Diuretics Flashcards
Carbonic anhydrase inhibitor
Acetazolamide
NaK 2Cl symport inhibitor
Furosemide
Na Cl symport inhibitors
Hydrochlorthiazide
Chlorothiazide
2 groups of K sparing diuretics
Epithelial Na channel inhibitors
Aldosterone antagonists
Epithelial Na channel inhibitors
Amiloride
Triamterene
Aldosterone antagonists
Spironolactone
Eplerenone
Osmotic diuretics
Mannitol
Vasopressin receptor antagonists
Demeclocycline
Tolvaptan
Endogenous OAT substrates (4
Urate
Bile acids
Oxalate
Prostaglandins
Exogenous OAT substrates (6)
Hydrochlorothiazide Furosemide Acetazolamide Probenecid Pencillin Aspirin
OCT endogenous substrates (3)
Creatinine
Epinephrine
Histamine
OCT exogenous substrates (5)
Amiloride Triamterene Cimetidine Atropine Quinine
Site of action is in proximal tubule, where it competitively inhibits carbonic anhydrase
Acetazolamide
Carbonic anhydrase is responsible for ___ reabsorption and __ secretion
NaHCO3, acid (H+)
Control vs. \_\_\_\_ Vol: 1 vs 3 (ml/min) pH: 6 vs 8 Na+: 72 vs. 302 K+: 22 vs. 260 Cl-: 85 vs. 95 HCO3-: 1 vs. 120
Acetazolamide (CA inhibitor)
Acetazolamide effect on renal hemodynamics
Increases NaCl delivery to macula densa, reducing RBF (afferent arterioles constricted) and GFR
Uses=
Open-angle glaucoma
Altitude sickness
Epilepsy
Acetazolamide
ADEs=
Renal stone formation (urinary alkalinization)
Potassium wasting
Worsens hepatic encephalopathy (diversion of ammonia into systemic circulation)
Acetazolamide
Site of action is in thick ascending limb of the loop of Henle, inhibits Na+-K+-2Cl- symporters
Furosemide (also abolishes trans-epithelial potential difference that drives paracellular transport of Ca and Mg)
Control vs. \_\_\_\_ Vol: 1 vs 8 (ml/min) pH: 6 vs 6 Na+: 72 vs. 1615 K+: 22 vs. 115 Cl-: 85 vs. 990 HCO3-: 1 vs. 1
Furosemide
Urinary effects:
Increase in Ca and Mg excretion
Decreased uric acid excretion (chronic effect, exacerbates gout)
Reduces ability of kidney to dilute urine when over-hydrated and concentrate urine during dehydration
Furosemide
Furosemide renal hemodynamic effects:
- Increases RBF and redistributes it to cortex (prostaglandin-mediated)
- Stimulates release of renin (blocks TGF by inhibiting salt transport into the macula densa)
Acutely increases systemic venous capacitance and decreases left ventricular filling pressure
May be beneficial to patients with pulmonary edema
Furosemide (prostaglandin mediated)
PK= highly protein bound
Delivered to apical membrane by OAT
Short half-life
“Post-diuretic” sodium retention
Furosemide