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renal II > Diuretics > Flashcards

Diuretics Flashcards

1
Q

CA inhibitors

A

Acetazolamide
Brinzolamide (topical opthalmic)
Dorxolamide (topical opthalmic)
Methazolamide

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2
Q

Loop diuretics

A

Ethacrynic acid
Furosemide (Lasiz)
Bumetanide
Torsemide

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3
Q

Thiazide diuretics

A 
Hydocholorthiazide
-thiazide
chlorothalidone
indapamide
metolazone
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4
Q

K sparring

mineralcorticoid (aldosterone) antagonists

A

spironolactone (adactone)

eplerenone

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5
Q

K sparring

inhibitors of renal NaCh

A

Amiloride

triamterene

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6
Q

osmotic diuretics

A

mannitol

isoorbide

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7
Q

hormone antagonists

A

conivaptan

tolvaptan

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8
Q

PCT fnx

A

resorption of
65% Na/K/Ca/Mg
85% NaHCO3
100% glucose, aa

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9
Q

PCT drugs and their targets

A

CA inhibitors

CA

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10
Q

DCT fnx

A

secretion and reabsoprtion of organic acids, bases, including uric acid and most diuretics

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11
Q

DCT drug targets

A

none

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12
Q

PCT transporters

A

Na/H exchanger (NHE3)

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13
Q

DCT transporters

A

acid and base transporters

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14
Q

tDL fnx

A

passive reabsorption of water

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15
Q

tDL transporters

A

aquaporins

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16
Q

tDL drugs/targets

A

none

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17
Q

TAL fnx

A

active reabsorption of
15-25% Na/K/Cl
secondary reabsoption of Ca and Mg

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18
Q

TAL transporters

A

Na/K/Cl cotransporter (NKCC2)

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19
Q

TAL drugs and their targets

A

Loop diuretics

Na/K/Cl cotransporter

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20
Q

DCT fnx

A

active reabsorption of
4-8% Na, Cl
Ca under PTH control

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21
Q

DCT transporters

A

Na/Cl cotransporter (NCC)

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22
Q

DCT drugs and their targets

A

Thiazides

NCC

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23
Q

CCT fnx

A

Na resorption coupled to K and H excretion

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24
Q

CCT transporters

A

ENaC
KCh
H transporters
aquaporins

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25
Q

CCT drugs

A

K sparring diuretics

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26
Q

MCT fnx

A

water reabsorption under vassopressin control

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27
Q

MCT transporters

A

aquaporins

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28
Q

MCT drugs

A

vassopressin antagonists

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29
Q

CA inhibitor prototype

A

Acetazolamide

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30
Q

Acetazolamide pharmacokinetics

A

well absorbed orally
excretion of drug is by secretion thru PCT (dosing must be adjusted for renal failure)
excreted druge is unchanged

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31
Q

Acetazolamide MOA

A

inhibit membrane bound and cytoplasmic CA -> abolition of NaHCO3 reabsorption in PCT -> decreased H in cells -> decreased NHE3 -> increased Na and HCO3 in lumen -> diuresis

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32
Q

Acetazolamide and pH

A

urine pH increased and body pH decreased

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33
Q

Acetazolamide and tolerance

A

w/in a few days become tollerant

34
Q

Acetazolamide toxicity

A

metabolic acidosis and bicarbonaturia
renal stones due to increased Na in CCT which increased K secretion
drowsiness and paresthesias
rare hypersensitivity reactions

35
Q

Acetazolamide contraindications

A

cirrhosis -> hyperammonia and hepatic encephalopathy

hypercholremic acidosis or COPD

36
Q

Acetazolamide clinical indications

A

diuretics- rarely used
glaucoma- most indicated use, reduces aqueous humor and decreases pressure, topical
urinary alkalization- excretion of uric acid or cystine, metabolic acidosis, acute mountain sickness, adjuvants in epilepsy

37
Q

loop diurectic prototypes

A

furosemide and ethacrynic acid

38
Q

loop diuretics pharmacokinetics

A
  • rapidly absobed PO
  • IV also utilized
  • eliminated by kidney via glomerular filtration and tubular secretion
  • act on luminal side after secretion so activity correlates w/kidney fnx
  • coadministration w/other weak acids (NSAIDs) may result in reduced loop diuretic secretion
39
Q

loop diuretic MOA

A

inhibit NKCC2 in TAL -> no NA, CL, K, transport -> no lumen postive charge -> no Mg Ca transport -> increased delivery of Na and H to DCT and CCT -> increased excretion of K -> induce PG synth -> increase RPF

40
Q

Loop diuretic toxcicty

A

-depletion of total body Na -> hyponatremia, reduced GFR, circulatory collapse, thrombohemolytic episodes, and hepatic encephalopathy in liver disease patients
-hypokalemic metabolic alkalosis
- hyperuricemia -> gout
dose-related hearing loss
-hypomagnesemia
allergic reactions
-dehydration

41
Q

loop diuretics contraindications

A
  • fuosemide, bumetanide, and torsemide and sulfonamides
  • deleterious to hepatic cirrhosis, borderline renal failure, or heart failure
  • avoid in postmenopausal osteopenic women due to hypocalcemic effects
42
Q

loop diuretic drug interactions

A

aminoglycosides (enhanced ototoxicity)
lithium (decrease or increase serum levels of lithium)
digoxin (increased toxicity due to electrolyte disturbances

43
Q

loop diuretics clinical indications

A 
among most efficacious diuretics
acute pulmonary edema
hypertension and heart failure
mild hyperkalemia
acute renal failure 
anion overdose (bromide, fluorise, iodide)
hypercalcemic states
44
Q

thiazide diuretics prototype

A

hydocholorothiazide

45
Q

thiazide diuretics pharmacokinetics

A

PO
not lipid soluble, so large dose
chlorthalidone longest acting t1/2=47hours
secreted by PCT

46
Q

thiazide diuretics MOA

A

inhibits NCC ->inhibits NaCl reabsoption -> enhanced Ca reabsorption in PCT and DCT
rarely causes hypocalcemia, but can maskhypercalcemia

47
Q

thiazide diuretics toxicity

A
  • Hypokalemic metabolic alkalosis and hyperuricemia
  • impaired carbohydrate tolerance -> hyperglycemia -> unmask latent diabeties
  • hyperlipidemia: increased total serum cholesterol and LDL, may normalize w/time (indapamide does not have this effect)
  • hyponatremia due to hypovolemia induced ADH
  • weakness, fatigue, paresthesias, impotence
  • sulfonamide hypersensitivity
48
Q

thiazide contraindications

A

diabetics
efficacy may be reduced when combined w/NSAIDs
excessive use dangerous in hepatic cirrhosis, borderline renal failure, heart failure

49
Q

thiazide clinical indications

A

HTN and heart failure
nephrolithiasis due to idiopathic hypercalciuria
DI

50
Q

thiazide w/DI

A

inhibits Na/Cl transporter in DCT -> increase diuresis -> reduce ECF -> less volume filtered at glomerulus and decreased GFR -> increase PCT Na and water reabsorption -> less Na and water delivery to CDs and decrease urine output

51
Q

K sparring diuretics MR antagonist prototype

A

spironolactone

52
Q

K sparring diuretic NaCh inhibitor prototype

A

amiloride

53
Q

Pharmacokinetics spironolactone and eplerenone

A

PO

inactivation in liver and several days needed before effect is seen

54
Q

eplerenone

A

spirnolactone analog w/greater sensitivity for MR

55
Q

amiloride and triamterene

A

PO

triamterene is metablized extensivly in liver and has shorter half life then amiloride

56
Q

spirnolactone and eplernone MOA

A

Synthetic steroids act as competitive inhibiotrs of aldosterone binding MR -> reduce Na reabsorption in CCT -> reduce K secretion
only diuretic that does not need access to tubular lumen to work

57
Q

MR

A

nuclear hormone receptor

regulated expression of ENaC and Na/K ATPase pumps in DCT and CCT

58
Q

amiloride and triamterene MOA

A

directly inhibit Na entry by blocking ENaC in CCT

therefore reduce K secretion

59
Q

K sparring toxicity

A

mild, moderate, or even life threatening hyperkalemia (higher risk w/renal disease, B-blockers, NSAIDs, ACEIs, ARBs)
metabolic acidosis due to reduced H secretion
gynecomastia, impotence, BPH
triamterene precipitates -> stones

60
Q

Triamterene drug interactions

A

indomethacin -> acute renal failure

61
Q

K sparring contraindications

A

chronic renal insufficiency
concomitant use of K sparring diuretics w/beta blockers, NSAIDS, ACEIs, or ARBs
patients w/liver disease
strong inhibitors of CUP3A4 and can increase eplerenone

62
Q

K sparring indications

A

states of mineralcorticoid excess or hyperaldosteronism
thiazides and loop diuretics can cause hyperaldosteronism, which increases K wasting so can be combined w/K sparring
MR antagonists are used to treat heart failure

63
Q

Osmotic agents prototype

A

mannitol

64
Q

mannitol pharmacokinetics

A

poorly absorbed and must be given parenterally

not metabolized, excreted in glomerular filter w/in 30-60min

65
Q

mannitol MOA

A

increases osmotic pressure pulling water into PCT and descending limb
oppose ADH effects in CCT
increase in water diuresis increased flow rate also reduces Na reabsorption
natriuresis < diuresis therefore leads to hypernatremia

66
Q

mannitol toxcicity

A

prior to diuresis -> ECF expansion and hyponatremia

dehydation, hyperkalemia, hypernatremia

67
Q

mannitol contraindications

A

severe renal disease, severe dehydration, severe pulmonary edema or congestion

68
Q

mannitol clinical indications

A

promoting urinary excretion of toxic substances
reduction of intracranial and intraoccular pressure
use for prevention of acute renal failure/promote diuresis not recommended

69
Q

antidiuretic hormone agonists

A
  • increased water reabsorption
  • vasopressin and desmopressin mediate vasoconstriction of vascular smooth m and increase water permeability and reabsorption in CCT
70
Q

antidiuretic hormone agonists indications

A

-treatment of choice for cDI, polyuria, polydipsia, hypernatremia, nocturnal enuresis

71
Q

antidiuretic hormone antagonists

A

Conicaptan and tolvaptan ADHR antagonists

  • Conivaptan parenteral t1/2 5-10hrs
  • tolbaptan PO
  • MOA: conicaptan V1a and V2 in CCT, tolvaptan selective for V2
  • variety of medical conditions cause water retention as result of ADH excess -> hyponatremia
  • Toxicity: can cause hypernatremia, nDI
72
Q

loop agents + thiazides

A

if patients fail or become refractory to usual dose of loop
effective bc:
-salt and water reabsorption in TAL (blocked by loop) or DCT (blocked by thiazides) leads to overactivity of the other, therefore combining them has a more then additive affect
-thiazides often produce mild naturesis in PCT that is usually masked by increased absorption in TAL, but blocked by loop
-metolazone (thiazide) is popular choice for combo
NOT recommended for outpatient b/c secer hypokalemia common

73
Q

K sparring w/loop or thiazides

A
  • hypokalemia common side effect of loop agents and thiazide
  • if hypokalemia unmanagable via diet and supplementation can be combined w/K sparring diuretic
  • generally safe, but avoided in patients w/renal insufficiency and those receiving angiotensin antagonisits
74
Q

edematous states treated w/diuretics

A

heart failure
kidney disease
hepatic cirrhosis

75
Q

heart failure

A

reduces CO -> decreased BP and blood flow to kidney -> sensed as hypvolemia -> RAAS -> retention of salt and water -> pulmonary interstitial edema occurs when plasma volume increases and kidney continues to retain salt and water

76
Q

kidney disease

A
  • renal diseases usually cause water and Na retention
  • insufficient GFR to sustain natriuretic response and diuretics are of little benefit
  • patients w/mild cases of renal disease may benefit
  • diuretics are beneficial in glomerular disease such as SLE or SM
  • loop and thiazide diuretics are beneficial w/hyperkalemia in early stage renal disease
77
Q

hepatic cirrhosis

A
  • diuretics are useful with edema and ascites

- aggressive use of diuretics can be disastrous in patients w/liver disease

78
Q

edematous states that are treated w/diuretics

A

HTN
Nephrolithiasis
hypercalcemia
DI

79
Q

HTN

A

thiazides are often used b/c of their mild diuretic and mild vasodilator activity
loop often reserved for patients w/mild renal insufficiency or heart failure
diuretics are often used in combo w/vasodilators b/c vasodilators cause significant salt and water retention

80
Q

nephrolithiasis

A

2/3 of kidney stones contain Ca phosphate or Ca oxalate

thiazides enhance Ca reabsorption in DCT and reduce urinary Ca

81
Q

hypercalcemia

A

loops reduce Ca reabsoption and promote Ca excretion, can cause marked volume contraction when used alone
saline can be administered simultaneously

82
Q

DI

A

thiazides can reduce polyuria and polydipsia in both types of DI

renal II (4 decks)

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