NERVOUS SYSTEM NERVOUS SYSTEM. Somatic nervous system. Brain Spinal Cord Autonomic nervous system. Sympathetic nervous system
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1 SYNAPTIC
2 NERVOUS SYSTEM NERVOUS SYSTEM CENTRAL NERVOUS SYSTEM PERIPHERAL NERVOUS SYSTEM Brain Spinal Cord Autonomic nervous system Somatic nervous system Sympathetic nervous system Parasympathetic nervous system
3 Acetylcholine (ACh): Synthesis and Breakdown Synthesis requires the enzyme choline acetyltransferase (ChAT) Made from choline (Ch) and acetyl coenzyme (acetyl CoA) in the axon terminal then filled into synaptic vesicles. Once released into the cleft, its rapidly broken down by the enzyme acetylcholinesterase (AChE). Ch is transported back into the axon terminal and reused to make ACh.
4 NEUROMUSCULAR JUNCTION ((( NMJ ))) Transmission of neural impulse at the nerve terminal translated into skeletal muscle contraction at motor end plate
5 NEUROMUSCULAR JUNCTION Junction between the terminal of a motor neuron and a muscle fiber. One kind of synapse. Also called myoneural junction.
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7 Acethylcholinesterase Synthesis in the muscle, under the end plate Secreted from the muscle but remains attached to it via thin stalk of collagen fastened to the basement membrane Destroy Ach that do not react immediately with receptor & that are released from binding sites. Ach is destroyed in < 1 ms after it is released.
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9 INTRODUCTION BRIEF HISTORY PRINCIPLES OF NEUROMUSCULAR TRANSMISSION MUSCLE RELAXANT Ideal properties Indications & Contraindication Mechanism of action Side effect
10 Before neuromuscular blocking introduce: High concentration of inhalational anesthetic agent Regional anesthesia 1942 curare (tubocurarine) introduce Less anesthetic administered
11 What is a Muscle Relaxer? A muscle relaxer, also known as a muscle relaxant, is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain.
12 Muscle Relaxer block neuromuscular transmission paralysis presynaptically via the inhibition of acetylcholine (ACh) synthesis or release. postsynaptically at the acetylcholine receptor. adjunct to anesthesia to induce paralysis
13 IDEAL PROPERTIES OF MUSCLE RELAXANT Rapid onset (1 min) To avoid hypoxia & aspiration of gastric content Nondepolarizing Predictable duration Easily antagonized, fully reversed No drug interaction Non-toxic Free of side effect eg. CVS, respiratory Stable pharmacokinetic and pharmacodynamic in the present of renal or hepatic disease No accumulation Safe in pregnancy
14 Muscle Relaxers and the Nervous System Muscle relaxers refer to two major therapeutic groups: neuromuscular blockers and spasmolytics
15 Two Therapeutic Muscle Relaxers Neuromuscular blockers act by interfering with Neuromuscular transmission at Blockers the neuromuscular end plate and have no central nervous system activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause temporary paralysis. Spasmolytics, also known as "centrally Spasmolytics acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions.
16 Neuromuscular Blockers Most neuromuscular blockers function by blocking transmission at the end plate of the neuromuscular junction. Normal end plate function can be blocked by two mechanisms := Non depolarizing agents, such as tubocurarine, block the agonist, acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization.
17 Neuromuscular Blockers Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction.
18 Neuromuscular Blockers Both of these classes of neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in pancuronium (a nondepolarizing agent).
19 Spasmolytics Spasmolytic agents generally work by either enhancing the level of inhibition, or reducing the level of excitation. Inhibition is enhanced by mimicking or enhancing the actions of endogenous inhibitory substances, such as gamma-aminobutyric acid (GABA).
20 Spasmolytics GABA is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays a role in regulating neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone. Spasmolytics are referred to as centrally acting muscle relaxants because they can be used to target specific regions of the body such as low back and neck.
21 Skeletal muscle relaxants Classification Peripherally acting (Neuromuscular blockers). Centrally acting Sk. M. relaxants Baclofen -Diazepam Direct acting Sk. M. relaxants. Dantrolene
22 Peripherally acting A) Presynaptic neuromuscular blockers 1) Inhibit Ach synthesis. Triethylacholine -hemicholinium 2) Inhibit Ach release. Mg, aminoglycosides, botulinum toxin, B) Postsynaptic neuromuscular blockers 1) Competitive (non depolarizing blockers). 2) Depolarizing blockers.
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24 Postsynaptic Neuromuscular Blockers Competitive NM blockers. d-tubocurarine. Gallamine. Atracurium. Pancuronium. Vecuronium. Depolarizing NM blockers. Succinylcholine (suxamethonium ).
25 Uses of NMB blockers control convulsion in psychotic patient. electroshock therapy Relieve of tetanus and epileptic convulsion. facilitate endoscopy As adjuvant in general anesthesia to induce muscle relaxation orthopedic surgery.
26 Competitive NM blockers Mechanism of Action competitive antagonists: compete with Ach at the Nicotinic receptors of NMJ. No depolarization of postjunctional membrane. Cholinesterase inhibitors can reverse blockade (Neostigmine).
27 Pharmacokinetics They are polar comp. inactive orally &taken parenterally. No cross placenta & CNS Metabolism depend upon kidney or liver EXCEPT atracurium -mivacurium (cholinesterase).
28 Pharmacological actions : 1- Skeletal muscle relaxation. 2- CVS :- Hypotension (Histamine release). d.tubocurarine. Mivacurium. Atracurium. H.R Gallamine Pancuronium
29 Gallamine ( Flaxedil ) 1-Less potent than curare ( 1/5 ). 2-Metabolized mainly by kidney 100% (((# in renal failure)))). 3-Long duration of action. 4-Tachycardia due to : Atropine like action.
30 d Tubocurarine 1-More potent than gallamine 2-Long duration of action ( 1-2 hr. ) 3-Eliminated by kidney 60% -liver 40%. 4-Histamine releaser : Bronchospasm. Hypotension. 5-Blocks autonomic ganglia (Hypotension).
31 Atracurium 1- As potent as curare (1.5) 2-Has intermediate duration of action (30 min). 3-Eliminated by non enzymatic chemical degradation in plasma ( Spontaneous hydrolysis at body ph). 4-used in liver failure & kidney failure ( drug of choice ). 5-Liberate histamine ( Transient hypotension ). 6-No effect on muscarinic receptor nor ganglia.
32 Mivacurium 1- Chemically related to atracurium 2-Metabolized by pseudo cholinesterases. 3-Fast onset of action 4-Short duration of action (15 min). 5-Transient hypotension (histamine release). 6-Longer duration in patient with liver disease or genetic cholinesterase deficiency.
33 Pancuronium 1-More potent than curare ( 6 times ). 2-Excreted by the kidney ( 80 % ). 3-Long duration of action. 4-Tachycardia : Antimuscarinic action.
34 Vecuronium 1-More potent than tubocurarine ( 6 times ). 2-Metabolized mainly by liver. 3-Intermediate duration of action. 4-Has few side effects. No histamine release. No ganglion block. No antimuscarinic action.
35 Depolarizing Neuromuscular Blockers Mechanism of Action Phase I ( Depolarizing ) combine with nicotinic receptors depolarization of motor end plate initial muscle twitching Persistent depolarization paralysis. Phase I block is augmented not reversed by anticholinestrases.
36 Phase II ( Desensitization Block ) Continuous exposure to succinylcholine depolarization decreases and the membrane become repolarized, but the membrane cannot be depolarized by Ach as long as succinylcholine present desensitization of the membrane. This phase reversed by anticholinesterase.
37 Succinylcholine ( suxamethonium ) Pharmacological Actions :- 1. SK. muscle: fasciculation spastic paralysis. 2. Hyperkalemia: Cardiac arrest. 3. Eye: intraocular pressure. 4.GIT: intragastric pressure regurgitation of gastric content to esophagus. 5. CVS: arrhythmia.
38 Pharmacokinetics Short onset of action ( 1 min. ). Short duration of action (5-10 min.). Destroyed by pseudocholinesterase.
39 Side Effects 1-Hyperkalemia. 2-CVS arrhythmia (Bradycardia, extrasystol and cardiac arrest ). 3-Malignant hyperthermia. 4-Succinylcholine apnea due to? liver disease (neonates elderly). Malnutrition. Organophosphorous poisoning.
40 Spasmolytics Baclofen: Centrally acting (GABA agonist Sp. cord). Diazepam (Benzodiazepines): Centrally acting (facilitate GABA action on Sp. Cord & CNS). Dantrolene:direct action on sk. muscles.
41 Uses of spasmolytics : reduce muscle spasm in 1-Spinal cord injury. 2-Stroke. 3-Cerebral palsy.
42 Dantrolene Mechanism of Action 1. It interferes with the release of calcium from its stores in sk. muscles (sarcoplasmic reticulum). 2. It inhibits excitation-contraction coupling in the muscle fiber. Uses Malignant Hyperthermia. Spastic states. IV, orally t ½ = 8-9 hrs.
43 Malignant hyperthermia Inability to bind calcium by sarcoplasmic reticulum in some patients due to genetic defect. Sensitive to some drugs general anesthesia e.g. halothane neuromuscular blockers e.g. suxamethonium Ca release, intense muscle spasm, rise in Temp.
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