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USMLE
BRS Renal Phys
| Question | Answer |
|---|---|
| what happens to osmolarity of ECF if person is infused with isotonic saline solution? | stays the same |
| what happens to osmolarity of ECF if person has loss of isotonic fluid? (example) | diarrhea stays the same |
| what happens to osmolarity of ECF if person has high NaCl intake? | incresaes |
| what happens to ECF osmolarity if person is sweating in the desert? | increases (sweat is hyposmotic... more water than salt is lost) |
| what happens to ECF osmolarity in SIADH? | decreases |
| what happens to ECF osmolarity in adrenocortical insufficiency (NaCl loss)? | decreases (lack of aldosterone), kidneys excrete more NaCl than water |
| what happens to plasma protein [] and hematocrit in infusion of isotonic NaCl? | decreases (overall increase in fluid) |
| what happens to plasma protein [] and hct in diarrhea? | increases (from volume contraction) |
| what happens to plasma protein [] and hct in high NaCl consumption? | decrease (ICF shrinks to accommodate the increased osmolarity in ECF, this dilutes out the plasma protein) |
| what happens to plasma protein [] and hct when swaeting in desert? | protein increases hct stays same b/c fluid leaves rbcs to offset fluid loss |
| what happens to plasma protein [ ] and hct in siadh | decreases stays same |
| what happens to plasma protein [] and hct in adrenal insuff? | plasma protein increases hct increases (from decreased ECF volume and rbc swelling from water entry) |
| how does vasoconstriction of renal arterioles affect RBF? how is this achieved? | decreases RBF SNS |
| how does AII affect renal arterioles | preferentially constricts efferent arterioles unless it is a situation where there is a massive hemorrhage. then, so much AII is released that it constricts both efferent and afferent arterioles |
| how does ACE affect renal arterioles | preferentially constricts efferent arterioles |
| what effects does AII have on GFR? | increases it |
| what effect do ACE-I have on GFR | decreases it by dilating efferent arterioles |
| what does afferent arteriole constriction do to RPF? | decreases |
| what does efferent artiorole constriction do to GFR? | increases (by increasing Pgc) |
| what does increased plasma protein do to GFR? | decreases it by increasing osmotic pressure in GC |
| what does decreased plasma protein do to GFR? | increases it by decreasing osmotic pressure in GC |
| what does increased plasma protein do to RBF? | nothing |
| what does decreased plasma protein [] do to RBF? | nothing |
| what does efferent arteriole constriction do to RBF? | decreases it |
| what happens to the filtration fraction in afferent arteriole constriction? | (GFR/RBF) GFR decreases, RBF decreases FF no change |
| what happens to FF in efferent arteriole constriction | GFR/RBF GFR increases, RBF decreases FF increases |
| what happens to FF in increased plasma protein concentraton | GFR/RBF GFR decreases, RBF no change FF decreases |
| what happens to FF in decreased plasma protein [] | GFR/RBF GFR increases, RBF no change FF increases |
| what happens to FF when ureter is constricted? | GFR/RBF GFR decreases, RBF no change FF decreases |
| what things are reabsorbed in the PCT? | glucose AA's most of the HCO3 |
| describe how HCO3 is handled in PCT | HCO3 is in the lumen and combines with H that is secreted into the lumen --> H2CO3 Carbonic anhydrase --> H20 + CO2 which re-enters the tubule and reforms as H2CO3 with CA the H is then secreted into the lumen and the HCO3 is reabsorbed |
| what happens in the TAL? | NKCC pump (blocked by furosemide): aids in reabsorbing Na, Cl, K K flows back out into lumen and the gradient drives the absorption of Mg and Ca also aids in the running of the NKCC pump |
| is the TAL permeable to water | no |
| what is the thin descending loop permeable to? | water, but not Na |
| what is happens in the early distal convaluted tubule | actively reabsorbs Na, Cl Ca absorption is controlled by PTH receptors found here |
| what happens in the collecting tubules | Na is reabsorbed in exchange for K/H (regulated by ALDOSTERONE!!!) reabsorption of water regulated by ADH (aquaporins) |
| which part of the nephron is impermeable to water? | TAL (and collecting tubule if there is no ADH) |
| where in kidney is EPO released from | endo cells of peritubular capillaries |
| what enzyme converts 25-OH vitamin D to its active form? | 1-alpha hydroxylase |
| what do JG cells do? | secrete renin in response to low renal blood pressure |
| what does the macula densa do? | senses the amt of Na |
| where is the macula densa | part of the DCT |
| what do PGs do to the kidney | vasodilate the afferent arterioles (that's why NSAIDS can --> ARF by inhibiting PG) |
| what effect does aldosterone have on H | more H is secreted |
| where does aldosterone work in kidney? | DCT |
| where does PTH work? | PCT to decrease PO4 reabsorption DCT to increase Ca reabsorption stimulates 1-alpha hydroxylase in PCT |
| where is ACE released from? | lung |
Created by:
Asclepius
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