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M2 Renal/FEK > 9. Diuretics PHARM > Flashcards

9. Diuretics PHARM Flashcards

1
Q

what are some causes of edema?

A

heart failure, hepatic cirrhosis, renal disease, sympathetic activation, hypoalbuminemia

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2
Q

how does sympathetic activation contribute to edema?

A

contributes to Na retention, vasoconstriction of the efferent arteriole (same as AtII). also, renin release via B1 receptor

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3
Q

how are diuretics delivered to their site of activity? three methods

A
  • glomerular filtration of drugs –> tubule
  • prox tubule secretion by carriers
  • reabsorption by diffusion
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4
Q

why do diuretics that work more proximally have a higher max capacity?

A

more Na is absorbed proximally than distally

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5
Q

Example of an osmotic diuretic? how does it work?

A

Mannitol.

filtered, but not reabsorbed. reduces tonicity of the renal medulla, decreases water reabsorption

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6
Q

what are OATs?

A

organic anion transporter proteins. can carry drugs from blood into the prox tubule

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7
Q

Mannitol: mechanism?

A

can pull water out of cells, into vasculature, and then diurese through kidney. contrast with albumin, which can maintain vasculature volume but cannot cause osmotic diuresis (too big to filter, stays in serum)

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8
Q

mannitol: therapeutic uses?

A

glaucoma, cerebral edema

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9
Q

carbonic anhydrase inhibitors: example medication?

A

acetazolamide

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10
Q

CA inhibitor: location of action? mechanism?

A

prox tubule. block bicarb reabsorption, reduce Na reabsorption as a result. increase urinary excr of bicarb, Na

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11
Q

CA inhibitors: why limited use/short term effect?

A

they cause metabolic acidosis (due to bicarb loss). once you have lost enough bicarb, they are less effective

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12
Q

Ca inh: how do they cause hypokalemia?

A

at collecting duct, Na is reabsorbed in exchange for K – since there is more Na present, more is reabsorbed here and more K is wasted. Increased urinary K secretion/excretion.

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13
Q

CA inhibitors: side effects?

A

hypoK
calcium stones due to alkalization of urine
hypersensitivity reactions due to sulfonamide residue

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14
Q

Thiazide: mechanism of action

A
  • inhibits NaCl symporter in distal convoluted tubule
  • increases Na/Cl excretion
  • blocks urinary diluting capacity
  • some degree of carbonic anhydrase inhibition
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15
Q

Thiazide: name of drug?

A

hydrochlorothiazide

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16
Q

Thiazide: side effects? how does it cause these?

A

hypokalemia, hyponatremia
prevents reabsorption of Na at the Na/Cl symporter, so more Na arrives at the collecting duct. More is reabsorbed there so K is wasted. But overall more Na is excreted than usual.
Hypersensitivity reactions: not sure how, but know it anyway.

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17
Q

Thiazide: impact on calcium?

A

can cause hyperCa. because less Na reabsorbed at distal tubule, so Ca is reab in order to maintain electroneutral cytosol

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18
Q

Therapeutic uses for thiazides

A

hypertension, increasing bone density in elderly women, edema, calcium stones

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19
Q

loop diuretic: prototypical drug?

A

furosemide

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20
Q

loop diuretic: mechanism?

A

blocks Na-K-Cl symporter in ascending LOH
increases Na/Cl excretion
increases K excretion

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21
Q

what effect do loop diuretics have on Ca and Mg excretion?

A

increase excretion of Ca, Mg due to decreased paracellular absorption in ascending limb

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22
Q

what diuretic class has the highest max efficacy?

A

loop diuretics

act at the site of highest Na reabsorption

23
Q

loop diuretics: therapeutic use?

A

acute pulmonary edema
edema from other causes
HTN refractory to other diuretics

24
Q

side effects of loop diuretics?

A

volume depletion (because they are so effective)
hypoK
excess Ca and Mg excretion

25
Q

effect of loop diuretics on tubuloglomerular feedback?

A

decr Na arrival at macula densa

–> renin secretion goes up, GFR goes down because of less Na concentration at macula densa (counter to diuretic effect)

26
Q

how does furosemide travel through the bloodstream?

A

95% bound to albumin

only 5% cleared through glomerulus and available for activity

27
Q

duiretic efficacy in chronic renal insufficiency?

A

decreased renal blood flow and anionic metabolites reduce diuretic renal excretion rate, can decr concentration of drug

28
Q

diuretic efficacy in nephrotic syndrome?

A

hypoalbuminemia decr renal excretion rate

29
Q

do thiazides and loop diuretics both cause hypocalcemia?

A

no, only loop diur

30
Q

are thiazides and loop diur both uricosurics?

A

no, only loop

31
Q

do thiazides and loop diur have the same natriuretic emax?

A

no, loop are more potent

32
Q

do thiazides and loop diur both cause hypokalemia?

A

yes

33
Q

do thiazides and loop diur both decrease renin release?

A

loop diur increase renin release

34
Q

where is the location of action for K sparing diuretics?

A

the collecting duct

35
Q

how do K sparing diuretics work?

A

inhibit Na reabsorption by principal cells of late distal tubule and collecting duct
decr K excretion

36
Q

which K sparing diuretic blocks the mineralocorticoid receptor?

A

spironolactone

37
Q

which K sparing diuretic blocks the ENaC?

A

amiloride

38
Q

why are K sparing diuretics used in combination with lithium?

A

to block Li uptake into principal cell, inhibit Li-induced diabetes insipidus

39
Q

what is the mechanism of the K sparing effect?

A

antagonism of mineralocorticoid receptor, blocks aldosterone effect
blocks ENaC expression, insertion
blocks activation of ENaC
blocks Na/K ATPase expression

40
Q

what diuretic is a common add-on with heart failure patients?

A

spironolactone. showed to prolong survival

41
Q

side effects of spironolactone?

A

hyperK
gynecomastia
impotence

42
Q

what is the med that is an alternative to spironolactone, and does not cause gynecomastia and impotence?

A

eplerenone

43
Q

do both ENaC and MR blockers cause hyperkalemia?

A

yes

44
Q

what is the braking phenomenon?

A

diuretic resistance: decreased potency over time

45
Q

ways to manage diuretic resistance?

A

incr dose
use in combination
restrict fluid, Na

46
Q

what meds are used to prevent renal impairment?

A

ACE inhibitors, ARBs

47
Q

what meds are indicated for prevention of diabetic nephropathy?

A

ACE inhibitors, ARBs

48
Q

what is the mech by which ACE Inhs and ARBs prevent diabetic nephropathy?

A

selective efferent arteriolar vasodilation –> decr glo cap pressure

49
Q

treatment of central DI?

A

desmopressin. selective for V2 receptor

50
Q

what receptor does ADH use?

A

V2

51
Q

treatment of nephrogenic DI?

A

thiazides, amiloride. cannot use desmopressin because it is the ADH receptor (V2) that is the problem

52
Q

excessive vasopressin secretion leads to what?

A

hyponatremia

53
Q

morphine toxicity may occur in patients with renal impairment because morphine…

A

is converted into an active glucoronide, which is cleared by the kidney

M2 Renal/FEK (20 decks)

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