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)

Twenty-two patients were given progressively increasing doses of Cytembena to determine toxicity patterns and to establish a dosage which produces definite but clinically tolerable toxicity when the drug is given by intravenous injections in a 5-day intensive course. Toxicity consisted primarily of nausea, vomiting, arm pain, and transiently decreased renal function. At higher doses, an "autonomic-storm" phenomenon was observed consisting of hypertension, tachycardia, tachypnea, hyperperistalsis, frequent explosive defecation, facial flushing and paresthesias, and chest pain with accompanying ischemic EKG changes. There was no evidence of mucocutaneous, hepatic, or hematologic toxic effects. Toxicity was dose-related, first being recognized at a daily dose of 300 mg/m2 and becoming clinically intolerable at a daily dose of 475 mg/m2. No permanent damage was observed in any of the organ systems monitored. An acceptable treatment regimen for most patients is 400 mg/m2/day for 5 days. Patient discomfort can be reduced by dividing each day's dose into two intravenous injections given at an interval of at least 6 hours. Coronary artery disease and impaired renal function should be contraindications to Cytembena therapy, and caution should be employed in the patients with significant impairment of liver function. Two of 22 patients, both with far-advanced carcinoma and previous chemotherapy failures, showed a favorable objective response to Cytembena therapy. Phase II studies to assess the magnitude of the drug's antineoplastic activity seem warranted.
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PMID:A phase I study of cytembena. 94 91

The case is reported of a non-diabetic young woman who attempted suicide by ingesting 2,500 mg of phenformin. The most marked clinical and laboratory findings during the first 24 hrs included nausea, vomiting, anxiety, agitation, polydipsia, polyuria, increased appetite, tachycardia, tachypnea, persistent lactic acidosis, hypoglycemia and hypokalemia. Treatment at the ICU 10 hrs after ingestion of the overdose was essentially symptomatic and included measures to correct acidosis and hypoglycemia. The patient recovered completely.
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PMID:Acute self-poisoning with phenformin. 102 Jun 9

A 19-year old woman who developed rapid nausea, vomiting, tachypnea, and alkalosis within 90 min of taking 3.25 g quinine S04 to induce abortion, was found to have an elevated anion gap and other electrolyte abnormalities. She was normovolemic, and had benign findings on drug screen except for quinine. Her abnormal laboratory values were high serum anion gap of 20 (normal 8-14), high urine anion gap of 171, low HC03- of 29 mEq/L, high Pa)@ of 130 mm Hg, alkalotic pH of 7.5, and hypokalemia of 2.6 mEq/L. Her hypokalemia was judged due to diuresis and vomiting. She was successfully treated with intravenous fluids and supportive care and was discharged on the third day. Quinine intoxication can also cause cinchonism, which is marked by tinnitus, vertigo, blurred vision and scotomata, and possible optic atrophy or death. The toxic dose is 2 g, and the lethal dose 8 g.
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PMID:Self-induced abortion and an elevated anion gap. 249 93

Following the ingestion of an alleged aphrodisiac known as "yo-yo," a 16-year-old girl experienced an acute dissociative reaction accompanied by weakness, paresthesias, and incoordination. Subsequent symptoms included anxiety, headache, nausea, palpitations, and chest pain. Hypertension, tachycardia, tachypnea, diaphoresis, pallor, tremors, and an erythematous rash were noted on physical examination. Serum epinephrine and norepinephrine levels were found to be elevated. Symptoms resolved spontaneously but lasted approximately 36 hours. The ingested substance was identified as yohimbine. The pharmacology of yohimbine and the treatment of yohimbine poisoning are discussed.
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PMID:Yohimbine: a new street drug. 403 64

Four adults, including a pregnant woman, and three children were admitted to hospital following accidental exposure to mercury vapour produced by heating mercury-gold amalgam. Initial symptoms and signs included a paroxysmal cough, dyspnea, chest pain, tachypnea, nausea, vomiting, fever and leukocytosis. Pulmonary function testing performed on the second day after exposure revealed air-flow obstruction and minor restrictive defects in three patients. The diffusing capacity of the lung for carbon monoxide was reduced in two of these patients. The mean initial blood mercury level (+/- one standard deviation) for the seven patients was 30.8 +/- 1.5 micrograms/dl. A computer analysis showed mercury to behave as a two-compartment system, the compartments having half-lives of 2 and 8 days. The four adults received chelation therapy with D-penicillamine, which did not affect the urinary excretion of mercury. The pregnant woman's infant, born 26 days after exposure, had no detectable clinical abnormalities. The levels of mercury in the blood of the mother and infant at birth and 6 days later were comparable, indicating free transfer of the metal across the placenta.
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PMID:Accidental inhalation of mercury vapour: respiratory and toxicologic consequences. 688 61

Pentachlorophenol (PCP) is a pesticide commonly used as a wood preservative. Although exposure has been well controlled in large chemical manufacturing plants, over-exposures have recently becomes a concern at smaller facilities. Five cases of PCP poisoning, including two fatalities, occurred in two small wood preservative plants. All cases presented with fever, including severe hyperpyrexia in two; an increased anion gap and renal insufficiency were noted in two others. PCP may uncouple oxidative phosphorylation, resulting in a poisoning syndrome characterized by hyperpyrexia, diaphoresis, tachycardia, tachypnea, abdominal pain, nausea, and even death.
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PMID:Pentachlorophenol poisoning. 688 56

Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness.
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PMID:Carbon monoxide intoxication. 769 50

We describe a case of keto- and lactic acidosis in a 22 year old, healthy woman hospitalized for preterm labor at week 32 of gestation. One former pregnancy was normal. Blood glucose level at admission was 115 mg/dl after 8 mg of betamethasone. Continuous salbutamol infusion was used for management of preterm labour. 18 hours later, the patient complained about nausea and dyspnoea followed by tachypnoea and hyperventilation. Blood gas analysis showed severe metabolic acidosis (ph 7.25, BE-17.5, pO2 114 mm Hg, pCO2 15.5 mm Hg). At this moment blood glucose level was 178 mg/dl. Ketone bodies in urine were positive, serum lactate level was also elevated at 8.6 mmol/l. Cesarean section was performed because of prolonged fetal bradycardia. 6 months post partum type-I-diabetes could be excluded. We conclude that this case of acidosis was due to both, beta-2-adrenergic treatment and beginning gestational diabetes.
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PMID:[Metabolic acidosis in the 32nd week of pregnancy--uncontrolled diabetes in pregnancy, dehydration or sequela of tocolysis?]. 784 85

102 patients were divided into 3 groups: epileptics, psychotics and epileptics with psychotic symptoms. All had long been monitored for a number of clinical and laboratory parameters. Though different in many respects, all share states of sudden dysphoria, cacophoria, panic anxiety, horror, and EEG (stereo-EEG, too) signs of epileptic or other gross anomalies, often correlated to those affective disorders. Attacks of dysphoria, epilepsy, and psychosis come spontaneously and in response to biological (hypoglycemia, sleep deprivation, alcohol, menses) or psychosocial stimulation (agitation, quarrels, fear of redundancy, psychic trauma). These states (attacks, dysphoria, "neurotic" or even psychotic episodes) often provoke one another. -Calling this syndrome epileptosis, we believe its mechanism is due to lesions of the limbic and brainstem modulation systems. At the start of the process there is an epileptic focus in the amygdalo-hippocampal complex (AHC) which in itself can trigger simple or complex partial paroxysm but also-by means of electric stimulation of the AHC-states of dysphoria, anxiety, and psychotic hallucinations. Besides, a form of pathological learning develops in premorbid "hypersensitive" personality which can be put down to associative learning and to Overton's phenomenon of "state-dependent retention of learned responses". This may give rise to mutual stimulation where epileptic focal activity in AHC can provoke dysphoria while an external psychosocial situation can trigger epileptic activity there, too (AHC). Since there need not always be mydriasis (though other vegetative signs such as tachycardia, tachypnoea, nausea, blush and others are frequent) or unconsciousness, and some psychomotor manifestations may be out of the ordinary, and scalp EEG may be normal, such patients are often regarded as "hysterics" or malingerers.
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PMID:"Epileptosis"--a syndrome or useless speculation? 871 19

A 92-year-old woman was admitted to our hospital due to hypertension, nausea, pain in the anterior part of the chest, epigastralgia, and tachypnea. During the initial examination of the patient in the emergency ward, she was very excited, howled, and both her hands were numb. Arterial blood gas analysis revealed a marked alkalemia (pH greater than 7.55) and hypocapnia (Pco2 24.1 mmHg). After paper bag re-breathing, the pH and Pco2 were within normal limits. Because there was no lesion in the lungs or the brain that would account for hyperventilation and convulsions, the attack was considered to be a manifestation of hyperventilation syndrome should be carefully considered in the differential diagnosis of disturbance of consciousness even in elderly patients.
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PMID:[Hyperventilation syndrome in a very old woman]. 915 99


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