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)

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

A rare case with the episodes of vertebrobasilar TIAs which were caused by carotid ulcerative lesion and by persistence of proatlantal intersegmental artery is reported. This 69-year-old man was admitted on 14th Feb. 1985 with complaints of three attacks of vertigo, diplopia, nausea, vomiting and dysequilibrium lasting about 1 hour. His past history and family history were unremarkable. On admission, physical and neurological examinations revealed nothing particular, except bilateral carotid bruits. On the right side, innocent low pitched bruit was detected, however on the left side, carotid bruit was high pitched and was regarded as pathological. Blood pressure was 180/80 mmHg. Pulse rate was 66/min and cardiac arrhythmia was not detected by EKG. He also had no history of cardiac arrhythmia as mentioned above. CT scans and MRI showed only mild brain atrophy and no brain stem nor cerebellar lesions. Left carotid angiogram revealed ulcerative lesion of the common carotid bifurcation which was compatible with high pitched bruit. And at the level of the C2 vertebra, persistent proatlantal intersegmental artery originated from the left internal carotid artery which, after running upward, joined to the horizontal portion of the left vertebral artery above the atlas. Internal carotid and the vertebrobasilar vasculature beyond the proatlantal intersegmental artery were normal except slight irregularity of carotid siphon. Right carotid and vertebral angiograms revealed no abnormality and basilar artery was opacified clearly again via right vertebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of transient cerebral ischemia of the vertebrobasilar system caused by carotid ulcerative lesion and persistent proatlantal intersegmental artery: a case report]. 360 Sep 93

Appropriate use of carbamazepine for the treatment of epilepsy is based on correct identification of the patient's seizure type. Carbamazepine is effective against partial seizures and against generalized tonic clonic seizures. Therapy should begin gradually, with initial doses increased slowly over 1 or 2 weeks, as tolerated. Side effects include fatigue, dizziness, ataxia, double vision, nausea, and vomiting. Most practitioners agree that, because of carbamazepine's relatively short half-life, the total dosage should be administered in at least two divided doses. This avoids too high a peak blood level that would occur with a single dose. Carbamazepine therapy is associated with the development of two hematologic conditions. Leukopenia, which may be transient or persistent, requires careful monitoring but is not cause for immediate discontinuation of therapy. Aplastic anemia occurs rarely but is potentially fatal, and therefore diligent monitoring of hematologic function is indicated. Aplastic anemia is an idiosyncratic, non-dose-related side effect that is most likely to occur within the first 3 or 4 months of initiating therapy. Once seizures are controlled, plasma levels of carbamazepine should be measured to establish optimum levels for individual patients being treated with this drug.
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PMID:How to initiate and maintain carbamazepine therapy in children and adults. 369 21

Aneurysm of the vertebrobasilar system is not a rare lesion but constituting 5-10% of all intracranial aneurysms. Aneurysm at the peripheral part of the anterior inferior cerebellar artery (AICA), however, is rare and only 20 cases have been reported previously. In this report, two cases of aneurysm arising at the junction between the AICA and internal auditory artery and extending into the internal auditory meatus are reported. The first patient was a 51-year-old male who was admitted because of sudden onset of dizziness, rt. tinnitus and deafness. Left vertebral angiograms demonstrated an AVM in the rt. cerebellar hemisphere and two aneurysms on the feeding arteries, one on the superior cerebellar artery and the other on the meatal loop of the rt. AICA. Removal of the AVM and neck clipping of the aneurysms, which were found unruptured, were performed through the rt. suboccipital approach. The second patient was a 42-year-old female who was admitted because of sudden onset of severe headache and vomiting followed by rt. tinnitus, deafness and double vision. CT scan showed subarachnoid clot mainly located in the rt. cerebellopontine angle. Repeated vertebral angiograms revealed an aneurysm at the meatal loop of the rt. AICA. Complete neck clipping was carried out. The clinical features of the aneurysms of this location can be divided into three subgroups according to the characters of onset: sudden onset with subarachnoid hemorrhage, insidious onset of the VII th, VIII th, nerve palsies by the mass effect of the aneurysm, intermittent episodes of the VIII th nerve disfunction due to the insufficiency of the internal auditory artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Aneurysm of the anterior inferior cerebellar artery at the internal auditory meatus: report of two cases]. 378 69

Chronic intracranial hypertension in the presence of hydrocephalus and/or arachnoiditis is a rare presentation of neurobrucellosis. The present case is exceptional because neither hydrocephalus nor arachnoiditis were present. Brucellosis was diagnosed by serological tests. The patient developed asthenia, anorexia, weight loss, violent headaches, explosive vomiting, bilateral papilloedema, diplopia with paralysis of the abducens nerves, left supranuclear facial paralysis and left hemiparesis. A skull radiograph showed destruction of the sella turcica. Rapid recovery was attained with the use of antibiotics. The pathogenesis of this intracranial hypertension syndrome with destruction of sella turcica is discussed.
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PMID:Chronic intracranial hypertension secondary to neurobrucellosis. 381 88

Isolated fourth ventricle is an untoward but interesting complication caused by the shunt procedure, which has been recognized since the introduction of CT scanning. Auditory brain stem evoked potentials (BAEPs) were recorded in a patient with isolated fourth ventricle for assessment of brain stem function. Case 1. A 9-year-old boy. He had undergone repair of the lumbosacral meningocele at birth, followed by shunting procedures, including repeated shunt revision, for hydrocephalus which subsequently developed. CT scanning on admission revealed typical findings of isolated fourth ventricle, while neurological examination disclosed no abnormalities. BAEPs on admission revealed normal waves both in amplitude and latency. This patient has been doing well without further shunting procedures. Case 2. A 17-year-old male was admitted with complaints of headache, diplopia, nystagmus and ataxic gait. He had a history of operation for radical removal of cerebellar astrocytoma and lateral ventriculo-peritoneal shunt at 9 years of age. CT scanning on admission revealed a typical isolated fourth ventricle, and fourth ventricle-peritoneal shunt was performed. Postoperative serial BAEPs revealed gradual improvement of brain-stem function. Clinically he has been symptom-free thereafter except for slight nystagmus. Case 3. A 2-year-old female suffering from hydrocephalus developed after neonatal intraventricular hemorrhage and ventriculitis. After repeated revision of a lateral ventriculo-peritoneal shunt, she was admitted in semicoma with vomiting and opisthotonic posture. CT study revealed an isolated fourth ventricle and preoperative BAEPs showed marked abnormalities. Although fourth ventricle-peritoneal shunt was performed, no remarkable change in BAEPs was obtained, and neurological deficit of considerable degree persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain stem auditory evoked potentials for assessment of isolated fourth ventricle in three patients]. 387 52

A 36-year-old housewife in the U.S.A. was diagnosed as having gastric cancer with meningeal carcinomatosis and admitted to our hospital in September, 1982. She had severe headache, nausea, vomiting, diplopia and neck stiffness. She was treated by intrathecal chemotherapy using methotrexate, cytosine arabinoside and prednisolone, and by systemic chemotherapy using adriamycin and ftorafur, resulting in complete disappearance of cancer cells from the cerebrospinal fluid and partial response for the primary tumor. She lived for more than 1 year following the first symptoms of her disease and for 10 months following the initiation of chemotherapy. This case suggested the usefulness of employing an intrathecal chemotherapy using methotrexate and cytosine arabinoside with simultaneous systemic chemotherapy for meningeal carcinomatosis of gastric cancer.
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PMID:[Case report of meningeal carcinomatosis of gastric cancer successfully treated with intrathecal and systemic chemotherapy]. 391 54

Animal studies have indicated a "vomiting center" situated in the dorsal portion of the lateral reticular formation of the medulla at the level of the dorsal nucleus of the vagus. There is also a chemoreceptor trigger zone in the floor of the fourth ventricle in the area postrema which influences the vomiting center. A 63 year old man with a three year history of metastatic malignant melanoma presented with nausea, projectile vomiting, gait ataxia and diplopia associated with horizontal and vertical nystagmus. CT scan showed a solitary brainstem metastasis without hydrocephalus and he was treated with radiotherapy with resolution of his vomiting after four weeks. At post mortem three months later a metastasis was found in the right middle cerebellar peduncle and lateral tegmentum of the pons; there was no pathological change in the area of the vomiting center or area postrema. It is postulated that this lesion caused projectile vomiting because of involvement of either afferent projections to the vomiting center. The neuroanatomy of vomiting is discussed.
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PMID:The neuroanatomy of vomiting in man: association of projectile vomiting with a solitary metastasis in the lateral tegmentum of the pons and the middle cerebellar peduncle. 407 83

A 39-year-old woman was admitted to hospital with headaches, vomiting, psychic impairment and diplopia. Three hydatid cysts of the lung had been previously removed. An avascular mass in the left hemisphere with left-to-right displacement of the anterior cerebral arteries was noted during a brain angioscintigraphy. A computed tomography (CT) brain scan showed two cystic lesions situated in the left-frontal and occipital regions. A CT abdominal scan showed multiple cysts in the liver, spleen and both kidneys. At operation, two brain cysts were totally extirpated without rupture. The definite pathological diagnosis was secondary hydatid cysts. The headaches, vomiting and diplopia were persistent in the post-operative period. Seven days after the operation, a CT brain scan showed an infratentorial cyst. The patient rejected any surgical intervention.
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PMID:Multiple cerebral hydatid cysts. 652 56

Two children and 29 of 31 crew members aboard a grain freighter became acutely ill after inhaling the toxic fumigant phosphine; one child died. Predominant symptoms were headache, fatigue, nausea, vomiting, cough, and shortness of breath. Abnormal physical findings included jaundice, paresthesias, ataxia, intention tremor, and diplopia. Focal myocardial infiltration with necrosis, pulmonary edema, and widespread small-vessel injury were found at postmortem examination of the dead child. The surviving child showed ECG and echocardiographic evidence of myocardial injury and transient elevation of the MB fraction of serum creatinine phosphokinase. Illness was significantly associated with living or working amidships or on the forward deck areas of the vessel. Phosphine gas was found to have escaped from the holds through a cable housing located near the midships ventilation intake and around hatch covers on the forward deck. The outbreak illustrates the hazards associated with shipboard fumigation.
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PMID:Acute phosphine poisoning aboard a grain freighter. Epidemiologic, clinical, and pathological findings. 738 74


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