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Skeletal Muscle Relaxants

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Skeletal Muscle Relaxants

Veröffentlicht in: Gesundheit & Medizin
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Skeletal Muscle Relaxants

  1. 1. Skeletal Muscle Relaxants DR.M.USMAN KHALID DPT,MS-NMPT
  2. 2. Classification  Neuromuscular Blockers  Non Depolarizing:  Long Acting e.g Tubocurarine  Intermediate Acting e.g.Rocuronium  Depolarizing(Succinylcholine)
  3. 3.  Spasmolytics  Chronic Use:  CNS Action e.g.Baclofen,Diazepam,Tizanidine  Muscle Action:  E.g.Dantrolene
  4. 4. Neuromuscular Blocking Drugs  Pharmacokinetics:  Given Parenterally,Highly Polar(Can’t cross BBB)  High levels it may cause seizures
  5. 5. Mechanism of Action  Prevents action of Ach at the skeletal muscle end plate  They compete with Ach  Some drugs may also directly plug the ion channel operated by Ach receptor  Post tetanic potentiation is preserved,Tension during tetanus fades rapidly  Larger muscles are more resistant to neuromuscular blockade
  6. 6. Depolarizing Neuromuscular Blocking Drugs Pharmacokinetics:  Parenteral:  short action  inactivated by plasma esterases
  7. 7. Mechanism of action  —Succinylcholine acts like a nicotinic agonist and depolarizes the neuromuscular end plate  When given by continuous infusion, the effect of succinylcholine changes from continuous depolarization (phase I) to gradual repolarization with resistance to depolarization (phase II) (ie, a curare-like block.
  8. 8. Reversal of Blockade  Readily reversed by increasing the concentration of normal transmitter at the receptors.  Neostigmine or pyridostigmine
  9. 9. Adverse effects  Respiratory paralysis  Autonomic ganglia stimulation  Histamine release  Muscle pain  Hyperkalemia  Increased intragastric and intraocular pressure
  10. 10. Non depolarizing drugs Mechanism of action:  Competitive antagonists at skeletal muscle ACh-N receptor.
  11. 11. Pharmacokinetics:  Parenteral use  variable disposition  Spontaneous inactivation (atracurium, cisatracurium)  Plasma ChE (mivacurium)  Hepatic metabolism (rocuronium, vecuronium)  Renal elimination (doxacurium, pancuronium, tubocurarine)
  12. 12. Adverse effects  Histamine release (mivacurium, tubocurarine)  Laudanosine formation (atracurium)  Muscle relaxation is potentiated by inhaled anesthetics, aminoglycosides and possibly quinidine.
  13. 13. Spasmolytic drugs Mechanism of action:  Three of the drugs (baclofen, diazepam, and tizanidine) act in the spinal cord.  Baclofen acts as a GABAB agonist at both presynaptic and postsynaptic receptors, causing membrane hyperpolarization.  Presynaptically, baclofen, by reducing calcium influx, decreases the release of the excitatory transmitter glutamic acid.  At postsynaptic receptors, baclofen facilitates the inhibitory action of GABA.
  14. 14. Mechanism of action:  Diazepam facilitates GABA-mediated inhibition via its interaction with GABAA receptors.  Tizanidine, an imidazoline related to clonidine with significant α2 agonist activity, reinforces presynaptic inhibition in the spinal cord.  Dantrolene : Weakens muscle contraction by reducing myosin-actin interaction.
  15. 15. Pharmacokinetics  Oral  Diazepam may also be given parenterally.
  16. 16. Adverse effects  Sedation  Muscle weakness  CNS depression

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