(From Baby Katzung and lecture, 10 Feb 2001, by Brian Buschman)
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Acetazolamide blocks carbonic anhydrase in the proximal tubule as well as in other tissues. In the kidney it leads to increased HCO3- excretion and K+ wasting. This results in a metabolic acidosis.
It also results in decreased HCO3- secretion into the aqueous humor thereby helping treat glaucoma. Glaucoma is the only clinical use for acetazolamide. It is not used for dieresis because of the acidotic side effects.
Adverse affects are focused on metabolic acidosis and on potassium wasting.
Furosemide and ethacrynic acid work to inhibit the cotransport of Na+, K+ and Cl- back into the blood from the nephron. This not only causes excretion of more of these ions but it also messes up the luminal potential and inhibits the reuptake of Ca++. This whole process messes up the salt system and causes excess renin secretion.
The duration of loop diuretics is very short. The only last about 4 hours or less.
Loop diuretics cause a metabolic alkalosis.
Furosemide and ethacrynic acid are used in the treatment of states with edema like CHF and ascites. They also cause pulmonary vasodilatation so they become very useful in pulmonary edema. In causes of hypercalcemia due to malignancy you can administer furosemide with electrolyte replacement.
Adverse affects include hypokalemic metabolic alkalosis. Potassium wasting can be severe. If overused they can cause hypovolemia.
Hydrochlorothiazide (or any thiazide) and chlorthalidone as well as thiazide-like drugs like indapamide all inhibit NaCl reabsorption in the early distal tubule. The urine has more NaCl. This causes reabsorption of Ca2+. Therefore loop diuretics waste Ca2+ and thiazides increase Ca2+.
Thiazides work great when used with a loop diuretic. They are used in hypertension and are great at lowering blood volume and prompting vasodilatation. Since they reduce urine Ca2+ it also reduces chronic renal calcium stone formation.
Adverse affects include massive Na+ dieresis and hyponatremia. (Don’t hike the grand canyon while you are taking thiazides.) It will have it’s share of potassium wasting and some metabolic acidosis.
Spironolactone is an aldesterone antagonist. It thereby turns off Na+/K+ pumps in the collecting duct.
Amiloride and triamterene block the Na+ channels in the collecting duct.
Both types increase Na+ clearance while decreasing K+ and H+ excretion hence the name K+-sparing. They cause a hyperkalemic metabolic acidosis.
These drugs are used with patients who are on other drugs and experiencing hypokalemia that is uncontrolled by other means (like diet). Spironolactone is also used with hyperaldesteroneism. Adverse affects are related to hyperkalemia. Never give a potassium sparing diuretic and K+ supplements to the same patient. Other adverse affects include gynecomastia.
Mannitol is a drug that is filtered but not reabsorbed. This makes it great for getting rid of free H2O. mannitol will also extract water from tissues into the blood. This will help reduce intracranial pressure. This method may cause hyponatremia by pulling other solutes that are not actually reabsorbed right along with it.
ADH and desmopressin are ADH agonists. Demeclocycline and lithium ions are ADH antagonists. ADH causes increased cAMP that leads to more free water reabsorption in the collecting duct.
ADH and desmopressin reduce urine volume and are used with pituitary diabetes insipidus (hyperantidiuretic hormone). Lithium ion and demeclocycline are V2 antagonists used to counteract ADH secreting tumors. Adverse affects are related to volume disturbances.
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