Urine colour

Patients taking some anthraquinones may notice their urine coloured brown (if acid) or red (if alkaline). Prolonged use can cause melanosis of the colon. 

The pre-purification of barbiturates to be isolated from urine can likewise be carried out by acid ether extraction [43, 56, 166]. Methylene dichloride has been employed also [34]. Acidification with hydrochloric acid is preferable since, if this is performed with weaker, organic acids, amphoteric medicinal components like sulphonamides, are extracted at the same time [166]. After drying the organic phase with sodium sulphate, further purification on a charcoal or alumina column can be carried out [43, 166]. Urine colouring materials can be removed by shaking the ethereal solution with 5% lead acetate solution [56]. After purification, the... 

Routine lab Urine colour red-brown with pink fluores- f +... 

A retrospective study of amoxicillin renal toxicity among children <6 years of age was conducted using information reported to the National Poison Data from 2004 fo 2008. Nearly 15,000 children were identified as having been exposed to amoxicillin, but only five children developed minor renal symptoms (urine colour change in four patients, increased serum creatinine in one patient, urine oxalate crystals in one patient and haematuria in one patient). The authors state that it is unknown if haematuria was linked to amoxicillin exposure. In all of the patients, symptoms resolved within 3 days. The authors conclude that patients should be monitored for these symptoms and followed up closely. These data support the fact that renal toxicity in paediatrics is very rare with amoxicillin exposure [30 ]. 

C. Excreted in the urine in the rare hereditary disease alkaptonuria. Homogentisic acid is easily oxidized in the air to dark-coloured polymeric products, so that urine from patients with alkaptonuria turns gradually black. It is formed from tyrosine and is an intermediate in tyrosine breakdown in the body. Alkaptonuria is due to the absence of the liver enzyme which cleaves the aromatic ring. 

The method is based on the conversion of urea to amnionium carbonate and the estimation of the latter by titration with standard acid. For this purpose, two equal quantities of urea (or urine) are measured out into two flasks A and B. A is treated with 10 ml. of a strong urease preparation and some phenol-phthalein, warm water is added and the mixture is adjusted by the addition of V/io HCl from a burette A until the red colour is just discharged. This brings the mixture to about pH 8 (the optimum for urease) and also prevents loss of ammonia. 

Bacterial action in the large gut converts the conjugated bilirubin into bilinogens and then to yellow-brown coloured bilins which finally leave the body through in the faeces (as stercobilin) and urine (as urobilin). A small proportion of the bilin produced in the gut is passively reabsorbed into the portal system and re-excreted as the blood flows through the liver. 

It is indicated for treatment of scurvy, for prophylaxis of vitamin C deficiency, to acidify urine, anaemia of vitamin C deficiency, as antioxidant to protect natural colour and flavour of many foods, dental caries and increased capillary fragility. 

When injected, it forms a stable water-soluble iron complex (ferrioxamine) that prevents the iron from entering into further chemical reactions and is readily excreted in the urine giving the urine a characteristic reddish colour. Some of it is also excreted in the faeces via the bile. It can also chelate aluminium and thus is useful in aluminium overload. It is primarily a chelator used in acute iron poisoning and chronic iron overload as in thalassemia patients needing multiple transfusions. 

There have been no fatalities in industry attributed to bismuth and it is regarded as relatively non-toxic for a heavy metal.246 The toxic problems which have been recorded have in the main been iatrogenic illnesses. A characteristic blue-black line on the gums, the bismuth line , which may persist for years, is a feature of bismuth overdosage. Soluble salts are excreted via urine and may cause mild kidney damage. Less soluble salts may be excreted in the faeces, which may be black in colour due to the presence of bismuth sulfide. Table 31 contains some toxicity data. 

A 27-year-old woman presents a prescription for nitrofurantoin tablets 50 mg q.d.s. for 3 days and asks to speak to the pharmacist. She explains that her GP has checked her urine with a coloured strip and diagnosed a urinary tract infection (UTI). She is suffering considerable discomfort on urination due to a burn-ing/stinging sensation and her GP has suggested she purchase some Effercitrate over the counter. A friend has recommended she also purchase cranberry extract tablets and the patient would like your advice. 

The incidence of gastrointestinal side-effects including nausea, vomiting and diarrhoea with nitrofurantoin is as high as 30% with standard microcrystalline formulations and patients should be advised to take the doses with food. Other important but less common adverse reactions include pulmonary fibrosis, peripheral neuropathy and hypersensitivity. Patients should also be warned that nitrofurantoin can colour the urine yellow or brown. 

Ehrlich s aldehyde test can be used to confirm a diagnosis of acute intermittent porphyria. Equal volumes of urine and Ehrlich s reagent are mixed a pink colour indicates raised urinary concentration of either porphobilinogen or urobilinogen. In acute intermittent porphyria, raised porphobilinogen is present and the pink precipitate formed is insoluble in chloroform. 

A similar method is used for the determination of inorganic phosphates in urine. 1 to 5 c.e. of the urine, containing about 0-5 milligram of phosphorus, are diluted and treated with a solution of ammonium molybdate in 15 per cent, sulphuric acid (5 c.c.), 1 c.c. of 1 per cent, hydroquinone solution and 1 c.c. of 20 per cent, sodium sulphite solution. The blue colour is compared in Nessler glasses with that developed by the same solutions when mixed with a standard phosphate solution of which 5 c.c. contain 0-5 milligram of phosphorus. 

On further testing, a specimen of urine showed a normal colour and the patient did not appear to be jaundiced. In addition, a CT (computerized tomography) scan showed that her liver and bile duct were normal, and she had no history of stomach (peptic) ulcers. 

Q3 What signs could indicate that Jude was jaundiced and why is the colour of her urine significant ... 

Q3 Signs of jaundice jaundice gives a yellowish colour to the skin and mucous membranes, usually easiest to see in the cornea. The yellow colour is due to the presence of breakdown products of haemoglobin such as bilirubin in tissues, which the liver usually removes from the blood. Jaundice is indicative of liver disease, obstruction of the bile ducts or haemolytic disease. Bilirubin stains not only the tissues but also all body fluids, including plasma and urine, and the patient s urine can become really dark. 

Symptoms include exercise intolerance and episodes of myoglobinuria (rust-coloured urine, indicating breakdown of muscle tissue) a skin rash is common. Inheritance is autosomal recessive. 

Dark urine occurs in obstructive jaundice because the water-soluble conjugated bilirubin cannot be excreted through the faeces. Excretion from the body is compensated for by increased kidney elimination, and hence the urine is a darker colour than normal. 

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