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العنوان
Analytical Look for Complications of Muscle Relexants
الناشر
Ain Shams University. Faculty of Medicine. Anesthesiology Department,
المؤلف
Abd-Aullah, Nihad Tarek
هيئة الاعداد
باحث / Nihad Tarek Abd-Aullah
مشرف / Amir Ibrahim Mohamed Salah
مشرف / Reem Hamdy Mohamed Al-Kabarity
تاريخ النشر
2008 .
عدد الصفحات
109p.
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
التخدير و علاج الألم
تاريخ الإجازة
1/1/2008
مكان الإجازة
جامعة عين شمس - كلية الطب - Anesthesiology
الفهرس
Only 14 pages are availabe for public view

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from 166

Abstract

Historically, neuromuscular blocking drugs (NMBDs) were thought to be lethal toxic substances rather than being drugs until the introduction of mechanical ventilation (Betcher, 1989).
About 40% of the body is skeletal muscle. Skeletal muscles are made of numerous fibers ranging from 10 to 80 micrometers in diameter. Myofibrils are large polymerized protein molecules that are responsible for muscle contraction, thick filaments are the myosin and the thin filaments are the actin. Adult human muscles have only one neuromuscular junction per cell. Neuromuscular junction-motor end plate consists of a prejunctional motor nerve ending separated from highly folded postjunctional membrane of the skeletal muscle by a synaptic cleft. It is specialized on both sides, on the nerve side and on the muscle side, to transmit and receive chemical messengers. Acetylcholine receptors are ion-gated channels, large glycoprotein complex, composed of 5 protein subunits arranged in a rosette or a donut (Standard, 1986).
Suxamethonium, has a variety of complications, the most life threatening of which is ”malignant hyperthermia”. Malignant hyperthermia (MH) (Autosomal dominant trait) is a pharmacogenetic condition that manifests as a life threatening hypermetabolic reaction when a susceptible individual is exposed to a volatile anaesthetic or depolarizing muscle relaxants (Denborough et al, 1966). A condition if left untreated leads to dissiminated intravascular coagulopathy, acute renal failure and eventually death (Hopkins, 2000).
Pseudocholinesterase deficiency is an inherited autosomal recessive, enzyme abnormality that results in abnormally slow metabolic degradation of exogenous choline ester drugs such as succinylcholine and mivacurium (Barasch et al., 2001)