Overview Of Diuretic

Diuretics are used clinically to treat hypertension (see Chapter 32) and to reduce edema associated with cardiac, renal, and hepatic disorders. Three fundamental strategies exist for mobilizing edema fluid: correct the underlying disease, restrict Na+ intake, or administer diuretics. The most desirable course of action would be to correct the primary disease; however, this often is impossible. Restriction of Na+ intake is the favored nonpharmacologic approach to the treatment of edema and hypertension and should be attempted; however, compliance is a major obstacle. Diuretics therefore remain the cornerstone for the treatment of edema or volume overload, particularly that owing to congestive heart failure, ascites, chronic renal failure, or nephrotic syndrome.

The clinical situation dictates whether a patient should receive diuretics and what therapeutic regimen should be used (i.e., type of diuretic, dose, route of administration, and speed of fluid mobilization). Acute pulmonary edema in patients with left-sided heart failure is a medical emergency requiring rapid, aggressive therapy including intravenous administration of a loop diuretic. In this setting, use of oral or less potent diuretics is inappropriate. On the other hand, mild pulmonary and venous congestion associated with chronic heart failure is best treated with an oral loop or thiazide diuretic, the dosage of which should be titrated carefully to maximize the benefit-to-risk ratio. Loop and thiazide diuretics decrease morbidity and mortality in heart failure; MR antagonists also reduce morbidity and mortality in heart failure patients receiving optimal therapy with other drugs. Periodic administration of diuretics to cirrhotic patients with ascites may eliminate the necessity for or reduce the interval between paracenteses, adding to patient comfort and sparing protein reserves that are lost during the paracenteses. Although diuretics can reduce edema associated with chronic renal failure, increased doses of the more powerful loop diuretics usually are required. In the nephrotic syndrome, the response to diuretics often is disappointing. In chronic renal failure and cirrhosis, edema does not pose an immediate health risk. Even so, uncomfortable, oppressive, and/or disfiguring edema can greatly reduce quality of life, and the decision to treat will be based in part on quality-of-life issues. In such cases, only partial removal of edema fluid should be attempted, and the fluid should be mobilized slowly using a diuretic regimen that accomplishes the task with minimal perturbation of normal physiology. Figure 28-7 provides an algorithm for diuretic therapy in patients with edema caused by renal, hepatic, or cardiac disorders.

Diuretic resistance refers to edema that is refractory to a given diuretic. If diuretic resistance develops against a less efficacious diuretic, a more potent diuretic can be substituted (e.g., a loop diuretic for a thiazide). However, resistance to loop diuretics can result from several causes. NSAIDs block prostaglandin-mediated increases in RBF and increase expression of the Na+-K+-2Cl- sym-porter in the TAL, resulting in resistance to loop diuretics. In chronic renal failure, reduced RBF decreases diuretic delivery to the kidney, and accumulation of endogenous organic acids competes with loop diuretics for transport at the proximal tubule. Consequently, the concentration of diuretic at the active site in the tubular lumen is diminished. In nephrotic syndrome, protein binding of diuretics may limit drug response. In hepatic cirrhosis, nephrotic syndrome, or heart failure, nephrons may have diminished responsiveness to diuretics because of increased proximal tubular Na+ reabsorption, leading to diminished delivery of Na+ to the distal nephron.

Faced with resistance to loop diuretics, the clinician has several options. Bed rest may restore drug responsiveness by improving renal circulation. An increase in the dose of loop diuretic may restore responsiveness; however, nothing is gained by increasing the dose above that which causes a near-maximal effect (i.e., the ceiling dose) of the diuretic. Administration of smaller doses more frequently or a continuous intravenous infusion of a loop diuretic will increase the length of time that an effective concentration of the diuretic is present at the site of action. Combination therapy to sequentially block more than one site in the nephron may result in a synergistic interaction between two diuretics. For instance, combining a loop diuretic with a K+-sparing or a thiazide diuretic may improve therapeutic response; however, nothing is gained by the administration of two

Moderate or severe CH F

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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