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Excretion renal, acceleration

Aceta2olamide, the best example of this class of diuretics (69,70), is rarely used as a diuretic since the introduction of the thia2ides. Its main use is for the treatment of glaucoma and some minor uses, eg, for the a1ka1ini2ation of the urine to accelerate the renal excretion of some weak acidic dmgs, and for the prevention of acute high altitude mountain sickness. [Pg.210]

The sterile peritoneal dialysis solutions are infused continuously into the abdominal cavity, bathing the peritoneum, and are then continuously withdrawn. The purpose of peritoneal dialysis is to remove toxic substances from the body or to aid and accelerate the excretion function normal to the kidneys. The process is employed to counteract some forms of drug or chemical toxicity as well as to treat acute renal insufficiency. Peritoneal dialysis solutions contain glucose and have an ionic content similar to normal extracellular fluid. Toxins and metabolites diffuse into the circulating dialysis... [Pg.389]

Drugs that alter the pH of urine can significantly affect the renal excretion of other drugs. Acid urine increases the effectiveness of mercurial diuretics. It also accelerates the excretion of basic drugs such as meperidine, tricyclic antidepressants, amphetamines, and antihistamines. Acidic drugs, such as aspirin, streptomycin, phenobarbital, sulfonamides, nalidixic acid, and nitrofurantoin have been shown to increase renal clearance in alkaline urine (61). The possible effects of urine pH on the renal excretion of drugs has been illustrated by the observation that if urine is rendered sufficiently alkaline, the excretion of amphetamine is markedly delayed and effective blood levels, after a single dose, can be maintained for several days (62). [Pg.259]

Hyperuricaemia occurs (with precipitation of gout) due to accelerated degradation of adenine nucleotides resulting in increased production of uric acid and its precursors. Only at high alcohol concentrations does alcohol-induced high blood lactate compete for renal tubular elimination and so diminish excretion of urate. [Pg.183]

Oral contraceptives accelerate the renal excretion of paracetamol, reducing its effect (SEDA-9, 90). [Pg.2689]

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. [Pg.2649]

Sulfadiazine is readily excreted by the kidney in both the free and acetylated forms, rapidly at first and then more slowly over a period of 2-3 days. About 15 0% of the excreted sulfadiazine is acetylated. This form is excreted more readily than the free fraction, and alkalinization of the urine accelerates the renal clearance of both forms by further diminishing their tubular reabsorption. [Pg.718]

D. Enhancement of Elimination Enhancement of elimination is possible for a number of toxins, including manipulation of urine pH to accelerate renal excretion of weak acids and bases. For example, alkaline diuresis is effective in toxicity due to fluoride, isoniazid, fluoroquinolones, phenobarbital, and salicylates. Urinary acidiflcation may be useful in toxicity due to weak bases, including amphetamines, nicotine, and phencyclidine, but care must be taken to avoid acidosis and renal failure in rhabdomyolysis. Hemodialysis or hemoperfusion enhances the elimination of many toxic compounds, including acetaminophen, ethylene glycol, formaldehyde, lithium, methanol, procainamide, quinidine, salicylates, and theophylline. Cathartics such as sorbitol (70%) may decrease absorption and hasten removal of toxins from the gastrointestinal tract. [Pg.520]

We therefore suggest that high levels of bromide in the body of experimental animals could influence their iodine metabolism in two parallel ways by a decrease in iodide accumulation in the thyroid and by a rise in iodide excretion by the kidneys. A high surplus of bromide ions in the blood, which was, under our experimental conditions, several thousand times greater than the concentration of iodide, could competitively inhibit the access of iodide into the thyroid and could replace a part of the iodide in the gland with bromide. By accelerating the renal excretion of iodide, excessive bromide could also influence the pool of exchangeable iodide in the thyroid (Pavelka et al.,... [Pg.593]

Early studies by Lieber and MacLachlan presented evidence suggesting that ethanol led to hyperlactic acidemia and decreased the excretion of uric acid l>2 Delbarre indicated the possibility of increased urate production and a study by Grunst, et al. suggested that ethanol infusion lead to increased release of uric acid from the liver. We have reexamined whether ethanol-induced hyperuricemia may be related to decreased renal excretion of uric acid, increased urate production by either accelerated degradation of nucleotides or increased novo synthesis or both mechanisms together. [Pg.457]

Overall, despite elevated solubility (134 pgmL ) and high effective permeability (logPe —4.5 cms ) of ester 11a, fast metabolic ester hydrolysis (ti/2<15 min) reduces its therapeutic potential. Especially, the accelerated renal excretion of the polar metabolite i.e. free carbo q late) impedes the maintenance of the therapeutic concentration in the bladder over an extended period of time. [Pg.278]

Alcohol is an important factor in causing thiamin deficiency because it inhibits the active transport of thiamin across the gut and when abused it impairs the quality of the diet consumed. Diuretics accelerate the excretion of thiamin and appear to override the renal conservation mechanism. Their use is of potential concern in elderly people whose diet may be poor for other medical reasons and their physicians may be unaware of their need for supplemental nutrient. [Pg.384]


See other pages where Excretion renal, acceleration is mentioned: [Pg.210]    [Pg.111]    [Pg.768]    [Pg.24]    [Pg.506]    [Pg.13]    [Pg.1031]    [Pg.121]    [Pg.500]    [Pg.503]    [Pg.623]    [Pg.238]    [Pg.631]    [Pg.129]    [Pg.277]    [Pg.597]    [Pg.3]    [Pg.326]    [Pg.587]    [Pg.614]    [Pg.132]    [Pg.467]    [Pg.326]    [Pg.131]    [Pg.263]    [Pg.287]   
See also in sourсe #XX -- [ Pg.3 , Pg.3 ]




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