EDUCAT - DRUGMAN.ZIP - DIURETIC

 
Output of file : DIURETIC contained in archive : DRUGMAN.ZIP



6. Renal Drugs: Diuretics And Other Drugs Acting On The Kidneys
BG Katzung and David G. Warnock

ÚÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄ¿
I. Agents that increase salt and water excretion
A. Thiazides
Drug Table ,
Thiazide combinations
B. Loop agents
Drug Table
C. Potassium-sparing diuretics
Drug Table
D. Carbonic anhydrase inhibitors
Drug Table
E. Osmotic Diuretics
II. Agents acting on water excretion
A. ADH and analogs
B. Demeclocycline
ÀÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÙ


(PgDn key for more text)

Drugs that act on the kidneys are used in a variety of diseases; the
greatest number of prescriptions are for hypertension and congestive fail-
ure. The major classes of diuretics are the thiazides, loop agents,
potassium-sparing diuretics, carbonic anhydrase inhibitors, and osmotic
diuretics. Mercurial diuretics, though still available, are obsolete and
should never be used. They are not discussed in this book. Carbonic an-
hydrase inhibitors, though mostly used for other conditions, are also
diuretics and are discussed in this chapter. Important agents that in-
fluence water excretion by the kidney are antidiuretic hormone and its
analog desmopressin, and a miscellaneous group of ADH antagonists.

Pathophysiology And Therapeutic Rationale For The Use Of Diuretics

* Salt and water retention: This condition is usually associated with in-
creased levels of aldosterone, secreted in response to a decrease in
"effective" circulating blood volume, eg, in congestive heart failure,
cirrhosis, and nephrotic syndrome. The increase in total body sodium
and water may be expressed as edema or ascites, in addition to an in-
crease in total blood volume. The increased workload on the heart and
the physical effects of pulmonary edema or massive ascites often re-
quire that the excess salt and water be removed.

(PgDn key for more text)

However, over-enthusiastic use of diuretics may cause potassium wasting
and impair cardiac output. Restriction of salt intake is often a more
rational and effective therapy, especially in cirrhosis and nephrotic
syndrome.

* Hypertension: The underlying pathophysiology is fully not understood
but reduction of blood volume and other effects of diuretic drugs are
important aspects of therapy . In addition, other
antihypertensive agents may cause salt and water retention; this effect
may be reversed by diuretics.

* Hypercalcemia and hypercalciuria: Hypercalcemia usually results from
nonrenal causes, eg, metastatic cancer. Hypercalcemia is a potentially
lethal condition: CNS depression can rapidly progress from lethargy to
coma and respiratory arrest. Rapid reduction of serum calcium with loop
diuretics may therefore be necessary while the un-
derlying cause is treated and long-term therapies are begun. Chronic
hypercalciuria is often associated with nephrolithiasis; it may result
from underlying metabolic disease, eg, hyperparathyroidism or excessive
ingestion of milk or vitamin D. Recurrent stone formers may benefit
from treatment with thiazides. See also Chapter 15, Section VI.

(PgDn key for more text)


* Diabetes insipidus and inappropriate secretion of ADH: While pituitary
diabetes insipidus is best treated with antidiuretic hormone,
nephrogenic diabetes insipidus is, by definition, resistant to ADH.
Furthermore, the nephrogenic form is a relatively common adverse effect
of several drugs, eg, lithium carbonate. Drugs acting on renal salt
transport mechanisms have beneficial effects on both forms of the dis-
ease. The syndrome of inappropriate ADH secretion (SIADH) is associated
with some tumors, eg, oat cell carcinoma of the lung and with a number
of drugs, including oral hypoglycemic agents, carbamazepine, and vin-
cristine.

* Drug intoxication: Some drugs that are cleared by the kidney can be
eliminated more rapidly by forced diuresis, especially if their reab-
sorption from the tubule can be reduced by changing urine pH. Examples
include amphetamine, salicylate, and phenobarbital.






(PgDn key for more text)


References
1. Acetazolamide for acute mountain sickness. FDA Bull 1983; 13: 27.
2. Ashraf N et al: Thiazide-induced hyponatremia associated with death or
neurologic damage in outpatients. Am J Med 1981; 70: 1141.
3. Brater DC: Determinants of the overall response to furosemide:
pharmacokinetics and pharmacodynamics. Fed Proc 1983; 42: 1711.
4. Beerman B, Groschinsky-Grind M: Clinical pharmacokinetics of diuretics.
Clin Pharmacokinet 1980; 5: 221.
5. Chaffman M et al: Indapamide: Review of its pharmacodynamic properties
and therapeutic efficacy in hypertension. Drugs 1984; 28: 189.
6. DeTroyer A: Demeclocycline: treatment for syndrome of inappropriate
antidiuretic hormone secretion. JAMA 1977; 237: 589.
7. Greene MK, et al: Acetazolamide in prevention of acute mountain sick-
ness: a double-blind controlled cross-over study. Br Med J 1981; 183: 811. 8. Maclean D, Tudhope GR: Modern diuretic treatment. Br Med J
1983; 286: 1419.
9. Narins RG, Chusid P: Diuretic use in critical care. Am J Cardiol 1986;
57: 26A




(PgDn key for more references)

10. Schuster C-J, et al: Blood volume following diuresis induced by
furosemide. Am J Med 1984; 76: 585.
11. Tiller DJ, Mudge GH: Pharmacologic agents used in management of acute
renal failure. Kidney Int 1980; 18: 700.


















(Home key to return to top of file)