Carbonic Anhydrase Inhibitors

1. Carbonic Anhydrase Inhibitors
Carbonic anhydrase converts H2O and CO2 into H+ and HCO3-, allowing Na+ and HCO3- to be reabsorbed into the interstitum. Acetazolamide blocks this conversion and causes HCO3- and Na+ to be excreted. The drug crosses the blood brain barrier and is eliminated in the proximal tubule (site of action). It is a weak diuretic since the Loop and Henle can compensate for the lack of reabsorption. The effects are also self-limiting. Inhibition of carbonic anhydrase will lead to increase solute delivery to the macula densa which will trigger the TGF and decrease GFR. The loss of HCO3- also leads to hyperchloremic metabolic acidosis. The body decreases the amount of HCO3- being filtered leading to enhanced NaCl reabsorption in other parts of the nephron.

Carbonic anhydrase inhibitors can be used to treat:
-open angle glaucoma
-urinary alkalinization
-metabolic alkalosis
-acute mountain sickness (by increasing ventilation)
-epilepsy
-edema
-solubilized uric acid

Adverse effects of carbonic anhydrase inhibitors include:
-metabolic acidosis
-renal stones (calcium phosphate)
-renal K+ wasting
-hypersensitivity with sulfonamide allergies

Contradictions to carbonic anhydrase inhibitors include:
-hypersensitivity with sulfonamide allergies
-acidosis
-renal disease
-cirrhosis (increase ammonium in blood)