Friday, December 12, 2014

WILTIMS #230: ♫♪ And now, the end is near... ♪♫

Last WILTIMS post before winter break! Woohoo!
Last post before first semester finals of dooooooom!!! Woohoo?

Thank you for my first complete calendar year of getting to share the highs, lows, and science of med school with you. I know I've said that I write this partly for myself, but if I never got any views, I'm sure I would have ended this crazy run by now. So, unless I get ambitious and write over break, see you in 2015!

TIL: Kids with congenital heart malformations more often die from a fatal arrhythmia due to the scar from a life saving surgery than from the malformation itself. To be clear, very few of them die from this at all now and most would have died in infancy without surgery. But because we now do such a good job identifying and correcting the surgery, all of these kids outlive their malformation and a few eventually die from a rare long-term  complication from surgery.

Every heart attack patient is greeted in the ER by "MONA":
Morphine - for pain
Oxygen - to combat ischemia
Nitroglycerin - for vasodilation both of peripheral veins and coronary arteries
Aspirin - to prevent clotting and limit inflammation

The reason that heart valves specifically get endocarditis compared to other tissues of the heart is that they are nearly acellular. The white blood cells of the immune system can't get to this tissue to clear the infection. You might reasonably ask how blood cells have a problem getting to valves that are literally bathed in blood. This is where some immunology comes in handy. The way immune cells target and invade infected tissues involves a complex dance along the endothelial cells that line blood vessels. The fibrous tissue of the valves just doesn't have the external markers to slow down and hold on to white cells long enough for them to invade the tissue and do their thing.


TIL: If you do a pericardiocentesis (use a big needle to drain the area around the heart of blood or other fluid) and are concerned you accidently pierced a chamber of the heart, there is quick way to tell. Splash the draining blood on the table and see if it clots. Blood in the pericardial space won't have any circulating clotting factors and won't clot.

A lot of people come into the ER with complaints that sound vaguely like a heart attack, but it would be ridiculous (and prohibitively expensive) to do a full diagnostic work-up on all of these patients. Extensive research has been done to show which risk factors are most predictive of an actual ischemic attack. The TIMI risk score correlates 7 groups of risk factors with the likelihood of death within two weeks.

The risk factors are:
  1. Age >65
  2. ≥3 coronary artery disease risk factors
  3. Prior coronary stenosis of ≥50%
  4. ST-segment deviation on EKG
  5. 2 instances of chest pain within 24hrs
  6. Use of aspirin within the last 7 days
  7. Elevated cardiac blood test markers
Most of these probably make sense (or sound really jargon-y, if you're not medically inclined), but take a look at #6. Why would using aspirin, a very good drug for treating a heart attack, be a risk factor? Well, the patient is definitely complaining of something; that's why they're in the ER. And if they are in distress or have any of the other risk factors while already being on aspirin, then their underlying level of disease is probably worse than it appears.

If you have none of the TIMI risk factors after presenting with heart attack-like symptoms, then your chance of death in the next two weeks is 4.7% whereas if you have all seven, it's 40.9%.

Wednesday, December 10, 2014

WILTIMS #228: I'm not an ambi-dilator

TIL: "Coronary steal" is not the new look of Derek Zoolander, but a physiologic phenomenon caused by vasodilation medications (drugs that make your blood vessels expand). These drugs have a variety of effects on the cardiovascular system  but the one you might reasonably think would be useful is opening up the coronary arteries supplying the heart in a patient with athlerosclerotic plaques causing angina (chest pain) which could lead to a myocardial infarction (heart attack). But if you give these drugs to such a person, it will likely make the condition worse.

This counterintuitive result is due to the body being one step ahead of you. When the heart is ischemic (not getting enough nutrients via blood), the body automatically fully dilates the coronary arteries to maximize their blood flow. So, when you prescribe the vasodilator, it has no effect on the coronaries that you were targeting, but still works beautifully on all the other healthier blood vessels in the body. The other vessels widen and divert even more blood away from the coronaries, quite the opposite of the desired effect.

This seemingly nasty side effect (more like downright failure of the drug) actually has a silver lining; by administering this drug class in a controlled setting, you can test the heart's response to ischemic stress. This is one type of cardiac stress test.

Tuesday, December 9, 2014

WILTIMS #227: JVD or is your neck just happy to see me?

Today was one of our monthly-ish preceptor sessions, where we don our mini white coats and disperse among the real doctor folk of the area. It's really gotten fun at these sessions now that we somewhat know things. My preceptor is an adult general practitioner and most of his patients have either some infectious or cardiovascular problem and, luck would have it, those two topics are precisely what our big first semester final is on next week.

TIL: "Splinting" is a term for when a patient guards one side of their chest from expanding when taking a breath.

Jugular-venous distention (JVD) is a great external indicator of right-sided heart failure (as well as tricuspid valve stenosis and constrictive pericarditis). This is when blood backs-up in the large veins as it tries to come back to the heart. This pressure travels back up the jugular veins (among others) and causes them to visible bulge in the neck.

But the jugular can be visible normally, so how do you officially classify JVD? First, you must have the patient sitting back at 45° and at rest. If the jugular is visible 4.5cm above the sternal angle, then the patient is positive for JVD.

WILTIMS #225: Think before you think

I've noticed a change in the way that I think, and I'm not sure if I like it. I've started wanting an H&P (history and physical) on my friends and relatives. Now, I don't mean that I literally want to peek into their medical records; it's more that I have come to expect a certain amount of background information before addressing a problem. When I'm asked for advice by people I know, I go into "doctor mode" and immediately want more information than it's socially acceptable to ask for.

One of the most important things you learn early in medical school is that your ability to diagnose and treat is most directly affected by the quality of your history and physical. You can't rule out or rule in anything if you don't have all the appropriate information. Doctor-patient privilege is a powerful thing, allowing you to ask anything - with the understanding that the conversation is confidential, useful, and may help to solve the problem at hand.

I want that same ability for certain situations. I want to be able to call timeout on our normal relationship and deploy this higher standard of listening, but that's just not socially feasible most of the time. Now, I think this is usually fine when the problem is medical; people naturally expect to have to share details if they bring up a medical problem on their own. But with interpersonal problems, issues at work, or in academics, there is a level of discretion employed that you simply get to bypass in medicine.

If a friend is asking for serious non-medical advice, I go into "problem solving mode" (a close relative to "doctor mode"). It's fun. It turns even terrible situations into puzzles. If I can just see all the pieces, eventually I will solve it. But this is a false analogy. There are times when the broken pieces will never add up to a full picture. When problem solving doesn't help. When all a person needs is comfort and understanding. This is a scary route to desensitization and it is plotted out by the most benign and even well-meant reasoning.

For years we are trained to elicit a problem, break it down into useful pieces of information, elicit more info if needed, and then start offering solutions. That's great, usually. But in real life, we aren't hearing the problem from an exam prompt or even a patient in a clinical setting. These everyday questions come from friends, from family. They probably aren't telling you their troubles because you're a doctor or medical student, but because you are a person close to them who they can trust to listen and reassure them. Sometimes they already know the answer to their problem. Sometimes they aren't sharing everything because the problem is too personal and you figuring out the solution (using your mighty problem solving skills) will only bring more pain, not less.

To any med students reading this, try to keep in check the wonderful, powerful ability you are honing to someday save untold lives. Your ability to problem solve is part of what makes you special and able to apply the vast knowledge you are accumulating, but it also can isolate you from your fellow humans if you let it dominate your thought process.

TIL*: Uremic pericarditis kills dialysis patients in blizzards. This is part of why only certain vehicles are supposed to be on the road in snowstorms. The average healthy peron can go a couple days bundled up and playing board games. But if a person in renal failure can't get to a dialysis clinic (thanks to roads blocked by accidents or stranded cars) they die - often from this form of pericarditis (inflammation in the tissue and space surrounding the heart). Stay off the roads in an emergency!

*It's a new record! I'm three days late on posting this one, but I'll be damned if I don't maintain my post-per-day-of-class run. Apologies for the delay!

WILTIMS #226: Eye eye, captain.

Why do doctors always look in your eyes? It seems like whatever you go in for - a fever, a headache, high blood pressure - they need to peek in the peepers. Well, just as the eyes are your window to the world, they're our window to blood vessels. The blood vessels in the retina are the only ones in the body that can be viewed directly. It's like we can look straight through the skin and watch disease processes do their damage.

With hypertension, a fundoscopic exam (eye exam) is especially useful thanks to a whole spectrum of symptoms that can tell us about the progression of this widespread medical condition. AV nicking shows venous damage around intersections with hypertensive arteries. Cotton wool spots are tiny infarcts of retinal tissue due to blood vessels pinching off parts of nerve cells. Finally, the retina can hemorrhage causing tiny blobs of blood to escape the vasculature. These can be tiny and unnoticed (until a doctor sees them during an eye exam) or so large that they severely reduce the persons vision.

TIL: Stages of heart failure were recently renamed so that stage A heart failure is really just a warning of predisposing risk factors. Stage A means you don't actually have any symptoms or structural damage, but have one or more of the high risk warning signs that, if left untreated, are likely to cause the other, more legitimate stages of heart failure.

Pulsus alternans is an interesting, if ominous, effect of left systolic heart failure whereby the heart alternates strong and weak beats thanks to a poorly executed compensatory response. When the heart fails to pump out enough blood, some blood is left in the ventricular chamber. When the heart tries to refill that chamber, it now overfills it because of the leftovers from the previous beat. This stretches the muscle out (using the Frank-Starling mechanism) causing the heart to beat harder. This tuckers out the already failing heart and it pumps rather feebly the next time, starting the cycle over again.

Friday, December 5, 2014

WILTIMS #224: De-defects

As a nice little follow-up to yesterday's heart congenital defects post, today I learned about some of the repair procedures for these defects. Most of these conditions require multiple procedures because a baby born with one of these deformities is typically premature and would not survive the main surgical correction. So, frequently, a less invasive procedure is done as a stopgap measure to keep the baby alive long enough to develop and grow a bit more.

TIL: The stopgap procedure used for transposition of the great arteries is to purposefully punch a hole in the atrial septum. This is the malformation from yesterday where you need a shunt of some kind between the parallel circuits of blood flow in order to survive. To better the outcome and stall until bigger procedures can be attempted.

Seemingly paradoxically, the first procedure developed for the permanent fix of this condition involves the rerouting of the left and right atria to the opposite ventricles. I have yet to hear a good expansion for why they didn't start with what is now the more common procedure: simply switching the great arteries back to where they normally are.

I say simply, but this surgery is very complicated (I still don't think it's more complicated than construction two crisscrossing atrial chambers while maintaining proper pacemaker production through the heart, but hey what do I know?). The incision must be made above the great arteries valves which presents us with a problem; the coronary arteries, which supply the heart with nutrients, come off the aortic valve. That valve is being left behind and converted into a new pulmonic valve, which won't be able to oxygenate the heart tissue. So in addition to the switching off the aorta and pulmonary arteries, the coronary arteries must also be moved over to the old pulmonic valve.

Thursday, December 4, 2014

WILTYIMS #223: Defects

We had a lecture today yesterday was on congenital heart defects. Here are some of the facts I found particularly interesting:

TIL: A person can be born with a double aortic arch. You might rightly think this shouldn't be a major problem because it's simply a redundant (if super large) blood vessel. Problems arise not because of blood flow, but because the second arch completes a circle around the the esophagus and trachea/bronchi. This leads to problems swallowing and breathing.

Coarctation of the aorta is a narrowing of the superior descending aorta and is one of the only things that will make you listen for the heart sounds through the patient's back. The aorta naturally arcs backwards and the stenosis occurs just on the downturn so that the noise of the blood whooshing through is best heard on the back, between the scapulas.

Ventricular septal defect (VSD) causes left sided volume loading because the volume ejected during systole never returns to the RV. Blood squeezed through the defect from left to right will go straight into the pulmonic valve and back to the left side.

A "tet spell" is a temporary event that occurs in children with the condition called tetralogy of Fallot, a fairly common constellation of heart malformations. Tet spells are caused by increased resistance through the pulmonary artery (it's not known why this happens) which causes all the deoxygenated blood longing for the lungs to go through a hole in the septum. The deoxygenated blood just cycles back to the body, causing the child to turn blue and faint.

And finally, when is the one time you want a septal defect? If you are born with a transposition of the great arteries (the aorta and pulmonary artery) you need a septal defect to survive long enough for surgery.Transposition of great arteries sucks. In effect, the two paths of blood from the heart are switched creating two parallel and thus useless circuits. Oxygenated blood from the lungs goes right back to the lungs and deoxygenated blood from the body returns to the body. The only way to survive is if you have another birth defect: a hole between the two sides of the heart.

Wednesday, December 3, 2014


Today was pretty awesome - we got our first crack at the super fancy medical mannequins that our school recently invested in. On monday I got to play around with "Harvey" the cardiovascular mannequin and, though he was indeed adept at making heart sounds and murmurs, he was lacking in both liveliness and limbs.

Today's nameless plastic patients had all their arms and legs (and pulses in each of them to boot!), dilatable eyes (that blink too!), breathing lungs and a beating heart. These are the sort of mechanical wonders that can be programmed on the fly from behind a mirrored window to behave as any sort of patient and get better or worse as we attempt to treat them.

A doctor lead our activity today by giving us the briefest of histories and then stepping back to see how we would do (rather poorly at this point, in case you were wondering). He would offer non-committal advice as we crowded around the mannequin listening with our stethoscopes, asking for test results, and trying to remember all that reading we haven't done yet. But I've never been more receptive to learn as when there is a dying (plastic) woman in front of me and we can (theoretically) save her.

Quote of the day:
 "If you can think and pee, your heart's working well enough to wait on getting a pacemaker." -our course clinical cardiologist when describing the most important organs that your heart perfuses.

TIL: Don't restart atria without anticoagulating first (if possible). When the atria are not contracting productively, as in atrial fibrillation, the blood can sit and clot. If you start up the atria right away, you will scatter these clots throughout the capillary beds of the body, notably in the lungs and brain, potentially causing a stroke if not killing the patient outright. That's why, if the afib is non-emergent (i.e. not already causing significant symptoms), you send the patient home on anticoagulants for a few weeks to dissolve any potential blood clots before trying to start the atria again.

And from yesterday's comments (yes, I do respond to questions in the comments! hint, hint, nudge nudge):
Q: What does it feel like to be defibrillated while awake? Is it terrible? 
A: We just learned this today actually! It really depends on the type of arrhythmia. If a person is in afib, you can reset the heartbeat with a relatively small shock - something that would make the person go "Ouch. That hurt!" If they are in v-tach, you may need to use 5- or even 10-times the power. Now, to be fair, if the person is in v-tach, they will almost definitely not be conscious. Regardless, this level of shock is the sort of thing you see portrayed on TV (although less dramatic): all the muscle cells in the heart are depolarized and will hopefully reboot, but with this level of shock, a bunch of the other muscle cells in the proximal body depolarize too, causing a fairly sizable full-body twitch. This would feel very much like being electrocuted... through your chest. So more of a "*#@$%!!!" than an "Ouch!"

Tuesday, December 2, 2014

WILTIMS #221: Physics - The Revenge!

The average med student regards physics is a necessary evil - a penance to placate the MCAT gods and then promptly forget. After all, most of us got into this business because we liked biology, not math. And yet as I've progressed through my first two years, I've noticed that hidden among the touchy-feely biologists are a handful of physics-heavy specialists who actually use those long forgotten equations to do their jobs.

Today we got a nice refresher on fluid dynamics from a cardiologist who specializes in echocardiography (using sound waves to image the heart, much like sonar in submarines). The following equations came up while discussing the flow of blood between the atria in a patient with an atrial septal defect:
P = Q × R   ∴   Q = P / R
A septal defect is when there is an abnormal hole in the heart connecting either the two atria or ventricles, neither of which are supposed to be connected. Generally, the left side of the heart is under more pressure than the right, so one might assume that blood would flow from the left to the right when there is gaping hole in the septum. With a big enough hole, the pressures equalize and you'd expect the flow through gap to stop... but it doesn't!

This is when the cardiologist coyly grinned as we all scratched our heads. Why would there be a flow of blood when there is no pressure difference? To the physics! Looking back at the equations above (or just remembering from physiology), flow (Q) is related to both pressure AND resistance. So, if the pressure is the same between the connected chambers and blood is still flowing, then the resistance must be different, and this, in fact, is the case.

TIL: Replacement valves last longer in place of the aortic valve than mitral valve. This is fairly counterintuitive because the aortic valve is generally dealing with bigger pressures. BUT, the mitral valve deals with a bigger change in pressure (AV: 120/80 vs MV: 120/12), and it's this that really causes the wear and tear.

Don't defibrillate people when they're awake. Generally not considered good bedside manner. If a shock would be good to reset their arrhythmic heart, knock them out first.

Rivaroxaban and apixaban have their mechanism in their names. What?! An intuitively named drug?! Crazy, I know! These anticoagulants counteract or ban Factor Xa. ban Xa → Xa ban → "-xaban". Tada!

Wednesday, November 26, 2014

WILTYIMS #220: NYMedTalks

Yesterday was a special day for my school. Every year, the second-year class hosts a day of scientific talks with a residency/specialty fair during lunch. This year's event was put on by my class and rebranded from the simultaneously enigmatic and uninteresting SPAD (Student Physician Awareness Day) to NYMedTalks (à la the popular TED Talks).

Our student senate put in way more work than anyone expected of them, getting some fantastic speakers and even convincing medical students to voluntarily attend anything. Normal classes were cancelled for first- and second-year students and third- and fourth-years were excused from their clerkships, should they want to attend. That's roughly 800 people alone. At most, I think we had maybe 125 people in the auditorium at once (for the "Watson" talk, if you were wondering), but to be honest that was way more than most people, including myself, expected.

The presenters were, on average, great speakers with interesting areas of research. Here's a rundown of the day and highlights I took away from the talks:

8:30 – 9:00 Introduction by Deans and Chancellor Halperin
  • As he himself so eloquently put, there is a difference between saying a few words and having a few words to say. Chancellor Halperin once again gave a surprising mini-speech on the merits of keeping an open mind, of disregarding one's societal station, of gracefully handling criticism, of branching out into many fields, and of doing all this at any age - all as tied together through the life and actions of Benjamin Franklin. Bold, interesting and well-spoken as always.
9:00 – 9:30 “Unnatural Killer Cells: TRAIL-coated Leukocytes that Kill Cancer Cells in the Circulation" by Dr. Michael King (Cornell University)
  • This was a great research presentation on a new way to defend against metastasis of cancers by, in a way, arming the body's natural immune defense cells with a cancer-targeting system. Specifically, they trick cancer cells into sticking to the white blood cells by adding a blood vessel protein to the cell membrane and then they give the white blood cells apoptosis-inducing weaponry to kill the cells that stick to the trap.
9:35 – 10:05 “Early Life Microbiome and Obesity" by Dr. Martin Blaser (New York University)
  • This guy is a rockstar in biomedical research. He is the head of the Human Microbiome Project, the follow up to the human genome project that seeks to quantify and categorize the various combinations of bacteria that inhabit our bodies with us. He is a phenomenal speaker and made a solid case for misuse of antibiotics having a leading role in the current obesity epidemic, among others. Here he is in a Daily Show interview* promoting his recent book.
*I'm not actually a big fan of Jon Stewart as a science-interviewer, and think this could have been better a better interview, but still it's cool that I just saw that guy in my classroom yesterday, after watching him on TV a few months ago.
10:15 – 11:00 Public Health Panel on (paraphrasing) issues in primary/geriatric care and incarcerated populations by Drs. Pedro Laureano and Kenneth Knapp (NYMC) moderated by our dean of public health, Dr. Robert Amler.
  • This was a rather blah panel, but the speakers did bring up some interesting points. Specifically, I had never really thought about the burden that unhealthy ex-prisoners put on their communities when they are released and how poorly we take care of them once they are.
11:05 – 11:35 “SpeechOmeter: a Google Glass Application” by Mansoor Pervaiz (Northeastern University)
  • This was a cool presentation by a PhD student on an app they made for the Google Glass platform where they could monitor and modify the speech patterns of people with disabilities that cause speech pathologies. An example he gave is of how parkinson's patients often lose a sense of how loud they are talking and with this technology, you can give them a big colorful display in the corner of their eye with volume and speed feedback. The patient can then get instant impartial feedback and the clinician can get a recording to see if the speech therapy techniques are working, are being used correctly, or need to be further adjusted.
11:40 – 12:10 “Updates in Obesity Medicine; Epidemiology, Metabolic Disease, and Clinical Applications” by Dr. Rekha Kumar (Weill Cornell Medical College)(and NYMC alumna)
  • This was a fairly simple description of the new, mostly pharmacologic options for treating severe obesity, as given by a fairly recent alum of our school who now practices on the upper east side in an obesity focused office.
12:10 – 1:10 Residency/Specialty Fair and Lunch
  • Lunch had an impressive turnout by many of the dozens of residencies that our school offers. Students could roam around and ask about the pros/cons of different specialties and learn what they need to do to better their chances of matching, come fourth-year.
1:15 – 2:15 “Watson: The Jeopardy! Challenge and Applications to Healthcare” by Dr. Eric Brown (IBM)
  • This was easily the coolest talk. The project leader of IBM's Watson supercomputer came to talk about the progress toward healthcare applications for Watson's powerful information systems. This is of course the computer that beat Ken Jennings and... that other guy in Jeopardy a few years ago. The remarkable thing about that feat was the ability of this computer system to navigate the complex and purposefully tricky wording of Jeopardy clues and then search a vast store of knowledge in just a few seconds to come up with an accurate answer.
  • In healthcare we have the problem that there is far more research done and patient information recorded than is reasonable for even a whole team of doctors to parse through in any reasonable amount of time. Enter Watson, who can almost instantly sort through the entirety of medical literature and years of patient charts to offer up a answer to a question and explain its reasoning, This could be not just powerful, but indispensable in coming years.
  • Our school has actually been part of the team training Watson's new healthcare algorithm. Every time the still-training Watson is given a query, a panel of experts with rate how well it did and provide feedback on how it could have been better. Then the computer scientists try to figure out how to incorporate that feedback into Watson's processes. So that's cool!
2:20 – 2:50 “Schizophrenia and Depression as Diseases of the Mind?” by Dr. Liah Greenfeld (Boston University)
  • This was simply a weird and poorly articulated talk. Either of those is excusable, but having both made it hard to even sit through. Eh, it happens.
2:55 - 3:25 "Biomaterials and Clinical Applications: New Approaches to the Prevention of Lung Tumor Recurrence Following Surgical Resection" by Dr. Mark Grinstaff (Boston University)
  • This poor fellow lost most of his audience do to the preceding train-wreck of a talk, which is unfortunate because it was an interesting subject. The goal of this research was to come up with a way to help prevent the recurrence of tumors that are surgically removed. The age old problem in this area is that the more you cut out, the less the chance of missing one or more still-cancerous cell. But the more you cut, the less healthy organ there is left for the patient to use during and after recovery. Dr. Grinstaff came up with an idea to coat the surgical wound with a nanoparticle infused mesh. The tiny particles are then slowly absorbed by the surrounding tissue where they release powerful chemotherapy directly to the worrisome tissue. And rather than lose all of that tissue, the chemo selectively targets the cancer cells, allowing more of the tissue to remain healthy.
3:35 – 3:55 “Toward Optimal Neuroprosthetics” by Dr. Ramana Vinjamuri (Stevens Institute of Technology)
  • This was a cool talk about the current state of prosthetics regarding brain machine interfaces (BMIs) that allow the wearer to move the mechanised limb just with their thoughts. We went through the various current options and talked about the balance between invasiveness and utility. For example, though you may be able to wear a funny looking hat to open and close a hand, you can fully move and grasp in three dimensions if you get a rather cumbersome implant that needs to be plugged in to large wires through your skull. Hopefully, time will blend the best of both worlds.
4:00 – 4:30 “Virtual Reality and Video Games for Stroke Rehabilitation” by Dr. Judith Deutsch (Rutgers)
  • Finally, we heard about how video games and virtual reality are being used to aid in physical therapy and rehabilitation. One of the more amusing takeaways was that it is often easier for engineers in this field to wait for the next generation of commercial video game consoles to come out rather than design and build their own custom equipment/software. Then when platforms like the XBOX Kinect release the specifications for designing custom games and programs, you can quickly make a cheap, fun, useful program for patients to use in nearly any space. Nintendo has kept the Wii locked from this application, so even though the Wii would be great for these applications, physical therapists have to adapt their programs to the already made games, like Wii Sports or Wii Fit, which are not designed well for rehab.
So there you go! Looooooong day, but it was a blast and I'm so impressed with how well it was put together by students who are dealing with everything else I have complained about in this blog (classes, exams, etc.). There was so much more discussed for every topic above, but I need to cut myself off somewhere. So, if you have any questions or want elaborations, just leave a comment or send me an email.

Happy Thanksgiving and I shall resume the blog next week!

Tuesday, November 25, 2014

Storm delay

Thanks to the lovely slush-storm heading my way, school has been canceled for tomorrow and I get an even longer holiday weekend! I have a ton of things to write about from today, so rather than losing sleep tonight trying to get out a post, I'll take my time with it tomorrow. See you then!

To everyone traveling tomorrow: stay safe!

Monday, November 24, 2014

WILTIMS #219: All the fun facts!

It's funny and awkward being at this teenage stage of my medical education. An example is of how my vocabulary has changed in the last year and a half. Words that I once defined as part of my "TIL" facts last year are so familiar that I get in trouble forgetting to defining them to the uninitiated in current posts in this same blog. See below where, when trying to describe a pulmonary embolism, I used the word occlusion, which no one else in the room was able to use in a sentence. So, I've obviously learned a few things (and must make sure to check that I don't overuse jargon, both in this setting and during future patient care).

But at the same time, nearly every day a professor does the same thing to my entire class. She will use a very basic term from her discussed field, something that we simply have never had occasion to learn, and then have to stop and backtrack once she sees the confused looks and quiet whisperings between classmates. Today's word was claudication (just as angina means chest pain, claudication is leg pain).

TIL: There are two different nuclear dyes used in cardiac stress tests to image the heart. They each have their own pros and cons, but one was particularly entertaining. Depending on the location and travel plans of a patient, you may want to use technetium-99mTc instead of thallium-201 because, with the latter, the patient will be "nuclear" for a week. These two drugs have the same radioactive dose, similar cost, and the same effectiveness. But thallium has a longer half-life and will set off nuclear detectors (such as those in high profile airports or the Lincoln tunnel) for a week post-procedure.

Mitral valve prolapse (MVP) can cause premature ventricular contractions (PVCs). MVP is when the mitral valve, between the left atrium and ventricle, is pushed back into the atrium as the ventricle contracts, much like an umbrella inverting in a heavy wind. As it does this, it pulls on the cords and muscles that normally tether the valve in place. These papillary muscles stretch out and stress the wall of the ventricle, which can cause the heart muscle to send out an emergency wave of contraction (that's its somewhat knee-jerk response to pretty much any stress). This wave can result in a single weird beat of the heart, or more seriously trigger a dangerous arrhythmia.

The force parentheses were strong with this one, so lets take it without them first: More people die during or immediately following air travel due to pulmonary embolism as a result of a deep vein thrombosis than of airplane crashes. Ok, got the basic structure? One more time: More people die of pulmonary embolism (the occlusion (blocking off) of an artery in the lungs due to a piece of debris getting lodged in the progressively narrowing blood vessels) as a result of a deep vein thrombosis (a big blood clot forming in a large vein which often breaks off small emboli (chunks of stuff) when agitated (like during air travel)) than of crashes in commercial air travel.

Lastly, you can use right heart catheterization to measure left atrial pressure. This may not seem sensical at first, but hear me out. Think about where a balloon would travel if you let it into the right atrium. First, it would float through the tricuspid valve to the right ventricle. Then it would be pumped through the pulmonary valve to the pulmonary artery. Then it would wander into smaller and smaller arteries as it approaches the lungs before getting lodged (much like the pulmonary embolism we just discussed). Once it's stuck in the lung arteries, the downstream pressure will equalize all the way to the left atrium. This balloon has a sensor on it that measures this pressure and Voila! Left atrial pressure.

Saturday, November 22, 2014

WILTYIMS #218: Listen up!

"Harvey": the cardiopulmonary patient simulator
The professor who taught us about cardiac murmurs today should take up beatboxing... wait... maybe he got his start as a beatboxer before becoming a doctor... so that he can use his powers of noise imitation to save lives through medical education! 

It's a little sad that the theme for the day was about how a super fancy mannequin can teach this material even better, but I honestly don't believe it. Over the next couple weeks we get to go in small groups to our school's new simulation center to practice doing a cardiovascular exam on "Harvey", a mannequin which can imitate heart and lung sounds, blood pressure and various pulses around the body. But I think Harvey has already been upstaged by our professor's uncanny ability to imitate any heart sound, at any speed, at a moment's notice.

In the words of one of the course directors, who was sitting behind me in lecture, I can't wait to see the transcription for this lecture:
Dr. M: And stenosis sounds more like [rhythmic noises] whereas regurgitation is more of a [other noises]. Now, if you have the patient make a fist, the sound will change from [quieter noises] to [louder noises]...
TIL: All about murmurs!

A murmur is essentially any unusual sound made by the heart and its surrounding vasculature. The most common murmurs are made from malfunctioning valves. For example, if the aortic valve gets all crusty and doesn't open all the way any more (aortic stenosis), then the blood will make a loud whoosh as it is squeezed through the smaller opening. Alternatively, if the mitral valve is leaky and lets blood flow backwards from the left ventricle to the left atrium (mitral insufficiency/regurgitation), you will hear a noise as the blood forces it's way back upstream.

Murmurs have a 6-level grading system for intensity:
  1. barely audible - softer than the normal "lub-dub"
  2. about the same intensity as the normal "lub-dub"
  3. louder than "lub-dub"
  4. you can feel the murmur with your hand
  5. you can hear it distantly in the body via the skeleton (like putting your ear to the railroad track)
  6. you can hear it without a stethoscope
That scale is crazy. If you can hear your own heartbeat through your chest (and not just through the arteries in your ears ('cause that's actually a-whole-nother problem)), you should probably go to the doctor.

Friday, November 21, 2014

WILTIMS #217: The EKGs Strike Back

Today we revisited a topic we covered back in physiology: EKGs. I definitely don't remember everything involved, but it's nice that at least the concepts are familiar this time. I'll need to really master interpreting those squiggly lines this time though, because now we are not just looking at what a healthy heart looks like, but how each of the innumerable heart dysfunctions look from an electrical perspective.

One totally useless slide from lecture today was particularly interesting to me: a ye olde EKG machine, circa 1895. The patient sat with three limbs in buckets of salt solution (these were the equivalent of the little sticky paper/metal leads of today) while the electrocardiographer looked through a viewer so as to draw by hand a vague approximation of what the electrical signal was showing.

TIL: A bunch of slight differences in terminology:

Sinus tachycardia vs supraventricular tachycardia: Tachycardia is an elevated heart rate. A sinus rhythm is simply any rhythm where all the peaks are in the right places. A problem comes, however, if an otherwise sinus rhythm is just too fast; the beats are so close together that they overlap and you can't see all the peaks distinctly. Since you can't at that point say whether it is or is not a sinus rhythm, you have to call it something else: the deceptively vague "supraventricular" tachycardia (because, just like in sinus rhythm, the rhythm generating pacemaker is in the atrium, hence supra- (above) the ventricle). 

Atrial flutter vs atrial fibrillation: A flutter occurs when the atrium is beating too fast and the ventricle can't keep up, so it only beats every 3 atrial beats (sometimes 2, sometimes 4, but always consistent). Afib occurs when the atrium is essentially beating non-stop so that there isn't even a signal that the ventricles can go off of. The ventricle then tries its best to keep a rhythm, but fails at it, resulting in an erratic heartbeat.

Atrial vs junctional vs ventricular escape: The heart has three normal pacemakers: the SA node, in the atrium; the AV node, between the atria and ventricles; and a baseline rhythm by the ventricles. The SA node overrides the AV node and either node overrides the ventricular rhythm, so that usually, the whole heart goes off the SA node. If for whatever reason, the SA node fails to fire, other nearby atrial cells can pick up the slack and make a new rhythm (atrial escape). If the whole atrium is slacking, then the AV node will lead the way (junctional escape). Lastly, if something is horribly wrong and nothing above is giving it a signal, the ventricles will beat on their own (ventricular escape).

Thursday, November 20, 2014

WILTIMS #216: "P"s get MDs

Hopefully you correctly interpreted my week of silence as: EXAMS! This round of 7 hour testing was exclusively microbiology and antibiotic pharmacology. And assuming my math is right and I didn't catastrophically fail a miniboard exam, I think I'm finally done with micro!

Our micro professor after the final, celebrating with the home-brew we started during fungi
This marks a fun transition in our curriculum for pathology too. Up to this point we have mainly been studying "general principles" of medicine: inflammation, principles of cancer, anemias, etc. Now begins the organ systems: cardiovascular, renal, reproductive, etc. Today we started cardio and it was lovely. It felt like back in anatomy or physiology, when we were learning big, impactful medicine that was complex, but able to be reasoned-out. It is really hard to put this feeling into words...

It's not that the things we learn in biochem or the immunological parts of micro aren't important - in aggregate, all the tiny malfunctions of our biological underpinnings add up to untold suffering and death at the population level. But once you understand the cell biology involved, each of those conditions boils down to a very simple, typically unfixable problem - this enzyme doesn't work, that protein doesn't fold properly. Those tiny changes can have huge system-wide consequences, but because of how many of them we need to get through, we have to move on before discussing the complex treatment of and interplay between the larger effects.

When we deal with things on a organ system basis, we actually have time to riddle-out, not just that there are downstream effects, but how their nature changes given the disease process. It may just be the way I'm wired, but I love the diseases that result from entire organs failing. It reminds me that the entire body is actually connected; that it is a giant, moving, ever changing puzzle and we get to try to put the pieces back together.

TIL: Oxygen takes up 21% of the dissolved space in blood. That is exactly the same as the percent oxygen in the atmosphere. This makes some sort of very, very long term evolutionary sense.

Lovingly borrowed from WebMD
Bicuspid and unicuspid aortic valves can lead to aortic stenosis. The heart has four valves and they're all a little different. The aortic valve normally has three cusps (tricuspid) but there are rare birth defects that result in bicuspid or, far less commonly, unicuspid aortic valves. One of the main problems with this birth defect is that that the valve doesn't open as well which prevents blood from leaving the heart efficiently. This makes the heart work harder and can lead to several serious complications including left ventricular hypertrophy, where the left ventricle grows super big to compensate. But, this compensation usually does more harm than good in the longterm.

Mitral stenosis (hardening of the heart's mitral valve), has a "fish mouth" appearance upon gross examination.

Friday, November 14, 2014

WILTIMS #215: It's never lupus, but apparently always TB

Today was one of our last "lectures" in microbiology and instead of being talked at for another hour, we got to play to role of a (really bad) detective. The guest lecturer was a doctor who turned off the Powerpoint, and simply had us try to unravel a mystery. We were given an incredibly vague history of a fake patient and then were prompted to ask questions until we figured out what the patient had.

It was very slow going, but by using the facts we've learned this semester, we were able to come to a diagnosis of TB. Apparently TB has such varied and complex constellation of possible symptoms, that it should always be somewhere on one's differential diagnosis.

This was weird and awkward at first, but eventually very rewarding just to see how much we had grown this semester. We didn't immediately figure out the cause of the infection, but we knew how to rule-out some of the hundred of potential causes we had learned in the past few months. If someone asked, "Does the man have pets?" or "Are his lymph nodes swollen?" everyone knew the slew of diseases that the questioner was trying to rule in/out from that line of questioning. I'm calling that progress!

TIL: If a heroin user shows up at the ER with a fever and a chest x-ray showing a patchy infiltrate of the lungs, think staph aureus! This bug is found on the skin and enters the venous drainage via the heroin needle track marks. From there, it infects the heart, specifically the tricuspid heart valve, causing endocarditis. That infection of the valvar surfaces can cause chunks of virus-infected material to break off from the damaged valve and get caught in the lung, resulting in a patchy infection of the lung.

Wednesday, November 12, 2014

WILTIMS #214: Incoldenza

Thank you all for the kind response to yesterday's post. This probably isn't the best week to stay up writing, but I'm glad I did.

The highlight from today was a fantastic lecture on ebola from the director of our school's Center for Disaster Medicine. I won't bore you with the details, because this is already so saturated in the news right now. If you have any questions about anything ebola, write a comment or send me an email and I'd be happy to explain what I know, both about the disease and the response to it.

TIL: The cold is not the flu... unless it is. This is one of those big points that we try to ram home because it relates to low vaccination rates. People often confuse the cold and the flu, feeling that since a cold is no big deal, there's no need to get a flu shot. But the flu is WAY worse than a cold. The flu kills thousands to tens of thousands of people in the US every year. And these aren't just children, the elderly or people with weakened immune systems. The flu also kills perfectly healthy adults.

So all that being said, it's funny that one of the viruses that bears the influenza name, is actually better described as one of the (far less common) causes of the common cold. The influenza A and B viruses cause the full-blown, feel-like-you're-gonna-die flu. But the much rarer C-type of influenza virus causes symptoms so much weaker than its big, bad relatives, that it is considered one of the causes of the common cold. Most cases of the cold are caused by a rhinovirus or coronavirus, but several others can also cause those less-severe, non-specific symptoms, including RSV, adenovirus, coxsackievirus and others.

WILTIMS #213: Unfair advantage with unfair news

Sorry, I don't have a TIL for this post. Instead I want to write about a topic that I know a little too much about.

Today we talked about how to break bad news to patients. After a short lecture, we broke up into small groups with real patients, in my room's case a breast cancer survivor, who had been given difficult news in the past. It was weird having someone come in and speak whom I could very much have replaced, had there been a need. I also felt like I was cheating when it was our turn to ask questions.

"I feel like that period between your initial irregular test result and your actual diagnosis must have been scary and confusing..." I say like a lawyer leading my witness. "Could you describe to us how you felt?"

The afternoon after my biopsy (a "fine"-needle aspirate of my mediastinal mass) was the most pain I've ever been in. I hurt in every way. My chest hurt where they stabbed me, my swollen sentinel lymph node still radiated pain down my arm, I was terrified that it was something even worse than it turned out to be, and I was surrounded by loving, equally-scared family who wanted nothing more than to help me, but who sat watching helplessly as I sobbed in the fetal position on my grandparents' couch. I just wanted to go home after winter break like I was supposed to, but my life had changed on that fateful Friday, three days prior.

And that was one of the big takeaways today. It doesn't take a metastatic cancer diagnosis to make for a difficult diagnosis discussion. Anything that will change someone's lifestyle or plan can be hard to handle. We need to amputate. You will need to take this medication for the rest of your life. You won't be able to play that sport/ do your job/ get around unassisted anymore.

I got my final diagnosis by phone, because the doctor wanted, as soon as possible, to reassure me that it wasn't something worse. So, I never really experienced that "bad news" talk from the patient perspective; my cancer diagnosis was relatively good news! I have, however been closer than most to the other side of the conversation.

After I recovered from my treatment, I volunteered with the Cancer Resource Center in the Ithaca. Among other things, I volunteered on thyroid clinic days, where 5-10 people would come in for a biopsy on potentially cancerous nodules on their thyroid. About five of every six patients would come in, be nervous for an hour or so, and leave relieved. But nearly once per clinic, someone would test positive. They were diagnosed with cancer, right there.

The doctors at this center were great; they would deliver the news and take as much time as was needed for the patient. But when they reached a comfortable stopping point, they would offer the assistance of volunteers like myself to talk with the newly diagnosed patient in a private room about the steps ahead and the resources available to them as they started this struggle.

We really never expected people to understand anything we said. Once someone says the C-word, everything else is white noise. We really were there for three reasons: to just be present for the patient as they start to digest the news (i.e. hold the Kleenex), to offer up support as someone who has been in there shoes and had come out alright, and to make sure they left with a big packet of materials that they could open up once the shock had abated.

That was another takeaway from today's discussion that I hope my classmates remember: The moment of diagnosis is so overwhelming that you need to assume the patient understands nothing, but will probably want to know everything once they have gone home, grieved, and begun to process the change that is about to happen in their life. Some people weep, others are stoic, none are grasping the details right then. So make sure they know, at bare minimum, when and where their next appointment is and that they have access to all the information you are telling them once they get home.

Lastly, and a point that I feel wasn't greatly stressed in our lecture today, when it's appropriate in the conversation, bring up family and friends. Some people are far less concerned about themselves than how their spouse, their children, their parents will handle the news. The patient's care should be topic #1, but a diagnosis like this is usually devastating to more than just the person in the room.

These conversations are very difficult and emotionally draining, but I've never felt more useful to a person than when I could help someone take the very first steps on the road back to normal, in the moments after they've never felt more lost. If you do it well, nothing is more rewarding.

Tuesday, November 11, 2014

WILTYIMS #212: Static

Apologies for the repeat tardiness; headaches don't make for productive bloggers. I actually got some sleep last night [gasp!] and am feeling much better.

Yesterday I learned: antibiotics are complicated:
Click to see the full-resolution original
I made another thing, but this one is just for me (and classmates who read my blog, I guess). It's nowhere near complete yet, but gives you an idea of some of the common drugs used to treat microbiotic infection and their mechanisms of action.

Tetracyclines (including the eponymous tetracycline and also the popular doxycycline), macrolides (including erythromycin and azithromycin), and clindamycin all target bacterial ribosomes. But whereas clindamycin and the macrolides disable the 50S subunit, tetracyclines go after the 30S subunit. None of these drugs are actually bactericidal - they don't kill bacteria.

What use are they if they don't kill bacteria? you might ask. By targeting the ribosome, these drugs stop the bacteria from effectively making proteins, thus stopping most cellular function and division. this can give your body enough time to take out the infection on its own. That can be for the best if you are trying to build up a robust immune response and create immunity through antibodies.

Sunday, November 9, 2014

WILTDBLIMS #211: Hepatitis and productive procrastination

This is the tardiest I've even been for this blog, but I was working on something else that I'm quite proud of:

Click to go to the full resolution Google Drawing
That diagram is just the classification information on most of the viruses we need to know for our microbiology final next week. Of course, we also need to know the pathology and treatment for each of the diseases these viruses cause - not to mention all the bacteria and parasites we need to review in the meantime... Gonna be a "fun" week!

What I learned the day before last: Hepatitis! Everyone has heard of hepatitis and probably even knows that there are three common types: A, B and C. But do you know what hepatitis actually is? Hepat- means liver and -itis means inflammation, so any hepatitis is an inflammatory process of the liver. The lettered bits refer to specific viruses that affect the liver, causing a form hepatitis.
{brace yourself for all the TLAs*}
Something that I didn't know until Friday was that the viruses that cause hep A, B and C are totally unrelated. Hepatitis A virus (HAV) is a tiny picornavirus, HBV is an hepadnavirus, and HCV is a flavivirus. HAV and HCV use RNA for their genetic material, meanwhile HBV uses DNA. HAV is transmitted from feces; HBV and HCV are passed on through blood and bodily fluids. Most importantly, HAV is quickly recovered from while HBV and HCV often lead to chronic, lifelong infections and severe liver damage.

There are also viral hepatitises D and E, as well as a few other viruses that are suspected of being associated with hepatitis but have not earned a letter yet. And all of these are very different as well. Isn't virology simple? (in case the sarcasm didn't just drip from that last sentence, take another glance at that chart above)

*three-letter acronyms

Friday, November 7, 2014

WILTIMS #210: ♪♫ Stool-day, bloody stool-day ♪♫♪

TIL: Blood in stool is more complicated than one might think. When my pathology small group leader asked us whether the bloody stool described in a case study was left-sided of right-sided, one of my brighter classmates turned to me and mouthed, "What the f*%#?" I nodded in confusion. How can you tell which side of the colon is bleeding from a description of the bloody stool?

With a little bit of more explanation we both got it. You can tell where in the GI tract the patient is bleeding by how digested, and thus black, the blood is. If it's still red, then it's relatively fresh and likely to be located near the end of the colon or around the anal opening (generally toward the lower left side of the body). If it's black, then it has been digested by its passage through the GI tract. Black blood can originate anywhere upstream, like the stomach or small intestine, but if it is in the colon, then it's on the right side of the body.

Wednesday, November 5, 2014

WILTIMS #209: Violet! You're turning violet, Violet!

TIL: If you see an ear defect at birth, look at the kidneys. These two structures develop at the same time, so if something non-congenital like an infection or teratogenic substance (alcohol, drugs, tobacco) caused a malformation of the ears, it is likely to have altered the development of the kidneys as well.

Rubella causes blueberry muffin babies. They are not tasty or part of some twisted fairytale, but bleeding from small blood vessels under the skin, giving them bruise-like marks reminiscent of a buried blueberry in a muffin.

Stridor is a high pitched squeak typically heard upon inspiration and caused by an upper airway obstruction. This is in comparison to a wheeze which is usually heard on expiration and caused by a lower airway obstruction, as with asthma. The prototypical cause of stridor in young children is croup (aka laryngotracheobronchitis), a viral respiratory infection of the vocal cords and windpipe.

There was a moment today, which happens periodically, when a professor assumes we know some basic term that, due to our complete lack of experience, we don't. Today's was "coryza," which is the fancy medical term for having a runny nose and watery eyes.

And lastly:
TORCH is yet another really dumb mnemonic. This one is for the types of infections that can be transferred from mother to child during pregnancy or birth.
    Other (parvovirus B19, varicella, clamydia, ghonorea, etc)
    Herpes, HIV, Hepatitis

Tuesday, November 4, 2014

WILTIMS #208: Stupid, fat hobbit. You ruins it!

Quote of the day: "Death is not good." ~Pathology course director

TIL: Coney island is named for rabbits (the old dutch name was Conyne Eylandt and the english one was Conney Isle; both versions of Coney mean rabbit). The rabbits used to cause a significant number of cases of tularemia, a bacterial infection that's carried by rabbits, in the Brooklyn/NYC area.

Recurrent and recrudescent are very similar words used to describe infections. The former means an infection that has returned due to repeated exposure to the infectious agent; the latter is a breakout that originates from within the person due to the original infectious exposure. 

Monday, November 3, 2014

WILTIMS #207: A pox upon you!

Herpes is a word that has morphed many times in my mind. In early sex-ed classes, I associated it with the barrage of sexually transmitted infections that the teachers accost your senses with (hopefully just sight), like gonorrhea, chlamydia, and syphilis. Then in high school, as with so many "facts," I learned that it wasn't quite so simple: herpes is also the cause for cold sores. It was a great conversation piece for all those herpes conversations that came up...

But as I experienced more and more of biology and medicine, both in high school and undergrad, I heard the word herpes come up over and over with all manner of seemingly unrelated illnesses. I had kind of accepted that it must be some broad term that isn't used by the general public. Turns out, I wasn't far off!

TIL: Herpesviruses are a broad family of viruses that include many disease-causing bugs of which you may have heard. There are eight types of human herpesvirus (HHV):
  1. cold sores
  2. genital sores
  3. chicken pox/shingles
  4. Epstein Barr (causes mono and several lymphomas)
  5. cytomegalovirus (usually asymptomatic in the immunocompetent)
  6. roseola (aka "sixth disease," one of the principle rash-causing diseases in infants)
  7. also causes roseola
  8. Kaposi sarcoma (used to be super rare, until the rise of AIDS)

And don't think that it's that simple, either. Type 1 (cold sores) can be found on the genitals and type 2 (STD) can cause cold sores (this cross-contamination shouldn't be too surprising given some common sexual practices). Furthermore, given the opportunity, either of the above can cause systemic infections including viral meningitis.

A one-dermatome rash caused by shingles (HHV-3)
Zoster, as in the varicella-zoster virus that causes chickenpox and shingles, means belt. It is used to describe the shingles form of the infection because of the telltale belt-like rash often seen in symptomatic patients. Herpes often sits latently in nerves throughout the body. When the HHV-3 becomes reactivated it will cause a rash throughout the area innervated by that one nerve. This leads to some anatomically interesting rashes that only affect one dermatome (the area serviced by one spinal nerve segment).

Poxviruses are a broad classification of viruses that include smallpox (as well as cowpox, monkeypox, etc) and moluscum contagiosum. By the way, unlike cowpox and monkeypox which are carried by and contracted from those respective animals, chicken pox has no connection with chickens. In fact chickens are immune to chickenpox. It is thought that the name cropped up as a way of indicating how mild the disease is compared to the better known pox, smallpox.

It was weird talking about smallpox today, because the last known diagnosis of the disease was in 1977. And it's kinda sad that the only reason we learn about it is for in the event of a bioterrorist attack.

Friday, October 31, 2014

WILTIMS #206: Witches' warts for Halloween!

And so the lame-duck week has come to an end. When crazy tests are put on a Wednesday, I don't think anyone expects much to get done on Thursday and Friday. Very few people stuck around for lecture and the presentations were held to mostly introductory topics. We learned our first 3 of untold scores of virus categories today: papillomavirus, polyomavirus, and adenovirus.

HPV by electron microscopy
The only one of these you're likely to know is (human) papillomavirus, aka HPV. These viruses can cause warts (yes those warts too), a slimy infection of mucous membranes (yes those membranes too), and cervical cancer (there's only one cervix, but for the sake of completeness: yes that cervix too).

TIL: The way HPV can cause such diverse conditions is that each subtype of virus encodes a specific subset of genes from its tiny genome. Subtypes 16 and 18 cause cancer because they express genes for three oncoproteins. These use the same techniques as cancer to convince the infected cell to replicate unchecked. The virus doesn't actually care if the cell divides and/or becomes cancerous; it just needs the cell to replicate its own DNA so the virus can then use the cell's replicative machinery to reproduce itself.

WILTYIMS #205: Thank you, sir, may I have another?!

Yesterday was another marathon exam session (hence my silence earlier in the week (actually, my posts are almost always silent (wait! I found an exception!))). We had exams from 9 to 5 with an hour lunch spent cramming for the tests we hadn't yet taken. Livin' life to the fullest right here.

Anyways we did, in fact, have class today because reasonable recovery time is for losers, apparently. We started our final chunk of microbiology with lectures on fungi today to be followed by an introduction to viruses tomorrow (or mycology and virology, respectively). To be honest, I don't think my brain had fully reset yet before lecture today and I retained absolutely nothing from sitting in class. But for the sake of you, my determined reader, I dug back through the lecture slides* and found a thing:

TIL: Ringworm is a complete misnomer. Unlike roundworms, pinworms, and hookworms, which are all horribly gross macroscopic worms that can live, grow and breed inside people, ringworms are not actually worms. Ringworm is the colloquial term for a large group of cutaneous (skin) infections caused by fungi. Amusingly though, the colloquial term has its origin in the actual medical name for the disease.

The different types of ringworm are classified by the Latin word tinea, followed by the Latin term for the body part they infect. So athlete's foot, which is a type of ringworm is called tinea pedis, which literally means "foot worm" even though there is no worm involved.

* Dug all the way to slide number 3
 Seriously, wear shoes or larvae will puncture your bare feet, swim to your lungs, crawl out of your trachea, to be swallowed into your intestines and grow into worms that feed and grow while releasing eggs in your poo. Yay parasites!

Friday, October 24, 2014

WILTIMS #204: ✌♒ These aren't the symptoms you're looking for...

Today I spent far more time with my study group than in class and here is the result of 3½ hours of work:

Totally makes sense, right? Myeloid neoplasms still to come...

TIL: "B symptoms" are a weird term for symptoms used in lymphoma staging. They include intermittent fever, night sweats, and unintentional weight loss. If those are the 'B symptoms', what are the 'A symptoms'? you might reasonably ask. There aren't any! Or, more precisely, "A" indicates the lack of symptoms. So a stage IIA lymphoma is less severe than a stage IIB which presents with some or all of the symptoms listed above.

Say you want to check if a CT scanner malfunctioned during a scan or you're treating a nuclear power facility worker who was briefly exposed to a radioactive source. How could you tell if damage was done when outwardly these patients look and feel totally fine? Well, it turns out that the most sensitive cells to a massive full-body radiation exposure are leukocytes (T cells, B cells and natural killer cells of the immune system). So by doing a complete blood count (CBC) you can quickly see if these canaries in the proverbial coal mine have keeled over, indicating more serious systemic cell death to come.

WILTYIMS #203: Translocate THIS

T At some point IL and today IL more about: There are a whole slew of chromosomal translocations that cause leukemias and lymphomas. These dangerous mutations occur when one gene, usually involved with cell proliferation, is grafted into another locus that encodes for some highly expressed protein.

Think of it as though some cellular proteins are painstakingly made by hand while others are mass-produced on an assembly line. Then some cancerous businessman comes in and finds a way to slip the blueprints for the handmade protein into the assembly line. Suddenly the shoddily made copies of the rare protein flood the market using the machinery of a simpler (gene) product.

In real life the assembly line protein is some important part of the immune system, like a piece of the antibody molecule of which we need to be able to produce immense quantities to fight infections. Then a mutation swaps-in a normally highly regulated molecule that controls cell growth and division, like cyclin D. The growth protein is then made at levels reserved for antibodies causing cells to divide in the uncontrolled manner of cancer.

The image to the right (from Wikipedia, amazingly) is a nice graphic showing the locations of the chromosomal fragments that swap, as connected by the disease that the swap causes. Notice that a bunch of diseases are connected to chromosome 14; this is where the immunoglobulin heavy chain (IgH), a part of all antibodies, is normally encoded. A translocation between part of chromosome 8 and this region of chromosome 14, or put more succinctly t(8;14), causes Burkitt's lymphoma. t(11;14) causes mantle cell lymphoma and t(14;18) causes follicular lymphoma.

The t(9:22) translocation is particularly interesting. This is called the Philadelphia chromosome (after the city of its discovery) and it's associated with chronic myelogenous leukemia.  Here, the gene that's swapped in is not just expressed more but, due to some convenient splicing, actually made more potent. The gene product is a tyrosine kinase, an enzyme that phosphorylates other proteins, and because of this translocation it is constitutively turned on, having widespread and, it turns out, cancerous results.

Thursday, October 23, 2014

WILTIMS #202: Shivers and smiles

Today was not a productive day. Well, it wasn't a productive day toward the goal of passing my upcoming exams, but I did do couple things. I started by giving a presentation on preventing lung cancer to a class of middle schoolers through our school's Cancer Education Awareness Program. It's always fun to scare some silence into a rambunctious class by pulling out my cancer souvenirs.

Then my team played our last flag football game of the season. It was 50-something degrees with 20+ mph winds and somewhere between drizzle and teeming rain. Ever since high school and rainy water polo games (yes, east coast people, we always played outdoors), I've thought rain makes any game more epic. But even though this was a playoff game, this just felt fun. The team we played was from our year and we all knew each other. Everyone was cold, drenched and just wanted to put in our hour on the field and go warm up at home.

But home is not where I went. Tonight was our weekly volunteer evening at the juvenile detention center. So I dug out a towel from the trunk of my car*, changed into drier clothes and headed over to the facility to spend some time with a very different set of kids than the ones I had taught this morning. Though I love giving my little cancer spiel for CEAP, playing games with the kids at the detention facility is probably more fun and possibly more rewarding for everyone involved.

TIL: (and I am literally looking this up right now so that I have something to show for the day, knowledgewise) Elephantiasis is caused by the parasite Wuchereria bancrofti. These roundworms are introduced into the bloodstream by a mosquito bite and then travel to lymph nodes to mature, mate and reproduce. After repeated cycles of reproduction, the dead remains of older generations of worms block the lymphatic drainage resulting in edema (swelling) of the lower extremities and scrotum (on persons with scrotums).

Also learned elephantiasis is called elephantiasis not elephantitis. Just now.
♒☆ The more you know! ♒☆

*This is one frood who always knows where his towel is.

Wednesday, October 22, 2014

WILTYIMS #201: FCM and a comic

Today was a full day of FCM (Fundamentals of Clinical Medicine, the "how to be a doctor" class). We had a brief lecture on how to talk to difficult patients, for instance patients who you suspect of prescription drug abuse or who decide to pursue a treatment plan other than the one you recommend. The latter is often called "patient non-compliance" which has become a sort of dirty word due to the obviously negative connotation. The doctor and patient need to be a team and come to a joint decision on the best course of action for that individual based both on medical science and the personal or cultural considerations of the patient.

The rest of the morning we practiced these skills in small groups with standardized patients. Though the actors' stories are theoretically "standardized," it was interesting hearing from different groups about how uniquely each actor played their part. Some were defiant but willing to budge, others were argumentative and some sounded downright hostile. Our Step II clinical board exams after 3rd year will have similarly difficult patients, but thankfully the vast majority of real world patients will be much more willing to work with us to navigate treatment decisions.

Finally, the afternoon was taken up by our first preceptor session of the year. During each of our first two years we are assigned a local doctor to shadow and learn from for an afternoon every 3-4 weeks. This year I am learning in Mount Vernon, a city in Westchester County just over the county line from the Bronx. Last year I did pediatrics, so it's nice to mix it up and see adults this year.

This first visit was once again frustrating because we have yet to learn much of pathology, but it was already so much better that last year when we were truly useless. I enjoyed talking with patients and riddling through the doctors questions for me about topics I haven't covered in enough detail yet. Hopefully by the end of the year I will feel more comfortable before actually starting our clinical education in July.

TIL: Hypertension (high blood pressure) can come in several forms. One categorization is of whether the increase in pressure is seen in systole (heart contraction) or diastole (heart filling). The former is usually seen in older patients (>50yo) due to atherosclerosis (hardening) of the aorta from the accumulation of plaques. Each time the heart pumps blood out the aorta pushes back and these plaques make it less accommodating, thereby putting pressure on the heart to pump harder. Hypertension caused by other chronic conditions usually increases the diastolic pressure and these conditions are often seen at an earlier age.

Monday, October 20, 2014

WILTIMS #200: Writings, reminiscence, and zombie amoebae

Bicentennial post! My blog now has as many med school posts as the US had years of existence in the seventies! That's a terrible comparison but I'm going to run with it. Both started at dubiously defined times (US: Declaration of Independence vs ratification of the Constitution; WILTIMS: move-in week rather than day 1 of classes), both didn't align with the larger time division (US: 200yrs in 1976; WILTIMS: #200 in October), and both very nearly didn't make it this far (US: Civil War; WILTIMS: neuro... ugh neuro). And yet, here we are!

Amusingly, today was the release date of our school's student journal the Quill & Scope in which my remarks from the Convocation of Thanks were reprinted. That was one of my most meaningful moments of the past 200 school days and it was all thanks to this blog. Writing every day, even if it's only short paragraphs filled with sesquipedalian (needlessly multisyllabic (apparently there is no word for this that isn't self-descriptive)) scientific words, is the only reason I was able to write that piece (though clearly I haven't learned to control my use of parentheses (or irony)).

A second throwback milestone for the day was learning in pharmacology about the chemotherapy that I was taking just over two years ago. It was very surreal watching classmates take notes on the symptoms that I knew - and still remember - all too well. Nausea is three-pronged: pre-treatment, acute, and delayed. Hair-loss sucks. We were told that low blood cell counts can leave you immunocompromised or anemic, but they didn't mention the psychologic distress of waiting for permission from the lab tech to get the treatment you hate.

I am still so glad I wrote about chemo as I was going through it because, as we broach these topics as student clinicians, I can integrate my experiences with my medical education and that of my friends. Also, I have a head start on the material!

TIL: Naegleria fowleri is a single celled parasite found in warm freshwater that will eat your brain! These creatures get into your head when the unsuspecting swimmer gets water way up his or her nose. The amoeba then burrows up through the very thin cribriform plate of the skull and starts munching on the brain. The amoebae don't want or need to live off of a human host, but when life gives you brains, make brain-ade? Unfortunately for us, infections are almost always fatal.

Alkylating chemotherapy agents are derived from the chemicals in mustard gas from WWI. Well, it does kill cells.

Thursday, October 16, 2014

WILTIMS WILYIMS #199: Short week recap

As we again have Thursday and Friday off this week thanks to obscure Jewish holidays, I thought I'd spread out my three blog posts a bit and publish this one today. I, in no way, just didn't write anything yesterday due to being lazy and/or enjoying date night with the SO. Nope. Wasn't that at all...

Anyways, though this week was fewer in days, it was all the denser in interesting experiences.

Go Little Giant Cells!
First up was the annual first-year vs second-year powderpuff flag-football game. We became the first class to go 2-0 in school history (after being the only class to upset the second-years, last year). It's a good thing we don't generally have competitive teams for med school students because if a "friendly" competition between classes at the same school is this contentious, I'm pretty sure interschool games would turn bloody.

Earlier that day we had an unusual standardized patient (SP) interaction where rather than each of us dressing up in white coats and interviewing one of these actor-instructors individually, we met as a group and interviewed a SP en masse. They had each student ask one question and then the next person was supposed to proceed logically and continue the interview. That was weird. Props to the two SPs we had for staying in character despite the ludicrous situation of being interviewed simultaneously by 8 unqualified med students in neon pink football paraphernalia.

LEFT HEAD: In that case I shall have to kill you.
RIGHT HEAD: Oh, I don't think so.
MIDDLE HEAD: Well, what do I think?

The takeaway lesson from this for me was that asking all the appropriate questions in succession will do you no good if you don't listen and adapt to the patient. That's the skill that's hard to learn. Anyone can read a checklist and write down answers, but learning how to disarm and effectively communicate with a stubborn or defensive patient takes people skills and practice. This is almost impossible to do as an eight-headed med student monster.

Yesterday we had our last required microbiology lab session (though there is an optional lab manual for "How to make pale ale" for when we start studying fungi). We did several stains on tiny bacteria and could only see a haze of red or speckles of blue, neither of which we were supposed to see. The picture below was the most interesting thing we observed all day. What an interesting bacterial growth pattern, you might think. Actually, that growth is the inorganic crystals of the very appropriately named crystal violet dye that we use to perform a Gram-stain. It's an artifact of poor staining technique and it was absolutely fascinating compared to the reddish wisps that were all over the rest of the slide.

The Artifact (nothing to see here)
Lastly, today I got to be a patient again but still learned a thing or two. It was interesting going back to my oncologist for my 4 month check-up, now that we are learning about lymphomas in pathology. Since it's common knowledge amongst my classmates that I had Hodgkin's lymphoma a few years ago, I've had quite a few friends ask excitedly which subclass of the disease I had. Somewhat embarrassingly, I had no idea, so I was looking forward to my appointment today to ask my doc for the details on my long past diagnosis. Then I got a kind reminder that the stuff that we work so hard to learn these first two years is sometimes absolutely useless when it comes to the real world treatment of patients.

TIL YIL: Turns out that with one rare exception, the subtypes of Hodgkin's lymphoma are clinically irrelevant because the treatment, ("ABVD" chemo +/- radiation) is exactly the same regardless of cellular pathology. That doesn't mean I won't be memorizing those subtypes for my exams!

Wednesday, October 15, 2014

WILTIMS #198: Tardy as usual...

Apologies once again. I failed miserably at writing a post yesterday. And it was a fantastically eventful day too! But occasionally sleep wins out. I shall make it up to you today/tomorrow. 'Til then, here's a tidbit to tide you over:

A smudge cell surrounded by healthy RBCs
TIL: One test that is run to diagnose hematopathology disorders (anemias and blood/lymph cancers (leukemias and lymphomas)) is a peripheral blood smear. This one doesn't really need translating. Lab techs literally take blood from a peripheral blood sample and smear it onto a slide. They can then look at the composition of cells and their morphology to try to see if either the comparative amounts of different cells or the shapes of one particular cell type explains a patient's symptoms.

One such morphological indicator is the presence of "smudge cells." This actual scientific term is used to describe diseased B-cell lymphocytes (a kind of white blood cell) that are so fragile that when they are smeared across the slide their cell membrane shreds apart, leaving behind a highly stained blob of DNA from their nuclei. The presence of smudge cells is diagnostic for chronic lymphocytic leukemia (CLL).