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

Last WILTIMS post before winter break! Woohoo!
-or-
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.