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)

Decompression sickness (DCS) is a well-known hazard of exposure to significant variations in ambient pressure. The diagnosis and management of DCS is frequently a source of confusion. Although the majority of cases are manifested by joint or limb pains (Type I DCS), patients may present with a wide array of symptoms, such as neurologic deficits, headache, fatigue, nausea, and respiratory difficulty. A thorough knowledge of the differential diagnosis and a strong index of suspicion are crucial to the proper management of DCS. Presented herein are two cases of altitude-related DCS which were confused initially with a viral syndrome. A discussion of the symptoms of DCS is included.
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PMID:Decompression sickness presenting as a viral syndrome. 199 34

Propofol or methohexitone was given to the same twenty patients on two separate occasions during total intravenous anaesthesia for microlaryngeal surgery. With propofol the quality of induction was superior. Fewer patients required supplementation. Heart rate and blood pressure were well controlled at levels of 110-120% baseline. There were fewer side-effects during maintenance and recovery. Patients were able to return home earlier. However, apnoea and pain on injection occurred frequently, the latter when injection was made into the dorsum of the hand. With methohexitone, apnoea, abnormal movement, nausea, vomiting, headache, restlessness and confusion were common. Cardiovascular variables were poorly maintained at levels of 170-180% baseline. The results suggest that propofol is suitable as the sole anaesthetic agent in patients undergoing microlaryngeal surgery.
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PMID:Comparative evaluation of propofol or methohexitone as the sole anaesthetic agent for microlaryngeal surgery. 201 95

Morphine-6-glucuronide is an active metabolite of morphine that has analgesic properties and is measurable in the plasma and cerebrospinal fluid of patients treated with this opioid. Decreased clearance of the compound has been observed in patients with renal insufficiency, and this has been associated with an increase in the ratio of morphine-6-glucuronide to morphine. Clinical effects from accumulation of morphine-6-glucuronide have not been described with the exception of case reports in which patients with renal failure were noted to develop opioid toxicity with high plasma levels of the metabolite and low levels of the parent drug. We describe a patient who experienced chronic nausea and an episode of confusion while treated with a small, stable dose of oral morphine in the setting of mild renal insufficiency. Relatively high levels of morphine-6-glucuronide were measured and all symptoms resolved promptly as the concentration of this metabolite declined. This case provides suggestive evidence that morphine-6-glucuronide can produce clinically significant effects in patients with mild renal insufficiency.
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PMID:Chronic nausea and morphine-6-glucuronide. 201 56

Sixty unpremedicated outpatients undergoing elective extracorporeal shock wave lithotripsy using an unmodified Dornier HM-3 lithotriptor were randomly assigned to receive an intravenous infusion of either alfentanil or ketamine as an adjuvant to midazolam for sedation and analgesia. Although both drug regimens allowed the maximal number of shock waves and energy level, the alfentanil group had significantly better calculi fragmentation (78% vs. 50% of patients with fragments less than 2 mm). Ketamine infusion provided superior intraoperative cardiorespiratory stability; however, it was associated with more disruptive movements (22 vs. 5) and dreaming (35% vs. 5%) during the procedure (P less than 0.05). Postoperatively, confusion also occurred more frequently in the ketamine-treated patients (31% vs. 5%, P less than 0.05). Alfentanil infusion was associated with more episodes of hemoglobin oxygen desaturation to less than 90% (12 vs. 2, P less than 0.05), itching (23% vs. 4%, P less than 0.05), and ability to recall intraoperative events (45% vs. 12%, P less than 0.05). The incidence of postoperative nausea was decreased (not significantly) in the alfentanil group (32% vs. 54%). The mean anesthesia time was similar in both groups; however, discharge times (means +/- standard deviations) were shorter in the alfentanil group (142 +/- 42 min vs. 161 +/- 31 min, P = 0.05). These data suggest that although both techniques proved effective for anesthesia in outpatients undergoing immersion lithotripsy, alfentanil is superior to ketamine as part of a sedative-analgesic technique because of the improved recovery profile and calculi fragmentation.
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PMID:Comparison of alfentanil and ketamine infusions in combination with midazolam for outpatient lithotripsy. 204 57

Ranitidine was first marketed in 1981; since then many patients have been treated such that much experience has been accumulated on the safety of this histamine H2-receptor antagonist in the treatment of gastroduodenal disease. A wide array of ranitidine-associated side effects has been described, but infrequently. As so much information is now available, the aim of this review is to assess the weight of evidence for a causal link between ranitidine and the reported side effects. Overall, ranitidine is well tolerated. The incidence of general side effects at less than 2% is very similar to placebo. Headaches, tiredness, dizziness and mild gastrointestinal disturbance (e.g. diarrhoea, constipation and nausea) are among the most frequent complaints, but have very seldom resulted in stopping treatment. Cardiovascular side effects are extremely rare and unpredictable with the usual doses of oral ranitidine (at most 1 in 1 million patients). They mostly comprise sinusal bradycardia and atrioventricular blockade, especially after rapid intravenous administration, receding after cessation of the drug. Clinical studies, however, have not shown a significant pharmacological effect of ranitidine on the cardiovascular system via H2-receptors, even though individual sensitivities cannot be ruled out in a few isolated reports. Ranitidine is unlikely to be directly hepatotoxic: a transient change in liver function tests has been noted in only 1 in 100 to 1 in 1000 patients. Several cases of mixed hepatitis have been reported, but very few were fully documented. The incidence of ranitidine-associated acute hepatitis has been estimated to be less than 1 in 100,000 patients. Neuropsychiatric complications may be less common and clinically quite similar to those reported with cimetidine, i.e. confusion, disorientation, hallucinations, delirium. These side effects have occurred especially in critically ill and multiple-therapy patients, or patients with chronic renal or hepatic failure, so that the direct causal link with ranitidine treatment was often difficult to ascertain. Even though an H2-receptor-mediated effect is an attractive hypothesis (since similar complications were noted with other H2-receptor antagonists), other mechanisms have been suggested to play a role, e.g. cholinergic or histaminic effects. The overall incidence of neuropsychiatric complications is probably markedly less than 1%. White cell injury (i.e. agranulocytosis) appears to be the most frequent haematological complication, even though case reports are very few and poorly documented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Side effects of ranitidine. 204 87

The responses of thirteen patients with bulimia nervosa and sixteen controls matched for age and weight are described following the ingestion of a carbohydrate and a calorie-free placebo mixture in simulated binges. Psychological, hormonal and biochemical parameters were measured before and at 15 minute intervals for two hours after the simulated binge. At baseline, the bulimics were clearly more symptomatic than the controls. The control population showed a specific satiating effect of carbohydrate upon hunger ratings. Bulimic patients responded differently showing a blunting of the normal sensation of hunger and an enhanced rating for nausea. Prolactin, growth hormone (GH) and cortisol failed to show a carbohydrate-mediated stimulation in either population. The bulimic patients showed a different pattern of GH release, but this was independent of the challenge condition. Large neutral amino acid (LNAA) levels fell following carbohydrate ingestion, but produced an increase of up to 20% in the tryptophan: LNAA ratio in both bulimic patients and the control group. Thus, while this increase in tryptophan availability failed to provoke hormone release, the time course of the carbohydrate specific effect on the sensations of hunger and nausea is compatible with a mechanism based on increased tryptophan availability. The confusion of satiety with nausea may provide a useful focus for the future treatment of patients with bulimia nervosa.
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PMID:Psychological, hormonal and biochemical changes following carbohydrate bingeing: a placebo controlled study in bulimia nervosa and matched controls. 204 88

The new fluorinated adenine analog, fludarabine, has been tested for efficacy in many tumor types over the past ten years. Two other similar nucleoside analogs are currently available for commercial use. Cytarabine is used principally as an antileukemic agent, and vidarabine as an antiviral. Unlike vidarabine, fludarabine is resistant to deactivation by adenosine deaminase. Data from Phase I and II trials suggest that fludarabine is potentially effective in a number of leukemias, including acute lymphocytic leukemia, acute nonlymphocytic leukemia, and chronic lymphocytic leukemia (CLL). Unfortunately, the doses required to achieve adequate response in the acute leukemias (greater than 75 mg/m2) were above the maximum tolerated dose, resulting in intolerable granulocytopenia, thrombocytopenia, and a life-threatening neurotoxic syndrome. In CLL: however, the dose required to achieve a satisfactory response is well within tolerated limits. Long-term survival statistics are not yet available, but historical perspective strongly correlates response to other agents with increased survival times. Toxicities seen at dose regimens of 15-40 mg/m2/d for five consecutive days include somnolence, metabolic acidosis, confusion, fatigue, nausea, vomiting, increase in serum creatinine and aminotransferase concentrations, and pulmonary and hepatic abnormalities. Mild to severe hematologic toxicity has been observed at all dose levels.
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PMID:Fludarabine: a review. 206 37

Diazepam (0.21 mg/kg; group 1) and midazolam (0.03 mg/kg; group 2) was applied for sedation in two groups of urological patients (n = 10 in each) requiring transurethral resection (urine bladder, prostata) using spinal or peridural anaesthesia. Before anaesthetic procedure, 500 ml hydroxyethyl starch were administered for precluding severe vascular depression. Patients receiving midazolam began to sleep within one minute. Heart rate dropped in both groups after injection of both benzodiazepines which was considered a physiological sleeping effect. No hypotensive reactions were registered. Using this therapy maximum PaO2 values of 14.9 kPa in group 1 (diazepam) were registered and of 14.0 kPa in group 2 (midazolam). During the operation all patients were arousable. Side-effects such as nausea, vomiting and confusion were not observed.
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PMID:[The effect of diazepam and midazolam on the circulation and respiration during spinal and peridural anesthesia]. 208 5

Nineteen patients receiving cancer chemotherapy were randomized in a double-blind fashion to receive either (a) dronabinol, 10 mg plus placebo q.i.d.; (b) prochlorperazine, 10 mg plus placebo q.i.d.; or (c) dronabinol plus prochlorperazine, each 10 mg q.i.d. There were six evaluable patients in each of the two single-agent groups and five in the combination group. The median duration and severity per episode of nausea was significantly greater in the group receiving prochlorperazine alone versus the other two groups. The median duration per episode of vomiting was also significantly greater in the prochlorperazine group than in the other two groups. The proportion of patients vomiting was the same in all groups; however, only one patient in the combination group versus three each in the single-agent groups experienced nausea (p = NS). The majority of side effects were associated with the CNS, including somnolence, dizziness, and confusion. Side effects were somewhat more common in both groups receiving dronabinol, though they were not statistically different from the side effects in the group receiving prochlorperazine as a single agent. Efficacy, as measured by duration of nausea and vomiting and by severity of nausea, was significantly greater in both groups receiving dronabinol.
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PMID:Dronabinol and prochlorperazine alone and in combination as antiemetic agents for cancer chemotherapy. 217 91

Hypercalcemia is a potentially lethal endocrine disorder occurring in 10% to 20% of cancer patients at some time during the course of their disease. Clinical manifestations vary in severity, depending on the degree and duration of hypercalcemia, rapidity of onset, patient's age, performance status, sites of metastases, previous antineoplastic therapy, and the presence of hepatic or renal dysfunction. The clinical features of hypercalcemia are protean and affect multiple organ systems, resulting most prominently in neurologic, gastrointestinal, renal, cardiovascular, and musculoskeletal morbidity. Recognition of the disorder requires a high index of suspicion because many of its symptoms, such as nausea, anorexia, weakness, fatigue, lethargy, and confusion, are non-specific and, in the patient with a malignancy, can result from other complications of the primary disorder. If identified appropriately as being related to hypercalcemia, such symptomatology is potentially reversible with treatment. Whereas in the ambulatory general medical population the most common cause of hypercalcemia is primary hyperparathyroidism, in cancer patients and hospitalized patients in general, the most common cause is malignancy. Hypercalcemia in cancer patients is, in most cases, due to advanced metastasized disease. Diagnostic tests are useful in the differential diagnosis of hypercalcemia, and such tests, together with an accurate history and careful clinical observation, permit the best therapeutic approach to an individual patient.
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PMID:Clinical manifestations of cancer-related hypercalcemia. 218 49


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