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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemistry, microbiology, pharmacokinetics, therapeutic use, adverse effects, and dosage of amoxicillin-potassium clavulanate, a beta-lactamase-resistant antibiotic combination, are reviewed. Clavulanic acid is a "suicide" inhibitor of bacterial beta-lactamase enzymes and has been effective in preventing destruction of penicillins by these enzymes. Clavulanic acid alone has weak antibacterial activity against most organisms. After oral administration, clavulanic acid is rapidly absorbed; amoxicillin appears to increase its absorption. Absorption of amoxicillin-clavulanic acid is not affected by food. Amoxicillin-clavulanic acid is effective in treating both acute uncomplicated and complicated urinary-tract infections and exacerbations of chronic bronchitis caused by amoxicillin-resistant organisms in adults. It appears to be comparable in efficacy to cefaclor for treating uncomplicated urinary-tract infections in adults and children, acute bronchitis and bronchopneumonia, and acute sinusitis, otitis media, and skin and soft-tissue infections in children. Other infections for which the combination has been effective include cellulitis and intra-abdominal and pelvic sepsis caused by mixed aerobic/anaerobic organisms. Amoxicillin-clavulanic acid has also successfully cured urethritis in men caused by penicillinase-producing Neisseria gonorrhoeae and is superior to amoxicillin alone for beta-lactamase-positive Haemophilus ducreyi infections (chancroid). Diarrhea or loose stools is the most common side effect seen with amoxicillin-clavulanic acid; nausea, vomiting, and skin rash may also occur. Nausea, vomiting, and diarrhea may be lessened by taking the combination with food.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amoxicillin-potassium clavulanate, a beta-lactamase-resistant antibiotic combination. 639 83

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia was reported and literatures were reviewed. The case was 61-year-old nonalcoholic female who had taken an operation of craniopharyngioma 23 years ago. Fifteen years later, she received re-operation for the recurrent tumor, followed by replacement therapy of corticosteroid and clofibrate. She was otherwise well until two weeks before entry, when she noticed abrupt onset of high grade fever, nausea, vomiting and general malaise. She was admitted to an emergency hospital because of weakness, disorientation and a slight impairment of consciousness, but she was able to speak and to take some food per os. Laboratory studies disclosed urinary tract infection and showed a serum sodium level of 117 mEq/l, potassium 2.9 mEq/l, a serum osmolarity 232 mO sm/l and urine osmolarity 141 mEq/l. She was diagnosed to have an exacerbation of adrenal insufficiency with hyponatremia and hypotonic dehydration triggered by urinary tract infection. Intravenous administration of vitamin B complex, electrolytes including KCL, 5% glucose solution and physiological saline with a large amount of corticosteroid was performed aggressively. Serum sodium concentration was raised to 161 mEq/l in two days, and the increased level had been maintained more than five days, resulting in coma and flaccid quadriplegia. During this period, there was no episode of hypotension, hypoglycemia, hypoxia nor hepatic failure which could have caused brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6

The author volunteered to experience on himself the effect of short-term, i.e., 36 consecutive days, oral administration of cesium chloride. Cesium chloride was given 6 g per day into two equally divided doses. The drug was dissolved in 8 ounces fluid and consumed immediately after the morning and evening meals which were diet-restricted to wheat bran and certain grain products, to attain approximately 1% potassium intake, for the initial 3 weeks. Bread products were discontinued and yogurt and cottage cheese products were reinstituted for the two week period that followed prior to reinstituting of the preceding food regimens. There was an initial general feeling of well-being and heightened sense perception. A gradual decrease in appetite was noted initially before it was stabilized at a later date. Discontinuation of rich bread meals resulted in pre-nausea sensation which was followed by diarrhea 48 hr later. The institution of high potassium nutrition decreased the feeling of nausea and abolished diarrhea. A "tingling" sensation in the lip and cheek regions was experienced 15 min subsequent the cesium chloride dosage compared to same sensation occurring at moderate intensity in hands and feet at end of the experiment. No adverse effects of CsCl were noted in performance of mathematical analyses or in driving skill. It is concluded that CsCl is devoid from toxicity provided adequate diet and supplements are administered.
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PMID:Effect of oral intake of cesium chloride: a single case report. 652 28

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma prolactin responses to acute changes in central blood volume in man. 664 22

The effects of three different hypocaloric diets on serum electrolytes, metabolites and enzyme activities were investigated for 3 weeks in 40 overweight patients. A 600 kcal mixed diet was as effective with regard to daily weight reduction as complete fasting or a low-energy protein diet. Only the patients of the last two groups complained of orthostatic dysregulation, nausea, headache and dryness of the skin. Neither a decrease in serum potassium, an increase in creatinine nor any other side-effects were observed in the mixed diet group. - Since the 600 kcal mixed diet can be carried out under ambulant conditions it is preferable to the other reducing diets.
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PMID:[The effects of various reducing diets in adiposity (author's transl)]. 678 Aug 23

40 patients, who underwent maxillo-facial surgery, were fed with the native physiological diet Nutro-Drip via nasogastric tubes for 10 days. Due to intolerance in 5% of the patients, the nutrition had to be interrupted. The other patients received 1500-2500 ml Nutro-Drip per 24 h (= 1605--2675 kcal = 6780-11300 J). Transient side effects were: diarrhoe 3,8%; nausea 0,8%; eructation and/or heartburn 1,1%; squeezing of the stomach 1,1%. In these patients nutrition with Nutro-Drip was not interrupted. The mean frequency of defecation was 0,81/day. There were no significant changes in body weight, serum electrolytes, water balance, blood sugar, liver enzymes, serum cholesterol, and acid-base balance during the feeding with Nutro-Drip. Immediately after surgery there was a statistically significant decrease in potassium, protein, and albumin levels in the serum with the tendency to normal values during Nutro-Drip feeding. During the postoperative period the urea content of the serum increased continuously without altering creatinin levels in the serum. Nutro-Drip seems to be very suitable for tube-feeding in patients with normal gastro-intestinal tract.
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PMID:[Trials with the native physiological tube-feeding diet Nutro-Drip after maxillofacial operations]. 679 1

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

Gossypol is a phenolic compound isolated from the seeds, stems, and roots of the cotton plant. The chemical has been known for years as the toxic principle left in the cottonseed cake after cottonseed oil extraction. It is also present in the cold pressed cottonseed oil from which it may be removed through reactions with alkali. Extremely low birthrates in China's Hebeth province were traced to the use of crude cotton seed oil for cooking purposes. After prolonged investigation, it was determined that male infertility was related to the gossypol content of the oil. After a short period of animal studies, the Chinese in 1972 undertook widespread clinical trials of gossypol as a contraceptive agent. Over 4000 men have undergone treatment with the drug, some for as long as 4 years. Infertility resulted after 2 months of a daily dose of 20 mg and then the participants were maintained on 150-220 mg/month in divided doses. The drug apparently did not decrease libido in most test subjects and had not been reported to impair potency. Semen analysis at various intervals showed a decrease in motile sperm, malformed spermatozoa, and then a decrease in sperm count, leading to azoospermia. On discontinuation of the substance, the antifertility effect completely reversed itself within 3 months. No obvious toxic effects of pathological changes were observed in human and animal studies. Levels of luteinizing hormone and testosterone were unchanged and apparently indicated that gossypol does not affect hormonal balances. Adverse reactions reported to date include transient and reversible weakness in 10% of the test subjects on initiation of therapy. In addition, appetite changes, gastric discomfort, and nausea have been noted. A few cases of slight EKG changes and disturbances in potassium metabolism have occurred. No chromosomal changes have been observed nor have tests shown any mutagenic effects of the drug. In conclusion, preliminary data indicated that gossypol may offer an excellent new approach to contraception. Further testing is required to elucidate the drug's mechanism of action and to determine its adverse and possible toxic effects.
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PMID:Gossypol as an oral contraceptive for men. 692 15

Although thioguanine has been in clinical use for over 20 years, few data are yet available on the clinical pharmacology of thioguanine administered orally. We have studied the plasma thioguanine levels in acute myelogenous leukemia patients during remission induction (daunomycin 60 mg/m2 on day 1, arabinosylcytosine 200 mg/m 2. day for 7 days by infusion, thioguanine 100 mg/m2 PO every 12 h for 7 days) and remission maintenance (arabinosylcytosine 200 mg/m2 . day for 4 days by infusion, thioguanine 100 mg/m2 PO every 12 h for 4 days). Hourly blood samples were taken after thioguanine administration, and plasma thioguanine levels were measured by high-performance liquid chromatography with an anion-exchange column. Prior to the chromatography the thioguanine was oxidized by alkaline potassium permanganate to the corresponding 6-sulfonate, which was monitored by means of fluorescence detection. Peak plasma levels of thioguanine were observed 2-4 h after administration and varied from 0.03-0.94 microM. Plasma levels of thioguanine were markedly lower in patients with severe nausea and emesis. Food intake at the same time as thioguanine administration also tended to lower plasma drug levels. The 30-fold range in thioguanine plasma levels observed in this study suggests that intermittent IV administration may provide a better means of standardizing the dosage of thioguanine.
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PMID:Clinical pharmacology of oral thioguanine in acute myelogenous leukemia. 694 61


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