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

Long marketed antiemetics, which are still used in medicine or veterinary medicine and whose sites of actions were either assumed to be peripheral or unknown, were subjected to evaluation as antiemetics, against oral copper sulfate emesis. In cats, ethyl aminobenzoate 0.5 g/head, cerium oxalate 0.1 g/head, pinelliae tuber 0.5 g/head and gelatin 2.0 g/head were not effective. In dogs, ethyl aminobenzoate 0.5 g/head, pinelliae tuber 2.0 g/head and hange-syasintoo 2.0 g/head were not effective. Cerium oxalate 0.1 g/head was found to have a slight antiemetic action.
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PMID:[Effectiveness of several antiemetics in vomiting induced by orally administrated copper sulfate in cats and dogs]. 98 88

On about one fourth of the patients ureteral colics caused by oxalate and phosphate calculi lead to a reversible hyperuricemia. This result seems to be important, because we might wrongly diagnose a uric acid calculus. The reason for hyperuricemia is a temporary diuretic disturbance of the uric acid. It cannot be explained by the functional loss of the obstructed kidney, because a nephrectomy does not change the uric acid level. As a possible reason we suppose a ketose by food deficiency and vomiting caused by renal colic.
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PMID:[Reversible hyperuricemia in case of ureteral colics (author's transl)]. 115 68

The clinical picture as well as the principles of treatment in ethylene glycol poisoning differ with the time after ingestion. These time-related differences are illustrated by two case reports. During the first hours of ethylene glycol poisoning, the patient suffers from drunkenness, vomiting and somnolence due to the intoxicant effect of ethylene glycol on the central nervous system. In the following hours a poisoning with glycolate and oxalate develops, with increasing acidosis, renal and brain damage. A patient admitted within a few hours of an overdose, with no or only slight metabolic acidosis, may be successfully treated with ethanol. If the serum concentration of ethylene glycol is very high, hemodialysis may be deferred until the necessary staff and equipment are available. If the patient is admitted with severe metabolic acidosis, hemodialysis must be started immediately. The need for ethanol administration during hemodialysis merits reevaluation.
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PMID:Considerations for the treatment of ethylene glycol poisoning based on analysis of two cases. 205 10

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.
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PMID:4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs. 258 8

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

Two brothers, aged 16 and 11 years, had recurrent episodes of vomiting, diarrhoea and abdominal pain, starting in infancy. In spite of extensive investigations no cause of their enterocolitis could be established. After several years symptomatic treatment was discontinued without any recurrence of symptoms. Their father and several paternal relatives have had kidney stones. Both boys developed urolithiasis and an oxalate-containing stone was removed from the elder brother's kidney. He had no hypercalciuria. His glomerular and tubular function tests were normal. Gas chromatography of urine from both brothers revealed massive excretion of L-5-oxoproline (pyroglutamic acid). Glutathione levels in erythrocytes of both patients were normal. The activities of enzymes of the gamma-glutamyl cycle were analysed in erythrocytes, leukocytes and cultured skin fibroblasts. The level of glutathione synthetase was normal, as was the affinity of this enzyme for its substrate gamma-glutamyl-cysteine. Feedback inhibition of gamma-glutamyl-cysteine synthetase by glutathione was also normal. Both patients had a specific deficiency of 5-oxoprolinase, the activity of which was 2-4% of that of control subjects. Their parents had intermediate 5-oxoprolinase activities in fibroblasts, indicating a recessive mode of inheritance. Thus, 5-oxoprolinuria in these two patients was due to a lack of 5-oxoprolinase, i.e., a new inborn error in the gamma-glutamyl cycle.
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PMID:5-oxoprolinuria due to hereditary 5-oxoprolinase deficiency in two brothers--a new inborn error of the gamma-glutamyl cycle. 611 26

At the University of Minnesota under the supervision of one staff surgeon both jejunoileal bypass (JIB) and gastric bypass (GIB) operations have been performed for weight reduction in morbidly obese individuals. During the last 14 years 727 patients underwent end-to-end (40 to 4 cm) JIB and more than 570 patients underwent GIB. This report is based on a comparison of 205 JIBs performed between July 1975 and July 1979, 106 Alden-loop type GIBs (GIB-loop) performed between July 1975 and July 1979, 53 loop GIBs with enteroenterostomies between the limbs of the loop (GIB-EE) performed between May 1980 and May 1981, and 57 Roux-en-Y GIBs (GIB-Roux) performed between May 1981 and May 1982. Adequate weight loss occurred in 80% of the patients who returned for follow-up in all groups. The percentage of excess body weight loss was similar for the first year (65% for JIB, 62% for GIB-loop, 69% for GIB-EE, and 71% for GIB-Roux). The operative mortality and the immediate morbidity rates were uniformly low. The long-term complications for JIB were 37.7% arthralgia, 7.1% oxalate urolithiasis, 5.6% incisional hernia, and 1.4% liver failure. The complications for GIB-loop were 10.2% nausea/vomiting, 1.9% bile reflux gastritis, and 2.8% anastomotic problems; for GIB-EE 23% nausea/vomiting, 7% bile gastritis, 4.6% incisional hernia, and 3.7% anastomotic problems; and for GIB-Roux 16% nausea/vomiting and 1.7% anastomotic problems. The anastomotic problems consisted of afferent loop obstructions and stomal stenosis; there were no leaks. At 1 year plasma cholesterol reduction for JIB averaged 42% (p less than 0.001), GIB-loop 14% (p less than 0.001), GIB-EE 7% (NS), and GIB-Roux 17% (p less than 0.001). One year after operation 49% of 88 JIB patients showed progression of liver disease on sequential biopsy specimens and 20% improvement. In the 78 GIB patients with sequential biopsies, liver disease progressed in 8% and improved in 65%. In summary, comparable therapeutic weight reduction occurred with all the assessed procedures; however, the GIB-Roux was associated with far fewer serious long-term complications. At this time the GIB-Roux procedure is the weight reduction operation we recommend.
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PMID:Searching for the best weight reduction operation. 648 6

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

1. A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2. The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a beta-hydroxybutyrate dominated ketoacidosis. 3. Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4. The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5. The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6. The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7. It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recommended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication.
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PMID:Severe metabolic acidosis in the alcoholic: differential diagnosis and management. 879 30


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