-
CycleTrack and SDN are teaming up to make medical school admissions more transparent and accessible! Read the announcement to learn how we’re supporting the future of CycleTrack’s free application-tracking tools .
Step I why...?
Started by goodies
Get help with your application
Use all the free resources available to you from SDN: articles, guides, expert advising, forums discussions, and school research.
God's will.
from what Goljan has to say, the uterus undergoes both hypertrophy and hyperplasia so makes sense if during menses that both apoptosis and atrophy are occurring. Though on a test if given the choice between the two, i would go with atrophy as that's usually the classification its placed under.
[SIZE=-1]prolonged hypercalcemia tends to cause high gastrin levels which increases acid secretion.
[/SIZE]
why would high ca increase gastrin levels?
the only thing I could think of was that more serum calcium means Ca entering voltage-gated Ca channels -> more Ach release -> more m3 stimulation of G-cells -> more gastrin release.
the problem is that if i'm not mistaken, hypercalcemia also systemically suppresses neuronal activity (that's why you get neurological sx right). Anyone help?
I think this will help.
out of curiosity, what book is that? I looked in a bunch of different books and nowhere did i see gastrin as a stimulant for calcitonin secretion or Ca as a stimulant for gastrin secretion. Are both secondary effects?
Found it thru google. Same pic was in my notes from last year, I remember my prof saying something about how "that's why people get addicted to rolaids. they put calcium in them to keep you using them" that's the way I've always remembered it. 😉 So Cute's right about the MEN sd, that will also give you an elevated gastrin even in the absence of a gastrinoma.
