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Additional information about the drug Acetazolamide

Acetazolamide, sold under the trade name Diamox among others, is a medication used to treat glaucoma, epilepsy, altitude sickness, periodic paralysis, idiopathic intracranial hypertension, and heart failure.
Common side effects include numbness, ringing in the ears, loss of appetite, vomiting, and sleepiness.
Acetazolamide came into medical use in 1952.
1 Medical uses
1.1 High altitude sickness
1.2 Pregnancy and lactation
2 Side effects
2.1 Contraindications
2.2 Interactions
3 Mechanism of action
4 References
Medical uses
It is used in the treatment of glaucoma, drug-induced edema, heart failure-induced edema, epilepsy and in reducing intraocular pressure after surgery.
In epilepsy, the main use of acetazolamide is in menstrual-related epilepsy and as an add on to other treatments in refractory epilepsy.
It has also been used to prevent methotrexate -induced kidney damage by alkalinalizing the urine, hence speeding up methotrexate excretion by increasing its solubility in urine.
High altitude sickness
In the treatment of mountain sickness, acetazolamide forces the kidneys to excrete bicarbonate, the conjugate base of carbonic acid. By increasing the amount of bicarbonate excreted in the urine, the blood becomes more acidic.
Pregnancy and lactation
Acetazolamide is pregnancy category B3 in Australia, which means that studies in rats, mice and rabbits in which acetazolamide was given intravenously or orally caused an increased risk of fetal malformations, including defects of the limbs.
Limited data are available on the effects of nursing mothers taking acetazolamide. Therapeutic doses create low levels in breast milk and are not expected to cause problems in infants.
Side effects
Common adverse effects of acetazolamide include the following: paraesthesia, fatigue, drowsiness, depression, decreased libido, bitter or metallic taste, nausea, vomiting, abdominal cramps, diarrhea, black feces, polyuria, kidney stones, metabolic acidosis and electrolyte changes ( hypokalemia, hyponatremia ).
Contraindications include:
Hyperchloremic acidosis
Hypokalemia (low blood potassium)
Hyponatremia (low blood sodium)
Adrenal insufficiency
Impaired kidney function
Hypersensitivity to acetazolamide or other sulfonamides.
Marked liver disease or impairment of liver function, including cirrhosis because of the risk of development of hepatic encephalopathy. Acetazolamide decreases ammonia clearance.
It is possible that it might interact with:
Amphetamines, because it increases the pH of the renal tubular urine, hence reducing the clearance of amphetamines.
Other carbonic anhydrase inhibitors — potential for additive inhibitory effects on carbonic anhydrase and hence potential for toxicity.
Ciclosporin, may increase plasma levels of ciclosporin.
Antifolates such as trimethoprim, methotrexate, pemetrexed and raltitrexed.
Hypoglycemics, acetazolamide can both increase or decrease blood glucose levels.
Lithium, increases excretion, hence reducing therapeutic effect.
Methenamine compounds, reduces the urinary excretion of methenamines.
Phenytoin, reduces phenytoin excretion, hence increasing the potential for toxicity.
Primidone, reduces plasma levels of primidone. Hence reducing anticonvulsant effect.
Quinidine, reduces urinary excretion of quinidine, hence increasing the potential for toxicity.
Salicylates, potential for severe toxicity.
Sodium bicarbonate, potential for kidney stone formation.
Anticoagulants, cardiac glycosides, may have their effects potentiated by acetazolamide.
Mechanism of action
Carbonic anhydrase ( ribbon ) complex with a sulfonamide inhibitor ( ball-and-sticks ). Proximal convoluted tubule. Urinary space is on left.
Acetazolamide is a carbonic anhydrase inhibitor, hence causing the accumulation of carbonic acid.
H 2 CO 3 ⇌ H 2 O + CO 2
hence lowering blood pH, by means of the following reaction that carbonic acid undergoes:
H 2 CO 3 ⇌ HCO 3 − + H +
which has a pK a of 6.3.
The mechanism of diuresis involves the proximal tubule of the kidney. The enzyme carbonic anhydrase is found here, allowing the reabsorption of bicarbonate, sodium, and chloride. By inhibiting this enzyme, these ions are excreted, along with excess water, lowering blood pressure, intracranial pressure, and intraocular pressure. By excreting bicarbonate, the blood becomes acidic, causing compensatory hyperventilation with deep respiration (Kussmaul respiration), increasing levels of oxygen and decreasing levels of carbon dioxide in the blood.
In the eye this results in a reduction in aqueous humour.
Bicarbonate (HCO 3 − ) has a pK a of 10.3 with carbonate (CO 3 2− ), far further from physiologic pH (7.35–7.45), and so it is more likely to accept a proton than to donate one, but it is also far less likely for it to do either, thus bicarbonate will be the major species at physiological pH.
Under normal conditions in the proximal convoluted tubule of the kidney, most of the carbonic acid (H 2 CO 3 ) produced intracellularly by the action of carbonic anhydrase quickly dissociates in the cell to bicarbonate (HCO 3 − ) and an H + ion (a proton ), as previously mentioned. The bicarbonate (HCO 3 − ) exits at the basal portion of the cell via sodium (Na + ) symport and chloride (Cl − ) antiport and re-enters circulation, where it may accept a proton if blood pH decreases, thus acting as a weak, basic buffer. The remaining H + left over from the intracellular production of carbonic acid (H 2 CO 3 ) exits the apical (urinary lumen) portion of the cell by Na + antiport, acidifying the urine. There, it may join with another bicarbonate (HCO 3 − ) that dissociated from its H + in the lumen of the urinary space only after exiting the proximal convoluted kidney cells/glomerulus as carbonic acid (H 2 CO 3 ) because bicarbonate (HCO 3 − ) itself can not diffuse across the cell membrane in its polar state. This will replenish carbonic acid (H 2 CO 3 ) so that it then may be reabsorbed into the cell as itself or CO 2 and H 2 O (produced via a luminal carbonic anhydrase). As a result of this whole process, there is a greater net balance of H + in the urinary lumen than bicarbonate (HCO 3 − ), and so this space is more acidic than physiologic pH. Thus, there is an increased likelihood that any bicarbonate (HCO 3 − ) that was left over in the lumen diffuses back into the cell as carbonic acid, CO 2, or H 2 O.
In short, under normal conditions, the net effect of carbonic anhydrase in the urinary lumen and cells of the proximal convoluted tubule is to acidify the urine and transport bicarbonate (HCO 3 − ) into the body. Another effect is excretion of Cl − as it is needed to maintain electroneutrality in the lumen, as well as the reabsorption of Na + into the body.
Thus, by disrupting this process with acetazolamide, urinary Na + and bicarbonate (HCO 3 − ) are increased, and urinary H + and Cl − are decreased. Inversely, serum Na + and bicarbonate (HCO 3 − ) are decreased, and serum H + and Cl − are increased. H 2 O generally follows sodium, and so this is how the clinical diuretic effect is achieved, which reduces blood volume and thus preload on the heart to improve contractility and reduce blood pressure, or achieve other desired clinical effects of reduced blood volume such as reducing edema or intracranial pressure.

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