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

Survival following attempted suicide in a 50-year-old man by ingestion of 12.4 g of mexiletine, 620 mg of nifedipine and 50 to 100 tablets of sublingual nitroglycerine 1:150 is reported. Initial presentation was that of mental obtundation, vomiting, tonic-clonic seizure, high-degree atrioventricular block, profound vasodilation and cardiovascular collapse. Treatment consisted of intravenous calcium gluconate and aggressive fluid management. Maintenance of cardiovascular stability required continuous infusion phenylephrine, dopamine and epinephrine. The patient made a full recovery and was medically discharged on the fourth hospital day. This case represents the largest overdose of mexiletine to date to end in patient survival.
 ...
PMID:Survival following severe overdose with mexiletene, nifedipine, and nitroglycerine. 189 1

A 44-year old woman had pain in the epigastric region under the thorax aperture on the left side 6 weeks prior to admission. Her doctor had prescribed Rewodina and Myocuran without success. Then she suffered circulatory collapse twice. Upon hospitalization, she experienced colicky upper abdominal pain and vomiting. She had been taking oral contraceptives (OCs) for 13 years. Spontaneous liver rupture attributable to adenoma was suspected, based on computer tumograms, and laparotomy bore out the suspicion. However, the cause was peliosis hepatis: the left half of the liver was more altered than the right, and a 10cm parenchyma defect was located under the left lateral liver lobe to which a large intrahepatic cavity filled with coagulum was attached. There was a copious amount of blood in the upper abdomen and another hole was filled with old blood. Partial liver resection was performed. The patient returned 3 weeks after recuperation because of fluctuating inflamed swelling developed on the right side. An incision was made to remove the abscess, but instead of finding pus, massive bleeding ensued whose source could not be located; it was squelched by tampons. Removal of the tampons 7 days later started another rupture with signs of liver insufficiency, and the patient died. Although the role of OCs in inducing liver changes has not been conclusively proven, the fact that she had taken OCs for years without any medical supervision seems to implicate this contraceptive method.
 ...
PMID:[Liver rupture in peliosis hepatis]. 190 60

Gemeprost vaginal suppositories (16,16-dimethyl-PGE1 methyl ester) were compared with intraamniotic Pgf2alpha in 20% saline after Dilapan tents for termination of 14-16 week pregnancies in 58 women. After randomization there were 44% multigravidae in the Gemeprost group and 58% in the Pgf2alpha-saline-Dilapan group; the Gemeprost group averaged 23.4 years, the Pgf2alpha group 26.2%. Gemeprost 1 mg vaginal pessaries were inserted at 3 hr intervals for a maximum of 5 doses. Pgf2alpha 20 mg in 40 ml 20% NaCl was injected intraamniotically under ultrasonic control immediately after Dilapan was inserted in the cervix. If abortion had not occurred within 24 hours, management by iv oxytocin, iv Pgf2alpha, intraamniotic Pgf2alpha or saline or both was at the physician's discretion, as was post-abortion treatment with oxytocin, ergometric or surgical evacuation of the placenta if not delivered within 2 hours. Successful abortion, defined as induction abortion intervals of 24 hours, occurred in 58% of the Gemeprost group and 90% of the PG-saline group, for mean induction-abortion intervals of 12.6 and 11.7 hours. 6 more Gemeprost patients aborted within 27.8 hours without additional treatment, while the last 2 patients to deliver took 42 and 50 hours, compared to a 32-hour maximum interval for PG-saline patients. Much of the difference in intervals was accounted for by primigravidas, who took 15.84 hours on average with Gemeprost, compared to 13.7 hours with PG-saline. Gastrointestinal side effects were more common in the Gemeprost group: diarrhea in 58% and vomiting in 62%, compared to 7% with diarrhea and 34% with vomiting in the PG-saline group. Retained placenta, hemorrhage 300 ml and pain requiring narcotics were similar in both series. The outcomes in terms of induction-abortion intervals were not significantly different. Gemeprost was considered the agent of choice, since it is not invasive, and avoids the risk of sudden collapse or death, intrauterine infection, saline intoxication or clotting disorders, which occur on rare occasions in Pgf2alpha- or saline-induced midtrimester abortions.
 ...
PMID:Second-trimester termination with 16,16 dimethyl-PGE1-methyl ester (gemeprost), compared with a regimen that included intra-amniotic PGF2 alpha and hypertonic saline. 207 46

In a cineradiographic analysis of the vomiting reflex in response to i.v. administration of an emetic drug (lanatoside C, 12 mg/kg) in cats, it was shown that the vomiting act is preceded by cyclic periods of abnormal peristaltic activity of the small bowel and inhibition of gastric peristalsis. It was further observed that massive antiperistalsis of the upper small bowel with reflux into the stomach is a common occurrence in the period immediately preceding vomiting. The emetic act itself is composed of phases of esophageal dilation, gastric emptying, gastric reflux, and esophageal collapse in cyclic repetition. The response of the esophagus and the stomach during emesis is passive, with external pressures and forces apparently providing the expulsive forces, the gastric bolus being contained by contraction of the pylorus and probably an upper esophageal or pharyngeal barrier. Earlier studies were conducted in cats in which observations were made on changes in thoracic venous pressure, abdominal venous pressure, and arterial blood pressure associated with vomiting induced by Veratrum alkaloids. Retching was characterized by a growing series of brief negative intrathoracic pressure pulses mirrored by positive pressure pulses in the abdomen. Expulsion then occurred and was followed with a sudden reversal of intrathoracic pressure from negative to positive. Expulsion involved a more sustained abdominal contraction, but both retching and expulsion were brought about by the same set of muscles, according to their EMG profiles. From results observed following phrenicotomy and spinal cord section at T5, it was concluded that the diaphragm, acting together with the inspiratory muscles against a closed glotis is responsible for the negative intrathoracic pressure that occurs in retching.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Mechanics of vomiting: a minireview. 217 46

Nicotine poisoning is a rarely reported toxicosis. The clinical signs and symptoms are complex and are mostly of central nervous system derangement. In addition, animals may have hypersalivation, vomiting, diarrhea, tachycardia, tachypnea, hypertension and hyperthermia. Some animals are presented in total collapse with slow and shallow respirations, hypotension, dilated pupils, and a weak, rapid and irregular pulse. Treatment is directed toward removing the unabsorbed poison and diluting, and counteracting or controlling the animal's signs. This report emphasises the comparative ease with which a dog would readily ingest chewing tobacco, which is sweet in taste, and come down with nicotine poisoning, as compared to cigarette tobacco which is nonpalatable and therefore less of a threat. The report further discusses clinical nicotine toxicosis, its incidence, clinical manifestations, diagnosis, prognosis and treatment.
 ...
PMID:Nicotine poisoning in a dog. 226 69

We report a case of nearly fatal cardiovascular collapse attributable to an idiopathic anaphylactic reaction in a 76-year-old man. The event began with gastrointestinal symptoms of abdominal cramps, diarrhea, nausea, and vomiting as manifestations of IA. The patient subsequently progressed to develop urticaria, flushing, cardiovascular symptoms of chest pain, hypotension, and eventually cardiovascular collapse and myocardial infarction over a five-hour interval. This case emphasizes that the potential for life-threatening cardiovascular events from IA exists in patients without previously defined cardiac risk factors.
 ...
PMID:Nearly fatal idiopathic anaphylactic reaction resulting in cardiovascular collapse and myocardial infarction. 237 90

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
 ...
PMID:Primary hypoadrenocorticism in ten cats. 246 93

Medical records, radiographs, and bronchial cytologic abnormalities of 65 cats with bronchial disease were reviewed. Bronchial disease was defined as abnormality of the lower airways to the exclusion of disease originating or mainly involving the alveoli, interstitium, vasculature, or pleura. Cats with bronchial disease were more likely to be female and older. Siamese cats were overrepresented and had more chronic disease. In order of frequency, the following clinical signs were reported: coughing, dyspnea, occasional sneezing, wheezing, and vomiting. Radiography revealed prominent bronchial markings, with some cats having collapse of the middle lobe of the right lung (n = 7), overinflation of the lungs (n = 9), or aerophagia (n = 13). Of 65 bronchial washes, 58 were considered exudative, with the predominant cell type being eosinophil in 24%, neutrophil in 33%, macrophage in 22%, and mixed population of cells in 21%. Cultures for bacteria were considered positive in 24% of the cats. Circulating eosinophilia was not helpful in predicting the predominant cell type in bronchial cytologic exudates. Hyperproteinemia without dehydration was present in a third of the cats, indicating an immunologic response. Half the cats had resolution of clinical signs, whereas half the cats required continuing medication with bronchodilators, antimicrobial agents, or corticosteroids.
 ...
PMID:Clinical, radiographic, and bronchial cytologic features of cats with bronchial disease: 65 cases (1980-1986). 247 Jul 10

T-2 toxin, a trichothecene mycotoxin, was injected iv or ip in the single lethal dose of 2 mg/kg. Vomiting was elicited in normal and decerebrate cats with an average onset time of 26.6 min. Chronic ablation of the area postrema significantly delayed the emetic latency to 304 min. Polygraph recording revealed a steady decline in mean arterial blood pressure and pulse pressure to an extreme shock level resulting in death after 5 to 15 hr. Heart rate varied unremarkably throughout the course of circulatory failure, and the cardiac beat persisted after respiratory arrest. No protection against the lethal response was afforded by midbrain decerebration, area postrema ablation, section of the carotid sinus and vagus nerves, and high spinal cord transection supported with artificial ventilation. Effects of T-2 toxin on central and reflex control of breathing were evaluated through changes in VT/FACO2 and f/VT relationships generated by delivery of CO2 enriched gas for inhalation. Central CO2 responsiveness was well maintained under all tested neurological conditions up to the stage of terminal collapse with late decreases in delta VT/delta FACO2 gain and FACO2 setpoint. A toxin-induced progressive increase in resting frequency and an associated decrease in delta f/delta VT gain was found in unanesthetized decerebrate cats, though resting f did not change remarkably in the anesthetized brain-intact cats. In vagotomized brain-intact cats, the delta f/delta VT gain was sustained at zero. These findings indicate that T-2 toxin exercised minimal influence on the brain stem CO2-VT regulator but it caused an acceleration of the central respiratory oscillator after interruption of forebrain connections.
 ...
PMID:Neural factors in acute emetic, cardiovascular, and respiratory effects of T-2 toxin in cats. 251 68

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
 ...
PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>