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!

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!

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.

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.

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).

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.

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.

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.

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.

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

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.

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.
    Toxoplasma
    Other (parvovirus B19, varicella, clamydia, ghonorea, etc)
    Rubella
    CMV
    Herpes, HIV, Hepatitis

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. 

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.