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PMCOL 343 > Renal 2 > Flashcards

Renal 2 Flashcards

1
Q

what mainly happens in descending limb of henle

A

water reabsorption

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2
Q

can water reabsorb in the ascending limb of henle

A

no

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3
Q

what is the main transporter in the thick ascending limb

A

NKCC2

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4
Q

what is special about K+ in ascending limb and what does it cause

A

K excreted into lumen which makes it ++++ so then Mg++ and Ca++ can be reabsorbed

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5
Q

how does K+ enter the blood in the loop of henle

A

alongside Cl

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6
Q

what do loop diuretics attack and where

A

NKCC2 in the thick ascending loop of henle

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7
Q

what are theraputic uses for loop diuretics

A 
hypercalcemia 
hyperkalemia
pulmonary edema
hypertension
heart failure
renal failure
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8
Q

adversive effects of loop diuretics

A

hypokalemia
hypomagnesia
metabolic alkalosis

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9
Q

how can loop diuretics cause metabolic alkalosis

A

increase in Na+ delivery to collecting duct causes increased urinary excretion of K and H

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10
Q

what are main transporters in distal convoluted tubule

A

NCC and apical calcium channel

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11
Q

what channel does PTH stimulate and where

A

apical Ca channel in the distal convoluted tubule

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12
Q

how does Ca enter the blood in the distal convoluted tubule

A

Na/Ca antiport

Ca/H ATP antiport

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13
Q

what do thiazides target and where in nephron

A

NCC transporter in distal tubule

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14
Q

what is NCC transporter and where is it

A

Na Cl co transpor in the distal tubule

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15
Q

what is the NKCC2 transporter and where is it

A

Na K 2Cl cotransporter in the loop of henle

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16
Q

where is the TRPV5 transporter (ca apical)

A

distal tubule

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17
Q

what does thiazides do to Na and Cl reabsorption

A

reduce

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18
Q

what does thiazides do to Ca reabsorption

A

increase (increases Na Ca basolateral exchange cause Na is reduced)

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19
Q

what are uses of thiazides

A

hypertension
edema
kidney stones
heart failure

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20
Q

what are adverse effects of thiazides

A

hypokalemia
hyponatremia
Metabolic alkalosis

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21
Q

where in the nephron is most important for K excretion

A

collecting tubule

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22
Q

where is the ENaC pump

A

collecting tubule

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23
Q

what does the ENaC pump exchange

A

just brings Na into principal cells in collecting tubules

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24
Q

what receptor is in principal cells

A

aldosterone

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25
Q

what does aldosterone do in principal cells

A

increase ENaC

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26
Q

what part of nephron has aldosterone receptors

A

principal cells of collecting tubules

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27
Q

what part of nephron has PTH receptors

A

distal convoluted tubule

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28
Q

what does Na+ exit from lumen do for the principal cells

A

drives negative lumen which increases K excretion and Cl-reabsorption into interstitium

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29
Q

what happens with volume depletion (aka what does this cause/or effect)

A

aldosterone secretion, which then increases K+ excretion

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30
Q

what 2 pumps are in A cells in collecting tubules

A

H-ATP sending H into lumen

HCO3-/Cl- antiport sending HCO3- into blood

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31
Q

what 2 pumps are in B cells in collecting tubules

A

H-ATP sending H into blood

HCO3-/Cl- antiport sending HCO3- into lumen

32
Q

which cells of the collecting tubule react with acidemia and what do they do

A

A dominate to secrete excess H+

33
Q

which cells of the collecting tubule react with acidemia and what do alkalemia do

A

dominates to secrete excess bicarbonate

34
Q

what does aldosterone do to apical proton pump in type A cells

A

increases the # of them

35
Q

what are the 2 potassium sparing diuretics

A

ENaC inhibitors and Aldosterone antagonists

36
Q

how can antagonists of aldosterone cause metabolic acidosis

A

they reduce the amount of A cell type H+ pumps (less H+ pumped out into lumen)

37
Q

what is the most efficacious diuretic agent

A

loop diuretics

38
Q

what do loop diuretics do to na and cl reabsorption

A

reduce

39
Q

what do loop diuretics do to ca and mg reabsorption

A

reduce

40
Q

what types of diuretics cause vasocilation

A

loop diuretics and thiazides

41
Q

what do thiazides do to na and cl reabsorption

A

reduce

42
Q

what do thiazides do to ca reabsorption

A

increase

43
Q

what receptor does aldosterone activate /potentialte

A

ENaC

44
Q

what does increased Na into collecting tubules do to K

A

increases K excretion

45
Q

what does volume depletion do to K and why

A

increases K excretion because it increases aldosterone secretion (which increases ENaC)

46
Q

what does aldosterone do to H+ ATP pump

A

make more of them on apical side

47
Q

how do ENaC inhibitors reduce K+ excretion

A

because less Na+ exit from lumen makes the lumen more positive so K doesnt enter

48
Q

what are some theraputic uses for potassium sparing diuretics (both types)

A

hypertension
hyperaldosteronism
heart failure
-really just whenever K+ loss is a concern

49
Q

what are the 2 types of potassium sparing diuretics

A

ENaC inhibitors and aldosterone competitive antagonists

50
Q

what are adverse effects of potassium sparing diuretics

A

hyperkalemia

51
Q

where are aquaporin 2

A

apical membrane of collecting tubules

52
Q

where are aquaporin 3 and 4

A

basolateral membrane of collecting tubules

53
Q

where does ADH act on

A

V2 receptors on basolateral membrane

54
Q

what is another name for ADH

A

vasopressin

55
Q

what is another name for vasopressin

A

ADH

56
Q

what does V2 activation cause

A

increased cAMP then increase AQP2 in apical membrane

57
Q

what happens with increased AQP2 in apical membrane

A

promotes water reabsorption

58
Q

what does V2 antagonist do to water and Na

A

reduces water reabsorption, increases plasma Na concentration (i think cause less water just makes na more concentrated)

59
Q

when do you use V2 antagonists therapeutically

A

syndrome of innappropriate ADH secretion

hyponatremia

60
Q

adverse effects of V2 antagonist

A

hypernatremia

hypotension

61
Q

what do carbonic anhydrase inhibitors do to ph of body

A

decrease

62
Q

what do loop agents do to ph of body

A

increase

63
Q

what do thiazides do to ph of body

A

increase

64
Q

what do K+ sparing agents do to ph of body

A

decrease

65
Q

relationship between blood and urine pH

A

opposite (one high other low)

66
Q

which diuretics increase NaCl in urine the most

A

loop agents and thiazides

67
Q

which agents increase K+ in urine the most

A

loop agents and thiazides (but not a lot of them do it a lot)

68
Q

which agents increase H3CO- in the urine the most

A

carbonic anhydrase inhibitors

69
Q

which agents decrease K+ in blood the most

A

K sparing agents

70
Q

what can be a bad side effect of heart failure

A

besides death, pulmonary edema

71
Q

what is the best treatment for kidney stones and why

A

thiazide because it decreases Ca in urine

72
Q

what are used for patients with mild renal insufficiency or heart failure

A

loop diuretics

73
Q

what do diuretics do to ACE inhibitors

A

enhance

74
Q

what are good drugs used to treat hypercalcemia

A

loop diuretics (reduce ca reabsorption) (less K+ making lumen ++++ so Ca Mg dont reabsorb)

75
Q

why is ca and mg reabsoprtion inhibited by loop diuretics

A

reduce luminal positive potential (inhibit NKCC2) so less ca and mg reabsorption

PMCOL 343 (31 decks)

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