Diuretics Flashcards
Mannitol MOA
MOA: Osmotic diuretic. inhibits water reabsorption throughout the tubule. Increases urine volume.
Target: descending LOH and PCT
Carbonic Anhydrase Inhibitors and MOA
acetazolamide and dorzolamide
carbonic anhydrase inhibition in PCT
Urinary Electrolytes:
↑ Na+ ↑K+
↑↑ HCO3
Blood: Acidosis
Carbonic Anhydrase Inhibitors Uses
Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri.
Mannitol Use
Use: Drug overdose, elevated intracranial/intraocular pressure.
Side effects and ADR of Mannitol
Side effects: acute hypovolemia
ADR: Pulmonary edema, dehydration. Contraindicated in anuria, HF.
Carbonic Anhydrase Inhibitors side effects:
Side effects:
- Hyperchloremic metabolic acidosis
- Renal stone: due to increase urine phosphate and calcium
- Hypokalemia
- Decreases urine NH4 + excretion, worsening hepatic coma
- Cross-allergy with sulfonamide
- Paresthesias
CA inhibitors contraindications
Contraindications:
Hepatic encephalopathy
Sulfonamide allergy
Loop diuretics and MOA
Furosemide, bumetanide, torsemide
Ethacrynic acid - no sulfonamide-like
Inhibit cotransport system (Na+/K+/2Cl−) of thick ascending limb of loop of Henle.
Urine: ↑↑ Na+ ↑K+ ↑ Ca2+ ↑ Mg2+ ↑ Cl-
Blood: Alkalosis
Loop diuretics uses
Uses: Edematous state Hyperkalemia Hypercalcemia (Loops Lose Ca2) Acute renal failure Acute heart failure Hypertension emergency
Loop diuretics ADR: OHH DAANG
Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), metabolic Alkalosis, Nephritis (interstitial), Gout.
Loop diuretics drug interactions:
Drug interactions
– Aminoglycosides (enhanced ototoxicity)
– Lithium (chronic loop administration,↓clearance)
– Digoxin (↑ toxicity due to electrolyte disturbances)
Thiazides and MOA
Hydrochlorothiazide, chlorthalidone, metolazone.
Na+/Cl− transporter inhibition in early DCT
Urine:
↑ Na+ ↑K+
↑ Cl-
↓ Ca2+
Blood: Alkalosis
Thiazides Uses
USES: Hypertension MOA: Short term is due to decrease of Blood Volume Long term is due to direct decrease in vessel tension (possible by K+ channel opening) Kidney stone or hypercalciuria Nephrogenic diabetes insipidus Chronic heart failure
Thiazides ADR (HyperGLUC)
HyperGLUC
Hypokalemic metabolic alkalosis, hyponatremia,
hyperGlycemia,
hyperLipidemia,
hyperUricemia,
hyperCalcemia.
Sulfa allergy.
K sparing diuretics MOA - The K+ STAys
Aldosterone antag: Spironolactone and eplerenone
ENaC direct inhibitors: Triamterene, and Amiloride
Spironolactone and eplerenone competitive aldosterone receptor antagonists in cortical collecting tubule.
Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule.
Combining K+-sparing diuretics with ________ may cause hyperkalemia.
ACEIs or ARBs
Uses of K sparing diuretics:
Hyperaldosteronism, K+ depletion, HF, hepatic ascites (spironolactone), nephrogenic DI (amiloride), antiandrogen.
spironolactone and eplerenone decrease chronic heart failure (CHF) mortality- increase long term survival
ADR of K sparing diuretics
Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (eg, gynecomastia, antiandrogen effects)
How do B Blockers effect RAAS ?
BBs reduce renin, angio I, angio II, ald and do not affect bradykinin
Aliskren MOA and effect on RAAS
inhibits renin
increase renin increase angio I decrease anio II decrease ald No effect on BradyK
ACE inhibitors MOA and effect on RAAS
inhibit ACE
increase renin increase angio I decrease anio II decrease ald increase BradyK
Angio II receptor 1 blocker (ARB) effect on RAAS
increase renin increase angio I increase angio II decrease ald increase BradyK
Angio II receptor 1 blocker (ARB) ADR - (CATCHH)
Captopril’s CATCHH.
Cough, Angioedema (due to bradykinin; contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), Creatinine ( GFR), Hyperkalemia, and Hypotension.
No use in renal artery stenosis, will cause renal failure
Uses of ACE inhibitors
Hypertension, HF ( mortality), proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension.
