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drzed
(B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases.
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kevin
I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up
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lolmedlol
i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well.
https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction
and amboss shock description
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trichotillomaniac
^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA.
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trichotillomaniac
Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible
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submitted by โtaediggity(44)
So this patient is essentially in hypovolemic shock because he's hemorrhaging blood from the aorta.
A) You'd have increased ADH to conserve volume B) You'd have increased BUN:Cr ratio b/c due to a decrease in blood flow C) Increased TPR naturally due to less pressure on barorecptors D) Decreased Capillary hydrostatic pressure b/c they have decreased volume E) Decreased Carotid sinus firing rate b/c less pressure F) The Answer: RAAS is activated -