Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A titration assay with two end points is described for comparison of the emetic and lethal potencies of digitalis-like drugs.2. A drug was infused at constant rate to a conscious, unrestrained cat, through an indwelling venous cannula. At the moment of vomiting the cat was rapidly anaesthetized and infusion continued at the same rate until the moment of cardiac arrest.3. With very slow and very fast infusions, the emetic and lethal doses tended to rise. In the range between these extremes (which varied from drug to drug) they were independent of time.4. The observations could be accounted for by analogue computation, assuming that the drugs entered an initial pool and were distributed at finite rates to receptors in the CNS (vomiting centre) and heart.5. Half times of metabolic loss derived from this computation for digitoxin, digoxin and ouabain (17, 9.9 and 1.8 h, respectively) were in the same ratio as the threefold longer half times reported for these drugs in man.6. When measured with infusion rates in the time independent range, the ratio of lethal to emetic doses did not vary between the drugs studied. All caused vomiting at 40% of the lethal dose.7. From a review of the literature, the emetic and cardiotoxic actions of digitalis-like drugs appear inseparable and probably share a common biochemical mechanism.8. It is concluded that foreseeable improvements in digitalis-like drugs are small and would depend on the elimination of any local emetic effect on gut receptors which they may have.
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PMID:Cat assay for the emetic action of digitalis and related glycosides (digitoxin, digoxin, lanatoside C, ouabain and calactin). 558 Jun 99

2 cases of midgut infarction in patients taking oral contraceptives are reported. Case 1 was a 38-year-old married woman with 3 children. After 2 isolated bouts of severe abdominal pain and diarrhea, examination revealed only minimal epigastric and left loin tenderness. Blood counts were normal. Other tests were negative. She had been taking cyclical tablets of 2.5 mg norethynodrel and .1 mg mestranol (Con ovid-E) for 48 months and continued after 8 days in the hospital. 18 weeks later severe abdominal pain, vomiting, and diarrhea occurred with abdominal tenderness and rigidity. The white-cell count was 25,000 with 85-90% segmented forms. Other blood tests were normal. At operation the superior mesenteric artery was found to be occluded distal to the origin of the middle colic artery. The thrombus was removed and the circulation to the gut seemed adequate. Intravenous heparin was given. Reoperation at 12 and again at 36 hours revealed viable intestine. 8 days after hospital admission ileus symptoms occurred. Reoperation revealed gangrene of almost all of the small intestine and part of the large intestine. The patient died 3 days later. Autopsy showed thrombosis of the superior mesenteric artery which was apparently not associated with local atheroma. Minimal atheroma in the aorta and an infarct of the spleen were noted. Case 2 was a 45-year-old married woman with 2 children who complained of severe abdominal pain and vomiting of 8 hours duration. A similar attack 1 week earlier had subsided in 6 hours. She had been taking tablets of 5 mg ethinyl-esternol (lynestrenol) and .15 mg mestranol (Noracyclin) for 11 months. There was no fever. The white-cell count was 19,500 with 85% segmented forms. Other laboratory tests and X-ray were normal. A loud bruit was heard over the upper abdomen. Bowel sounds were hyperactive. A diagnosis of acute small-bowel obstruction was made. At operation a definite diagnosis could not be made. Symptoms became worse. Reoperation 10 days later revealed gangrenous small intestine and part of the large intestine. The gangrenous parts were removed. After a complicated convalescence the patient recovered, but has moderate steatorrhea. Histologic examination of the resected intestine showed no evidence of atheroma in the mesenteric vessels. Considering these 2 cases with premonitory warning symptoms and without evidence of an atheromatous cause but associated with oral contraceptive therapy the immediate discontinuance of such therapy in women who develop acute abdominal pain is irecommended.
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PMID:Infarction of the midgut associated with oral contraceptives. Report of two cases. 568 97

Cholera is a disease state caused by the Vibrio cholerae. The vibrios remain in the gut lumen, and the disease is atypically afebrile. The main symptom is a profuse isotonic diarrhea of rice-water character with an output rate of as much as 1 liter/hour. Early signs in the untreated patient are skeletal muscle cramps (presumably due to electrolyte loss) and vomiting. Mortality rate in untreated cases may be as high as 80%, and in treated cases, 20%. The U.S. Navy method of treating chlera has reduced the mortality rate to zero in the uncomplicated cases. U.S. Navy scientists have demonstrated that the cholera stool is remarkably constant from patient to patient and throughout the course of the disease. The simplicity of the Navy method for treating cholera makes it well suited for use in epidemics in populations with no experience in cholera. The method measures plasma specific gravity by the copper sulfate method. The Navy scientists found that there is a sodium transport inhibitor in cholera stools, and that there is decreased sodium transport from the gut lumen to plasma in the acute phase of cholera. Unlike other forms of shock, the mesenteric circulation in cholera must continue as there is a danger of loss of protein-free plasma, eventually leading to death. Tetracycline and other antibiotics have been shown to halve the course of the disease and fluid requirements for its therapy.
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PMID:Cholera in the perspective of 1966. 592 97

Space sickness is generally considered a variant of motion sickness although not fully proved as such. Understanding space sickness requires objective and quantitative characterization of the disorder. Vomiting is a quantifiable physiological event performed by the respiratory muscles which generate the pressures that evacuate the gut. Vomiting from all causes is coordinated by the vomiting center in the medulla oblongata. The emetic chemoreceptor trigger zone (CTZ) in the area postrema is thought to be an indispensable element in the afferent pathway of motion sickness. About 30 potential neurotransmitters exist in the vomiting control mechanism which includes at least eight chemical transmission steps through the reflex pathway of motion sickness. Individual synaptic transmitters do not likely mediate specific functions, but particular combinations of those transmitters might well serve distinct functions. Adaptation to the cause of space sickness probably results from readjustment of a cerebellar circuit or of a humoral factor acting on the CTZ, rather than from stimulus-receptor desensitization. Space sickness must, for purposes of investigation, be treated as a unique disorder engendered by weightlessness until proved equivalent to any emetic syndrome that occurs on earth.
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PMID:A 1983 neuropharmacologic perspective of space sickness. 614 69

Eleven patients with recurrent malignant glioma were treated with single high doses of BCNU ranging from 600 to 1400 mg/sq m. To prevent the characteristic late myelosuppression observed after conventional doses of BCNU, autologous bone marrow harvested just before drug treatment was infused 24 to 36 hours after therapy. Higher doses of BCNU causes earlier and more profound myelosuppression; one patient died on pancytopenia, breakdown of the gut epithelium, and Clostridium septicemia 10 days after receiving 1400 mg/sq m of BCNU. All patients experienced transient emesis; four developed transient elevation of hepatic enzymes, two reversible interstitial pulmonary infiltrates, and two who received 1400 mg/sq m BCNU suffered irreversible cortical damage. Eight patients receiving 600 to 1200 mg/sq m demonstrated reconstitution of polymorphonuclear leukocytes an platelets within at least 30 days after treatment. With a follow-up time of up to 19 months, four patients improved, three stabilized, and three deteriorated and died. The median survival time was 7 months. Computerized tomography performed on patients receiving constant corticosteroids showed diminished contrast enhancement and mass effect in eight patients. High-dose BCNU at doses up to 1200 mg/sq m with marrow rescue is a feasible approach to the treatment of patients with glioblastoma.
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PMID:High-dose BCNU with autologous bone marrow rescue for recurrent glioblastoma multiforme. 625

Pyrazolone intoxication accounts for most (52 percent) mild analgesic poisonings in West Germany. Severe and fatal intoxication with pyrazolones is, however, rare. In the German literature, only 50 cases have been described in the past 62 years; 80 to 90 percent of these were caused by aminopyrine, which was withdrawn from the West German market in 1978 and replaced by propyphenazone. Up to now, no fatal poisoning with propyphenazone has been reported. However, the signs and symptoms of severe intoxication are similar for both propyphenazone and aminopyrine. The acute toxicity of dipyrone is slightly lower than that of propyphenazone, whereas phenylbutazone and oxyphenbutazone clearly cause less severe reactions. Characteristic symptoms include impaired consciousness progressing to coma, and convulsions. In addition, arrhythmia and cardiogenic shock may occur. Severe aminopyrine intoxication may also be complicated by sudden apnea. Liver damage may develop after a latent period of about 24 hours, especially after phenylbutazone and oxyphenbutazone poisoning. Therapy involves supportive measures as well as gastric emptying by emesis or lavage, installation of medical charcoal, and induction of diarrhea or gut lavage. Although exact clinicotoxicologic data on hemoperfusion are not available as yet, distribution volumes, plasma half-lives, and endogenous plasma clearances as well as results of in vitro trials all suggest the efficacy of this procedure. Hemoperfusion with uncoated amberlite XAD-4 resin is, therefore, recommended for patients with severe pyrazolone intoxication.
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PMID:Acute toxicity of pyrazolones. 635 72

When vomiting is not related to preventing the entry of physically or chemically unsuitable substances into the absorbing gut, it may be regarded as pathologic. The commonest causes of chronic vomiting are structural lesions affecting the mucosa of the upper gastrointestinal tract (often with luminal obstruction) and psychogenic disorders. Diseases affecting extrinsic and intrinsic neural control of gut motility and visceral smooth muscle may also cause unexplained vomiting. A stratified management approach to patients with vomiting is suggested. The first assessment is aimed at exclusion of mucosal lesions of the upper gut and systemic or psychiatric disease that may affect it. Second is a therapeutic trial, usually with a prokinetic agent. The final phase, reserved for recalcitrant undiagnosed patients, is evaluation at special centers with gastric emptying studies, gastrointestinal manometry, other electrophysiologic studies, and, in a few patients, laparotomy with examination of full-thickness biopsy specimens of the small intestine.
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PMID:Unexplained vomiting: a diagnostic challenge. 637 6

Four silver-silver chloride electrodes were surgically implanted at 5-cm intervals on the jejunal serosa of 7 neonatal pigs. Daily recordings, 7 h in duration, were made from each piglet beginning 3 days after surgery. Characteristic migrating motility complexes and short, distinct (2.5-5.0 s), rapidly aboral migrating bursts of intense spike activity ("migrating action potential complexes") were seen in all preinfection recordings. Piglets were inoculated with a 1-ml oral dose of a 0.1% gut suspension from coronavirus (transmissible gastroenteritis) infected pigs. This resulted in inappetence, vomiting, and diarrhea, most marked on the second day postinfection, but which had abated by the third day. When compared to recordings from both fed and fasted noninfected (control) animals, infection significantly altered jejunal myoelectrical activity by (a) shortening the duration of the migrating motility complex on day 1 postinfection and prolonging it on day 2, (b) increasing the number of abnormal activity fronts, and (c) decreasing the number of migrating action potential complexes. Slow wave frequency and the duration of phase 3 of the migrating motility complex were unaffected. When compared to fed control animals, infected piglets also showed a slight shortening of phase 1 of the migrating motility complex on day 1 postinfection and a prolongation on days 2 and 3, as well as a shortening of phase 2 on the second and third days postinfection. Changes in myoelectrical activity were not solely due to decreases in food intake, as abnormalities persisted when food intake returned to normal on postinfection day 3, and disruption of the activity front and migrating motility complex duration were purely transmissible-gastroenteritis-virus-induced phenomena. These findings suggest that infection with transmissible gastroenteritis virus disrupts organized propulsive activity in the jejunum of the neonatal pig.
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PMID:Influence of coronavirus (transmissible gastroenteritis) infection on jejunal myoelectrical activity of the neonatal pig. 673 81

Intestinal pseudo-obstruction (IP) is an uncommon disorder of gut motility which must be differentiated from mechanical intestinal obstruction. We have seen 11 such patients over the last 5 years. Characteristic symptoms, shared by mechanical obstruction, include abdominal distention and pain, nausea, and vomiting. Radiologic studies reveal dilated loops of bowel with air fluid levels. In most patients a major differentiating feature from obstruction may be the presence of diarrhea rather than obstipation. Steatorrhea is secondary to an overgrowth of anaerobic bacteria in the motionless dilated loops of bowel. IP has been associated with various disorders: in our series two patients had scleroderma, one multiple small bowel diverticula, one systemic amyloidosis, one celiac disease, and one spinal cord injury; in only two patients was the disorder considered "idiopathic." Three patients had previously undergone a jejuno--ileal bypass for morbid obesity. During the acute episode, the patients were treated symptomatically with decompression by nasogastric or rectal tube with fluid and electrolyte replacement. Malabsorption treated with broad spectrum antibiotics reversing the steatorrhea but not episodes of pseudo-obstruction. Magnesium deficiency was present in seven patients and its correction resulted in amelioration of the symptom complex. In two patients episodes of pseudo-obstruction were markedly reduced by metoclopramide which was not effective in two others.
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PMID:Chronic intestinal pseudo-obstruction. 679 59

One is tempted to believe that volvulus in elderly patients on many occasions may be preceded by inactivity and pseudomegacolon. Owing to psychiatric problems, chronic illness, or institutionalization, the patient is more likely to be subjected to treatment with sedatives and psychotropic drugs, causing decreased neuromuscular function of the gut. The basic principles in treating the volvulus are releasing the volvulus, deciding whether a nonoperative or an operative procedure should be employed, and treating complications. As far as surgical management is concerned, several techniques have been suggested, some of which are still controversial. Colonoscopy appears to have become an important method of treatment for volvulus with clearly established indications. Oddly enough, already hospitalized patients are occasionally subjected to delayed attention for volvulus. Therefore, physicians responsible for the care of geriatric patients should be alerted by even fairly mild symptoms of distention, abdominal pain, vomiting, and constipation. Clinical evaluation, including routine films of the abdomen, may avert a major catastrophe.
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PMID:Colon volvulus and the geriatric patient. 707 92


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