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Flashcards in Diuretics Deck (21):
1

Furosemide

MOA: blocks NKCC in ThAL
Effects:decreases renal vascular resistance and increases renal blood flow
Use: DOC for managing edema assoc w/ CHF, hepatic or renal dz, or moderate-b severe HTN (pt's that dont respond to thiazides)

2

Loop Diuretic Mechanism

Blocks Na+/2Cl-/K+ co-transporter (NKCC), increase in concentration of these ions in the tubular fluid = increase in H2O excretion
SE: hypokalemia, ototoxicity, alkalosis, hyperuricemia

3

Loop Diuretic Actions

Increased Ca2+ excretion, increased Mg2+ excretion, decreased renal vascular resistance, increased renal blood flow, increased PG synthesis

3

Loop Diuretic PK

Given PO and parenteral
t1/2 = 2-4h

4

Loop Diuretics SEs

Ototoxicity (d/t ion imbalance in the endolymph in ear), hyperuricemia, acute hypovolumia, hypokalemia, hypomagnesemia, allergic rxn's

4

Names of Thiazide Diuretics?

Hydrochlorothiazide / Chlorthalidone / Metolazone

5

Thiazide Uses

DI (produce hyperosmolar urine), premenstrual edema, first-line antihypertensive
*particularly useful in black and elderly pt's

5

Thiazide Mechanism

Acts on DCT, blocks Na+/Cl- co-transporter (NCCT)

6

Thiazide Effects

πŸ‘†πŸ½ Na+, Cl-, K+, Mg2+ excretion, πŸ‘‡πŸ½ Ca2+ excretion; πŸ‘‡πŸ½ PVR d/t decrease in blood volume initially but over time the volume recover but decreased BP effects remain

7

Chlorthalidone

Long duration of action (t1/2 - 40-60h)
Use: tx HTN once daily

8

Metolazone

Most potent, causes Na+ excretion in advanced kidney failure

9

Thiazide SEs

Hypokalemia, hyponatremia, hyperurecemia, hyperglycemia, hyperlipidemia, hypersensitivity

10

Torsemide

Loop diuretic

11

Amiloride and Triamterene

K+ sparing diuretic (Na+ channel inhibitors)
MOA: block Na+ transport channels, do not rely on aldosterone presence
Effects: decreases Na+/K+ exchange preventing K+ loss
SE: hyperkalemia, hyponatremia, leg cramps, GI upset, dizziness, puritis, HA, minor visual changes

12

Eplerenone / Spironolactone

K+ sparing diuretics (aldosterone antagonists)
MOA: act in collecting duct to antagonize aldosterone receptor sites
Effects: πŸ‘‡πŸ½Na+ reabsorption and πŸ‘‡πŸ½ K+ excretion, prevents cardiac remodeling
Use: HTN and HF (first line in pts w/ both)
SE: gastric upset, peptic ulcers, anti-androgen effects (acts as antagonist), hyperkalemia, nausea, lethargy, mental confusion

13

Spironolactone

Structural similarity to androgens so binds those receptors but acts as antagonist = anti-androgen effects

14

Acetazolamide

Carbonic anhydrase inhibitor
MOA: blocks CA in proximal tubule cells, so less Na+ is exchanged for the H+
Effects: decreased activity of Na/K-ATPase, HCO3-retained in lumen increasing urinary pH
PK: PO well absorbed, IV for acute tx of closed angle glaucoma, t1/2 = 3-6h
SE: metabolic acidosis, hyponatremia, hypokalemia, crystalluria, malaise, fatigue, depression, HA, GI upset, drowsiness, paresthesia

15

Mannitol

Osmotic diuretic
MOA: raises osmotic pressure of plasma drawing H2O out of body
Action: increased urine volume via osmotic diuresis
PK: IV
Use: inc urine flow in acute renal failure, reduce ICP and tx cerebral edema, promote excretion of toxins (e.g. Myoglobin in rhabdomyolysis)
SE: extracellular water expansion, tissue dehydration
Contra: CHF, pulmonary edema

16

Conivaptan

ADH antagonist at V1 and V2 receptors in collecting duct
PK: IV only, metabolized by and potent inhibitor of CYP 3A4
Use: euvolemic and hypervolemic hyponatremia, SIADH, HF (sometimes)
SE: thirst, a-fib, GI and electrolyte disturbances, nephrogenic DI, infusion site rxn
Contra: hypovolemic hyponatremia, ESRD

17

Eplerenone and Spironolactone Uses

HF: adjunct to prevent cardiac remodeling
HTN: adjunct
1Β° hyperaldosteronism: dx and tx
Edema: assoc w/ excess aldosterone

17

Thiazide PK

Orally effective, t1/2 = 40h (takes 1-3 wks to produce stable effect)