Diuretics MOA Notes Indications Side effects Drugs

1. Mannitol Inhibits water Increases urine Dec IOP in glaucoma- Acute hypovolemia Mannitol
reabsorption throughout volume promotes drainage of
the tubule aqueous chamber

Dec ICP

Olguric states
(rhadomyolysis)
2. Carbonic Carbonic Anhydrase Decrease formation of Glaucoma Bicarbnaturia Acetazolamide
Anhydrase inhibitor inhibition in PCT and H+ inside PCT Acute mountain sickness Metabolic acidosis Dorzolamide
Principal cells of CD Dec Na/H antiport (prophylaxis prior to Hypokalemia
Increase Na and HCO3 climb; acidosis is Hyperchloremia
excretion protective) Paresthesias (inhibits CA in
Increase diuresis Tx: Metabolic alkalosis CNS)
Alkalinizes urine and Renal stones (alkaline urine
causes rapid increases risk for PO4 stones)
metabolic acidosis
Contraindicated in sulfa
allergy

3. Loop diuretics Inhibits NaK2Cl Short half-life (not For high-volume diuresis Hypokalemia Furosemide
- enter through cotransporter in TAL of used in treatment of such as Pulmonary Metabalic alkalosis Torsemide
glomerulus / via loop of Henle; significant hypertension) edema or to decrease Hypomagnesemia Ethacrynic acid
secretion by OAT Natriuresis fluid overload in heart Hypocalcemia
(uric acid transport failure Ototoxicity (endolymph has
site) NaK2Cl cotransporter,
Used for treatment of blockage prevents normal
NaK2Cl cotransporter hypercalcemia due to it’s electrolyte balance)
creates an AP, calcium-wasting effect
opening paracellular (“Loops lose calcium”) Contraindicated in sulfa
spaces for allergy
reabsorption of Ca,
Mg and loss of this (+) EXCEPT Ethacrynic acid
potential decreases
reabsorption of Ca
and Mg
4. Thiazide diuretics Inhibits NaCl Long lasting but cause For treatment of Metabolic alkalosis (due to Hydrochlorothiazide
-enter through cotransporter at DCT, less diuresis (less hypertension because increased Na delivery to CD Chlorthalidone
glomerulus / via leading to natriuresis potent) than Loops rapid diuresis is not and inc gene expression of Indapamide
secretion by OAT and diminished necessary aldosterone; inc reabsorption
(uric acid transport intravascular blood Increase Ca resorption of Na in intercalated cells, inc
site) volume dec BP due to opening of Prevent stone formation H+ excretion in principal cells)
voltage-gated Ca in those with Hypokalemia
channel, leading to hypercacliuria and at risk Hyperuricemia (pharmacologic
decreased calcium for Ca Oxaloacetate inhibition, actively secreted by
excretion in urine OAT)
Nephrogenic diabetis Hypertriglyceridemia
insipidus (paradox: give Hypercalcemia
diuretic so that patient
will urinate less) Contraindicated in sulfa
allergy
5. Potassium- Sparing Amiloride- blocks Amiloride: heart failure Hyperkalemia Amioride and
Diuretics sodium channels in when hypokalemia is a Spironolactone- blocks Triamterene
Principal cells of CD concern testosterone receptor
causing natriuresis. (androgen antagonism, like Spironolactone and
Normally this sodium Spironolactone: heart gynecomastia) eplerenone
channels reclaims failure as well as
sodium at the expense aldoseterone-secreting Eplerone- aldosterone
of potassium tumors before surgical antagonist with NO
correction antiandrogen effects
Spironolactone- causes
blockage of aldosterone
receptor, preventing
upregulation of principal
cells and leading to
decreased sodium
reclamation
Note:
Sodium reabsorption:
PCT >60%; TAL > 25%; DCT <10%; CD <5%