia. My hope is that it'll remain informative, interesting, and just perhaps make someone curious to read and/or study more. Lastly, I will *not* be duplicating my med school class notes or anything here; this is just the "neat stuff" off the top without lots of the details. If you're curious of course I'm happy to try and answer followup questions.

And of course to any medical professionals or non-medical professionals who feel like it'd be fun to chip in, feel free.

So, let's kick it off with a congenital malformation:



Transposition of the Great Vessels (of the Heart)

Short 'n Sweet:
This is a congenital malformation (happens in embryo/fetal stages) in which a child is born with the Aorta attaching to the Right Ventricle and Pulmonary Artery attaching to the Left Ventricle.

Background Anatomy&Physio:
As we all know, the heart is a four-chambered pump that propels blood around the body. The basic path can be summarized as follows: Venous Return (from body) -> Right Atrium-> Right Ventricle -> Pulmonary artery -> Lungs (gets O2!) -> Pulmonary Vein(s) -> Left Atrium -> Left Ventricle -> Aorta -> "rest of body" ->Venous return. And so our circulatory system forms this nice "circuit", with oxygenation happening in the lungs (on the right sided heart circulation) and then O2 supply to the body (left sided heart circulation).

Why is this Interesting:
Think for a second what would happen if we made the switch I discussed earlier. Try to trace the blood flow:

Venous Return -> Right Atrium -> Right Ventricle -> Aorta -> "rest of body" -> Venous Return

Pulmonic vein -> Left Atrium -> Left ventricle -> Pulmonary Artery -> Lungs (O2 in) -> Pulmonic Vein.

At once the situation becomes clear: We now have *TWO* distinct circulations that are totally disconnected! Effectively we have two two-chambered hearts instead of one 4-chambered one. The pulmonary circuit will have excess oxygen . . .and the rest of the body will have none! It's a very serious condition that requires immediate care; and without an additional heart 'defect' that leaves a hole in the wall between the left and right side, the child will die very shortly after birth.



(I'm very open to feedback, please let me know if I'm using too high/low level jargon and if I ought to do this differently ... or not at all.)

[madd0ct0r]

This is interesting. and bringing on my hypochondria.

[Losonti Tokash]

Transposition of the Great Arteries is something that's stuck in my mind, and not just because I've met two sets of parents that had children born with it. No, it is because my pathology textbook reports that it is "a condition incompatible with post-natal life." Fortunately, it's very easy to detect in the fetus and (relatively) easy to fix by placing a shunt into the newborn's heart.

[PeZook]

This is interesting. and bringing on my hypochondria.

Did you miss the part where he said "without treatment or an additional defect, the child will die shortly after birth"?

Since you can read and write and use a computer, and obviously are alive, I assume you've survived past being a week-old infant and thus cannot have the defect, or already had it surgically corrected

[Sela]

So I'm gonna post something we learned a while ago instead of the stuff from today, mostly because it's more interesting and some of the stuff from today requires a lot of background.

Amblyopia

Short 'n Sweet:
A 'mild' defect with one of the six muscles responsible for moving the eye causes a child to have decreased functioning of the eye (or even blindness) without physically damaging the eye at all.

Background Anatomy&Physio:
There's quite a bit here, but let's plow through as best we can! So as we all know, we are capable of moving our eyeball around (left, right, up, down. . . and other stranger motions). This is achieved by a set of 6 muscles that attach to the eyeball from the left, right, top, bottom and move them in those directions (the other two are more complex). As with all muscles, it takes the *pair* to achieve useful motion, one to pull it in the direction you want to go, and the other to pull it back later (no pushing!). To achieve vision, we recieved light photons which are turned into chemical messages at the back of the eyeball (retina) and then transmitted up to the brain. Here the brain muxes the two signals together and merges them, providing a single useful picture and depth perception.
(again, this is a gross simplification, but again, that's the motto of this topic. Feel free to ask if you want to know more.)

How does it go bad?:
So let's say - for arguments sake, there's damage to the Lateral rectus muscle in the left eye. This means you can't turn your left eye left as much/ as well (damage doesn't mean it's absent!). What would happen if you looked to your left? Your right eye would go all the way, and your left eye would only go part way. This would have your two eyes looking at two seaparate images, the brain would see that and would give you 2x vision (since it knows it can't merge the two).

That's good for us, because we're all over 13, but childrens' brains are not as well developed (medically speaking) and are much more moldable at that stage. So you've got this 6 year old kid, and he develops this same muscle weakness; his eyes are *chronically* (as opposed to just occasionally when we might have crossed our eyes as kids) giving him mixed signals. When he's looking straight ahead or to the right he's fine; when he looks to the left, he gets a mixed signal in his brain. But at this point his brain has not yet molded itself to definitively recognize both signals! In other words his brain *mistrusts* the signal (which is frequently bad) and gradually downgrades its responsiveness to the defective eye. If left untreated, the brain will eventually shutdown that pathway altogether. . . and the eye will be perfectly healthy, but the patient will be quite blind in that eye for life.
This is what's cool to me: the eyeball is *perfectly* functional and healthy. No cataracts, no retinal issues, no cell death, etc. . . but the brain refuses to acknowledge it and so you go blind in that eye!

Treatment (also cool):
So we can't do high-tech neurosurgery to correct the brains misperception . . if we wait that long it's too late. We *can* do surgery to repair the muscle defects (depending on what caused it) and fix the underlying problem. The issue is that doing that surgery will not reverse the remodeling of the brain pathways.

So here's the treatment: You tell the kid to wear an eyepatch over his good eye! For a week or so, you totally block the "healthy" signal so the brain is forced to rely on (and thus upgrade the pathways of) the unhealthy eye. If you wait too long to treat, this isn't possible as they're physiologically blind in that eye (not physically, but physiologically). After that week or so, you can then correct the muscle problem and job's done. Typically this disease is caught and treated in time as the child complains of lazy-eye or double vision close to its onset and the mom is quick to bring him into the doctor's office.

[mr friendly guy]

Ok since we are going to go down this route, lets go for some of the rarer ones with funny names.

Broken heart syndrome. The proper name is Takotsubo cardiomyopathy, but you literally do have heart failure from an emotional broken heart (not the only cause, but interesting and rare). I haven't actually seen one of these before.

Transient global amnesia (TGA)

Transient global amnesia (TGA) is "one of the most striking syndromes in clinical neurology" whose key defining characteristic is temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness plus deeply-encoded facts of the individual’s past, such as his or her own name.

I have diagnosed about 2 people with this condition. Its quite weird, and its usually provoked by some stressful event. The "classic" is during intercourse, but of course they can't remember what they were doing. Although I have heard it said someone developed TGA while watching a tense game of football.

[Sela]

Neat stuff . I actually read up on Takutsubo's cardiomyopathy last year. We had a mock-patient and had to do a differential on what was basically an obvious case of bereavement with some coronary artery disease. Still, it showed up on an automatic diagnostic list and so I looked it up and made a case for it. It was awesome - and gave the teacher a great opportunity to discuss "hear hoofbeats think horses not zebras".


Anyway, here's my tidbit of the day:

Tic Dolereux aka: Trigeminal Neuralgia

Short 'n Sweet:
An dysfunction involving the Trigeminal nerve (fifth cranial nerve) either directly(rare) or indirectly(more often) causes it to falsely send a heavy pain signal constantly.

Background Anat&Physio:
Nerves are the body's way of sending signals (as we all know). For the most part, nerves that have to conduct over distance are myelinated, meaning they are covered in a sheath (of myelin) that effectively "insulates" their electrical signal and does not allow for "cross-talk between the wires".
Pain is a complex signal with many different types of signals the body can produce to transmit it. Seriously oversimplified, your skin has multiple kinds of sensation receptors as well as straight-up pain receptors (a different kind of sensor). Organs have visceral pain sensors as well, though they're less sensitive and fewer in number. All of these sensors send their signals to the nearby spinal cord segments via *nerves*, the spinal cord in turn transmits them up to the midbrain, which sends them to the cerebrum where the signals are dealt with, interpreted, and pain is actually "felt". This spinal pathway also has opiod receptors which allow the sensation of pain to be dulled or inhibited and is sensitive to the effect of both endgonously produced opiods/enkephalins as well as exogenously delivered ones (like morphine or heroin).

Above the level of the neck, pain is transmitted via the Trigeminal Nerve (cranial nerve 5) and the facial nerve (cranial nerve VII). Of these, CN5 does more surface area and 'deeper', whereas CN7 works primarily with the face and superficial. Though 100% distinct from blood vessels, it is not at all uncommon to see a set bundled together (ie: an artery, nerve, and vein all in one sheath) or adjacent to each other.


What goes wrong?:
While there can be other causes, in trigeminal neuralgia what happens is that blood vessel gets too big and effectively "clamps down" on the trigeminal nerve where they run adjacent to each other. This friction disrupts the myelin sheath . . .and allows the trigeminal nerve to fire erratically direcctly into the brain.This signal sends "wave upon wave" of excruciating pain. I can't emphasize this enough - the pain is really *REALLY* bad; this illness has the nickname "the suicide disease" because people would kill themselves at the pain's severity and consistency.

The thing that makes it so interesting though is that the pathway by which the pain is caused effectively short-circuits past all of the usual mechanisms! Patients will take painkillers, some will be put on opiods, and it will all have absolutely zero effect. The spinal-cord pathways that would have modulated an extreme pain signal (like how when you suffer a truly massive injury pain dulls after a moment, or you go into shock) are ineffective here, and even some of the midbrain level stuff to modulate pain response is all being short-circuited past!

Treatment:
So they were skimpy on this in class back then; basically 'surgery to fix it' was what they said. There are medications you can take, but they're not pain meds . . . they're anti-seizure meds. The idea is to dampen the excitability of the nerves (like you'd want in a seizure setting) and try to target the trigeminal nerve (which still has plenty of spillover and bad side effects). Eventually if a patient can't handle the meds or their side effects, surgical correction is in order.

[PeZook]

That thing with the eyes? My family has that in its genetic lineage...

[Sela]

The injury is cool in its own way, but a good part of this post explains "Acute MI" [heart attack], as its a leading cause of death in virtually all modernized countries and has been for many years.
Rupture of Free-Wall of the Ventricle secondary to Acute MI
Short 'n Sweet:
A weakening of the wall of the left ventricle causes the muscle to tear apart, leading to cardiac tamponade and death.


Background Anat&Physio:
The heart is a muscular pump that is supplied blood (and thus, oxygen) by a set of arteries termed the coronary arteries. If this supply of blood is interrupted (ie: by fat buildup, a blood clot, abnormal constriction of the blood vessel, etc.) the heart muscle in the area it normally supplies will temporarily recieve no oxygen. Depending how long this lasts, this can lead to irreversible muscle cell death. The areas supplied by these vessels, include all of the muscle of the heart: The left ventricle, right ventricle, left atrium, right atrium, and other associated internal structures. As I mentioned in a previous tidbit, the Left Ventricle is the last chamber of the heart (and typically the largest) - from there, blood is pumped to the entire body and so the pressure generated there is quite high.
When body tissues (most) anywhere in the body die from lack of oxygen, there's a process that follows termed "necrosis". [1]The tissues first are infiltrated by general cells from the immune system which begin the process of neutralizing all the noxious cell-contents that have been released from the dead/dying cells.
[2]Next more specialized immune cells enter/form to continue the cleaning process, dissolving away the underlying dead tissue and start laying down granulation tissue instead.
[3]Finally, a final type of cell lays down collagen and make a firm scar tissue in the place of the dead tissue. This collagenous scar tissue has none of the functioning of the original tissue, but it at least serves as a firm placeholder rather than leaving a gaping hole behind.


What goes wrong?:
In a Myocardial (heart-muscle) Infarction [termed MI], we get blockage of a coronary vessel. If the blockage persists for 30-60 minutes, some irreversible cell death begins to occur. It's worth noting that time really is of the essence here - in the first hour, <10% of the supplied muscle cells are likely to die . . . by the 3rd hour 80% or more will be beyond saving.
Once the blockage is cleared - say at the 90minute mark - the heart muscle is re-supplied and the repair process can begin. The necrotic process follows a very predictable timing and course in a post-MI patient. Going off the 3 stages (again - this is simplified) I discussed above, the first stage happens over the course of the first 3 days. The second stage happens from days 3-10, the final stage takes a 6months-1year to finish.
Now here's where it gets interesting, the first step to fixing the heart is to remove the offending debris and the useless dead bits right? So during the second stage, we find ourselves removing the original muscle tissue altogether to replace it with the far weaker granulation tissue - the precursor to the very strong scar tissue. It turns out the heart wall is at its weakest in this second stage. . . and thus prone to the pressure forces discussed earlier.

When a patient gets this secondary effect, the wall of the heart muscle literally *bursts* open, and the blood pours out. Since the heart is encased in a sac (the pericardial sac), it quickly fills that pouch and compresses the heart, leaving it virtually unable to pump (and leaking!).

The majority of post-MI deaths in the 3-10 day range are due to rupture of the free wall of the ventricle.


Why it's cool: Apart from the heart *actually* bursting, I thought it's really cool how the repair process temporarily leaves you weaker and just how delayed (3-10 days AFTER) the effects can be.



*edited for spacing and clarity*

[PeZook]

This really underlines just how much evolution doesn't give a shit

It's good enough to breed? Then it doesn't matter that the most critical organ in the body can get utterly destroyed by its own repair process!

[eion]

Fatal Familial Insomnia, my favorite prion disease. Summed up in three words: You stop sleeping.

[Sela]

Lol, interesting way to think of it. I mean, it's not like the body makes itself weaker or anything, mind. The process is designed to replace the damaged heart muscle with scar-tissue and that scar-tissue is really strong. There's just a window where it's weaker.

That said, you *really* DONT want to have an MI (obviously). In the first few minutes, well before there's any permanent damage (remember 30-60 minutes before the earliest cell death, and 4hours before any change you can see on a microscope) all the ion concentrations go off balance and the the risk of the heart-rhythm going out of whack is very high. In fact the MAJORITY of heart-attack related deaths occur before a patient gets to the hospital due to an arrythmia.

Also, even after a year when you have the "fully formed scar" phase, it's *still* not as good as the original muscle. The heart's contraction power is reduced, causing some increase in volume of blood that isn't being pumped, which can lead to either hypertrophy (overgrowing) of the remaining muscle fibers or dilation of the heart chamber . . . . both of which long-term can lead to congested heart failure. Also, the scar left behind is the perfect substrate for *additional* arrythmic problems or issues with the conducting system. Post-MI post 1yr, your yearly risk of death in modern times is still ~2-4% I think (gotta double chekc that, it could have been 1-3%).


I think it's more a matter of how we've sort of suspended our own evolutionary process, you know? Back in the good ole caveman days, how many cavemen do you think ate so damn much fat and cholestrol and got so little exercise that they could undergo a THIRTY YEAR process of plaque buildup in the arteries? Odds are good cavemen didn't have MI's often . . since they had serious other issues to deal with or die from. Not to mention in order to have a shot at getting to the repair stage you need to survive the heart attack first. If you don't remove that block in under four hours odds are good you *are* gonna die (depending on where exactly the block is and how serious it is).

[PeZook]

I think it's more a matter of how we've sort of suspended our own evolutionary process, you know? Back in the good ole caveman days, how many cavemen do you think ate so damn much fat and cholestrol and got so little exercise that they could undergo a THIRTY YEAR process of plaque buildup in the arteries? Odds are good cavemen didn't have MI's often . . since they had serious other issues to deal with or die from. Not to mention in order to have a shot at getting to the repair stage you need to survive the heart attack first. If you don't remove that block in under four hours odds are good you *are* gonna die (depending on where exactly the block is and how serious it is).

Yeah, this is all true, and again, it shows how evolution doesn't give a shit about potential problems, systems design etc. and really is a blind idiot god. I was getting at the creationist "LOOK AT HOW COMPLICATED IT ALL IS!!!" angle. Really, an omnipotent God could've been expected to design a special repair system for the heart, since he's all knowing and shit and probably could've foreseen civilization?

Anyway, some people get heart attacks even when healthy, it's just that the percentage is low enough not to destroy the viability of the species so hunter-gatherers (I hate "cavemen| ) could survive fine as a population.

[PainRack]

All of you are evil bastards who are trying to contribute to my case of insomonia.

So, here's the return favour

http://en.wikipedia.org/wiki/Transfusio ... ung_injury

You leak fluid into your lungs after a blood transfusion. I just love the acronym TRALI.

[Sela]

*shivers* That sounds like goodpasture's almost. Scary stuff.

[mr friendly guy]

*shivers* That sounds like goodpasture's almost. Scary stuff.

Um, only in the sense that both are immune mediated. Goodpastures can affect other organs, namely the kidneys.

[Sela]

Not a disease, but an "interesting medical tidbit". This came up both in Psych and in Human Sexuality discussions. I've had to review some stuff to make sure I don't get the facts wrong. Also, realize that this is *not* a 100%-totally widely known and accepted as fact thing. There's several peer-reviewed studies, and 4-6 papers in NCBI last I checked on the subject, as well as epidemiological data to support it; but this is not something like "transposition of the great arteries" which every doctor will tell you is 100% for sure true.
Without further ado:

Fraternal Birth Order Effect

Short 'n Sweet:
"Auto"-Antibodies against male-specific antigens are produced by the mother due to the sex-difference with the fetus. This leads to increased likelihood of homosexuality in the fetus.


Background Anat&Physio:
To greatly simplify things; the adaptive Immune System works by sampling small strings of amino acids, proteins, DNA, hormones - molecules from all over the body pretty much. In the first couple years of life, anything found is considered a "normal part" or "self-antigen". Once this phase ends, the body's definition of 'self' is set and does not expand. The constant sampling process continues, and any foreign particle is labeled as such and treated as an invader. Antibodies are made that bind that *specific* short segment that got sampled and serve as markers for immune cells to come and attack. Immune cells themselves are rather blind in their approach - they'll attack anything with an antibody sticking onto it.
This process of antibody production, however, is far from instantaneous. Enough 'samples' need to be brought in to prompt a response, and successfully making antibodies can take a long time. Once they're made, however, they stay on in memory-cells; ready to quickly respond to a second or third exposure, etc. In this manner, we see that the second exposure to something eliciting an immune response will be more rapid and severe than the first, and the third more than the second, etc.

Again, this is a huge oversimplification, if I discuss another immune process I may end up going into a lot more detail; for now this is plenty.


What goes wrong?:
There are some genes, proteins, and other 'bits' that are unique to males and/or females. When a mother is pregnant with a male fetus, the placental barrier for the most part shields the fetus from the sampling process of the immune system. For this reason, if the baby's blood type differs from the mother (Rh factor +/-), it's important to be sure that her body won't attack it as foreign. The first incompatible baby is safe (no pre-formed auto antibodies, no real risk till delivery of exposure), the next needs to be sure the mom is immnosurpressed.
The fraternal birth order effect is a theory which holds that - since the mother is female - her body naturally will consider all the "male-genes" in the fetus as potential immunity targets. Exposure can lead to production of auto-antibodies and an immune response. While not as severe as the hemolytic anemia of a blood reaction, without those "male genes", the fetus is more predisposed to growing up and being homosexual. The risk is virtually non-existent for the firstborn male, more likely for the second, much more likely for the third, and then it remains at roughly that level.

There's lots of supporting evidence for this effect, most interestingly the fact that it explains a sizable (though still minority) of the homosexual population [ie: they're second-born males or after]. Further, stepchildren show no parallel correlation nor is a 2nd or 3rd born sister more likely to be a tomboy (correlation-wise). Again, I should emphasize that this explanation -even if it is as I suspect 100% true- only accounts for a sizable minority of the homosexual population. There's more to homosexuality than just this effect, but I found this effect interesting nonetheless.

[Sela]

*shivers* That sounds like goodpasture's almost. Scary stuff.

Um, only in the sense that both are immune mediated. Goodpastures can affect other organs, namely the kidneys.

. You're absolutely right - I got goodpastures wrong here. I was thinking of the reaction you get when you're transfused the wrong blood type (serum sickness leading to a acute hemolytic transfusion reaction, yes?) but for some reason I ended up at goodpastures. Gotta review my immuno!

[PainRack]

Lol, the first time I read it out, I realised I pronounced it as TARDI. You know, just one s away from TARDIS.

[Literally Hitler]

Fraternal Birth Order Effect

That sounds pretty bizarre. I mean sure, all those Y-derived proteins are exogenous to the mother, she's never been tolerant to them. But that's hardly going to affect the kid's genes themselves, immune systems specifically attack foreign genes, they are optimised to attack foreign gene products (proteins). These anti-Y antibodies cross the placenta, and bind what proteins? It's not like there's a gene that encodes a protein that regulates sexuality (yet found), and if there were, that protein would probably jump back to the normal level by a couple of months after birth.

Maybe these antibodies affect higher level structures in the development of the fetal/neonatal brain, but we know so little and the causation is so weak that it is indeed completely speculative. I for one aren't buying it.

[Sela]

Well, I don't insist upon it - like I said at the beginning of that post; there's less evidence for this than for any other disease I posted by far. But yes, the idea is that H-Y antigen is needed for proper differentiation of quote: "sex-typical traits" and that having an anti H-Y (anti human Y-antigen) antibody will put a dampener on proper development.

But near as I recall they do indeed affect the neonatal brain. If you want to do more reading on it here are a few of the NCBI articles I mentioned:

http://www.ncbi.nlm.nih.gov/pubmed/11534970 "Fraternal birth order and immune hypothesis. . . ."
http://www.ncbi.nlm.nih.gov/pubmed/14994314 "Proportion of homosexual men who owe their sexual orientation to fraternal birth order . . ."
http://www.ncbi.nlm.nih.gov/pubmed/15302549 "Quantitative and theoretical analysis of the relationship . . . "
http://www.ncbi.nlm.nih.gov/pubmed/17148215 "The association between fraternal birth order in homosexuality and other markers . . . "


Personally, I'd be surprised if there were NO genetic component to homosexual orientation . . . I mean there's a genetic component to so darned much, it'd be unlikely in the extreme that you couldn't get predisposition of a sexual orientation off of some. But again, I emphasize that I don't know all too much.

[mr friendly guy]

saw this today

A WOMAN was temporarily partially paralysed by a love bite on her neck from her amorous partner.

The 44-year-old New Zealand woman went to the emergency department of Middlemore Hospital in Auckland last year after experiencing loss of movement in her left arm while watching television, doctors reported in the New Zealand Medical Journal.

Doctors concluded the woman had suffered a mild stroke but were puzzled about its cause until they found a small vertical bruise on her neck - a love bite or hickey - near a major artery.

She had received the love bite a few days earlier.

"Because it was a love bite there would be a lot of suction," one of the doctors who treated her, Teddy Wu, told the Christchurch Press.

"Because of the physical trauma it had made a bit of bruising inside the vessel. There was a clot in the artery underneath where the hickey was."

Dr Wu says the clot dislodged and travelled to the woman's heart where it caused a minor stroke that led to the loss of movement.

"We looked around the medical literature and that example of having a love bite causing something like that hasn't been described before," he said.

The medic said the woman recovered after being treated with an anti-coagulant.

Heh. A love bit causing paralysis, via clot formation leading to stroke, and the first of its kind reported in the literature. I think the Doctors need to check if her lover is secretly a vampire.

[Sela]

That *is* pretty messed up in a cool sort of way. We just had a lecture where we heard about a physical therapist who tried to relieve someone's leg pain via massage. . . .

But it turned out the leg-pain was occuring thanks to venous thromboses that had lead to congestion (or something like that). . . and the result of the massage was to dislodge them - turning them into pulmonary emboli.

[Sela]

Been a while since I posted on this, but I've got a really neat one today .

Refractory Hypertension due to Renal Artery Stenosis

Short 'n Sweet:
"Healthy" response of the kidney to a local limitation in blood supply results in systemic hypertension (high blood pressure).


Background Anat&Physio:
Be warned - lots of stuff here.
The kidneys cumulatively ('renal system', prefix 'nephro-') are composed of one million tiny units called 'nephrons'. Each kidney is supplied blood by a large artery - the renal artery - which then branches into several smaller arteries ending eventually in the renal afferent and renal efferent arterioles. Between these two ('glomerulus'), pressure from inside the arterial tube pushes fluid into the nephron itself where the fluid is drained of useful nutrients and then expunged from the body. The rate at which this occurs is called 'glomerulal filtration rate' (GFR) and there are several cells in each nephron that are designed to sense changes in this rate. For example, if less blood flows through the body, this means less blood gets to the kidney and thus GFR goes down. These cells detect this, and respond by certain regulatory mechanisms:
1.) Retaining sodium (and thus water), which results in increased blood *volume* -> increased blood pressure -> increased renal-artery blood -> increased GFR.
2.) Increasing the resistance (constricting) of the latter (efferent) arteriole after the filtration site. This increases the pressure before it, and thus increases GFR.
3.) Relaxing the resistance in the afferent arteriole (before filtration), again increasing the amount of blood to get in locally.

And in this way, a healthy person can continue to have totally normal kidney function despite blood pressures as low as 90 or as high as 200. Further, the kidney itself can help temporarily correct losses or gains in blood pressure.

What goes wrong?:
So, quite like in the case of MI, say our patient has fatty plaques building up in some arteries. In this case, they've got a physical blockage of one of the renal arteries. They'll have a normal overall blood pressure, since their whole body is pretty much fine. In fact, their kidney function should be pretty okay too, since one kidney still can do enough work (hence why live kidney donation is safe).

But that's not how our kidney sees it. From Mr. Blocked Left Kidney's point of view, the blood flow is incredibly low! After all, only a trickle of blood (relatively) is getting past the renal artery blockage! And all the way down at the level of the arterioles and the lumen, GFR is going to be looking very, very low. But kidneys are stupid. Instead of realizing they've got an upstream blockage and that overall GFR is still okay, the blocked kidney only senses lower blood flow. It interprets this as a *body-wide* drop in blood pressure instead of just a local one, and starts quickly trying to raise the blood pressure!

Now if it's just one kidney doing it, the other kidney can usually help. But most often, patients have major blockage in one renal vessel and *slight* blockage in the other, which is enough to tip the scale. The kidneys demand blood volume in the whole body increases, and the patient gets high blood pressure. But this *still* doesn't fix the blockage, and only very mildly increases the blood getting through. So instead of quieting down, the kidneys demand even further and further blood pressure increase. Needless to say, that kind of high blood pressure throughout the body is very bad for you. That sort of pressure on small weak blood vessels can make them rupture .. . and scar . . . and get blocked. . . leading to even more permanent, higher blood pressure.

Why it's cool:
I think there's two things that really are awesome about this. One is just how oblivious the kidney is (yes, I'm anthrapomorphizing (sp?) it's more fun that way.) to what it's doing to the rest of the body. It's working so hard to help when in reality it's putting everything else in serious danger. Second is the way it's a vicious cycle. The higher the hypertension is, the more likely damage elsewhere will cause more plaque formation. And that will actually raise the vascular resistance and thus the blood pressure further.

Treatment:
This kind of scenario is relatively refractory to drugs. At first glance, you'd think we could block the hormones the kidney is releasing that are bringing up the blood pressure. The fact of the matter, however, is that despite how much damage that hormone is doing via BP up (first adaptive mechanism), it simultaneously does the 2nd adaptive mechanism (Reff up->GFR up). Without it, the kidneys would fail at filtering out toxins altogether, and we'd have way more problems than just the high blood pressure.
After diagnosis, surgery(rare) or catheterization -sticking a long wire+balloon into an artery to "force" the blockage open and leave a metal mesh behind- is needed to re-open the blockage. This generally fixes the problem, but monitoring is needed to be sure that kidney function recovers.
Additionally, blood pressure medications (*after* the block is fixed), and anti-clotting meds are given to help correct the problem and prevent recurrence.


Good stuff. . . well, not good; but interesting.

[mr friendly guy]

Well if you are going to go with causes of secondary hypertension, I suggest phaeochromocytoma. Its the one people think about but rarely seen (I have seen it twice). Essentially a growth on the adrenal glands which makes it produce more hormones. Symptoms are the five "Ps" (get it, P for phaeochromocytoma). They are pallor, palpitations, perspiration, paroxysmal hypertension and pounding headache. You have to use a combination of alpha and beta blockade, before removing the gland. Oh, and you have to alpha blockade first before beta blockading because it makes it worse via a mechanism I can't remember. Note in my experience beta blocker antihypertensives are used more frequently than alpha blocker antihypertensives, so it this snippet might not be obvious.