Chloride urinary

FLECAINIDE AMMONIUM CHLORIDE Urinary acidification l flecainide levels Flecainide excretion is T in the presence of an acidic urine flecainide exists in predominantly ionic form, which is less readily reabsorbed from the renal tubules Watch for a poor response to flecainide... 

QHgNiOiS. Colourless crystals, m.p. 164 5-166-5" C. It is usually prepared by treating p-acetamidobenzenesulphonyl chloride with ammonia, and hydrolysing the acetyl derivative to the base. Used for the treatment of streptococcal infections, gonorrhoea, meningococcal meningitis and urinary infections. Liable to cause unpleasant reactions, such as nausea, cyanosis and skin rashes. 

Methybcanthine Diuretics. The mild diuretic effect of drinking coffee, from caffeine, and tea, mainly from theophylline, has been recogni2ed for along time. But the methylxanthines (Table 5) are of very limited efficacy when used as diuretics. The excretion of sodium and chloride ions are increased, but the potassium excretion is normal. Methylxanthines do not alter the urinary pH. Even though the methylxanthines have been demonstrated to have minor direct effects in the renal tubules, it is beUeved that they exert their diuretic effects through increased renal blood flow and GER (71). 

Carcinogens Cancer-producing agents Skin Respiratory Bladder/urinary tract Liver Nasal Bone marrow Coal tar pitch dust crude anthracene dust mineral oil mist arsenic. Asbestos polycyclic aromatic hydrocarbons nickel ore arsenic bis-(chloromethyl) ether mustard gas. p-naphthylamine benzidine 4-am i nodi pheny lam ine. Vinyl chloride monomer. Mustard gas nickel ore. Benzene. 

In an unusual variant on the Chichibabin reaction, treatment of 3-hydroxypyridine with sodium amide at 200° affords 2,6-di-aminopyridine (21). Coupling of the product with benzenediazo-nium chloride gives phenazopyridine (22). This drug is used as an analgesic for the urinary tract in conjunction with antibacterial agents for treatment of urinary infections. 

Harn-farbstoff, m. urinary pigment, -ganmg,/. fermentation of urine, -geist, m. ammonium chloride (old name), hamigi a. uric urinous, urinose. 

Chloride-responsive or volume-depleted states (urinary chloride concentration <10 mEq/L)... 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

Guay DRP. Trospium chloride an update on a quaternary anticholinergic for the treatment of urge urinary incontinence. Ther Clin Risk Manag 2005 1 157-166. 

Monitor the patient for resolution of hematuria after each successive therapeutic intervention. Frequency of monitoring is based on the severity of hemorrhaging. Monitor urinary output and serum chemistries (including sodium, potassium, chloride, blood urea nitrogen, and serum creatinine) daily for renal dysfunction. Check the CBC at least daily to monitor hemoglobin and platelet count. 

Chromium compounds interact synergistically or antagonistically with many chemicals. For example, potassium dichromate administered by subcutaneous injection potentiated the effects of mercuric chloride, citrinin, and hexachloro-1,3-butadiene on rat kidneys (USPHS 1993). Chromium effects were lessened by ascorbic acid and Vitamin E, and N-acetyl cysteine was effective in increasing urinary excretion of chromium in rats (USPHS 1993)... 

A number of workers have described methods for the determination of mercury in which the mercury is first reduced to the element or collected as the sulfide on a cadmium sulfide pad. It is then volatilized into a chamber for measurement. These techniques are extremely sensitive. Thillez108) recently described a procedure for urinary mercury in which the mercury is collected on platinum and then volatilized into an air stream. Rathje109) treated 2 ml of urine with 5 ml of nitric acid for 3 min, diluted to 50 ml, and added stannuous chloride to reduce the mercury to the element. A drop of Antifoam 60 was added and nitrogen was blown through the solution to carry the mercury vapor into a quartz end cell where it is measured. Six nanograms of mercury can be detected. Willis 93) employed more conventional methods to determine 0.04 ppm of mercury in urine by extracting it with APDC into methyl-n-amyl ketone. Berman n°) extracted mercury with APDC into MIBK to determine 0.01 ppm. 

In adult male rats, after mercuric chloride injection, in addition to tubular necrosis and rise in tubular cell counts, transient elevation of urinary glutamic-oxaloacetic transaminase activity has been found [230]. 

The rat has been used rather widely to study the relation between dietary protein, or acid salt feeding, and calcium loss. Barzel and Jowsey (19) showed that the rat fed a control diet supplemented with ammonium chloride excreted excessive urinary calcium, and experienced a concomitant loss of fat-free bone tissue. Draper, et al. (20) extending this work, reported an inverse relation between dietary phosphate and loss of bone calcium and dry, fat-free tissue. In subsequent studies (21), they reported that this process was accompanied by reduced serum calcium levels the high phosphorus, low calcium diet increased urinary calcium loss. Whereas, increasing the phosphorus content of the diet stopped the excessive urinary calcium loss. To test possible zinc loss that might result from this sort of acid salt feeding, Jacob and her coworkers (22) fed rats a supplement of ammonium chloride and then measured urinary zinc and calcium. The hypercalciuria occurred exclusive of an effect upon urinary zinc loss. 

Acidosis induced by salt feeding to humans influenced urinary calcium loss as effectively as feeding whole foods. Martin and Jones (25), for example, fed adult subjects a diet supplemented with ammonium chloride which resulted in marked hypercalciuria and an acidified urine. In a follow-up trial, feeding alkali as sodium bicarbonate, they also demonstrated that human hypercalciuria could be prevented by adding an alkaline supplement to the diet. 

Earlier animal work showed similar results in terms of urinary acid production from dietary precursors that could be converted into acid before excretion. However, most investigators used salts rather than foods containing the anion or its precursor. The addition of acid, in the form of hydrochloric, sulfuric, or ammonium chloride, acid phosphate salts, or ascorbate resulted in enhanced urinary acidity and concomitant calcium excretion. For example, in the detailed study of bone salt metabolism, Barzel and Jowsey (19) showed that the rat fed supplementary ammonium chloride subsequently lost more calcium, and developed markedly demineralized fat-free bone mass. 

This phenomenon also had been reported in human subjects fed acid ash foods. Farquharson, et al. (33) fed a high-protein (200 g) diet to human subjects who promptly excreted more urinary acid and calcium. This occurred whether the protein level was raised to 200 g, or an equivalent amount of ammonium chloride was fed. If, on the other hand, the acid ash in the protein were neutralized with sodium bicarbonate, the hypercalciuria did not occur. 

The experiments described above indicated amino acids were oxidatively deaminated in liver and their a-amino groups converted to urea. A start on investigations of the mechanism of urea biosynthesis was made by Schultzen and Nenki (1869) who concluded that amino acids gave rise to cyanate which might combine with ammonia from proteins to produce urea. Von Knieren (1873) demonstrated that when he drank an ammonium chloride solution, or gave it to a dog, there was an increase in the formation of urea, without any rise in urinary ammonia. His results were consistent with the cyanate theory but did not eliminate the possibility that urea arose from ammonium carbonate which could be dehydrated to urea ... 

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