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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic ketoacidosis is a frequently encountered metabolic disturbance that follows a prolonged intake of ethanol. Following a brief duration of abstinence, patients typically present with vomiting, abdominal pain, and shortness of breath. Examination reveals Kussmaul breathing, variable volume loss, and coincident manifestations of chronic alcohol usage. Characteristic laboratory findings include anion-gap metabolic ketoacidosis, normal serum glucose, and zero ethanol levels. Phosphate measurements may be depressed, particularly after institution of therapy. Intravascular volume restitution, delivery of dextrose, attention to electrolytes, and discovery of alcohol-related illnesses are the mainstays of therapy.
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PMID:Alcoholic ketoacidosis--a review. 331 91

A group of 28 Syrian children (19 males and 9 females; age ranging from 2.5 to 12 years) were diagnosed clinically and radiologically to have upper urinary tract stones. The commonest presentations were renal colic, vomiting, haematuria, pyrexia and vague abdominal pain. Family history of renal stones was present in 21% of cases. Haematological picture and chemical analysis of blood were within the normal limits for their age and sex. Urine analysis, however, showed significantly marked increase in the 24-hour excretions of calcium and uric acid. Microscopic examination showed haematuria and pyuria in 72% of the children with urolithiasis. Chemical analysis of removed stones revealed that most of them were mixed stones of calcium oxalate and urate or/and phosphate. Pure stones of calcium oxalate or calcium phosphate were less common. Radiologically, about 95% of all stones were demonstrated by plain X-ray, while 5% only after IVP.
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PMID:Some features of paediatric urolithiasis in a group of Syrian children. 358 9

To delineate the spectrum of clinical expressions of distal, type 1 renal tubular acidosis in children and to update progress in diagnosis, therapy, and prognosis, the medical records of 14 girls and 10 boys, seen over a 7 year period, who met the following criteria, were examined: persistent urinary pH more than 6, net acid excretion less than 70 microEq/min/1.73 m2, simultaneous serum total CO2 less than 17.5 mEq/1, and normal or mild impairment of the glomerular filtration rate. The mean age at diagnosis was 8 months. The presenting signs and symptoms were failure to thrive (50%), vomiting and/or diarrhea (37.5%), dehydration (12.5%), and poor feeding (8.3%). Mean values +/- SD of serum calcium (9.8 +/- 0.8 mg/dl), inorganic phosphate (5.6 +/- 0.8 mg/dl), and alkaline phosphatase (222.6 +/- 96.1 U/l) were normal. Hyperkalemia (serum potassium above 5.0 mEq/l) was present at diagnosis in 13 children. Type 4 renal tubular acidosis was ruled out by the inability to achieve a minimum urine pH. With a mean follow-up period of 28.1 +/- 25.3 months, after alkali therapy at 3.3-3.5 mEq/kg/day had been administered for at least 12 months, the growth parameters improved as follows: the percentile weight (mean +/- SD) increased from the initial 11.8 +/- 7.5 to the final 27.6 +/- 31.3 (p less than 0.003), and the length/height percentile increased from 11.5 +/- 7.3 to 29.7 +/- 24.2 (p less than 0.03). The relationship between urine calcium/creatinine ratio and serum total CO2 showed poor correlation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular acidosis in children. Diagnosis, treatment and prognosis. 377 38

A number of factors affect the concentration and distribution of magnesium in patients with chronic renal failure (CRF). Poor nutritional intake, impaired absorption from the intestine, vomiting, diarrhea, the use of diuretics and acidosis may result in a negative balance. More commonly, accumulation of magnesium may be the consequence of reduced renal excretion. Magnesium concentrations are increased in serum and red cells in CRF patients. Bone concentrations and total body magnesium also appear to be increased; muscle magnesium does not appear to be increased. Use of magnesium hydroxide-containing antacids as phosphate binders in patients with CRF was largely discontinued 2 decades ago after reports described increases in serum magnesium concentrations to toxic levels. More recently, the undesirable effects of aluminum-containing phosphate binders (encephalopathy, osteomalacia) have led several investigators to report favorable experiences using low concentrations of magnesium in dialysate and a combination of magnesium and aluminum-containing antacids, as phosphate binders, while closely monitoring serum magnesium concentrations.
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PMID:Chronic renal failure and magnesium metabolism. 380 22

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

Thirteen patients with hypercalcaemia due to carcinoma received inorganic phosphate, orally or intravenously, as palliative treatment for their high serum calcium levels. The serum calcium promptly fell in all patients fully treated, and there was a striking clinical improvement in most patients. The blood urea was usually unchanged or became nearer to normal, while the serum phosphate altered variably. Only two of the eight patients who were studied at necropsy had microscopical nephrocalcinosis; corneal calcification was evident in both before phosphate treatment was started.This oral inorganic phosphate (1 gramme thrice daily) is a safe and effective means of treating hypercalcaemia due to carcinoma. An intravenous infusion of 1 gramme over eight hours may sometimes be required initially for patients who are vomiting.
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PMID:Phosphate treatment of hypercalcaemia due to carcinoma. 417 70

In three patients with thyrotoxicosis and with symptomatic hypercalcaemia antithyroid therapy restored the plasma calcium concentration to normal, though initially in one case intravenous and oral neutral phosphate solution were required to curtail intractable vomiting.Nine cases have been recorded in which the plasma calcium concentration returned to normal after antithyroid treatment was started; all but one became normocalcaemic within eight weeks. It is suggested that in hypercalcaemic thyrotoxicosis a second pathological condition should be considered only if the plasma calcium concentration fails to return to normal within eight weeks.
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PMID:Symptomatic hypercalcaemia in thyrotoxicosis. 542 53

To assess the value of high-dose dexamethasone therapy in preventing the gastrointestinal (GI) side effects of chemotherapy, a randomized double-blind study was conducted in women receiving outpatient therapy for breast cancer. Single-dose dexamethasone sodium phosphate (10 mg) or placebo was administered intravenously in 57 trials in 22 women immediately before chemotherapy. Questionnaires (administered before therapy and 24 hours later) were compared for evidence of nausea, vomiting, and anorexia produced by chemotherapy. No GI intolerance to chemotherapy was noted in 24 (83%) of the 29 dexamethasone trials v 16 (57%) of the 28 placebo trials. Dexamethasone trials produced the following results: no side effects in 50% (14/29), insomnia the night after chemotherapy in 21% (6/29), an increase in energy levels in 24% (7/29), and an improvement in mood in 14% (4/29). High-dose dexamethasone therapy has useful application in alleviating the emetic effects of cancer chemotherapy.
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PMID:Antiemetic efficacy of dexamethasone therapy in patients receiving cancer chemotherapy. 634 9

Alcoholic ketoacidosis is a common condition which occurs predominantly in chronic alcoholics. The usual picture is an interval of increased ethanol intake followed by one or more days of abdominal pain, vomiting, dehydration and a marked decrease in caloric intake. Acidosis is frequently as severe as in diabetic ketoacidosis, but the serum Acetest measurement of ketones may be negative or only slightly positive because of the predominance of beta-hydroxybutyrate compared with acetoacetate. Treatment with intravenous glucose and saline are the essentials of management. Insulin, bicarbonate and phosphate are usually not needed. The major cause of morbidity and mortality is not the acidosis but rather failure to adequately treat concurrent medical or surgical conditions.
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PMID:Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment. 634 51

The basis of conservative treatment in chronic uremia is the restriction of protein, which lowers blood urea and diminishes nausea, vomiting and other uremic symptoms. Protein restriction to less than 25-30 g per day in adult patients may lead to negative nitrogen balance and protein depletion, which can be prevented by supplementing the diet with essential amino acids or a mixture of essential keto acid analogues and amino acids. The traditional view has been that low protein diet affords symptomatic relief in chronic uremia but does not effect the progression of renal failure. However, recent clinical results, mostly retrospective, suggest that protein restriction may retard or halt progression. This has led to a renewed interest in therapy with low protein diet and essential amino acids or keto analogues, since this form of treatment may postpone the time when the patient has to be started on dialysis, or even make dialysis unnecessary. It is not settled by which mechanism protein restriction effects progression of renal failure. According to one hypothesis, hyperphosphatemia (high Ca X P product) is harmful for the diseased kidneys; protein restriction is beneficial, since a low protein diet is generally also low in phosphate. An alternative hypothesis suggests that glomerular hyperfiltration in the remaining nephrons of the diseased kidneys is harmful and leads to glomerulosclerosis; low protein intake protects the kidney by abolishing glomerular hyperfiltration.
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PMID:Discovery and rediscovery of low protein diet. 636 67


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