Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This 74-year-old female suddenly complained of severe headache, nausea, vomiting and dizziness on June 19, 1981. She was brought to nearby hospital. During the following six days, the state of consciousness gradually worsened and left-sided hemiparesis and convulsion attack arose and she was admitted to our clinic on June 25, 1981. Cerebral angiograms revealed an aneurysm of the right middle cerebral artery. Diagnosis of subarachnoid hemorrhage due to the rupture of an aneurysm was tentatively made and conservative therapy was done. On the second hospital day, she had nasal bleeding and began to excrete tar-like stool. Laboratory examination revealed thrombocytopenia, increase of FDP and prolongation of prothrombin time. Her liver and renal functions gradually worsened after this episode. On the 13th hospital day, she expired. General autopsy showed wide spread adenocarcinoma with metastases to the lung, lymph nodes and bones. Examination of the head revealed an unruptured aneurysm and bilateral diffuse subdural clotted hemorrhage. The dura was tightly adherent to the skull and partially thickened. No abnormal findings were found in the brain. On microscopical examination of the dura, there were fresh hemorrhage and many of the innumerable dilated small vessels contained tumor in the inner dural layer. Even by extensive examination, the origin of the malignancy could not be identified. We concluded that the initial symptoms just like of subarachnoid hemorrhage were due to the dural metastasis and subdural hematoma. Sixteen cases of subdural hematoma secondary to metastatic neoplasm were reported previously. We made some discussion about the pathogenesis and symptomatology of this type of subdural hematoma.
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PMID:[Subdural hematoma due to metastatic dural carcinomatosis associated with DIC--a case report]. 662 89

A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3-4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.
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PMID:Acute trazodone poisoning: clinical signs and plasma concentrations. 671 57

This is a report of the safety evaluation of tocainide in the first 369 patients entered into the American Tocainide Emergency Use Program. This humanitarian protocol has made tocainide available for emergency use in the treatment of life-threatening, intractable ventricular arrhythmias in patients who were unresponsive to or unable to take the approved antiarrhythmic drugs. TAhe most frequent adverse experiences reported were neurologic and gastrointestinal in nature and included dizziness, lightheadedness, tremors, nausea, vomiting, and anorexia. Adverse experiences resulted in the discontinuation of tocainide in 16% of these patients and were transient and reversible with no conclusive evidence of permanent organ injury. Adverse experiences having special relevance to the safety assessment of new antiarrhythmic agents are discussed, including congestive heart failure, arrhythmias and conduction disturbances, convulsions, lupus erythematosus-like illness, and deaths while on therapy. No significant abnormal trends were observed in routine hematologic and biochemical laboratory screening tests or in ophthalmologic or chest x-ray examinations. An evaluation of the effects of chronic tocainide administration of ECG intervals showed no significant change in P-R or QRS intervals but demonstrated a statistically significant decrease in Q-T duration. It is concluded that in patients with life-threatening ventricular arrhythmias, tocainide is a safe agent with a favorable risk-benefit ratio.
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PMID:Safety evaluation of tocainide in the American Emergency Use Program. 677 92

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

For a long time there has been doubt the facultative enteropathogenicity of saprophytic bacteria of the genus Bacillus; even today, it is not generally recognized. The simultaneous presence of numerous factors is known to be required for the genesis of enteric diseases (food poisoning). Among bacilli, B. cereus is the most pathogenic one, however, other species may also be involved. In Central Europe, food poisoning caused by bacteria become manifest after a latent period of 6-10 h. Gastric and intestinal convulsions which last for 8-12 h hand diarrhea with watery stools are observed. Nausea, vomiting, headache, and fever are rare symptoms. Cases of food poisoning observed in America and England were mainly characterized by nausea and vomiting lasting 4-6 h after a latent period of 1-2 h. both types have shown a mild course. In the present communication, 5 comparatively severe cases are described, of which 2 occurred in children. In 3 cases. foods of animal origin were incriminated as vehicles of infection, which had not been stated for earlier cases. The potential of spore-forming organisms, in particular of B. cereus, for causing severe disease should not be overlooked.
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PMID:[Cases of severe enteric disease caused by spore-forming aerobic bacteria in Hungary (author's transl)]. 719 38

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

Salicylate poisoning remains a major clinical hazard, usually resulting from accidental ingestions in preschool children, suicidal overdoses in adults and teenagers, and therapeutically acquired intoxication in all ages. Alkalemia or acidemia, alkaluria or aciduria, hypoglycemia or hyperglycemia, and water and electrolyte imbalances may occur; nausea, vomiting, tinnitus, hyperpnea, hyperpyrexia, disorientation, coma, and/or convulsions are common. With chronic, therapeutically induced salicylism, these symptoms may be mistaken for symptoms resulting from the illness for which the salicylates were administered. For acute ingestions, the magnitude of the poisoning is clearly dose related. Blood level determinations are good prognostic indicators for acute ingestions but are of limited value in chronic, therapeutically induced salicylism. Fluid and electrolyte management is the mainstay of therapy. Diuresis, hemodialysis, and hemoperfusion are effective, but the latter two rarely are necessary.
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PMID:Acute and chronic effects of aspirin toxicity and their treatment. 746 27

Five young patients with primary hyperparathyroidism were treated in our hospital. Male to female ratio was 3 to 2 and the mean age was 12.2 years old. Hypercalcemia due to a single adenoma of the parathyroid gland was found in all cases. They showed various clinical symptoms, such as abdominal pain, nausea, convulsions and disturbance of walking. Parathyroid tumors usually could be easily identified with ultrasonography or CT scan or thyroid subtraction scintigraphy. But in two cases parathyroid tumor was not found during operation. Angiography and/or venous sampling were performed and they showed the right localization.
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PMID:[Primary hyperparathyroidism in young patients]. 775 82

We reported a rare case of multiple cavernous angioma accompanied with a convexity meningioma. A 41-year-old female developed generalized convulsion on October 8, 1985. Plain computed tomography (CT) scan revealed a round heterogeneous density mass in the right parietotemporal region, which was homogeneously enhanced. Angiography demonstrated a tumor stain fed by the right angular artery and the posterior branch of the right middle meningeal artery. Total removal of the tumor was performed. Since histological examination disclosed meningothelial cells, whorl formation, polymorphism and necrotic tissue, she received radiation therapy (total 50Gy) under the diagnosis of anaplastic meningioma. On November 10, 1988, she suddenly developed headache, nausea, motor weakness and homonymous hemianopia on the left side. CT scan revealed intracerebral hemorrhage (ICH) near the region where the meningioma used to be. Magnetic resonance image (MRI) demonstrated a high intensity mass at T1-weighted image and mixed intensity mass at T2-weighted image. Furthermore, there were multiple low intensity spotty lesions at the cerebral and cerebellar hemisphere in T1 and T2-weighted image. A few parts of these lesions showed central high intensity cores and perifocal low intensity areas, which were called ring formations or reticulated cores with black rims. The multiple lesions could not be detected by CT scan. ICH was evacuated. Histological examination revealed no specific pathology except necrotic tissue around the hematoma wall. Diagnosis of radiation necrosis was made. On October 25, 1992 she suddenly complained of left hemihypesthesia. CT scan demonstrated two high density spotty areas at the left caudate head and right thalamus. MRI showed these two lesions as reticulated cores with black rims.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multiple cavernous angiomas accompanied with a convexity meningioma: a case report]. 781 76

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46


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