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Renal II > Diuretics - Kruse > Flashcards

Diuretics - Kruse Flashcards

(65 cards)

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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
MOA: loop diuretics
- inhibition of luminal Na/K/2Cl cotransporter in TAL - induces synthesis of renal PGs - causes increase in RBF - some weakly inhibit carbonic anhydrase
26
AE: loop diuretics
- hyponatremia - hepatic encephalopathy in liver dz pts - otoxoicity - hypokalemic metabolic acidosis - gout - hypomagnesemia - allergic reactions
27
CI: loop diuretics
- sulfonamide sensitivity - doesn't work in hepatic cirrhosis, renal failure, heart failure - avoid in postmenopausal women
28
DI:loop diuretics
- aminoglycosides: increased ototoxicity - lithium - digoxin
29
CI: loop diuretics
- pulmonary edema - HTN - HF - ARF - anion OD - hypercalcemia - mild hyperkalemia
30
Carbonic anhydrase inhibitors
- acetazolomide - brinzolomide - dorzolomide - methazolamide
31
ROA: thiazide diuretics
oral - give in large doses d/t lack of lipid solubility
32
longest acting thiazide and it's T1/2
cholothalidone, 47 h
33
MOA: thiazide diuretics
- 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
AE: thiazide diuretics
- hypokalemic metabolic acidosis - impaired carb tolerance - hyperlipidemia: increase total serum cholesterol and LDL - hyponatremia - hypercalcemia - weakness, fatiugueability, parethesias, allergic reactions, impotence
35
the only thiazide diuretic that doesn't induce hyperlipidemia
indapamide
36
CI: thiazide diuretics
- caution in DM pts | - excessive use is dangerous is hepatic cirrhosis, boarderline renal failure pts, or HF pts
37
DI: thiazide diuretics
- reduced efficacy of: anticoags, anti-gout, insulin | - efficacy is reduced by: NSAIDs and COX-2 inhibitors
38
clinical uses of thiazide diuretics
- HTN & HF - nephrolitiasis d/t hypercalciuria - nephrogenic DI
39
mechanism of HCTZ in DI tx
- 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
DOA: MR K sparing diuretics
several days are needed before benefits are observed
41
MR K sparing diuretic with greater selectivity
eplerenone
42
Na channel inhibitor K sparing diuretic with shorter T1/2
triamterene
43
MOA: MR K sparing diuretics
- 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
Only diuretics that don't require access to the tubular lumen to induce diuresis
MR agonist K sparing diuretics - spirinolactone, eplerenone
45
MOA: Na channel blocking K sparing diuretics
- block epi ENaCs in the apical membrane of the CD | - reduce Na reabs and therefore K secretion
46
AE: all K sparing diuretics
- hyperkalemia | - metabolic acidosis
47
AE: MR K sparing diuretics
- gynecomasita - impotence - BHP
48
AE: triamterene
-kidney stones
49
DI: K sparing diuretics
- beta blockers and NSAIDs: reduce renin, increase risk of renal disease - ACEi and ARBs: decrease AngII activity
50
DI: triameterene
indomethacin: causes acute renal failure
51
CI: K sparing diuretics
- chronic renal insuff: severe hyperkalemia - concomitant use of K sparing drugs - liver dz - CYP34A inhibitors (increases elperenone blood level)
52
clinical uses for K sparing diuretics
- mineralcorticoid xs - hyperaldosteronism (primary or secondary) - HF - blunt K secretion in use of thiazide diuretics
53
MOA: osmotic agents
- inhibition of tubular reabsorption and electrolytes | - increased urine output
54
DOA: osmotic agents
excreted in glom filtrate w/in 30-60 min
55
AE: osmotic agents
- pre diuresis ECF vol expansion and hyponatremia | - dehydraiton, hyperkalemia, hypernatremmia
56
CI: osmotic agents
- increase/maintain urine V | - reduction of ICP and intraoccular P
57
effect of ADH agonist
increase H2O reabs
58
Tx: ADH agonist
- DI - polyuria, polydipsia - hypernatriemia - nocturnal enuresis
59
Tx: ADH antagonist
- HF | - SIADH
60
T1/2: conivaptan
5-10 h
61
MOA: conivaptan
antagonist of ADH receptors in the CD
62
Loop + thiazide
- 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
K sparing diuretics + loop or thiazide
- 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
edematous stated tx w/ diuretics
- HF - kidney disease - hepatic cirrhosis
65
nonedematous stated tx w/ diuretics
- HTN - nephrolithaisis - hyperCa - DI

Renal II (7 decks)

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