Mechanism of action<br />Reversibly inhibit CA enzyme in proximal convoluted tubule cause<br />- reduction in hydrogen ion for Na+--H+ exchange<br />- Suppress CO2 reabsorption from glomerular filtrate<br />- Na+-HCO3- excretion is increased<br /># lead to production of alkaline urine<br />
To maintain ionic balance, Cl- is retained by kidney cause<br />Hyperchloremic acidosis induce<br />Refractory state and decrease diuresis<br />
High concentration of CA occur in ciliary process of eye<br />CA enzyme involve in aqueous humor formation<br />CA inhibitors reduce intraocular pressure in glaucoma by decreasing production of aqueous humor.<br />
Therapeutic uses<br />Reduce the rate of aqueous humors formation in treatment of glaucoma<br />Use as adjuncts in treatment of metabolic alkalosis<br />
Pharmacokinetics <br />Acetazolamide and dichlorphenamide are absorb orally distributed to tissue with high CA concentration (renal cortex, eye and RBC)<br />Excreted by kidney by active secretion and passive reabsorption.<br />Onset of diuretic action is 30 mins with a duration of 6-12 hours in small animal.<br />
Administration <br />For glaucoma-acetazolamide, metazolamide, ethazolamide or dichlorphenamide given orally 2-3 times daily.<br />Acute cases: 1 IV dose of acetazolamide followed by an oral dosage.<br />
Adverse effect<br />Toxicity is rare.<br />GI disturbance- vomitting after oral administration.<br />Contraindicated in presence of liver disease because they may precipitate hepatic coma by diverting ammonia produce in kidney from the urine to the systemic circulation as a result of urine alkalinization.<br />
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