P seudocholinesterase Deficiency - SlideServe
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P seudocholinesterase Deficiency - SlideServe
P seudocholinesterase Deficiency. Etiology and considerations . Angela Hepler RN, BS Biology, SRNA Allegheny Valley Hospital School of Anesthesia. Objectives. 1. Review physiology, diagnosis, prevalence, and effects of pseudocholinesterase deficiency
Jul 18, 2014
Pseudocholinesterase Deficiency Symptoms
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One hypothesis for the mechanism of depression implicates deficits in γ-aminobutyric acid (GABA) and downstream alterations in monoaminergic neurotransmission; this hypothesis is supported by evidence in patients with depression and in patients who have died by suicide. Watch the Quick Take video, then see the trial: https://nej.md/2ku3or7 | The New England Journal of Medicine
2:05
One hypothesis for the mechanism of depression implicates deficits in γ-aminobutyric acid (GABA) and downstream alterations in monoaminergic neurotransmission; this hypothesis is supported by evidence in patients with depression and in patients who have died by suicide. Watch the Quick Take video, then see the trial: https://nej.md/2ku3or7 | The New England Journal of Medicine
FacebookThe New England Journal of
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med's go on Instagram: "Pseudocholinesterase (butyrylcholinesterase) is the enzyme responsible for rapidly breaking down succinylcholine, a depolarizing neuromuscular blocker. In patients with pseudocholinesterase deficiency—either genetic or acquired—the metabolism of succinylcholine is markedly slowed, leading to prolonged apnea and paralysis after administration. Non-depolarizing agents such as rocuronium, atracurium, and vecuronium are not dependent on this enzyme for metabolism. Therefore,
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med's go on Instagram: "Pseudocholinesterase (butyrylcholinesterase) is the enzyme responsible for rapidly breaking down succinylcholine, a depolarizing neuromuscular blocker. In patients with pseudocholinesterase deficiency—either genetic or acquired—the metabolism of succinylcholine is markedly slowed, leading to prolonged apnea and paralysis after administration. Non-depolarizing agents such as rocuronium, atracurium, and vecuronium are not dependent on this enzyme for metabolism. Therefore,
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