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Block 4 Pharm > Diuretics > Flashcards

Diuretics Flashcards

1
Q

MOA of Mannitol

A

filtered into tubular space and significantly increases osmolarity resulting in impairment of fluid reabsorption (and some Na+)

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2
Q

Nephron segments that mannitol acts on

A

Segments permeable to water: PCT, descending limp of Henle, and CT (w/ADH)

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3
Q

Route of administration of mannitol

A

IV (not orally absorbed)

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4
Q

Adverse effects of mannitol

A

increases plasma osmolarity (esp. with decreased GFR), if mannitol is in ECF it moves water out of cells and can worsen heart failure, hyponatremia

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5
Q

Contraindications of mannitol

A

CHF, chronic renal failure, acute pulm. edema

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6
Q

Indications of mannitol

A

Acute renal faillure, intracranial pressure, intraocular pressure (assuming BBB is intact), promote renal excretion of toxic substances

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7
Q

Name the 4 drugs in the carbonic anahydrase inhibitor class

A

acetazolamide, dichlorphenamide, methazolamide, dorzolamide

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8
Q

MOA of acetazolamide

A

CA inhibitor - blocks the reabsorption of HCO3 in the PCT

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9
Q

MOA of dichlorphenamide

A

CA inhibitor - blocks the reabsorption of HCO3 in the PCT

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10
Q

MOA of methazolamide

A

CA inhibitor - blocks the reabsorption of HCO3 in the PCT

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11
Q

MOA of dorzolamide

A

CA inhibitor - blocks the reabsorption of HCO3 in the PCT

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12
Q

Adverse effects of CA inhibitors

A

METABOLIC ACIDOSIS (due to loss of HCO3), and HYPOKALEMIA (due to increased Na+ in the lumen that gets exchanged with K+ in the CT), Ca2+ phosphate stones (due to alkalination of tubular fluid), drowsiness, paresthesias, hypersensitivity rxn

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13
Q

Contraindication of CA inhibitors

A

HEPATIC CIRROHOIS (due to increased urine pH leading to decreased NH3 secretions leading to increase NH3 in the serum –> hyperammonemia –> encephalopaties)

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14
Q

Indications of CA inhibitors

A

glaucoma, increased CNS pressure, therapeutic alkalination of the urine (ion trapping in drug ODs), altitude sickness (Bohr effect)

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15
Q

Rank the potency of the various CA inhibitors

A

Acetazolamide (x), Methazolamide (5x), dichlorphenamide (30x)

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16
Q

Which CA is used for topical prep for ocular use

A

Dorzolamide

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17
Q

What is the MOA of furosemide

A

(loop diuretic) blocks the Na+/K+/2Cl- co-transporter

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18
Q

What is the MOA of bumetanide

A

(loop diuretic) blocks the Na+/K+/2Cl- co-transporter

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19
Q

What is the MOA of torsemide

A

(loop diuretic) blocks the Na+/K+/2Cl- co-transporter

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20
Q

What is the MOA of ethacrynic acid

A

(loop diuretic) blocks the Na+/K+/2Cl- co-transporter

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21
Q

Besides causing diuresis what other therapeutic effect do the loop diuretics have

A

dilation of the venous system (renal vasodilation) mediated by PGs (improves RBF)

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22
Q

What portion of the nephron do the loop diuretics affect

A

Thick ascending loop of Henle

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23
Q

How are the loop diuretics secreted into the nephron

A

organic Acid transporter

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24
Q

Adverse effects of the loop diuretics

A

hyponatremia, HYPOKALEMIA, Ca2+ and Mg2+ depletion, METABOLIC ACIDOSIS, OTOTOXICITY, mild hyperglycemia

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25
Q

Contraindications of the loop diuretics

A

patients susceptible to hypokalemia, patients of digoxin

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26
Q

Indication for the loop diuretics

A

ACUTE pulm edema, edema with CHF, acute hypercalcemia, hyperkalemia, hypertension

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27
Q

What loop diuretic drug can you use for a patient that has a hypersensitivity rxn to other loop diuretics

A

Ethacrynic acid (last resort as it has nepho and ototoxicity)

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28
Q

What is the most efficacious diuretic that can cause up to 20% excretion of filtered Na+

A

Loop diuretics

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29
Q

What is the MOA of the thiazides and thiazide-like drugs

A

inhibit the Na+/Cl- co-transporter in the distal convoluted tubule (cortical TAL and early distal tubule)

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30
Q

What are the thiazide-like drugs

A

Metolazone, indapamide, and chlorthalidone

31
Q

Rank the order of half lives of the loop diuretics

A

Bumetanide (1hr)

32
Q

Which loop diuretic is the most potent

A

Bumetanide is 40x the potency of Furosemide

33
Q

What is the most commonly prescribed class of diuretics

A

Thiazides: because they are milder than loop diuretics and have a longer duration of action

34
Q

What conditions will decrease the bioavailability of the thiazides

A

renal disease, hepatic disease, and CHF

35
Q

Adverse effects of the thiazides

A

hyponatremia, HYPOKALEMIA, dehydration, METABOLIC ALKALOSIS, hyperuricemia, HYPERGLYCEMIA (linked to hypokalemia), HYPERLIPIDEMIA, weakness, fatigue, paresthesia, hypersen. rxn

36
Q

Contraindications of the thiazides

A

patient susceptible to hypokalemia

37
Q

Indications of the thiazides

A

hypertension, CHF, nephrotic syndrome and other Na+ retaining states, used to reduce tubular Ca2+ conc to prevent kidney stones

38
Q

What other electrolyte is decreased in the tubular fluid with the thiazides

A

Ca2+ (since the Na+/Cl- co-transporter on the apical side is blocked the cell becomes deficient in Na+ and therefore the activity of the Na+/Ca2+- co-transporter on the basolateral is increased, resulting in more Ca2+ transported out of the lumen and out of the cell on the basolateral side)

39
Q

Rank the potency of the thiazides and the thiazide-like diuretics

A

Chlorothiazide (0.1x), Hydrochlorothiazide (x), cholthalidone (x), metolazone (10x), and indapamide (20x)

40
Q

Which distal nephron diuretic can be efficacious in patients with sever renal insufficiency (can also be given in combo with loop diuretics)

A

Metolazone

41
Q

What condition will cause the thiazides to be relatively ineffective

A

Renal insufficiency (decreased GFR –> less fluid reaches the DT –> impact of thiazides)

42
Q

Rank the half lives of the thiazides/ thiazide-like diuretics

A

Chlorothiazide (1.5hr) , Metolazone (4-5hrs), Indapamide (10-22hrs), Chlorthalidone (44hrs)

43
Q

What is the MOA of spironolactone

A

competitive antagonist of aldosterone (binds to the cytosolic MR in principal cells and blocks aldosterone action of up regulating Na+/K+ pump and the H+ efflux pump in the intercalcated cells)

44
Q

What is the net effect of spironolactone on electrolytes in the DCT and CT

A

Decreases Na+ (and water) reabsorption, and increased K+ and H+ reabsorption (Potassium sparing diuretic)

45
Q

PK of spironolactone

A

takes up to 2 day to be effective. Half life of 20hrs. Taken orally

46
Q

Contraindications of spironolactone

A

HYPERKALEMIA

47
Q

Adverse effects of spironolactone

A

Hyperkalemia, metabolic acidosis, gynecomastia, amenorrhea

48
Q

Indications for spironolactone

A

LIVER CIRRHOSIS, patients with increased plasma levels of aldosterone, HTN w/ thiazides or loop diuretics

49
Q

MOA of epleronone

A

competitive antagonist of aldosterone (Potassium sparing diuretic)

50
Q

Major differences between spironolaction and epleronone

A

Epleronone does not cross react with androgen receipts and does not cause gynecomastia but is more expensive

51
Q

What drugs should NOT be co-administered with spironolactone

A

Any drugs that might also cause hyperkalemia: ACE INHIBITORS, K+ supplements, renin inhibitors, NSAIDs, etc)

52
Q

In what disease states should spironolactone be avoided

A

Any disease states that could cause hyperkalemia: diabetes mellitus, multiple myeloma, renal insufficiency

53
Q

What is the MOA of amiloride

A

blocks the Na+ channels in the apical membrane of the late distal tubule and CT (potassium sparing diuretic)

54
Q

What is the net effect of amiloride on the electrochemical gradient in the tubule

A

By blocking the Na+ channel the cells in the DT and CT become more negative and therefore attract more K+ and more H+ into the cell leading to increased reabsorption (potassium sparing diuretic) - relatively weak diuretic

55
Q

What is the MOA of triameterene

A

blocks the Na+ channels in the apical membrane of the late distal tubule and CT (potassium sparing diuretic) - relatively weak diuretic

56
Q

What are the half lives of amiloride and triameterene

A

21 hours and 4 hours respectively

57
Q

How are amiloride and trimeterene secreted into the nephron

A

secreted in the PCT via the organic base transporter

58
Q

What are the adverse effects of amiloride and triameterene

A

HYPERKALEMIA, metabolic acidosis, nausa, vomiting, hyponatremia

59
Q

Indications for amiloride and trimeterene

A

edema, usually given with another diuretic (often with thiazide or loop diuretic - combo and normalize K+ excretion)

60
Q

Contraindications of amiloride and trimeterene

A

HYPERKALEMIA, same as other K+ sparing diuretics avoid giving with disease conditions or drugs that can cause hyperkalemia)

61
Q

MOA of Demeclocycline in diuretic context

A

inhibits ADH in the CT (tetracycline ABX)

62
Q

Toxicity of Demeclocycline

A

Nephrotoxic

63
Q

MOA of Lithium in diuretic context

A

inhibits ADH in the CT (Psych drug for mania)

64
Q

Toxicity of Lithium

A

Nephrotoxic

65
Q

MOA of tolvaptan

A

V2 vasopressin (ADH) receptor antagonist

66
Q

MOA of conivaptan

A

V1a and V2 vassopressin (ADH) receptor antagonist

67
Q

MOA of mozavaptan

A

V2 vasopressin (ADH) receptor antagonist

68
Q

Indication for conivaptan

A

IV for euvolemic hyponatremia

69
Q

Adverse effects of V2 vasopressin receptor antagonists

A

hypernatremia, thirst, dry mouth, hypotension, dizziness

70
Q

Indications for the V2 vasopressin receptor antagonists

A

SIADH euvolemic or hypervolemic hyponatremia, CHF

71
Q

Physiological effect of V2 vasopressin receptor antagonists

A

induces increased dose-dependent production of dilute urine

72
Q

What diuretic is indicated for hepatic cirrhois

A

spironolactone

73
Q

Which thiazide/thiazide like drug is metabolized extensively by the liver

A

indapamide

Block 4 Pharm (9 decks)

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