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MUSCLE RELAXANTS AND ANTICHOLINERGIC DRUGS Q1) types of muscle relaxant& how they work (the difference), how to confirm position of endotracheal tube Type1: *Depolarizing , Non competitive, agonist.(Succinylcholine) *work :succinylcholine Bind nicotinic cholinergic receptors at end plate lead to depolarization of muscle fibers (so called depolarizing)>>In contrast to Ach ,it resists the hydrolysis by Ach-estrase enzyme so remains attached to receptors for longer time>>constant, continuous stimulation of receptors lead to repeated action potentials & initial phase of muscles fasciculation>>This continuous stimulation of receptors lead to receptors desensetization (unresponsiveness) then muscle exhaustion & paralysis>>Drug remains binding to Ach receptors causing desensatization till it diffuse away from end plate to plasma>>In plasma it undergo spontaneous hydrolysis by endogenous plasma cholinesterase (pseudocholieesterase), Type2: *Non depolarizing, Competitive, antagonist.(Tubocurarine ) work: These drugs combine with nicotinic receptors and prevent binding of acetylcholine so prevent depolarization of the muscle cell membrane so inhibiting muscle contraction, these drugs competitively block the receptors this means that you can overcome their action by increase Ach concentration by giving Ach esterase inhibitors such as pyridostigmine or neostigmine … Q2) What do you know about NMB in details? What the reverse? 1. Two classes: 1. Depolarizing, Non competitive, agonist. As Succinylcholine 2. Non depolarizing, Competitive, antagonist. As Tubocurarine 3. NMB’s are co-administrated with anasthetics in the induction phase to induce muscle paralysis 4. facilitate the surgery, especially intra-abdominal and intra-thoracic surgeries 5. Facilitate endotracheal intubation. It is reversed by anticholinesterases, neostigmine, and edrophonium Q3) What do you know about succinylcholine? MOA & Termination succinylcholine Bind nicotinic cholinergic receptors at end plate lead to depolarization of muscle fibers (so called depolarizing) In contrast to Ach ,it resists the hydrolysis by Ach-estrase enzyme so remains attached to receptors for longer time NOTES : • No drug to antagonize it. • It has shorter DOA compared to competitive blockers For more about MOA refer to HANDOUT & read about phase I & phase II12block . March This continuous stimulation of receptors lead to receptors desensetization (unresponsiveness) then muscle exhaustion & paralysis constant, continuous stimulation of receptors lead to repeated action potentials & initial phase of muscles fasciculation Drug remains binding to Ach receptors causing desensatization till it diffuse away from end plate to plasma In plasma it undergo spontaneous hydrolysis by endogenous plasma cholinesterase (pseudocholieesteras e), not acetylcholinesterase Dr. Med. Khaled Radaideh 11 Pharmacodynamics CNS : • MSS : • NO effect on consciousness, pain threshold & cerebral fnx ↑ IOP ↑ ICP • • • • • Skeletal muscles paralysis Myalagia Myoglobinemia, myoglobinurea Messeter muscle spasm Dynamics CVS : • • Bradycardia Dysarrythmia • Sinus arrest GU: • Resp: • March 12 Respiratory muscles paralysis Dr. Med. Khaled Radaideh Coz metabolites excreted by kidneys, pts with RF may have hyperkalemia 14 Indications: 1. Non Fasting (emergency, CS) 2. Predicted difficult intubation 3. Prior to ECT 4. Operations of short duration where muscle relaxation is needed. Absolute contra- indications: 1. Inability to maintain airways 2. Lack of resuscitative equipment 3. Known allergy / hypersensetivity 4. Positive Hx of malignant hyperthermia 5. Myotonia (M. congenita, M.dystrophica, paramyotonia congenita), why ? 6. Patient have risk of a hyperkalemic response to succinylcoline, previously mentioned. Relative contra- indications: 1. Known Hx of plasma cholinestrase deficiency 2. Myasthenia gravis & myasthenic syndrome 3. Familial periodic paralysis 4. Open eye injury Q4) What are the side effects for succinycholine ?? Bradycardia Dysarrythmia Sinus arrest myalagia myoglobinemia , myoglobinurea ↑ intra-ocular pressure ↑ intracranial pressure Q5) So why do we use it although it has a lot of side effects? o It’s hydrolyzed in plasma & the metabolites are excreted by kidneys. o Peak effect reached within 60 sec o The blocking effect dissipates over the next 5-10 min. o It is used in the following cases: Non Fasting (emergency, CS) Predicted difficult intubation Prior to ECT Operations of short duration where muscle relaxation is needed. Q6) what is the drug from non depolarizing muscle relaxant that is metabolized by hofmann elimination?? Atracurium Q7) mention 5 side effects of suxamethonium? Hyperthermia, apnea, hyperkalemia, constipation, muscle pain, acute rhabdomyolysis.. Q8) What do you know about atracurium? What is the most imp cause of post op airway obstruction, give other causes? Q9) talk about the uses and side effects of atropine and neostigmine ? Neostagmine: 1. In anesthesia at the end of an operation to reverse the effect of non polarizing muscle relaxants 2. It can be used for urinary retention resulting from general anesthesia 3. In the treatment of myasthenia gravis Side effects of neostagmine: 1. 2. 3. 4. 5. 6. 7. 8. Salivation Flushing Sweaty skin Meiosis Bronchospasm Bradycardia, decrease BP Abdominal pain, nausea Urinary urgency Atropine: 1. Blocks the effect of acetylchline that result from cholinesterase inhibitors like Neostigmine 2. Blocks secretions prior to surgery 3. Ophthalmic: mydiasis and cycloplegia to facilitate the examination of retina & optic disc 4. GIT: antispasmodic agents 5. Urinary: reduce hypermotility states f the urinary bladder and occasionally used in enuresis 6. CNS disorder: Parkinson and motion sickness 7. Antidote for organophosphate & some types of mushroom poisoning. Side effects of atropine: 1. 2. 3. 4. 5. 6. Dry mouth Blurred vision Tachycardia Constipation Confusion, delirium ,agitation Collapse of the circulatory & RS. Talk abt hypo/hyperkalemia? • Hypo..sym/signs: Autonomic neuropathy Skeletal muscle weakness Increased sensitivity to Digoxin Cardiac • Decreased myocardial contractility • Electrical conduction abnormalities • Arrhythmias • Tachycardia • Ventricular fibrillation • Hyper…sym/signs: Areflexia Weakness Paralysis Paresthesia Cardiac conduction abnormalities