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Cardio > Diuretics > Flashcards

Diuretics Flashcards

1
Q

the site of action for loop diuretics is the ____

A

thick ascending loop of henle

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2
Q

loop diuretics block what transporter

A

Na+/K+/2Cl- symporter

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3
Q

loop diuretics compete with ____ for binding to the Na+/K+/2Cl sympoter

A

Cl

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4
Q

approximately __% of filtered sodium is reabsorbed at the thick ascending loop of henle

A

25

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5
Q

the most serious side effects of loop diuretics are due to ______

A

fluid and electrolyte imbalance (an extension of the therapeutic effect)

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6
Q

what are the loop diuretics

A

furosemide, bumetanide, torsemide, ethacrynic acid

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7
Q

what is different about ethacrynic acid

A

it has no sulfa moiety

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8
Q

what is the most potent diuretic

A

loop

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9
Q

what are the side effects of loops

A

hypokalemia, hyponatremia, volume depletion, hypotension, hearing loss, hyperuricemia, hyperglycemia, increase cholesterol and triglycerides

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10
Q

clinical uses of loops

A

emergency treatment of acute pulmonary edema, edema associated w/ CHF, cirrhosis, and liver disease. use after less potent diuretics have failed to work, use in combo with other diuretics

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11
Q

what are the thiazides

A

chlorthalidone, indapamide, metolazone, chlorothiazide, hydrochlorothiazide

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12
Q

what site in the renal tubule do thiazides work

A

distal convoluted tubule

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13
Q

what protein do thiazides bind to

A

a carrier protein that symports Na and Cl out of the renal tubule

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14
Q

thiazides must ______ to exert effect

A

enter the renal tubule

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15
Q

thiazides are actively secreted by the ____

A

proximal tubule

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16
Q

thiazides inhibit ____ reabsorption from the luminal side

A

sodium

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17
Q

the diuretic effect of thiazides is max __%

A

5%; because most of the sodium has been reabsorbed before filtrate arrives

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18
Q

why are thiazides safe drugs

A

toxic doses are many times greater than the therapeutic dose

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19
Q

the most serious adverse effects of thiazides are due to ____

A

disturbances of fluid and electrolyte balance

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20
Q

what are the adverse effects of thiazides

A

hyponatremia, volume depletion, hypotension, hyperuricemia, decreased glucose tolerance, increased cholesterol and triglycerides

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21
Q

clinical uses of thiazides

A

hypertension; congestive heart failure (adjunct)

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22
Q

what are the two types of potassium sparing diuretics

A

aldosterone antagonists/mineralocorticoid receptor antagonists, and sodium channel blockers

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23
Q

what are the aldosterone antagonists

A

spironolactone, eplerenone, finerenone

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24
Q

what are the sodium channel blockers

A

triamterene, amiloride

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25
Q

what is the site of action of the potassium sparing diuretics

A

collecting duct

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26
Q

aldosterone antagonists are structurally related to ____

A

aldosterone

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27
Q

aldosterone antagonists bind to _____

A

cytoplasmic mineralocorticoid receptors

28
Q

how do aldosterone antagonists promote sodium loss and potassium conservation

A

they prevent aldosterone from stimulating sodium reabsorption, and the capacity of aldosterone to make more sodium channels is blocked so less sodium absorbed= potassium not eliminated

29
Q

what are the side effects specific to spironolactone; and WHY

A

gynecomastia, impotence, menstrual disorders; because it lacks specificity, also blocks androgen and progesterone

30
Q

what is the most common side effect of potassium sparing diuretics

A

hyperkalemia

31
Q

the risk of hyperkalemia with K+ sparing diuretics is INCREASED when used with what other drug class

A

RAAS inhibitors

32
Q

why does eplerenone not share the same side effects as spironolactone

A

is is a SELECTIVE aldosterone blocker, greater specificity for MR

33
Q

what makes finerenone different from the other aldosterone antagonists

A

it is nonsteroidal, more potent anti-inflammatory and anti-fibrotic effects

34
Q

what is finerenone approved for

A

reduce risk of sustained estimated GFR decline, end stage kidney disease, CV death, nonfatal MI, and hospitalization for HF in pts w/ CKD associated w/ T2DM

35
Q

what is the mechanism for the sodium channel blockers

A

they bind to and inhibit epithelial sodium channels. since less sodium is absorbed, potassium is not eliminated in exchange

36
Q

pearl for K+ sparing diuretics

A

weak antihypertensive activity, major benefit is when used in conjunction with thiazides or loops to reduce incidence of hypokalemia

37
Q

clinical uses of all K+ sparing diuretics

A

prevent hypokalemia from thiazides and loops

38
Q

clinical use of spironolactone

A

heart failure, primary aldosteronism, acne

39
Q

clinical uses of eplerenone

A

adjunct treatment of HTN & post-MI w/ HF

40
Q

what are the carbonic anhydrase inhibitors

A

acetazolamide, dorzolamide

41
Q

what is the site of action of the carbonic anhydrase inhibitors

A

proximal tubule

42
Q

what is the mechanism of the carbonic anhydrase inhibitors

A

inhibit carbonic anhydrase– both the membrane bound and cytoplasmic forms, which interferes with normal bicarb reabsorption, so the urine becomes alkaline and urine pH increases to 8. meanwhile, pH of blood decreases and may result in metabolic acidosis. the increased H+ concentration in the tubular fluid diminishes H+ concentration gradient which normally favors sodium reabsorption by the Na/H exchange transport proteins. more sodium is left in the tubular fluid as it travels toward other segments of the tubule

43
Q

why do carbonic anhydrase inhibitors have a mild diuretic action

A

much of the Na+ whose reabsorption is prevented in the proximal tubule can be reabsorbed thru compensation by the other downstream portions of the tubule

44
Q

pharmacologic uses of carbonic anhydrase inhibitors

A

glaucoma (dorzolamide), acute mountain sickness, metabolic alkalosis

45
Q

how do carbonic anhydrase inhibitors work for glaucoma

A

reduce the rate of aqueous humor formation by the ciliary process, and reduce intraocular pressure

46
Q

how do carbonic anhydrase inhibitors work for acute mountain sickness

A

they increase the breathing rate

47
Q

what are the osmotic diuretics

A

mannitol, urea (Ure-Na)

48
Q

how do osmotic diuretics work

A

they increase osmolarity of the tubular fluid and thereby attract water by osmosis in the tubule.

49
Q

osmotic diuretics are freely filtered at the ____

A

glomerulus

50
Q

osmotic diuretics are pharmacologically ____

A

inert

51
Q

what are the uses of mannitol

A

to decrease intracranial pressure in neurological conditions, decrease intraocular pressure before opthalmic procedures

52
Q

what is the use of urea

A

is is a medical food for hyponatremia

53
Q

why is mannitol used for intracranial pressure

A

it is trapped in the blood vessels and acts as an osmotically active agent to pull water into the circulation from the interstitial fluid of the brain

54
Q

why is mannitol used before opthalmic procedures

A

it takes advantage of its high concentration in the blood, causing water to be pulled from the eye into the blood

55
Q

why does urea treat hyponatremia

A

it helps to normalize serum sodium levels by inducing osmotic excretion of free water

56
Q

why is mannitol IV only

A

it is a 6 carbon sugar like glucose, but it is not a substrate for sugar transporters so it cannot be absorbed from the intestine. if it was given orally it would cause diarrhea by osmotically pulling water into the intestine

57
Q

what are the vasopressin antagonists

A

tolvaptan, conivaptan

58
Q

vasopressin antagonists are ____

A

aquauretics

59
Q

what does aquauretic mean

A

they promote free water loss but do not affect sodium excretion

60
Q

what are the vasopressin receptor subtypes

A

V1alpha, V1beta, V2

61
Q

___ vasopressin receptors are in the vascular smooth muscle, and their stimulation results in contraction

A

V1alpha

62
Q

____ vasopressin receptors are in the anterior pituitary, and their stimulation results in the release of ACTH and beta-endorphin

A

V1beta

63
Q

__ vasopressin receptors are located in the collecting ducts, and their stimulation results in increased water reabsorption

A

V2

64
Q

tolvaptan blocks __ causing what

A

V2, water diuresis

65
Q

conivaptan blocks ___, causing ____

A

V1 and V2, relaxation of blood vessels and water loss

66
Q

which vasopressin antagonist is IV only

A

conivaptan

67
Q

what are the clinical uses of vasopressin antagonists

A

they are used in hyponatremia. they are studied in patients with heart failure. they are not used for hypertension

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