Diuretics

Front 1

Carbonic Anhydrase (CA) Inhibitors

Back 1

Acetazolamide (RoA = PO, IV)

Dorzolamide (RoA = topical eye drops)

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MoA of CA Inhibitors

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Work @ the PCT; inhibit type II (cytoplasmic) and type IV (luminal membrane bound) CA --> inhibiting NaHCO3 reabsorption; increase renal excretion of Na, K, & HCO; alkaline urine, metabolic acidosis; decreases production of aqueous humor and cerebrospinal fluid

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Therapeutic Uses of CA Inhibitors

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Open angle glaucoma, acute mountain sickness, edema from heart failure, epilepsy, alkalosis from Loop Diuretics or Thiazides, familial periodic paralysis

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AE of CA Inhibitors

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Hypokalemia, hyperuricemia, nephrolithiasis, paresthesias, sulfa-type allergic reactions;
dorzolamide can produce a bitter taste and localized burning, stinging, or discomfort

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CI of CA Inhibitors

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Hepatic cirrhosis (b/c of urine alkalinization), COPD (b/c of metabolic acidosis), hypersensitivity to sulfa drugs, hypokalemic states

Front 6

Osmotic Diuretics

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Mannitol (RoA = PO, IV)

Front 7

MoA of Osmotic Diuretics

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0% bioavailability --> freely filtered by glomerulus so they limit water reabsorption in the TDL of LoH and the PCT; increase renal excretion of Na, K, Ca, Mg, Cl, HCO3, and PO4; more water diuresis than salt diuresis; acid urine; lead to an initial EC volume expansion followed by EC volume reduction

Front 8

TU of Osmotic Diuretics

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Cerebral edema, acute angle-closure glaucoma, prevention and/or treatment of oliguria or anuria in acute renal failure (to promote diuresis)

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AE of Osmotic Diuretics

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Initial EC volume expansion (cardiac or renal disease) = hypervolemia, hyponatremia, pulmonary edema;
Later EC volume contraction (with high doses) = hypovolemia, hypernatremia, dehydration

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CI of Osmotic Diuretics

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Severe renal failure, heart failure, pulmonary congestion/edema, severe dehydration

Front 11

Loop Diuretics

Back 11

Furosemide (RoA = PO, IV, IM); very short half-life!

Ethacrynic Acid (RoA = PO, IV); EA is NOT a sulfa drug!!

Front 12

MoA of Loop Diuretics

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Works in the TAL of LoH to inhibit the Na/K/2Cl symporter; increase renal excretion of Na, Cl, K, H, Ca; acid urine, metabolic alkalosis; venous vasodilation and maintenance of GFR (due to PG synthesis and release)

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Therapeutic Uses of Loop Diuretics

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Acute pulmonary edema, heart failure, ascites, HTN (when associated with renal insufficiency or heart failure), hypercalcemia; SYNERGISTIC effect when added to loop diuretics

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AE of Loop Diuretics

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Hypokalemic metabolic alkalosis, hyperuricemia, hypomagnesemia, hypovolemia; GI bleeding (EA); postural hypotension; ototoxicity; allergic reactions (sulfa drug - furosemide)

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CI of Loop Diuretics

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Serious hypovolemic or hyponatremic states; hypersensitivity to sulfa drugs; anuria unresponsive to loop diuretics (suggestive of kidney failure)

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Thiazides & Congeners

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Hydrocholorthiazide (RoA = PO)

Indapamide (RoA = PO)

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MoA of Thiazides

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Work at the EDCT to inhibit the Na/Cl symporter; also weakly inhibit CA; increased renal excretion of Na, K, H, Cl, HCO3, and decreased renal excretion of Ca; arteriolar vasodilation; alkaline urine, metabolic alkalosis

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Therapeutic Uses of Thiazides

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DOC for HTN!! Nephrogenic Diabetes Insipidus; edema, ascites; calcium nephrolithiasis, idiopathic hypercalciuria; Meniere's disease

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AE of Thiazides

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Hypokalemic metabolic alkalosis, imparied carb tolerance in DM patients, hyperlipidemia, hyperuricemia, hyponatremia; sexual dysfunction; sulfa allergic reactions (Stevens-Johnson syndrome, agranulocytosis, aplastic anemia)

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CI of Thiazides

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PREGNANCY; anuria, renal decompensation; hypersensitivity to sulfa drugs

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Potassium Sparing Diuretics

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Triamterene

Amiloride

Spironolactone

RoA for all = PO

Front 22

MoA of Organic Bases

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Triamterene & Amiloride; work at LDCT & CCT to inhibit ENAC channels

Front 23

MoA of Aldosterone Receptor Antagonist

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Spironolactone; works at the LDCT & CCT to inhibit aldosterone-induced proteins --> decreasing ENAC channel synthesis and Na/K ATPase pumps

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MoA of Potassium Sparing Diuretics

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Increase renal excretion of Na, Cl; decrease renal excretion of K, Ca, H; alkaline urine

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Therapeutic Uses of Potassium Sparing Diuretics

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All drugs = treatment and prevention of hypokalemic states in response to thiazide and loop diuretics;
Amiloride = Lithium induced nephrogenic diabetes insipidus;
Spironolactone = hyperaldosteronism

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AE of Potassium Sparing Diuretics

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Hyperkalemia, metabolic acidosis; asthenia, muscular weakness, diarrhea, bradycardia, AV block

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CI of Potassium Sparing Diuretics

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Hyperkalemic states, chronic renal insufficiency, patients receiving high doses of NSAIDs, severe hepatic disease

Front 28

Vasopressin/ADH Antagonists

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Conivaptan (RoA = IV)

Tolvaptan (RoA = PO)

Front 29

MoA of Vasopressin/ADH Antagonists

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Work at the medullary collecting duct to competitively block V2 receptors (conivaptan also does V1a) --> decreasing the synthesis of apical aquaporin channels; increase water diuresis; increase renal excretion of Na, K, Ca

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Therapeutic Uses of Vasopressin/ADH Antagonists

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SIADH; chronic euvolemic hyponatremia

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CI of Vasopressin/ADH Antagonists

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Hypovolemic hyponatremia; concurrent use with strong CYP inhibitors

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AE of Vasopressin/ADH Antagonists

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Infusion site reactions (C);
nausea, xerostomia (T); nephrogenic diabetes insipidus; postural hypotension; hypokalemia