Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Platelet responses to halothane in normal individuals and in patients susceptible to malignant hyperthermia were evaluated. Platelets in platelet-rich plasma from both normal controls and patients underwent aggregation in response to halothane. There was no significant difference in the degree of aggregation between normal subjects and patients. Aggregation by halothane was associated with a change in platelet shape, centralization of platelet granules, and phosphorylation of platelet actin binding protein, myosin light chain, and a 40 000-dalton protein. Aggregation induced by halothane could be inhibited by EGTA, PGE1, adenosine and verapamil, but not by aspirin. Aggregation induced by halothane could be potentiated by small doses of adrenaline or ADP and in some individuals by caffeine. However, previous exposure of platelets to halothane made them subsequently less aggregable to ADP. The results of these studies do not support a use of halothane-induced aggregation of platelets to detect an abnormality in individuals susceptible to malignant hyperthermia, but do provide new evidence of the effects of halothane on cellular function.
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PMID:Halothane stimulates the aggregation of platelets of both normal individuals and those susceptible to malignant hyperthermia. 665 14

This narrative symposium illuminates the problem of clinician moral distress. NIB editorial staff and narrative symposium editors, Cynda Rushton, PhD, RN, FAAN and Renee Boss, MD, MHS, developed a call for stories, which was sent to several list serves and posted on Narrative Inquiry in Bioethics' website. The request for personal stories from inter-professional healthcare providers asked them to: identify specific clinical situations that give rise to moral distress; discuss the sources of this distress; reflect on how they experienced moral distress-physically, psychologically, socially, or spiritually; assess how they managed their situations; and offer suggestions for avoiding future problems of a similar nature. Twelve stories are found in the print version of the journal and an additional eight supplemental stories are published online only through Project MUSE. The clinicians describe a wide range of experiences with patients, other clinicians, and their own professional and personal identities. Embedded in each of the narratives are deeply felt emotions that accompany their experiences of moral distress. Katherine Brown-Saltzman (a nurse), Alisa Carse (a philosopher), Zhanna Bagdasarov and Shane Connelly (industrial-organizational psychologists), and Nancy Berlinger (a bioethicist) provided commentaries.
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PMID:The many faces of moral distress among clinicians. 2440 71