A few things are new: first, we are getting a new bed. The current bed has gotten so bad that I spent last night on the floor in a sleeping bag. I would liken it to sleeping in a ladle. Your spine is bent laterally along its longitudinal axis, and also the anterior/posterior axis. If you lie on your back, your sacrum slowly drifts down so you have a nice anteriorly rotated pelvis. This, combined with my year old running shoes means that I live with constant back pain. Having slept a grand total of 5 (ish) hours Sunday evening, I said enough's enough, and moved to the floor where I slept soundly all last night.
To rectify this crappiness, Mindy and I bought a new mattress today. Hopefully this one will last through residency. I have been sleeping like the happy fellow above, and I'm tired of it.
On a more medical note, path and pharm are a lethal combination. There's just so much testable material! We're covering ANS (autonomic nervous system) agents right now, which will be useful if I go into anesthesia. This week we covered muscarinic agonists, antagonists, and acetylcholinesterase inhibitors. We're also covering the α and β agonists, antagonists, and re-uptake inhibitors. Perhaps a brief exposition will clarify and edify:
The ANS is divided into two main branches that govern all of our subconcious bodily functions, including sweating, heart rate, vascular tone, digestive secretions, eye focusing, dilating and contraction, and to some extent the reproductive organs, as well as many others. These two branches are respectively, the sympathetic, and the parasympathetic. These are mainly anatomical terms, referring primarily to the site of origin for the respective nerves. The parasympathetic nervous system is mostly in charge of the "rest and digest" functions, e.g. secreting gastric juices, slowing heart rate, contracting the pupil, constricting bronchiolar smooth muscle (sound familiar all you asthmatics?). The sympathetic nervous system, on the other hand, is in charge of the "fight or flight" response that you associate with fright or stress. This means it increases heart rate, dilates the pupil, dilates the bronchioles, constricts the peripheral vasculature to raise blood pressure, reduces gastric motility, reduces gastric secretions, etc. Still with me? Good.
The two systems also differ in the neurotransmitter secreted at the synapse or junction. The sympathetics release norepinephrine (mostly) and the parasympathetics release acetylcholine. What about adrenaline (which is epinephrine in the US)? It is mainly released by sympathetic stimulation of the adrenal medulla, a wee gland perched on your kidney. These chemicals elicit the effects described previously.
Once the transmitter has been released, it acts on a receptor, which is a molecule that protrudes from the cell membrane. When the transmitter binds the receptor, the receptor modifies other molecules inside the cell and elicits the appropriate response (e.g. secretion or contraction of muscle). Sympathetic drugs stimulate α and β receptors, while parasympathetic drugs stimulate muscarinic and nicotinic receptors (it's a little more complex, but this will suffice).
The real fun begins when you consider the multiple ways to antagonize or potentiate the effects of endogenous neurotransmitters. You can irreversibly inhibit a receptor which means you chemically modify it so it no longer recognizes acetylcholine or norepi. You can competitively inhibit it which means that Ach (acetylcholine) or NE (norepi) have to fight for a spot to bind with the drug. These facts are pretty straight forward though, in comparison with the real meat of the course
When it gets really interesting is when you start considering multiple drugs. What happens to heart rate and blood pressure if you agonize muscarinic receptors, while simultaneously blocking alpha receptors? What's going to happen in the GI if you do this? is the patient going to crap themselves because you overstimulated the parasympathetics?
Ahh fun.
Answer: (as I can figure it out): muscaranic agonization: slow HR due to Ach on M receptor. Increased GI motility. Alpha block prevents baroreflex from stimulating α1 vasoconstriction, so BP stays lower than normal. Also decreases sympathetic tone in GI, allowing paras to dominate. Not sure when you would want the patient hypotensive and bradycardic, but there you have it. Wow. look ma! I larned something!
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