Diuretics Pharmacology Flashcards

1
Q

Mannitol MOA

A

Osmotic diuretic. Increase tubular fluid osmolarity–> increases urine flow, decreases intracranial/intraocular pressure. Acts primarily in proximal tubule.

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2
Q

Mannitol clinical use

A

Drug overdose, elevated intracranial/intraocular pressure

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3
Q

Mannitol toxicity

A

Pulmonary edema, dehydration, contraindicated in anuria, HF.

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4
Q

Acetazolamide MOA

A

Carbonic anyhydrase inhibitor. Causes self limited NaHCO3 diuresis and decreased total bicarb stores. Acts in proximal tubule. Reduces bicarb and Na+ reabsorption

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5
Q

Acetazolamide clinical use

A

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, psuedotumor cerebri.

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6
Q

Acetazolamide toxicity

A

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.

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7
Q

Loop diuretics (3 names)

A

Furosemide, bumetanide, torsemide

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8
Q

Loop diuretic MOA

A

Sulfonamide loop diuretics. Inhibit cotransport system (Na+/K+/2Cl-) of thick ascending limb of loop of henle. Prevent concentration of urine by abolishing hypertonicity of medulla. Increases Na+, K+, H20 excretion. Stimulate PGE release (vasodilatory effect on afferent arteriole). Increase Ca++ excretion

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9
Q

Loop diuretic clinical uses

A

Edema (HF, cirrosis, nephrotic syndrome, pulmonary edema). HTN, hypercalcemia.

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10
Q

Loop diuretic toxicity

A

Ototoxicity, Hypokalemia, Dehydration, Allergy, Nephritis, Gout (OH DANG)

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11
Q

Ethacrynic acid MOA

A

Phenoxyacetic acid derivative. Same action as furosemide (but not sulfonamide)

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12
Q

Ethacrynic acid clinical use

A

Diuresis in patients with a sulfa allergy.

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13
Q

Ethacrynic acid toxicity

A

Similar to furosemide. Can cause hyperuricemia. Never use to treat gout.

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14
Q

Thiazide diuretics (3 names)

A

Chlorthalidone, hydrochlorothiazide, metaloxone

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15
Q

Thiazide MOA

A

Inhibit NaCl reabsorption in the early DCT. Decrease diluting capacity of nephron. Decrease Ca++ excretion. Opens K+ channels–> hyperpolarize vessels–>vasodilation

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16
Q

Thiazide clinical use

A

HTN, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

17
Q

Thiazide toxicity

A

Hypokalemic metabolic acidosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sufla allergy.

18
Q

How do thiazides cause hyperglycemia?

A

Bind to SUR on K+ channel controlling insulin release–> opens channel–> hyperpolarizes beta cell–> suppresses insulin release–> hyperglycemia

19
Q

K+ sparing diuretics (4 drugs)

A

Spironolactone and eplernone, triamterene, amiloride

20
Q

Spironolactone and eplernone MOA

A

Competitive aldosterone receptor antagonists in cortical collecting tubule.

21
Q

Triamterene and amiloride MOA

A

Block ENaC–> block the Na+ exchange for K+ and H+ in cortical collecting tubule.

22
Q

K+ sparing diuretic clinical use

A

Mild diuretics, hyperaldosteronism, K+ depletion, HF. Spironolactone used post-MI for cardiac remodeling

23
Q

K+ sparing toxicity

A

Hyperkalemia (can cause arrhythmias), hypercholeremic metabolic acidosis, endocrine effects with spironolactone (gynecomastia, antiandrogen effects). Triamterene + indomethacin can cause ARF, kidney stones

24
Q

ADH and congeners (Vasopressin and desmopressin) MOA

A

Stimulate GPCR–>Gs–>cAMP–>PKA–> increase aquaporins–> allows for concentration of urine. Act in the medullary collecting duct

25
Q

SGLT inhibitors (3 drugs)

A

Canigliflozin, dapagliflozin, gliflozin

26
Q

SGLT inhibitor MOA

A

Inhibit SGLT2–>reduce glucose reabsorption–> loss of glucose in urine. Acts in proximal tubule.

27
Q

ADH uses

A

Diabetes insipidus, bedwetting

28
Q

SGLT inhibitor clinical uses

A

Reduce blood sugar levels in DM (adjunctive), causes weight loss (loss of energy in form of glucose)

29
Q

SGLT inhibitor toxicity

A

Ketoacidosis, UTI, yeast infections, hypoglycemia

30
Q

Organic Anion Transport (OAT) inhibitors (2)

A

Probenicid, sulfinpyrazone

31
Q

OAT inhibitor MOA

A

Act in proximal tubule. Driven by symport/antiport exchange of molecules for dicarboxylates, facilitate excretion, suppress uric acid reabsorption, critical molecule = urate

32
Q

OAT inhibitor uses

A

Gout treatment

33
Q

Allopurinol MOA

A

Inhibits xanthine oxidase formation

34
Q

Colchicine MOA

A

Microtubule inhibitor w/anti-inflammatory properties