Carbonic anhydrase inhibitor gruop 5
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Carbonic anhydrase inhibitors like acetazolamide, methazolamide, and dichlorphenamide are sulfonamide derivatives that reversibly inhibit the carbonic anhydrase enzyme. This reduces hydrogen ion exchange and carbon dioxide reabsorption in the kidney, increasing sodium and bicarbonate excretion and producing alkaline urine. They are also used to treat glaucoma by decreasing aqueous humor production in the eye. Adverse effects can include vomiting and hyperchloremic acidosis due to chloride retention in the kidney.
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Diuretics act at different sites along the nephron to promote the excretion of sodium, chloride, and water. The main classes are carbonic anhydrase inhibitors, loop diuretics, thiazides, potassium-sparing diuretics, and osmotic diuretics. They are used to treat conditions like edema, hypertension, and liver cirrhosis. Each class has a distinct mechanism of action and side effect profile. For example, loop diuretics inhibit sodium reabsorption in the loop of Henle but can cause ototoxicity, while thiazides target the distal tubule and cause hypokalemia. The site and mechanism of the drug determines its clinical applications and adverse effects
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This document discusses the sites of action and mechanisms of various classes of diuretic drugs, including carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazide diuretics, potassium-sparing diuretics, and others. It describes how each class of diuretic targets a specific site along the nephron to inhibit reabsorption of sodium and water, thereby increasing urine output and reducing extracellular fluid volume. Adverse effects and therapeutic uses are also summarized for each diuretic class.
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Diuretics work by increasing urine output and the excretion of electrolytes like sodium and chloride. They are classified as thiazide diuretics, loop diuretics, potassium-sparing diuretics, carbonic anhydrase inhibitors, and osmotic diuretics. Thiazide diuretics such as hydrochlorothiazide work by inhibiting sodium and chloride reabsorption in the distal convoluted tubule. Loop diuretics like furosemide inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle. Potassium-sparing diuretics prevent potassium loss by inhibiting sodium reabsorption in the collecting ducts. Carbonic anhydrase inhibitors
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Loop diuretics such as furosemide act directly on the ascending loop of Henle to increase urinary output and reduce fluid volume and blood pressure. Thiazide diuretics such as hydrochlorothiazide act on the distal convoluted tubule to inhibit sodium reabsorption and increase the excretion of sodium, chloride, water and potassium. Potassium-sparing diuretics such as spironolactone competitively bind to aldosterone receptors to prevent potassium loss while sodium and water are excreted. Osmotic diuretics such as mannitol work by increasing the osmolarity of the renal filtrate to pull water from tissues into the renal tubules.
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This document summarizes different classes of diuretic drugs, including their mechanisms of action, sites of action in the nephron, and clinical uses. It describes how loop diuretics inhibit sodium reabsorption in the thick ascending loop of Henle, thiazide diuretics inhibit sodium reabsorption in the distal convoluted tubule, and potassium-sparing diuretics inhibit sodium reabsorption in the collecting ducts and tubules. The summary provides key details on the pharmacology and effects of major diuretic drug classes to treat conditions like edema, heart failure, and hypertension.
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Carbonic anhydrase inhibitor gruop 5
- 2. Preparation & Chemistry Acetazolamide Methazolamide sulfonamide derivatives Dichlorphenamide
- 3. Mechanism of action Reversibly inhibit CA enzyme in proximal convoluted tubule cause - reduction in hydrogen ion for Na+--H+ exchange - Suppress CO2 reabsorption from glomerular filtrate - Na+-HCO3- excretion is increased # lead to production of alkaline urine
- 4. To maintain ionic balance, Cl- is retained by kidney cause Hyperchloremic acidosis induce Refractory state and decrease diuresis
- 5. High concentration of CA occur in ciliary process of eye CA enzyme involve in aqueous humor formation CA inhibitors reduce intraocular pressure in glaucoma by decreasing production of aqueous humor.
- 6. Therapeutic uses Reduce the rate of aqueous humors formation in treatment of glaucoma Use as adjuncts in treatment of metabolic alkalosis
- 7. Pharmacokinetics Acetazolamide and dichlorphenamide are absorb orally distributed to tissue with high CA concentration (renal cortex, eye and RBC) Excreted by kidney by active secretion and passive reabsorption. Onset of diuretic action is 30 mins with a duration of 6-12 hours in small animal.
- 8. Horse - IV # Distribution t1/2:60 mins # Elimination t1/2:~ 7.5 hours - Orally # reach peak plasma level ~ 2 hours # bioavailability of acetazolamide:~25%
- 9. Administration For glaucoma-acetazolamide, metazolamide, ethazolamide or dichlorphenamide given orally 2-3 times daily. Acute cases: 1 IV dose of acetazolamide followed by an oral dosage.
- 10. Adverse effect Toxicity is rare. GI disturbance- vomitting after oral administration. 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.