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Renal II > Diuretics - Kruse > Flashcards

Diuretics - Kruse Flashcards

1
Q

ending of loop diuretics

A

-mide

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2
Q

ending of thiazide diuretics

A

-thiazide

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3
Q

K-sparing diuretics - mineralcorticoid antagonists

A
  • eplernone

- spirinolactone

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4
Q

K sparing diuretics - Na renal sodium channel inhibitors

A
  • amiloride

- triameterene

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5
Q

osmotic diuretics

A
  • mannitol

- isosorbide

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6
Q

ADH antagonists

A

conivaptan

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7
Q

what is reabsorbed in the proximal tubule?

A

PCT: NaHCO3, NaCl, K, H2O, glucose, AA, other organic solutes

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8
Q

what is reabsorbed from the tDL?

A

H2O

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9
Q

what is the TAL impermeable to?

A

H2O

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10
Q

what is the DCT relatively impermeable to?

A

H2O

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11
Q

What regulates Ca2+ reabsorption in the DCT?

A

PTH

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12
Q

What is the NCC NaCl transporter in the DCT sensitive to?

A

thiazide diuretics

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13
Q

The CD is the most important site of what?

A

K secretion

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14
Q

Action of aldosterone at the CD

A

increases ENaC and basolateral Na/K ATPase ( = Na reabs, K secretion)

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15
Q

ADH action in the CD

A

controls expression of AQP2 thereby controling the CD’s H2O permeability (w/out ADH the CD isn’t permeable to H2O)

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16
Q

site of carbonic anhydrase excretion

A

proximal tubule

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17
Q

MOA: carbonic anhydrase inhibitor

A

inhibition of membrane-bound and cytoplasmic forms of carbonic anhdrase = near complete abolition of bicarb reabs in proximal tubule

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18
Q

pH effects of carbonic anhydrase inhibitors

A

increase urine pH, decrease body pH

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19
Q

DOA: carbonic anhydrase inhibitors

A

effect wears off in a few days d/t Na+ reabsorption

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20
Q

AE: carbonic anhydrase inhibitors

A
  • metabolic acidosis
  • renal stones
  • hypokalemia
  • drowsiness and parathesias in large doses
  • hypersensitivity rxns (rare)
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21
Q

CI: carbonic anhydrase inhibitors

A
  • cirrhosis
  • hyperchloremic acidosis
  • severe COPD
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22
Q

clinical uses of carbonic anhydrase inhibitors

A
  • v rare as diuretic
  • used topically for glaucoma to decreaes intraoccular P
  • adjuvant in epilepsy
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23
Q

correlation of loop diuretics’ T1/2

A

kidney function - their elimination is indicative of secretion at proximal tubule

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24
Q

coadmin of loop diruretics with weak acids

A

reduction of diuretic secretion

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25
Q

MOA: loop diuretics

A
  • inhibition of luminal Na/K/2Cl cotransporter in TAL
  • induces synthesis of renal PGs
  • causes increase in RBF
  • some weakly inhibit carbonic anhydrase
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26
Q

AE: loop diuretics

A
  • hyponatremia
  • hepatic encephalopathy in liver dz pts
  • otoxoicity
  • hypokalemic metabolic acidosis
  • gout
  • hypomagnesemia
  • allergic reactions
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27
Q

CI: loop diuretics

A
  • sulfonamide sensitivity
  • doesn’t work in hepatic cirrhosis, renal failure, heart failure
  • avoid in postmenopausal women
28
Q

DI:loop diuretics

A
  • aminoglycosides: increased ototoxicity
  • lithium
  • digoxin
29
Q

CI: loop diuretics

A
  • pulmonary edema
  • HTN
  • HF
  • ARF
  • anion OD
  • hypercalcemia
  • mild hyperkalemia
30
Q

Carbonic anhydrase inhibitors

A
  • acetazolomide
  • brinzolomide
  • dorzolomide
  • methazolamide
31
Q

ROA: thiazide diuretics

A

oral - give in large doses d/t lack of lipid solubility

32
Q

longest acting thiazide and it’s T1/2

A

cholothalidone, 47 h

33
Q

MOA: thiazide diuretics

A
  • inhibits the Na/Cl cotransporter to stop luminal reabs of NaCl into DCT cells
  • enhances Ca reabs in PCT
  • some are weak carbonic anhydrase inbhibitors
34
Q

AE: thiazide diuretics

A
  • hypokalemic metabolic acidosis
  • impaired carb tolerance
  • hyperlipidemia: increase total serum cholesterol and LDL
  • hyponatremia
  • hypercalcemia
  • weakness, fatiugueability, parethesias, allergic reactions, impotence
35
Q

the only thiazide diuretic that doesn’t induce hyperlipidemia

A

indapamide

36
Q

CI: thiazide diuretics

A
  • caution in DM pts

- excessive use is dangerous is hepatic cirrhosis, boarderline renal failure pts, or HF pts

37
Q

DI: thiazide diuretics

A
  • reduced efficacy of: anticoags, anti-gout, insulin

- efficacy is reduced by: NSAIDs and COX-2 inhibitors

38
Q

clinical uses of thiazide diuretics

A
  • HTN & HF
  • nephrolitiasis d/t hypercalciuria
  • nephrogenic DI
39
Q

mechanism of HCTZ in DI tx

A
  • inhibits Na/Cl xporter in DCT
  • increases diuresis, decreases ECF volume
  • decreased ECF = decreased GFR
  • decreased GFR = increased Na + H2O reabs in PT
  • less H2O and Na+ to CD = decreased urine output
40
Q

DOA: MR K sparing diuretics

A

several days are needed before benefits are observed

41
Q

MR K sparing diuretic with greater selectivity

A

eplerenone

42
Q

Na channel inhibitor K sparing diuretic with shorter T1/2

A

triamterene

43
Q

MOA: MR K sparing diuretics

A
  • competitive inhibitors of MR
  • MRs regulate expression of ENaC and Na/K ATPase expression in the late DT and CD
  • agonists reduce Na reabs and K secretion
44
Q

Only diuretics that don’t require access to the tubular lumen to induce diuresis

A

MR agonist K sparing diuretics - spirinolactone, eplerenone

45
Q

MOA: Na channel blocking K sparing diuretics

A
  • block epi ENaCs in the apical membrane of the CD

- reduce Na reabs and therefore K secretion

46
Q

AE: all K sparing diuretics

A
  • hyperkalemia

- metabolic acidosis

47
Q

AE: MR K sparing diuretics

A
  • gynecomasita
  • impotence
  • BHP
48
Q

AE: triamterene

A

-kidney stones

49
Q

DI: K sparing diuretics

A
  • beta blockers and NSAIDs: reduce renin, increase risk of renal disease
  • ACEi and ARBs: decrease AngII activity
50
Q

DI: triameterene

A

indomethacin: causes acute renal failure

51
Q

CI: K sparing diuretics

A
  • chronic renal insuff: severe hyperkalemia
  • concomitant use of K sparing drugs
  • liver dz
  • CYP34A inhibitors (increases elperenone blood level)
52
Q

clinical uses for K sparing diuretics

A
  • mineralcorticoid xs
  • hyperaldosteronism (primary or secondary)
  • HF
  • blunt K secretion in use of thiazide diuretics
53
Q

MOA: osmotic agents

A
  • inhibition of tubular reabsorption and electrolytes

- increased urine output

54
Q

DOA: osmotic agents

A

excreted in glom filtrate w/in 30-60 min

55
Q

AE: osmotic agents

A
  • pre diuresis ECF vol expansion and hyponatremia

- dehydraiton, hyperkalemia, hypernatremmia

56
Q

CI: osmotic agents

A
  • increase/maintain urine V

- reduction of ICP and intraoccular P

57
Q

effect of ADH agonist

A

increase H2O reabs

58
Q

Tx: ADH agonist

A
  • DI
  • polyuria, polydipsia
  • hypernatriemia
  • nocturnal enuresis
59
Q

Tx: ADH antagonist

A
  • HF

- SIADH

60
Q

T1/2: conivaptan

A

5-10 h

61
Q

MOA: conivaptan

A

antagonist of ADH receptors in the CD

62
Q

Loop + thiazide

A
  • blocks Na+ reabs in all three segments (PCT, ascending loop, and DCT) when individual agents are enough alone
  • not used on out-pt basis
63
Q

K sparing diuretics + loop or thiazide

A
  • hypokalemia caused by loop or thiazide can be manages with K sparing diuretics when diet management isn’t enough
  • avoid in renal insuff pt and pts on angiotensin antagonists
64
Q

edematous stated tx w/ diuretics

A
  • HF
  • kidney disease
  • hepatic cirrhosis
65
Q

nonedematous stated tx w/ diuretics

A
  • HTN
  • nephrolithaisis
  • hyperCa
  • DI

Renal II (7 decks)

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