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)

Quinidine gluconate (total dose 4-4 to 9-1 mg/kg) was infused intravenously over 22 minutes in 20 patients with either frequent premature ventricular contractions or supraventricular arrhythmias, 16 of whom had bundle-branch block. Therapeutic plasma quinidine levels (3 to 7 mg/l) were achieved in 15. Heart rate, atrioventricular nodal, and infranodal conduction times did not change significantly. The QRS duration increased significantly from 128+/-30 to 134+/-29 ms at peak plasma quinidine levels (P less than 0.01). Mild hypotension occurred during infusion in most patients. Two patients had a severe but transient toxic response characterised by hypotension, nausea, vomiting, and diaphoresis. Atrioventricular dissociation with escape His bundle or fascicular rhythm occurred in 1 patient with sinus bradycardia. Bundle-branch block does not contraindicate administration of quinidine. Quinidine gluconate administered intravenously (0-3 to 0-4 mg/kg per min) is frequently associated with hypotenstion and should be used only in an intensive care setting and with careful monitoring of blood pressure.
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PMID:Clinical and electrophysiological effects of intravenous quinidine in man. 84 92

A case of digoxin overdose was described. Despite vigorous gastric lavage, the serum digoxin which was 0.8 ng/ml on admission rose to 7 ng/ml four hours later. The main side-effects were symptoms of nausea and anorexia and conduction defects including complete atrioventricular dissociation requiring pacemaker insertion. Opportunity was taken to study the site of heart block with His bundle electrography during the conduction disturbances. This showed that the site of block was situated above the His-Purkinje system in the atrioventricular (A-V) node.
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PMID:A case of self-induced digoxin poisoning: with His bundle studies of the site of heart block. 107 Nov 60

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.
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PMID:Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis. 122 84

A 45-year-old white man ingested approximately two cups of boric acid crystals dissolved in water in a suicide attempt. Nausea, vomiting, greenish diarrhea, and dehydration occurred shortly thereafter. Two days later, he presented to the hospital with hypotension, metabolic acidosis, oliguric renal failure, a generalized erythematous rash, and several superficial skin abrasions. His condition failed to improve despite intravenous fluids and vasopressors. He later developed atrial fibrillation with a rapid ventricular response and could not be converted to a sinus rhythm. This rhythm deteriorated to electromechanical dissociation, and the patient died 17 hours after admission. The urine and whole blood boric acid concentrations approximately 52 hours after ingestion were 160 and 42 mg/dL, respectively. These results are equivalent to urine and blood boron concentrations of 28 and 7 mg/dL, respectively. A postmortem urine boron concentration was 29.4 mg/dL. The autopsy report listed boron toxicity as the cause of death. This is the only adult reported to die from acute boric acid ingestion in recent years and may be atypical since the patient was untreated for 3 days and presented with dehydration and renal function impairment. This case suggests that lack of adequate urine flow and dehydration increases the risk of boron toxicity.
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PMID:Fatal ingestion of boric acid in an adult. 138 80

The authors describe the case of a mentally very labile boy suffering from strabism. When he was excited, the deviation of the affected eye increased, diplopia, nausea and headache developed. Hypnosis was applied and the condition improved after 12 sessions. His behaviour changed and progress in school improved. The authors draw attention to new therapeutic possibilities of some forms of strabism in mentally labile children by application of hypnosis.
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PMID:[Use of hypnosis in certain forms of childhood strabismus]. 148 30

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.
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PMID:Electrophysiologic effects of intravenous nicardipine on sinus node function and conduction in humans. 168 70

A case of traumatic carotid-cavernous fistula (CCF) which presented subarachnoid hemorrhage long after the injury is reported. A 24-year-old male was admitted to the National Yokohama Hospital with complaints of severe headache and nausea. CT scan and cerebral angiography showed subarachnoid hemorrhage due to ruptured CCF. His right visual acuity has disappeared after a traffic accident 5 years before, and he had hit his forehead again 3 years previously. He experienced severe headache twice for 2 weeks after his admission. He was transferred to Kanagawa Rehabilitation Center to be treated with intravascular surgery. Plain CT showed high density areas in the basal cisterns. CT after contrast infusion disclosed a small enlarged high density area in the right cavernous sinus, and showed an enhanced mass lesion in contact with the right ventrolateral side of the midpons. The right internal carotid angiogram showed high flow CCF, fed only by the internal carotid artery. It drained mainly into the basilar plexus, partially into the basal vein of Rosenthal and the inferior petrosal sinus. The CCF was found at the C4 portion of the right internal carotid artery. CT and the angiogram revealed a part of the CCF developing into a varix in the ventral side of the prepontine cistern. It ruptured and the patient developed subarachnoid hemorrhage 5 years after the head injury. The CCF was intravascularly embolized by a detachable balloon. Early treatment for CCF is necessary to prevent the occurrence of subarachnoid hemorrhage if a part of the CCF develops into a varix.
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PMID:[Traumatic carotid-cavernous fistula presenting subarachnoid hemorrhage 5 years after head injury; case report]. 189 23

Mexiletine is a Class IB antiarrhythmic which has basic and clinical electrophysiologic properties similar to lidocaine. Like other Class I antiarrhythmic agents, mexiletine blocks the rapid inward sodium current responsible for phase 0 of the action potential. It has been noted in the clinical electrophysiology laboratory to have minimal effect on sinus node function and AV nodal and His-Purkinje system conduction. Pharmacokinetic studies have shown that oral absorption is rapid with bioavailability of 80-90%. Mexiletine is predominantly metabolized by the liver with elimination half-life of 9 to 12 hours. The antiarrhythmic effects of the primary drug's metabolites remain to be defined. Hemodynamic studies have shown mexiletine to have a lesser negative inotropic effect than procainamide or disopyramide. Although mexiletine as a single agent successfully suppresses 60 to 80% of spontaneous ventricular arrhythmias, it has lower efficacy in suppression of induced ventricular arrhythmias. Multiple studies have shown that as monotherapy mexiletine is effective in preventing the induction of ventricular tachycardia in approximately 20% of patients. When used in combination with a Class IA antiarrhythmic drug for suppression of induced ventricular arrhythmias, multiple investigators have reported greater efficacy. Neurological side effects (tremor, dizziness, memory loss) occur in approximately 10% of patients while gastrointestinal side effects (nausea, anorexia, gastric irritation) occur in up to 40% of patients. Proarrhythmia or other serious toxicity from the drug is uncommon.
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PMID:Mexiletine: pharmacology and therapeutic use. 218 14

A patient with traumatic diaphragmatic hernia at right side was treated surgically. He was 63-year-old male. His illness was caused by a traffic accident one year ago. The major symptoms due to the injury were short breathness and pain at right lateral chest wall. One year later he complained of the nausea and abdominal discomfort. At the right thoracotomy, the herniation of liver and colon through the ruptured diaphragma was found. After the return of herniated organ into the abdominal space, ruptured diaphragma was closed directly.
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PMID:[A case of traumatic hernia of right diaphragma]. 230 52

Two cases of ruptured intracranial aneurysm with severe DIC were reported. One case recovered due to early treatment. A 65-year-old man was admitted to our hospital in June, 1987 because he was suffering from sudden severe headache and nausea. On admission, CT-scan angiograms disclosed moderate subarachnoid hemorrhage (SAH) and probable ruptured anterior communicating aneurysm. However definitive diagnosis was not made at that time. On the 15th day after SAH, he had high fever and low blood arterial pressure. His laboratory findings were consistent with DIC, and therapy of FOY was then started with transfusion of fresh blood two days after. His laboratory findings and clinical status improved gradually and he underwent uneventful operation of the aneurysm on the 42nd day after SAH. Another case concerns a 71-year-old woman who was admitted to our hospital in June, 1988 because she had lost consciousness. On admission, CT-scan disclosed severe SAH and next day an operation was performed. On the 6th day after SAH, she showed clinical and laboratory evidence of severe DIC and died two days later. The association between DIC and ruptured intracranial aneurysms have been rarely mentioned in past reports. But the association might occur more frequently than we have supposed, and so more immediate and careful diagnosis and proper treatment for DIC should be given.
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PMID:[Studies of two cases of ruptured intracranial aneurysm with disseminated intravascular coagulation]. 251 15


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