21-31 - Diuretics Flashcards
carbonic anhydrase inhibitor
acetazolamide
MOA acetazolamide
carbonic anhydrase inhibitor
decreases PCT reabsorption of HCO3-
also decreases formation of HCO3- and inhibits NH4+ secretion
end physiological actions of acetazolamide
decrease RBF and GFR
diuresis
increased K excretion
** metabolic acidosis
clinical indications for acetazolamide
- glaucoma
- acute mountain sickness
- induce urinary alkalinization
- edema (combine with NKCC or NCC inhibitor)
is carbonic anhydrase located only in the renal system?
no
also in ciliary body, kidney, erythrocytes, gut, choroid plexus, and glial cells
adverse effects of acetazolamide
- hyperchloremic metabolic acidosis
- renal stones
- renal loss of K+
contraindication for acetazolamide
cirrhosis
because increases plasma NH4+
osmotic diuretic example
mannitol
MOA mannitol
osmotic diuretic
MOA osmotic diuretics
increase tubular fluid osmotic pressure and thereby decrease water reabsorption
most potent diuretics
loop agents
indications for mannitol
- phophylaxis of acute renal failure
- cerebral edema
- dialysis disequilibrium syndrome
- acute attacks of glaucoma
why can osmotic diuretics be used for prophlylaxis of acute renal fialure?
expands the ECV, maintains the GFR, increases tubular fluid flow, prevent tubule obstruction from shed cell
reduces renal edema
adverse effects of osmotic diuretics
risk of pulmonary edema in pts with heart failure
hyponatremia or hypernatremia depending on speed of fluid loss
contraindications for mannitol
anuria due to real disease
impaired liver function
active cranial bleeding
NKCC inhibitor
aka loop diuretics
ex: furosemide
furosemide clasification
loop diuretic aka NKCC inhbitor
MOA furosemide
inhibits NKCC cotransporter –> inhibit reabsorption of solute
also venodilation (decreased RA pressue and pulmonary capillary wedge pressure)
what happens to calcium and magnesium with loop diuretics?
increases calcium excretion 30% (gradient potential change)
increases Mg excretion by 60% (b/c voltage dependent)
indications for loop diuretics
- pulmonary edema
- CHF
- acute renal failure
- hypercalcemia
major adverse effect of furosemide
hypokalemia
MOA NCC inhibitors
block NaCl cotransporter and decrease calcium excretion
chlorthalidone classification
NCC inhibitor
indications for chlorthalidone
HTN edema with CHF hypercalciuria nephrolithiasis Nephrogenic diabetes insipidus
NCC inhibitors aka
thiazides and sulfonamides
how does chlorthalidone treat nephrogenic diabetes insipidus?
increases renal sodium reabsorption
recovers aquaporin2 abundance
inhibitor of renal epithelial sodium channels
amiloride
MOA amiloride
block epithelial sodium channels on prinicpal cells in late DCT and initial connecting tubule and cotical collecting ducts –> omdest natriuresis and prevention of K loss
indications for amiloride
- hypokalemic alkalosis
- combo with loop diuretics and thiazides to prevent hypokalemia
aldosterone receptor agonist
spironolactone
MOA spironolactone
antagonize aldosterone receptos in renal collecting tubules
decreas sodium reabsorption –> K sparing diuretic
pleiotropic effects of spironolactone
- prevention of LV remodeling and cardiac fibrosis
- prevention of sudden cardiac death
- hemodynamic effects
- vascular effects
indications for spironolactone
- edema and HTN
- added to therapy for HF
- primary aldosteronism
- refractory edema associated with secondary aldosteronism
what is refractory edema with seconday aldosteronism?
CF, hepatc cirrhosis, nephrotic syndrome, and severe ascites all make the body think it doesn’t have enough water –> increased aldosterone secretion
treat with spioronolactone
adverse effect of spironolactone
hyperkalemia
other adverse effects include metabolic acidosis in cirrhotic pts, and effects due to binding to other steroid receptors including gynecomastia, hirsutism, deepened voice, etc.
