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)

We report a 17-year-old female case of ornithine transcarbamylase (OTC) deficiency who died of brain edema due to hyperammonemic attack. The patient had a brother with OTC deficiency who had died of hyperammonemia at 17 years of age. She firstly had a symptom of headache, nausea, vomiting and myalgia at 14 years old and twice thereafter. On admission she had a severe disorientation and vomiting. The plasma ammonia level was 89 micrograms/dl, then increased to 400 micrograms/dl in five hours. In addition to plasma exchange, hemodialysis and then peritoneal dialysis for next 5 days, parenteral sodium benzoate and arginine were administered. Although the plasma ammonia level improved gradually, her consciousness never returned and she died of severe brain edema with uncontrollable hypotension on day 8. Histology of a necropsy liver sample showed fatty metamorphosis of hepatocytes mainly with fine lipid droplets. Electron micrograph of hepatocytes showed crystalloid inclusions in mitochondria. Significance of the clinical course and the treatment during hyperammonemic crisis was discussed.
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PMID:[Abrupt onset and rapid deterioration in the course of congenital ornithine transcarbamylase deficiency: a case report]. 221 May 91

The syndrome of water intoxication may occur in psychiatric patients and various hypotheses regarding its aetiology have been postulated. Twenty-seven patients in Woodbridge Hospital were found to have this syndrome. The aim of the study was to describe the clinical and biochemical findings of this group of patients. 70.4% had schizophrenia, 25.9% had mental retardation and 3.7% had a history of alcohol dependence. Many of them were on antipsychotic medication. The symptoms of water intoxication included polyuria, nausea, tremors, weight gain, disorientation, coma and fits. A majority of the patients had hyponatraemia during the acute stages and the osmolality of urine and plasma were correspondingly low. A few patients had abnormalities in electroencephalogram and computerised axial tomography of brain. The management of patients with water intoxication is discussed briefly.
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PMID:Water intoxication in psychiatric patients in Singapore. 239 1

A case of a basilar bifurcation aneurysm associated with common carotid artery occlusion is reported. A 40-year-old woman was admitted to our hospital with severe headache and nausea. On admission, no neurological abnormality was observed. CT scan showed thin subarachnoid hemorrhage in the basal cistern. Left vertebral angiograms revealed a basilar bifurcation aneurysm located in the high position. Also, the left internal and external carotid arteries were supplied through the anastomotic muscle branches of the left occipital and vertebral artery. The trunk of the left common carotid artery was not visualised from its origin on the aortogram. CT scan at the level of C6 showed thinning of the left common carotid artery and contrast enhancement study indicated occlusion. Neck clipping of the aneurysm was successfully performed by right trans-sylvian approach. Right zygomatic arch was removed to obtain a wider operative field for avoiding further retraction of the brain tissue. The postoperative course was uneventful except transient disorientation for two weeks. It has been well known that internal carotid artery occlusion may be associated with cerebral aneurysm in some cases. However, it seemed to be a rather rare case that the common carotid artery occlusion due to arteriosclerosis was associated with cerebral aneurysm. Hemodynamic factor was positively suggested for aneurysmal formation in this case.
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PMID:[A case of a basilar bifurcation aneurysm associated with common carotid artery occlusion]. 239 17

A 68-year-old male was hospitalized because of headache, nausea, and disturbance of consciousness. Neurological examination on admission disclosed somnolence, disorientation, marked neck stiffness, papilledema, and quadriparesis. Computed tomography (CT) scanning demonstrated a round mass with marked contrast enhancement in the right sylvian fissure and small contrast-enhanced masses in the interpeduncular, quadrigeminal and ambient cisterns. CT also showed marked peritumoral edema, a midline shift, and hydrocephalus. The patient's consciousness level and respiration deteriorated 3 days after admission and a craniotomy was performed. The tumor, which was well demarcated, firmly attached to the sphenoidal ridge, and grossly appeared to be a meningioma, was totally removed. Histologically, the tumor had two well defined components, glioblastoma and fibrosarcoma. The patient underwent ventriculoperitoneal shunting, chemotherapy, and radiotherapy after surgery, but the primary tumor soon recurred, with scalp metastasis, and he died 5 months postoperatively. Autopsy revealed metastases to the liver, spleen, and spinal cord. The histogenesis of this mixed tumor and the mechanism of extracranial metastasis are discussed, and the literature is reviewed.
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PMID:[Gliosarcoma with multiple extracranial metastases. Case report]. 248 46

Reports of posteffects following training sessions in Navy and Army flight simulators were obtained from pilots to determine the time course of recovery from simulator sickness. Results imply that posteffects may be a more serious problem than previously considered; 45% of all those queried (N greater than 700) reported having experienced symptoms of simulator sickness; 25% of the symptoms lasted more than 1 h after leaving the simulator; and 8% lasted more than 6 h. Postexposure symptoms were classified into three categories: visuomotor (based on disturbances in oculomotor control; e.g., eyestrain), disorientation (based on disturbance in postural control; e.g., dizziness), and nausea (vagal/autonomic symptoms). A safety risk may be posed particularly by the moderately high frequency of symptoms involving postural disequilibrium. Guidelines for coping with risks are discussed.
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PMID:The time course of postflight simulator sickness symptoms. 281 93

From January 1979 through March 1988, our regional poison center, located many hundreds of miles from the nearest coastal salt water, documented 23 cases of envenomation by "Lionfish" (members of genus Pterois). All cases involved specimens which were maintained in the homes of amateur aquarists. A study of patient epidemiology showed the following: patient's sex 91.3% male, 8.7% female; patients ages ranged from 17 to 50 years with an average age for males of 29.8 years and 35 years for females; the site of the envenomation accident was always in the home; the only part of the body envenomated was the hand or finger; and all of the patients were symptomatic. Symptoms noted included sharp pain, swelling, redness, bleeding, nausea, numbness, joint pain, anxiety, headache, disorientation, and dizziness. One patient had a complication of cellulitis. Treatment provided included immersion of the effected area in hot water at 40 C for 60 to 90 min, analgesics, tetanus toxoid, and antibiotics. There were no deaths noted and treatment proved effective in all cases. This paper also discusses the natural history, clinical effects, and current treatment for envenomations from these beautiful but dangerous venomous fish, which can cause poisoning exposures that are likely to be encountered by poison centers anywhere in the world.
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PMID:Lionfish string experiences of an inland poison center: a retrospective study of 23 cases. 292 30

One of the important factors in outer space is the absence of gravity (OG). During longterm missions, this factor is responsible for the larger number of anatomical and physiological changes that astronauts experience. The cardiovascular system undergoes these changes with severe intensity, which is part of an adaptation process to the new environmental conditions. The modifications observed in both the anatomy of the cardiovascular system and its hemodynamics occur in two phases. The first phase begins when the astronauts enter into Earth orbit or in interplanetary trajectory and extends until the second or fourth day of the mission. It is characterized by an important shifting of fluids from the lower extremities to the cephalic regions which produces an increase of the venous return and the preload, the heart rate is increased, the blood volume in the thorax is also increased, the cardiac chambers become dilated, and by reflex action, the antidiuretic hormone diminishes, diuresis increases and leads to a virtual state of dehydration. Clinically, the first stage is manifested by headache, dizziness, space disorientation, nausea, anorexia, projectile vomiting, sweating and pallor. This constalation of data is known as "The Space Adaptation Syndrome". The second phase begins at the end of the first phase and finishes toward the fortieth or fiftieth day of the mission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Behavior of the cardiovascular system in outer space]. 295 26

A seventy-two-year-old man with hypertensive cerebral hemorrhage acutely developed severe headache, nausea, vomiting, agitation, and disorientation with abrupt rise in blood pressure on the sixth day after the onset. At that time, there were no remarkable changes in focal neurologic deficits, and repeated brain CT scans revealed a small hematoma located in the right basal ganglia without further enlargement or herniation. Blood chemistry and arterial gas analysis were within the normal ranges except for a slight rise in blood urea nitrogen. Similar episodes occurred three times within two days, and each time the cerebral symptoms disappeared in accordance with lowering of blood pressure by antihypertensive therapy. Complication of hypertensive encephalopathy was strongly suggested. The authors discuss the pathophysiology of this encephalopathy in relation to cerebral hemorrhage.
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PMID:Transient encephalopathy related to rapidly and markedly elevated blood pressure in acute stage of hypertensive cerebral hemorrhage--relationship to hypertensive encephalopathy--a case report. 317 64

A case of cryptococcal meningitis in a patient with the acquired immunodeficiency syndrome (AIDS) is described, as well as the epidemiology, pathogenesis, clinical manifestations, diagnosis, and therapeutic management of the disease. In July 1987 a 38-year-old white man was admitted to the hospital because of confusion, disorientation, and headache. His medical history was notable for a positive human immunodeficiency virus test. Culture of the cerebrospinal fluid was positive for Cryptococcus neoformans. The patient was started on amphotericin B 16 mg/day (0.3 mg/kg/day) intravenously and flucytosine 2 g every six hours (150 mg/kg/day) orally. Despite premedication with diphenhydramine and acetaminophen, he experienced rigors that were treated with hydrocortisone and meperidine. Three weeks later he was discharged on flucytosine 2 g orally every six hours and amphotericin B 50 mg intravenously every other day. One week later the patient developed fever and chills; blood cultures were positive for methicillin-sensitive Staphylococcus aureus, and his peripheral leucocyte count was 1.8 X 10(3)/cu mm. Flucytosine was discontinued, and he was treated with intravenous nafcillin while remaining on amphotericin B. In October the patient complained of nausea, vomiting, weakness, and agitation. A CSF latex agglutination titer for cryptococcal antigen was 1:32. He was treated with amphotericin B 50 mg daily until symptoms resolved and then continued on amphotericin B 50 mg twice weekly. Cryptococcosis is the most common life-threatening fungal infection among AIDS patients. In contrast to immunocompetent hosts, this population invariably develops disseminated disease, with 85% having meningeal involvement. The most effective therapy for cryptococcal meningitis in patients with AIDS has not been established.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of cryptococcal meningitis in patients with AIDS. 341 73

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


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