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Major Pharmacological Issues - Essay Example

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Summary
The essay "Major Pharmacological Issues" focuses on the analysis of the major disputable issues on pharmacological questions. Centrally acting muscle relaxants are: Benzodiazepines (diazepam), baclofen, mephenesin, chlormezanone, carisoprodol, methocarbamol, tizanidine, chlorzoxazone…
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Major Pharmacological Issues
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ification of Skeletal muscle relaxants Centrally acting muscle relaxants: Benzodiazepines (diazepam), baclofen, mephenesin, chlormezanone, carisoprodol, methocarbamol, tizanidine, chlorzoxazone 2. Neuromuscular blocking agents: (a) Non-depolarizing blocking agents: d-Tubocurarine, dimethyl tubocurarine, gallamine, pancuronium, alcuronium, atracurium, doxacurium, mivacurium, rocuronium, pipecuronium, rapacuronium, vecuronium. (b) Depolarizing blocking agents: Succinylcholine, decamethionium 3. Directly acting muscle relaxant: Dantrolene Sodium, Quinine (Tripathi, 2003). Mechanisms of action Centrally acting muscle relaxants: These drugs inhibit transmission in polyneuronal pathways controlling muscle tone. Thus, they inhibit spinal interneurones and promote inhibitory influences of the brain stem reticular formation on spinal motor neurones. They reduce spasm of skeletal muscles without affecting voluntary movement. Neuromuscular blocking agents: These drugs are competitive antagonists of Ach at nicotinic receptors of the motor endplate. They prevent end plate depolarization by Ach and induce flaccid paralysis. Depolarizing blocking agents: These drugs produce prolonged depolarization of the motor endplate and prevent any response to Ach. Normally, Ach, after release from the motor nerve ending, acts on the neuromuscular junction postsynaptic nicotinic receptors, and induces depolarization of the endplate membrane to generate endplate potential from the peak of which the action potential is initiated. Ach is rapidly inactivated by ChE and endplate returns to its resting potential. However, if there is prolonged depolarization induced by these drugs, there is no further generation of action potential after the initial twitch and there is loss of electrical excitability at the motor endplate. Directly acting muscle relaxant: They exert direct action on the skeletal muscle, by interfering with the release of Ca2+ from the sarcoplasmic reticulum, they interfere with the excitation-contraction coupling (Bhattacharya 2003). Respiratory paralysis due to neuromuscular blocking agents and its treatment Treatment of respiratory paralysis arising from an adverse reaction or overdose of a neuromuscular blocking agent should be by positive pressure artificial respiration with oxygen and maintenance of a patient airway until the recovery of normal respiration is assured. With the competitive blocking agents, this may be hastened by the administration of neostigmine methyl sulphate (0.5 to 2mg, intravenously) or edrophonium (10mg intravenously, repeated as required.) (Hardman 1996). Neostigmine Neostigmine is a quaternary ammonium compound that inhibits cholinesterase activity and thus prolongs and intensifies the physiological actions of acetylcholine. It probably also has direct effects on skeletal muscle fibres. To reverse neuromuscular blockade produced by competitive neuromuscular blockers, the usual adult dose in the UK is 50 to 70micrograms/kg given by intravenous injection over a period of 60 seconds; in the USA lower doses of 0.5 to 2mg are used. Additional neostigmine may be given until the muscle power is normal but a total of 5mg should not be exceeded. Similar doses may be used in children; the BNFC recommends a dose of 50 to 80micrograms/kg in neonates and children, to a maximum of 2.5mg in those under 12 years of age. The patient should be well ventilated until complete recovery of normal respiration is assured. To counteract any muscarinic effects in adults 0.6 to 1.2mg of atropine sulfate is given by intravenous injection with or before the dose of neostigmine; neonates and children up to 18 years of age may be given 20micrograms/kg of atropine sulfate (to a maximum of 600micrograms in those aged 1 month and over). It has been suggested that in the presence of bradycardia atropine sulfate should be given several minutes before neostigmine. Glycopyrronium bromide has been used as an alternative to atropine sulfate. Adverse effects The adverse effects of neostigmine are chiefly due to excessive cholinergic stimulation and most commonly include increased salivation, nausea and vomiting, abdominal cramps, and diarrhoea. Allergic reactions have been reported; rashes have been associated with the use of the bromide salt. Neostigmine penetrates the blood-brain barrier poorly and CNS effects are usually only seen with high doses. Overdosage may lead to a cholinergic crisis', characterised by both muscarinic and nicotinic effects. These effects may include excessive sweating, lachrymation, increased peristalsis, involuntary defaecation and urination or desire to urinate, miosis, ciliary spasm, nystagmus, bradycardia and other arrhythmias, hypotension, muscle cramps, fasciculations, weakness and paralysis, tight chest, wheezing, and increased bronchial secretion combined with bronchoconstriction. CNS effects include ataxia, convulsions, coma, slurred speech, restlessness, agitation, and fear. Death may result from respiratory failure, due to a combination of the muscarinic, nicotinic and central effects, or cardiac arrest. It has been reported that a paradoxical increase in blood pressure and heart rate may result from nicotinic stimulation of sympathetic ganglia, especially where atropine has been given to reverse the muscarinic effects Treatment of adverse effects If a life-threatening amount of neostigmine has been taken by mouth and the patient presents within 1 hour, the stomach may be emptied by lavage; giving activated charcoal to decrease absorption should also be considered. When necessary maintenance of respiration should take priority. Atropine sulfate should be given in usual doses of 1 to 2mg, preferably intravenously, or else intramuscularly and repeated as necessary to control the muscarinic effects; doses of up to 4mg have been suggested. Nicotinic effects, including muscle weakness and paralysis, are not antagonised by atropine; small doses of a competitive neuromuscular blocker have been suggested for the control of muscle twitching. Use of the cholinesterase reactivator pralidoxime as an adjunct to atropine has also been suggested. Further supportive treatment should be given as required. Edrophonium Chloride Edrophonium is a quaternary ammonium compound that is a reversible inhibitor of cholinesterase activity. It has actions similar to those of neostigmine but its effect on skeletal muscle claimed to be particularly prominent. It has a rapid onset but a short duration of action. Dosage, Adult (usual) Reversal of neuromuscular blockade, Nondepolarizing: 10 mg IV over 30 to 45 seconds; may be repeated as needed until a cholinergic response is detected; maximum dose, 40 mg. Adverse Effects C O M M O N Cardiovascular: Bradyarrhythmia, Hypotension Dermatologic: Sweating symptom Gastrointestinal: Abnormal gastric secretion, Diarrhea, Dysphagia, Excessive salivation, Nausea, Vomiting Neurologic: Seizure Ophthalmic: Excessive tear production Renal: Increased frequency of urination S E R I O U S Cardiovascular: Cardiac arrest Respiratory: Bronchospasm, Respiratory tract paralysis Edrophonium chloride was originally introduced for the reversal of neuromuscular blockade in anaesthesia. In the UK, the recommended dose in adults and children for the reversal of the effects of competitive neuromuscular blockers is 500 to 700micrograms/kg given by intravenous injection over several minutes either with or after atropine sulfate 7micrograms/kg (to a maximum of 600micrograms). In the USA, a dose of 10mg of edrophonium chloride is given over 30 to 45 seconds and repeated as required up to a maximum of 40mg. The brevity of its action limits its value. Where prolonged apnoea occurs in a patient treated with a depolarising neuromuscular blocker, such as suxamethonium, edrophonium 10mg may be given intravenously with atropine to determine the presence of phase II block. Treatment of adverse effects . (as for neostigmine). If a life-threatening amount of edrophonium has been taken by mouth and the patient presents within 1 hour, the stomach may be emptied by lavage; giving activated charcoal to decrease absorption should also be considered. When necessary maintenance of respiration should take priority. Atropine sulfate should be given in usual doses of 1 to 2mg, preferably intravenously, or else intramuscularly and repeated as necessary to control the muscarinic effects; doses of up to 4mg have been suggested. Nicotinic effects, including muscle weakness and paralysis, are not antagonised by atropine; small doses of a competitive neuromuscular blocker have been suggested for the control of muscle twitching. Use of the cholinesterase reactivator pralidoxime as an adjunct to atropine has also been suggested Further supportive treatment should be given as required. References Bhattacharya, SK, Parantapa, S & Arunabha, R 2003, Pharmacology, 2nd edn, India, Elsevier, A division of Reed Elsevier India Pvt Ltd, pp.232-38. Hardman, JG, Lee, EL, Perry, BM, Raymond, WR & Alfred, GG 1996, Goodman and Gilman's Pharmacological Basis of Therapeutics, 9th edn, New York, McGraw-Hill Health Professions Division, pp.189. Thomson MICROMEDEX 1974 - 2007. MICROMEDEX Healthcare Series Vol. 132. Tripati, KD 2003, Essentials of Medical Pharmacology, 5th edn, New Delhi, Jaypee Brothers Medical Publishers (P) Ltd, pp 309. Read More
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