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Topical– Brinzolamide, Dorzolamide

Loop Diuretics

Systemic– Acetazolamide, Methazolamide

Ethacrynic acid






Loop Diuretics (Furosemi de)

  • 40-100 mg up to 2 gm orally IM or IV
  • It is secreted from PT by organic anion transport and reaches AscLH where it acts from luminal side
  • Major site of actin is the thick AscLH (therefore called loop diuretics) where furosemide inhibits Na+-K+-2Cl cotransport
  • K+ excretion is increased mainly due to high Na+ load reaching DT
  • However at equinatriuretic doses, K+ loss is less than with thiazide
  • Furosemide increases Ca2+ and Mg2+ excretion
  • Hypokalemia: prevented by-
    • High dietary intake
    • Supplements of KCl
    • Concurrent use of K+ sparing diuretics
  • Acute saline depletion- cause dehydration and marked fall in BP
  • Dilutional hyponatremia
  • Hearing loss
  • GIT- N, V, D
  • CNS- Headache, giddiness, weakness, paresthesia, impotence
  • Allergic manifestations- Rashes, photosensitivity, blood dyscrasias
  • Hyperuricemia- lower incidence than thiazide
  • Hyperglycemia and hyperlipidemia
  • Hypocalcemia
  • Magnesium depletion
  • Brisk diuresis in cirrhotic patient- precipitate mental disturbances and hepatic encephalopathy
  • Edema- of any origin cardiac, hepatic or renal
  • Acute pulmonary edema (acute LVF, following MI)
  • Cerebral edema
  • Hypertension
  • Hypercalcemia of


  • Along with blood transfusion in severe anemia, to prevent volume overload


/Triamter ene

  • 5-10 mg/day
  • Luminal membrane of late DT and CD cells express a distinct amiloride sensitive Na+ channel
  • Amiloride and triamterene block luminal Na+ channel and indirectly inhibit K+ excretion
  • They increases excretion of Na+

and Cl-

  • Hyperkalemia
  • Diarrhea
  • Dry mouth
  • Skin rash
  • Edema disorders with diuretics
  • Pseudo-aldosteronism

Thiazide diuretics

  • Hydrochloro thiazide- 12.5-50 mg OD
  • Secreted via PT through organic acid secretory pathway; reach DT along with tubular fluid
  • Primary site of action in the cortical diluting segment or the early DT; here they inhibit Na+-Cl symport at the luminal membrane
  • Under thiazide action, increased amount of Na+ is presented to distal nephron, more of it exchanges with K+ -> urinary K+ excretion is increased parallel to natriuretic response
  • They decreases Ca2+ and increases Mg2+ excretion
  • Furosemide’s plus:
  • No-Hearing loss
  • Hyperuricemia- More incidence with thiazide
  • Hypercalcemia
  • Precipitate renal or hepatic failure
  • Edema- mild to moderate cases
  • Hypertension
  • Diabetes insipidus
  • Hyperalciuria
  • Chlorthalidone- used in correction of hypocalcemia due to hypoparathyroidism

Acetazolamid e

  • 250 mg OD/BD
  • It is sulphonamide derivative which noncompetitively but reversibly inhibits Case (type II) in PT cells resulting is slowing of hydration of CO2-> decreased availability of H+ to exchange with luminal Na+ through Na+-H+ antiporter.
  • HCO3 cannot be reabsorbed and is lost in

urine; so patient will develop metabolic acidosis.

  • Due to excess H+ now available for exchange distally. Hence it is self-limiting diuretic
  • Metabolic Acidosis
  • Hypokalemia
  • Drowsiness
  • Paresthesia
  • Fatigue
  • Abdominal discomfort
  • Hypersensitivity- fever, rashes
  • BM depression
  • Liver ds.- Precipitate Hepatic coma so contraindicated
  • Due to self-limiting action, production of acidosis and hypokalemia not used as diuretics
  • Glaucoma
  • To alkalinize urine- UTI, certain acidic drug poisoning
  • Acute mountain sickness- Symptomatic relief and prophylaxis
  • Periodic paralysis
  • Resistant epilepsy- Decreases CSF production


  • Not

absorbed orally; given IV

  • 25%

solution 1.5-2

gm/kg rapidly IV 100ml, 8

hr. ly

  • On IV administration it is freely filtered at glomeruli and undergoes limited reabsorption
  • Retains water iso-osmotically in PT- dilutes luminal fluid which opposes NaCl reabsorption
  • Inhibits transport process in the thick AscLH by an unknown mechanism
  • Expands extracellular fluid volume- increase GFR and inhibit renin release
  • Increase renal blood flow, especially to medulla- medullary hypertonicity is reduced- corticomedullary osmotic gradient dissipated -> passive salt reabsorption is


  • Pulmonary edema
  • Heart failure

Contraindicated in

  • ATN
  • Anuria
  • Pulmonary edema
  • Acute LVF
  • CHF
  • Cerebral hemorrhage
  • Headache, N, V
  • Mannitol is never used for treatment of chronic edema or as a natriuretic
  • Increased ICP- cerebral edema
  • Increased intraocular pressure
  • To maintain GFR and urine flow in impending ARF- prerenal cause
  • To counteract low osmolality of plasma/ECF due to rapid hemodialysis or peritoneal dialysis

Glycerol and isosorbide

  • Orally- 0.5-1.5 g/kg oral


  • Same as mannitol
  • IV glucose can cause hemolysis
  • Not suitable in


  • Raised IOP, ICP


  • 25-100

mg/day daily orally

  • Spironolactone acts from interstitial side of tubular cells in late DT and CD combines with MR and inhibit formation of Aldosterone induced Proteins in competitive manner; increases Na+ and decreases K+ excretion
  • It has no action in absence of aldosterone
  • Hyperkalemia
  • Acidosis
  • Drowsiness, ataxia, mental confusion
  • Epigastric distress, loose motion
  • Gynecomastia, ED or loss of libido in men
  • Breast tenderness, menstrual irregularity

in female

  • Conn’s syndrome
  • To counteract potassium loss due to thiazide and loop diuretic
  • Edema
  • Hypertension
  • CHF
  • Cirrhosis and nephrotic syndrome where there is secondary hyperaldosteronism


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