A Urinary acidifiers

The nurse measures the fluid intake and output, especially when the primary health care provider orders an increase in fluid intake or when a kidney infection is being treated. The primary health care provider may also order daily urinary pH levels when methenamine or nitrofurantoin is administered. These drugs work best in acid urine failure of the urine to remain acidic may require administration of a urinary acidifier, such as ascorbic acid. 

Unlabeled uses Vitamin C (at least 2 g/day) may be used as a urinary acidifier in conjunction with methenamine therapy. 

B. Proteus species produce urease (A) that produces ammonia and urea, alkalizing urine. Urine requires acidification for effective therapy. Hippuric (B), mandelic, or ascorbic acids or methionine are urinary acidifying agents. The normal acidic urinary environment is disturbed by recurrent Proteus in-... 

Methenamine mandelate, 1 g four times daily, or methen-amine hippurate, 1 g twice daily by mouth (children, 50 mg/kg/d or 30 mg/kg/d, respectively), is used only as a urinary antiseptic to suppress, not treat, urinary tract infection. Acidifying agents (eg, ascorbic acid, 4-12 g/d) may be given to lower urinary pH below 5.5. Sulfonamides should not be given at the same time because they may form an insoluble compound with the formaldehyde released by methenamine. Persons taking methenamine mandelate may exhibit falsely elevated tests for catecholamine metabolites. 

Mcthenamine is used internally as a urinary antiseptic for the treatment of chronic urinary tract infections. The free base has practically no hacteriostatic power formaldehyde relca.se at the lower pH of the kidney is required. To optimize the antibacterial effect, an acidifying agent. such as sodium biphusphatc or ammonium chloride generally accumpanies the administratiun of methenaminc. 

Intermittent self-catheterization with or without a concomitant anticholinergic agent is recommended in patients with large postvoid urine residual volumes (>100 mL) or when the urinary problem is hyporeflexic in nature (failure to empty). Patients with large postvoid residual volumes are at risk for developing urinary tract infections and often are prescribed urinary acidifiers such as vitamin C or antiseptics such as methenamine mandelate to prevent infections. 

Methenamine and methenamine mandelate are only effective as urinary antisepties if the pH is about 5.5 or lower, when formaldehyde is released. This is normally achieved by giving urinary acidifiers such as ammonium chloride, ascorbic acid, or sodium acid phosphate. In the case of methenamine hippurate, the acidification of the urine is achieved by the presence of hippuric acid. The concurrent use of substances that raise the urinary pH such as acetazolamide, sodium bicarbonate, potassium or sodium citrate is clearly contraindicated. Potassium citrate mixture BPC has been shown to raise the pH by more than 1 at normal therapeutic doses, thereby making the urine sufficiently alkaline to interfere with the activation of methenamine to formaldehyde. Some antacids (containing magnesium, aluminium or calcium as well as sodium bicarbonate mentioned above) can also cause a significant rise in the pH of the urine. ... 

Occurs widely in animals and plants. Good sources are citrus fruits and hip berries. Isol. from ox adrenal cortex, lemons and paprika. Vitamin (antiscorbutic) urinary acidifier. Used as a reducing agent, masking agent in photometric detn. of Ti, Nb. Mp 190-192°. 

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. 

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. 

Effects of pH on urinary drug elimination may have important applications in medical practice, especially in cases of overdose. For example, one can enhance the elimination of a barbiturate (a weak acid) by administering bicarbonate to the patient. This procedure alka-linizes the urine and thus promotes the excretion of the now more completely ionized drug. The excretion of bases can be increased by making the urine more acidic through the use of an acidifying salt, such as ammonium chloride. 

Alternatively, acidified urine can be collected on a filter paper. The urine is preserved with 20% HC1 as described above. Filter paper strips (3 x 5 cm filter paper backing, cat. No. 165-0921, Bio-Rad) are dipped into urine to 1 cm below the upper edge. Excess urine is wiped off, and the filter is left to dry at room temperature. Urinary filter paper spots are then cut into small pieces, shaken in 3 ml of water for 15 min at room temperature, and sonicated for 5 min at room temperature. The extracts are filtered through an Ultrafree-MC filter with 10-kDa cutoff (Millipore, USA) at 2000g for 10 min at room temperature. The clear supernatant is analyzed by HPIC. 

It is used in the treatment of scurvy, postoperative cases, and healing bedsores and chronic leg ulcers. Vitamin C increases the absorption of iron during anemia and is frequently combined with ferrous salts. It is used in urinary tract infections to acidify urine. Large doses of vitamin C have been tried to cure everything from the common cold to cancer, with not much success. The usefulness of vitamin C in asthma, cancer, atherosclerosis, psychologic symptoms, and fertility is doubtful. Ascorbic acid is well tolerated in large doses and may cause rebound scurvy on withdrawal. There is a possibility of forming urinary stones. 

The effect of urinary pH on drug ionization also has toxicological implications. For example, in cases of phenobarbital (a weak acid barbiturate) overdose the urine can be alkalinized (the pH elevated) by administering sodium bicarbonate to the patient. The resultant increase in pH shifts the dissociation equilibrium for this weak acid to the right, producing an increase in the proportion of the ionized form, less reabsorption in the kidneys, and more rapid elimination. Conversely, acidifying the urine with ammonium chloride will increase the excretion rate of drugs that are weak bases since they will be more protonated (ionized) and less reabsorbed (more polar, less lipophilic). 

Disposition in the Body. Absorbed from the gastro-intestinal tract but there is extensive first-pass metabolism bioavailability about 30%. It is metabolised to pethidine and norpethidine. Up to about 5% of a dose is excreted unchanged in the urine, with about 18% as norpethidine and 2% as pethidine, in two to three days. The urinary excretion of unchanged phenoperidine is increased to about 7% when the urine is acidified. 

When a dmg is in its unionised form it will more readily diffuse from the urine to the blood. In an acidic urine, acidic drugs will diffuse back into the blood from the urine. Acidic compounds such as nitrofurantoin are excreted faster when the urinary pH is alkaline. Amfetamine, imipramine and amitriptyline are excreted more rapidly in acidic urine. The control of urinary pH in studies of pharmacokinetics is thus vital. It is difficult, however, to find compounds to use by the oral route for deliberate adjustment of urinary pH. Sodium bicarbonate and ammonium chloride may be used but are unpalatable. Intravenous administration of acidifying salt solutions presents one approach, especially for the forced diuresis of basic dmgs in cases of poisoning. 

Tolbutamide is absorbed rapidly in rc.sponsivc diabetic patients. The blood sugar level reaches a minimum after. I 10 8 hours. It is oxidized rapidly in vivo to I-bulyl-3-(/7-carboxyphenyOsulfonylurca. which is inactive. The metabolite is freely. soluble at urinary pH if the urine is strongly acidified, however, as in the use of sulfosalicylie acid as a protein precipitant, a white precipitate of the l rce acid may be formed. 

Ephedrine, synephrine, and caffeine are excreted in the urine. The rate of urinary excretion of ephedrine is dependent on urinary pEI. The elimination half-life of ephedrine is 3 h when the urine is acidified to a pEI of 5.0 and 6h when the urinary pEI is 6.3. 

Some patients acidify urine at a submaximal rate, but at a rate that is generally sufficient to maintain acid-base balance. Potassium wasting, hypokalemia, and hyperchloremia are generally not present. However, when patients are stressed or are given an acid load, their ability to excrete acid and to lower urine pH is suboptimal and urinary pH may exceed 5.5. 

Calcium salts, such as calcium oxalate, precipitate in urine specimens during and after collection. Specimens may be collected in a container containing acid to prevent calcium salt precipitation. A commonly used acid is HCl, 6 mol/L, with 20 to 30 mL added to the container for a 24-hour collection (1 to 2 mL for a random specimen). The safety of the patient and the patient s family in handling such a container may be a concern. The measured urinary calcium concentration must be corrected for the dilution by the acid solution when the urinary volume is low. The specimen should be kept well mixed during collection. Specimens collected without acid should be acidified and allowed to stand for 1 hour before thorough remixing and aliquot-ing. Some have questioned the ability of postcollection acidification to redissolve all of the calcium salts with or without heating. ... 

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