| 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 |
Ch.18 LTI-MA 509
