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)

Violent shaking causes severe injury in infants, but the diagnosis of shaken baby syndrome is often difficult to make because of the lack of obvious external signs. Consultations by other specialists may not be helpful, since the findings of most organ systems, taken in isolation, are usually nonspecific. Shaken baby syndrome should be considered in infants presenting with seizures, failure to thrive, vomiting associated with lethargy or drowsiness, hypothermia, bradycardia, hypertension or hypotension, respiratory irregularities, coma or death. Shaken babies are usually less than one year old, and most are under six months of age. Head injury (notably subdural hemorrhage) and retinal hemorrhages are the hallmarks of the syndrome.
 ...
PMID:Shaken baby syndrome. 218 31

A novel type of intoxication in Canada in 1987 was traced to consumption of cultivated mussels contaminated with the excitotoxin domoic acid. Studies carried out in rats and monkeys revealed that parenterally administered domoic acid induces in rats neuroexcitatory phenomena culminating in seizures. Monkeys respond with gagging, emesis and less clearly evident seizure activity. CNS damage consisting of dendrotoxic and gliotoxic edema and nerve cell degeneration occurs in structures of the limbic system and the retina in both species. CNS lesion distribution similarities in animals treated with domoic acid or kainic acid suggest that these excitotoxins share a common pathogenesis mediated by glutamic acid, a putative endogenous excitatory neurotransmitter.
 ...
PMID:Neuropathology of excitatory neurotoxins: the domoic acid model. 219 36

Nonsalicylate, nonsteroidal anti-inflammatory drugs (NSAIDs) can be divided into 4 chemical classes: acetic acids, fenamic acids, oxicams and propionic acids. Most NSAID overdoses result in a benign outcome. Of 50,614 exposures reported to poison centres in the United States in a 2-year period, 131 (0.26%) had a major outcome, with 10 deaths. Despite the generally mild effects reported in large patient series, isolated case reports have documented serious toxicity, such as seizures, hypotension, apnoea, coma and renal failure. The majority of these consequences occur after ingestion of substantial quantities by adults attempting suicide. Rarely, with ibuprofen and piroxicam, children who ingest small amounts in accidental exposure develop serious toxicity. Typical signs and symptoms of NSAID overdose include nausea, vomiting, headache, drowsiness, blurred vision and dizziness. Seizures are rarely documented across all NSAID classes, with the exception of mefenamic acid (where seizures occur in over one-third of cases), or following massive ingestion of other agents. Drugs in the propionic acid group have produced metabolic acidosis, respiratory depression and coma in severe cases. Ibuprofen is the agent with the most published data on overdose, probably because it is available without a prescription in many countries. Symptoms are unlikely after ingestion of 100 mg/kg or less, and are usually not life-threatening unless more than 400 mg/kg is ingested. There is some relationship between plasma concentrations and the potential for development of symptoms, but plasma concentrations have no impact on treatment decisions. Treatment of NSAID overdose is entirely supportive. Recent trends in emergency department procedures regarding gastric decontamination are evolving towards the recommended administration of activated charcoal without gastric emptying in patients presenting more than 1 hour after ingestion, although gastric lavage, followed by administration of activated charcoal, may be advisable in patients who present earlier. Home administration of syrup of ipecac is still recommended if treatment is given shortly after ingestion, with a few exceptions: for example, ipecac is contraindicated after ingestion of mefenamic acid or ibuprofen in amounts greater than 400 mg/kg. Urine alkalinisation and diuresis have been recommended to enhance the elimination of NSAIDs, based on a pKa in the range of 3 to 5. However, because the drugs are universally highly protein bound, with little unchanged renal excretion, this technique is not likely to be beneficial. Haemodialysis is also unlikely to enhance elimination, but may be required if oliguric renal failure develops. Multiple dose activated charcoal may be useful in enhancing elimination of NSAIDs with long half-lives, such as piroxicam and sulindac.
 ...
PMID:Toxic effects of nonsteroidal anti-inflammatory drugs in overdose. An overview of recent evidence on clinical effects and dose-response relationships. 219 51

Despite the trend towards newer therapeutic agents, theophylline continues to play a major role in the treatment of reversible airway obstruction. Clinical use of the drug is complicated by a relatively narrow therapeutic range and a large pharmacokinetic variability between patients. Generally, however, theophylline toxicity is foreseeable and preventable. Most cases can be attributed to either inadvertent or intentional overdosing of the drug. Age, disease state and drug interactions are other factors which may contribute to its toxicity. Nausea, vomiting and tachycardia are common signs of mild theophylline toxicity; seizures, ventricular arrhythmias and hypotension are life-threatening manifestations of severe toxicity which may respond poorly to standard therapy. Although serum theophylline concentration correlates with toxicity in a general fashion, life-threatening adverse reactions are not readily predictable from the drug concentration alone. Treatment of theophylline toxicity primarily involves supportive care along with gastric lavage and administration of activated charcoal to facilitate drug removal. The early use of haemoperfusion may be life-saving in cases of severe toxicity.
 ...
PMID:Adverse reactions and interactions with theophylline. 219 52

Fifteen patients with neoplastic meningitis received a single intrathecal injection of between 11 and 60 mCi of a 131I radiolabelled monoclonal antibody (MoAb), chosen for its immunoreactivity to tumour. Major toxicity was manifest as nausea, vomiting and headache (7/15 patients), reversible bone marrow suppression (3/8 patients) and seizures (2/15 patients). Nine patients were evaluable for either a tumour or clinical response. Six of these demonstrated an event-free response that was maintained for periods of between 7 and 26 months.
 ...
PMID:Intrathecal administration of 131I radiolabelled monoclonal antibody as a treatment for neoplastic meningitis. 222 81

Margosa Oil is an extract of the seed of the Neem tree and is widely used as a traditional medicine by Indians in India, Sri Lanka, Burma, Thailand, Malaysia and Indonesia. Used mainly for external applications, it is often administered orally to neonates and infants regularly in small amounts. Margosa Oil causes toxic encephalopathy particularly in infants and young children. The usual features are vomiting, drowsiness, tachypnea and recurrent generalised seizures. Leucocytosis and metabolic acidosis are significant laboratory findings. Management is aimed primarily towards the control of convulsions although supportive management is equally important. Prognosis is usually good but fatalities and neurological deficits have been reported. We report here two infants with Margosa Oil poisoning presenting with encephalopathy.
 ...
PMID:Margosa oil poisoning as a cause of toxic encephalopathy. 225 44

Twenty-six cases of accidental 5-fluorouracil (5-FU) ingestions by dogs were reviewed from phone calls to the Illinois Animal Poison Information Center. Cases were collected from January 1, 1987 to December 31, 1988. Of the 26 calls involving 5-FU exposures, 12 were classified as "toxicosis," 13 as "suspected toxicosis," and one as "exposure." Dogs were the only species involved in 5-FU cases received during this time. Accurate estimates of the amount of 5-FU ingested by dogs could be made in 17 cases. Ingestion of more than 20 mg/kg of 5-FU was associated with the development of toxicosis. None of the 12 dogs that ingested oral doses in excess of 43 mg/kg (estimated) survived. Clinical signs associated with 5-FU poisoning in the dog were death, seizures, vomiting (with and without blood), tremors, diarrhea (with and without blood), ataxia, and depression. Clinical signs generally developed within 45 to 60 minutes after exposure, and deaths occurred 6 to 16 hours after ingestion.
 ...
PMID:5-Fluorouracil toxicosis in the dog. 226 27

To determine whether seizures are a reliable sign of increased intraventricular pressure in children with shunt-dependent hydrocephalus and meningomyelocele, we performed a retrospective chart review of 346 patients with meningomyelocele and shunt-dependent hydrocephalus. Fifty-one patients had seizures. Seizure episodes were investigated to determine whether they were temporally associated with shunt dysfunction. Episodes of actual or presumed shunt dysfunction were analyzed as to presenting symptoms, ventriculogram, computed tomography scan, and shunt film results. These 51 patients had 129 admissions for possible shunt dysfunction. One hundred one admissions were due to increased intraventricular pressure; nine (9%) of these, had a seizure as one of the presenting symptoms. All of the nine episodes had other common presenting symptoms of shunt dysfunction, such as headache, vomiting, lethargy, or respiratory compromise. We conclude that seizures alone are an inadequate predictor of shunt dysfunction in children with meningomyelocele, but can be seen as one of the presenting symptoms.
 ...
PMID:Seizures in relation to shunt dysfunction in children with meningomyelocele. 223 Dec 21

Congenital hyperargininaemia is a rare condition transmitted as an autosomal dominant trait. Following a one-year free interval, repeated vomiting, psychomotor regression and spastic paraparesis with talipes equinus progressively develop. The diagnosis, confirmed by arginine assays in blood and urine, is probably often missed. We report a case of homozygous arginase deficiency belatedly diagnosed at the age of 18 years, when treatment with sodium valproate (VPA) was instituted. This female patient presented with psychomotor regression since the age of 15 months and with paraparesis since she was 3 years' old. These symptoms rapidly became worse. At the age of 18 years, when she was bed-ridden, she was hospitalized for subintrant tonic seizures. EEG showed generalized, continuous spike-wave discharges at the rate of 3.5 c/s. Treatment with VPA was instituted. Five days later, she went into a state of stupor. Blood ammonia level was elevated at 362 mumol/l. VPA was discontinued, and this was followed by a regression of disturbances of consciousness and by a decrease in arterial ammoniaemia, although the ammonia levels remained high, fluctuating between 40 and 100 mumol/l. Several months after VPA treatment was interrupted, the patient had a second episode of stupor, and her ammoniaemia was 500 mumol/l. Serum amino acid chromatography showed hyperargininaemia at 501 mumol/l (N = 30-150 mumol/l). The diagnosis of arginase deficiency was confirmed by the rise of arginine in red cells, cerebrospinal fluid and urine and, above all, by the finding of a deeply depressed arginase activity in erythrocytes. In all cases of intolerance to VPA, arterial ammoniaemia should be measured after withdrawal of VPA, some time after the acute episode.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Late diagnosis of congenital argininemia during administration of sodium valproate]. 229 Oct 40

Toxicosis attributable to fenvalerate and N,N-diethyl-m-toluamide (Deet) exposure was suspected in 2 cats. Clinical signs of toxicosis developed within 4 to 6 hours of dermal application of the pesticide. Clinical signs of toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition, seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and brain tissues confirmed the presence of fenvalerate and Deet. The pyrethroid fenvalerate and the insect repellent Deet are used for the control of fleas and ticks on cats. Suspected fenvalerate/Deet toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting, depression, and seizures.
 ...
PMID:Fenvalerate/N,N-diethyl-m-toluamide (Deet) toxicosis in two cats. 229 39


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