7 - Diuretics Flashcards

1
Q

acetazolamide - mech

A

inhibit carbonic anhydrase in PCT
inc NaBicarb diuresis
can cause hyperchloremic metab acidosis

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2
Q

clinical uses of acetazolamide

A

glaucoma
urinary alkalinization (inc solubility of uric acid and cysteine)
metab alkalosis (diuretic induced)
acute mountain sickness

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3
Q

acetazolamide AEs

A

hyperchloremic metab acidosis

hypokalemia

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4
Q

how do most diuretics cause renal K wasting?

A

inc distal Na delivery drives K secretion (Na-K exchangers that aldosterone works on)

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5
Q

how do osmotic diuretics work?

A

prevent water reabs in PCT and dLoH
oppose ADH action in CD
inc urine flow rate > dec contact time btwn fluid and tubular epithelium > reduce Na reabs > diuresis

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6
Q

uses of osmotic diuretics (eg mannitol)

A

cerebral edema
acute congestive glaucoma
prevent oliguric phase in AKI (ex hemolysis, rhabdomyolysis)

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7
Q

osmotic diuretic AEs

A

EC volume expansion + hyponatremia

dehydration + hypernatremia

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8
Q

loop diuretic mechanism

A

inhibit Na/K/2Cl transporter in TAL of Loop
very potent - induces NaCl diuresis
inc Mg and Ca excretion b/c dec luminal positive potential
K wasting
induce renal PG synth > inc RBF and vasodilation

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9
Q

uses of loop diuretics

A

pulm edema
edematous conditions (heart failure, cirrhosis, nephrotic syndrome)
HTN - refractory, assoc w/ renal insuff or HF, HTN emergency
hypercalcemia and hyperkalemia
SIADH

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10
Q

how does furosemide work to counter SIADH?

A

block Na reabs in loop of henle >
abolish hyperosmolarity of medulla >
hinder Na reabs due to ADH in distal nephron

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11
Q

loop diuretics AEs

A

hypokalemic metab alkalosis
hypomagnesemia
hyperuricemia
ototoxicity (dose related)

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12
Q

thiazide diuretics mechanism

A

block Na/Cl cotransporter in DCT
induce NaCl diuresis
inc Ca reabsorption
renal K wasting

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13
Q

uses of thiazides

A

HTN
heart failure
renal stones due to idiopathic hypercalciuria
nephrogenic DI

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14
Q

how do thiazides work in nephrogenic DI?

A

thiazide induced Na loss stimulates Na reabs in PCT > dec urine formation over time

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15
Q

thiazides AEs

A
hypokalemic metab acidosis
hyperuricemia
hyponatremia
hyperglycemia
hyperlipidemia
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16
Q

mechanisms of both types of K sparing diuretics

A

spironolactone/eplerenone - direct antagonism of MR receptors (aldosterone)

amiloride/triamterene - inhibition of Na entry through ion channels in luminal membrane

both increase urine NaCl excretion
can cause hyperkalemia / metabolic acidosis

17
Q

K sparing diuretic use

A

primary and secondary hyperaldosteronism
heart failure
cirrhosis

18
Q

K sparing diuretic AEs

A

hyperkalemia
hyperchloremic metab acidosis (like type IV RTA)
gynecomastia (specifically spironolactone)

19
Q

approaches to diuretic resistance

A

make sure they are following salt restriction + med intake
discontinue NSAIDs
adjust dose of diuretic if renal impairment - protein bound diuretic gets wasted in albuminuria
switch to IV admin if absorption is a concern
continuous IV infusion for loop diuretic to avoid postdiuretic salt retention
combine loop diuretics w/ other diuretics (preferably thiazide)