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)

A review of the prelegal abortion scene in the US precedes discussion of the effect of injected soap, phenol, cresol, and their compounds. The latter is based on a review of 4 toxicology books. There is little difference in the symptoms after the instillation of phenols, cresols, or soaps. Any one of those agents can cause vaginal bleeding, abdominal pain and distension, nausea, vomiting, and cramps. The damage produced by the use of Lysol thus is due to both the phenol and soap components of the compound. Following instillation into the uterus, there is coagulation necrosis of the decidua and placental site. The toxin will invariable cause thrombosis of the intrauterine and parametrial veins. The thrombosis may spread to the entire pelvic vein plexus and paravaginal, paracervical, and ovarian veins. The liver and kidney are affected by the toxin. Icterus and bile pigments in the urine and clinical evidence of liver damage are seen often. Pulmonary edema has been described as have microscopic to massive pulmonary oil emboli and thrombosis. Depression of all bone marrow elements due to toxin has been reported. The red blood cells are further depressed in number because of hemolysis. Cerebral changes include oil emboli, cerebral coagulation, necrosis, and petechial hemorrhages. Until Studdiford and Douglas described gram-negative sepsis causing shock, patients admitted with hypotension accompanying septic abortion were thought to have concealed blood loss. Studdiford and Douglas showed that gram-negative septicemia could produce hypotension. With the advent of massive antibiotic therapy for septic abortion and septic shock, most of these patients could be saved. The kidneys, after exposure to phenolic-soap comounds, show mainly lower nephron changes. As long as the toxin is in the system those changes continue until irreversible renal damage occurs. It is essential to remove the source of the poison (the affected uterus) and then remove the circulating toxins. the main problem is removal of the circulating toxin. In addition to the problems produced by fixed and circulating toxin, it has been shown that most phenol-soap induced abortions are infected. Thus it is necessary to employ the optimal antibiotic therapy for septic incomplete abortion. The initial management phase moves along classic lines. First is monitoring the vital state and supporting the systems. This includes maintaining an intravenous solution with a large-bore needle, monitoring central venous pressure, measuring urinary output, monitoring the vital signs, maintaining adequate oxygenation, and supporting the blood pressure with blood vasopressors or other agents, as needed. Second is diagnosing the extent of the illness. Third is the initial treatment, which includes reestablishment of the blood volume with blood transfusions; aggressive coverage with double or triple antibiotic therapy; correction of hypofibrinogenemia with cryoprecipitate, fresh whole blood or fresh frozen plasma, as indicated; and avoidance of overhydration in the presence of actual or suspected renal failure. After antibiotic coverage has been established, removal of retained products of conception is indicated.
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PMID:Treatment of women who have undergone chemically induced abortions. 404 35

Severe renal failure caused by the mushroom Cortinarius speciosissimus was first recognised in 1972 and has been reported only from Scandinavia. In the summer of 1979 and following the consumption of the wild mushroom in Scotland, three previously healthy young adults developed the recognised features of cortinarius poisoning-namely, gastrointestinal upset after 36-38h, followed by nausea, anorexia, headache, rigors, severe burning thirst, muscle aching, and oliguria. One patient had a diuresis after 8 days and recovered completely. The two other patients did not present to hospital until 10 days after ingestion and severe renal failure had already developed. Both had a severe interstitial nephritis and neither recovered renal function. They were maintained on intermittent haemodialysis until they received renal transplants 9 months later. This form of mushroom poisoning has not so far been reported in the British Isles. With the increasing popularity of wild-mushroom eating, posters and publications on wild edible foods should contain warnings about the toxic nature of species of the genus Cortinarius.
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PMID:Poisoning by Cortinarius speciosissimus. 610 89

A combined modality of treatment utilizing cisplatin as a radiosensitizing agent concomitantly with full-course radical irradiation has been studied in 14 patients. Cisplatin at a dose of 15 mg/M2 body surface area was given intravenously on days 1 through 5 and 21 through 25 of the radiation therapy course. Among the 14 patients so treated, 11 patients had evidence of complete clinical regression of their tumors. Most remained in remission without evidence of recurrent disease for as long as 18 months. Recurrence in the field of treatment was even more rare. Symptomatic improvement was very encouraging in these patients. Most of them have had a significant improvement in their tolerance of pain and in the ability to swallow foods and maintain weight without a nasogastric feeding tube. Decannulation of the tracheostomy is usual. Problems included four patients with renal toxicity, one of whom died with renal failure. No patient required interruption of therapy due to mocositis or dysphagia. Nausea was rare. This encouraging data in our pilot study of a new therapeutic regimen justifies a full-scale clinical trial.
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PMID:Cisplatin sensitization to radiotherapy of squamous cell carcinomas of the head and neck. 619 3

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

The basis of conservative treatment in chronic uremia is the restriction of protein, which lowers blood urea and diminishes nausea, vomiting and other uremic symptoms. Protein restriction to less than 25-30 g per day in adult patients may lead to negative nitrogen balance and protein depletion, which can be prevented by supplementing the diet with essential amino acids or a mixture of essential keto acid analogues and amino acids. The traditional view has been that low protein diet affords symptomatic relief in chronic uremia but does not effect the progression of renal failure. However, recent clinical results, mostly retrospective, suggest that protein restriction may retard or halt progression. This has led to a renewed interest in therapy with low protein diet and essential amino acids or keto analogues, since this form of treatment may postpone the time when the patient has to be started on dialysis, or even make dialysis unnecessary. It is not settled by which mechanism protein restriction effects progression of renal failure. According to one hypothesis, hyperphosphatemia (high Ca X P product) is harmful for the diseased kidneys; protein restriction is beneficial, since a low protein diet is generally also low in phosphate. An alternative hypothesis suggests that glomerular hyperfiltration in the remaining nephrons of the diseased kidneys is harmful and leads to glomerulosclerosis; low protein intake protects the kidney by abolishing glomerular hyperfiltration.
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PMID:Discovery and rediscovery of low protein diet. 636 67

Thirty-six patients with recurrent or metastatic squamous cell carcinoma of the head and neck were treated with doxorubicin and cisplatin. The overall response rate (complete + partial) was 30%, with a median duration of response of 4 months. Median survival durations for responders and nonresponders were 15 and 4 months, respectively. Nausea, vomiting, and alopecia were common. Neither grade 4 myelosuppression nor irreversible renal failure was observed.
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PMID:Doxorubicin and cisplatin for recurrent or metastatic squamous cell carcinoma of the head and neck. 654 Oct 95

A continuous infusion schedule for cisplatin employing a portable infusion pump was studied in a phase-I trial designed to establish an optimal daily dose rate to deliver drug for protracted periods (up to 30 days). Fifteen trials were carried out in 14 patients at daily dose rates of 5, 6.5, 7.5, and 10.0 mg/M2 X day. The median duration of therapy at the respective doses was 21, 17, 8, and 7 days. Dose-limiting toxicity was recalcitrant and protracted nausea was observed in all patients receiving greater than 5 mg/M2 X day. One patient did develop mild thrombocytopenia (98,000) at day 35. Renal failure was relatively minor considering the absence of a concomitantly delivered hydration regimen but 3 patients did develop a transient rise in serum creatinine, 2 of whom had a solitary kidney or partial urinary tract obstruction. No patient developed renal failure at 5 mg/M2 X day. At the recommended dose of 5 mg/M2 X day, the cumulative dose of cisplatin delivered by a protracted infusion schedule is comparable to the intermittent high-dose regimen with less adverse drug complications.
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PMID:Phase-I study of protracted infusion of cisplatin. 654 24

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

A 50-year-old carpenter with stable pulmonary sarcoidosis for nine years underwent uneventful right total hip replacement. Four months later he developed nausea, renal failure, and hypercalcemia. The hypercalcemia and uremia promptly subsided with corticosteroid therapy and no other etiology except sarcoidosis could be established to explain the hypercalcemia. Hypercalcemia did not recur following discontinuation of corticosteroid therapy. These events suggest trauma to bone can precipitate hypercalcemia in patients with stable sarcoidosis, and serum calcium levels should be monitored for three-six months following trauma to bone from surgery or accidents in these patients.
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PMID:Hypercalcemia following bone surgery in a patient with stable pulmonary sarcoidosis. 688 6

Haemolytic transfusion reactions can be defined as the occurrence after transfusion of measurably increased destruction of red cells, of donor or recipient, by alloantibodies. They may be acute (occurring within 24 hours of transfusion) or delayed (when signs of red cell destruction do not occur until 4 to 10 days after transfusion). The severest signs and symptoms of acute reactions follow intravascular red cell lysis and progress to anaemia, fever, haemoglobinuria and jaundice. The subjective responses of pain, restlessness, nausea, skin flushing, dyspnoea and shock are mediated by cleavage products of complement (C3a, C5a) activated by red cell antigen-antibody reaction. The bleeding and renal failure complications that follow are multi-factoral in aetiology but also stem from the activation of intravascular clotting and from the vasomotor disturbances following histamine and kinin release.
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PMID:Clinical presentation of haemolytic transfusion reactions. 739 74


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