Diuretics

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Diuretics

 

agents that increase the excretion of urine and decrease the amount of fluid in the tissues and serous cavities. Natriuretics increase the excretion of sodium ions. Diuretics are used primarily to treat edema accompanying cardiovascular, liver, and kidney diseases. Depending on their effect, they are classified as renal diuretics, which act directly on the kidneys and have the most pronounced effect, and extrarenal diuretics, which act indirectly through other systems in the body.

Renal diuretics act by blocking the kidney enzymes responsible for the transport of electrolytes, as well as by inhibiting reabsorption in the terminal tubules, which intensifies the excretion of sodium, chlorine, and potassium ions. Among the renal diuretics are the mercury compounds Mercusal and Novurit and carbonic anhydrase inhibitors such as Diacarb and dichlorphenamide (Daranid)—sulfonamide derivatives that intensify the excretion of bicarbonate, causing a drop in the alkaline reserve in the blood and, in some cases, acidosis. Benzothiadizine and sulfamoylanthranilic and dichlorophenoxyacetic acid derivatives such as dichlothiazide (Hypothiazide), furosemide (Lasix), and ethacrynic acid (Uregit) are extremely potent diuretics that sharply increase the excretion of sodium and have a hypotensive effect. Pyrimidine and pteridine derivatives, such as Allacyl and triamterene (pterofen), inhibit tubular reabsorption of sodium and chlorine ions but do not affect the excretion of potassium. Aldosterone antagonists, including spironolactone (Aldactone and Verospiron), increase the excretion of sodium and decrease the excretion of potassium and urea.

Depending on how they act, extrarenal diuretics are classified as osmotic and other types of agents. Among the osmotic agents are potassium acetate, mannitol, and urea, which are excreted by the kidneys and absorb water. They cause the excretion of sodium and chlorine in proportion to the increase in volume of urine and are used to lower intracranial pressure and reduce cerebral edema. Acid-forming diuretics include ammonium chloride and potassium chloride, which act by the transformation of cations. The ammonium ion is transformed into urea in the liver, the calcium ion settles in the intestine in the form of phosphate or carbonate, and chlorine ions occur in excess in the blood plasma and are excreted by the kidneys with sodium.

Extracts and tinctures are sometimes prepared for use as diuretics from bearberry leaf (tincture or decoction), field horsetail (decoction or fluid extract), and Orthosiphon leaf (tincture).

References in periodicals archive ?
They have a milder action than loop diuretics, because most of the sodium has already been reabsorbed by this stage.
Loop diuretics and angiotensin-converting enzyme inhibitors increased risk for hospitalization for lithium toxicity.
Increased aldosterone activity (compensatory activation of RAAS) and loop diuretic intake promote excessive urine calcium and magnesium loss.
Table 4 Calcium Imbalances Hypocalcemia Hypercalcemia * Surgical hypoparathyroidism * Malignancies * Acute pancreatitis * Primary hyperparathyroidism * Hyperphosphatemia * Kidney transplant * Inadequate vitamin D * Immobilization * Alcoholism * Thiazides, lithium, large doses of vitamins A and D, theophylline * Sepsis * Hydration, mobilization, risk for * Loop diuretics, phenobarbital, cardiac arrest, risk for fracture, dilantin, citrate, calcitonin risk for digoxin toxicity * Do not mix IV calcium with sodium bicarbonate or phosphate (precipitate forms) Sources: Gooch, 2015; Metheny, 2012.
Unfortunately, loop diuretics are accepted as 'urine producers' among physicians in ICUs and are often used.
However, the onset of hypokalemia and hypomagnesemia with thiazides or loop diuretics may lead to increased ventricular ectopy and an increased incidence of sudden death."
Diuretic drugs, including loop diuretics and natriuretic peptides, are used frequently as a conventional therapy in patients with acute heart failure (HF).
Loop diuretics, thiazide diuretics, angiotensin receptor blocker, beta-blocker, and alpha-blocker were not associated with the risk of NOF.
The mechanism by which diuretics block the reabsorption of ions and the site of action varies; they may act at the proximal tubule (carbonic anhydrase inhibitors), loop of Henle (loop diuretics), distal tubule (thiazide diuretics), collecting tubule (potassium sparing diuretics), or combination of these sites [2].
Fluid restriction (n=39, 62.9%) with or without loop diuretics (n=34, 55%) were used in majority of patients whereas intravenous fluids mainly isotonic saline was used for volume depleted patients (n=23, 37.1%).Serum sodium level improved in 41 patients (66.1%), while 13 patients (21.0 %) showed partial improvement.
Increased urinary magnesium loss due to thiazides and loop diuretics inhibit magnesium re-absorption by the renal tubules.
Loop diuretics such as furosemide (Lasix[R]) are used commonly to treat uncomplicated hypertension in patients with renal disease.