Skeletal muscle relaxants
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- Rosemary Franklin
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1 Slide # : Revision for the Physiology of skeletal muscles: --Acetylcholine (Ach) works as a neurotransmitter for both the Sympathetic &Parasympathetic Systems. -- The Sympathetic system, at the synapses the preganglionic neurons release Ach. And In response to this stimulus postganglionic neurons release Norepinephrine ((with some exceptions)). --from wiki :The parasympathetic nervous system uses chiefly acetylcholine (Ach) as its neurotransmitter, although peptides (such as cholecystokinin) may act on the PSNS as a neurotransmitter. -- We also have a release of Ach in the Neuromuscular Junctionto initiate the contraction of the skeletal muscle. -- We also have different Receptors for Ach ((Nicotinic &Muscarinic receptors)), andin this lecture we will talk about the receptor at the skeletal muscle end plate which is the Nicotinic receptor. --Why we call them Nicotinic and Muscarinic Receptors? Because the Nicotine and Muscarine activate only these receptors respectively, but Ach works on both of them. --We can also find nicotinic receptors in the Sympathetic and parasympathetic ganglia That is one of the risk factor of Smoking, because the cigarettes have nicotine, so it can activate Sympathetic and parasympathetic receptors and cause serious complications such as Hypertension ((contraction of arteries)) and Heart attack. --As an action potential reaches the end ofmotor neurons, voltage-dependent calcium channelsopen allowing calcium to enter the neuron. Calcium facilitates vesicle binding and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. Invertebrates, motor neurons release acetylcholine (Ach), a small molecule neurotransmitter, which diffuses through the synapse and binds nicotinic acetylcholine receptors ((ion channels)) on the plasma membrane of the muscle fiber, by binding of Ach to these channels, they open and cause entry of Sodium and activationof other channels for the exit of Potassium. Note:sometimes the amount of Ach is not enough to cause contraction, sometimes it causes contraction fora small part of the muscle, or it can P a g e 1
2 contract the whole muscle, so it depends on how much of Ach has been released. --the nicotinic receptors consist of five unites. Slide#6: The first type : neuromuscular blockers which block the channels and prevent depolarization of the motor endplate. --We have two Subtypes ((Nondepolarizing and Depolarizing Drugs)) The second type:spasmolytics which mainly work Centrally (in the CNS). The third type:directly Acting Drug which work directly in the contraction process that happens within the muscle. Slide#7: *One or two quaternary Nitrogen's, i.e. Poorly lipid soluble or highly polar compounds. --Neuromuscular blockers are very similar to Ach structure. --that means these drugs: 1) cannot pass through the CNS. 2) If taken orally they will be poorly absorbed. Slide#8: --Tubocurarine((curarecomes from the South American Indian name for the arrow poison, "ourare"= tube because it was put in tubes ))was used by the native south American Indian, they put it at the tip of the arrow to kill the animals, because it paralysis the muscles,then they take the animals and eat them. Slide#9: --Succinylcholine is the only used Depolarizing muscle relaxant, and the rest of the drugs we are going to talk about in this.a Question for Smart People. When those people ate the animals, why their muscles were not be affected in the presence of tubocurarine? The Answer: because as we mentioned the Neuromuscular Blockers are highly polar and poorly absorbed when taken orally. P a g e 2
3 lecture are Polarizingdrugs. --look at the structures, and don t worry, you don t have to remember any of them. Slide#10 : --Now we have the Steroid Neuromuscular Blocking drugs, Pancuronium,Vecuronium,Pipecuronium, Rocuronium --There are two differences between these Drugs : 1)Duration of action 2)Onset of action So we decide what is the proper drug for the patient by these Differences ((Characteristics)),For example, in an emergency we want a drug with short duration of action to give its effect on the patient quickly. Slide# 11: *Compete with Ach at the nicotinic receptor sites at the NMJ. *In High doses, can enter the pore of the ion channel to cause a more intense blockade So it will be harder to degrade these compounds. Note: There are esterases that degrade these drugs such as Butyrylcholinesteraseand Psuedocholinesterase. *Can also block prejunctional sodium channels to interfere with the mobilization of acetylcholine at the nerve endings. Note: In the nerve terminals we have the prejunctional Sodium channels which are stimulated By Ach to enhance the release of Ach in the terminals. Slide#12: *Pharmacokinetics: Must be given parenterally because it is so polar. Excreted in the kidney or metabolized by the liver. One of them((mivacurium)) is metabolized by cholinesterase's. Note:In general, because the Nondepolraizing drugs are not metabolized by the cholinesterase and mainly conjugated by kidney and liver, they have longer time of action than Depolarizing drugs which P a g e 3
4 are highly sensitive to cholinesterase. *Atracurium is spontaneously broken down ((Hoffman elimination)) ((From Wiki : Hofmann elimination, also known as Exhaustive methylation, is a process where an amine is reacted to create a tertiary amine and an alkene by treatment with excess methyl iodide followed by treatment with silver oxide, water, and heat.)) Slide#13: --You just have to know the name of drugs in the table, and don t memorize any number. Slide#14: --Tubocurarine is not used that much currently and other improved drugs are used such as Pancuronium which causes the blockade of ach receptors so no depolarization of endplate, leading to the relaxation of skeletal muscles. --We need to keep the patient artificially ventilated because the Diaphragm and the skeletal muscles will be paralyzed. --In cases of overdose we have the Antidotes which are the cholinesterase inhibitors e.g.neostigmine. Slide#15: In this slide, we have to know in Phase I that there is an initial contraction that causes constant or permanent depolarization and prevention of subsequent depolarizations to happen, so the channels stay openleading to paralysis. Slide#16: Slide#17: this is a picture that shows the difference between the depolarizing and nondepolarizing blockers : --the nondepolarizing blockers bind to the receptors just like Ach ((compete with Ach)) but don t open the channels P a g e 4
5 --depolarizing blockers bind to the receptors and they either keep them open so that the muscle contracts causing flaccid paralysis or they can go to the channels and prevent further depolarization to happen. Slide#18: *Extremely Short duration (5-10 minutes) because we have normal esterases in our plasma that degrade nondepolarizing blockers such as Butyrylcholinesterase and psuedocholinesterase. *only a small percentage reaches the neuromuscular junction, where it diffuses away into the extracellular fluid. *Some patients have genetically abnormal variant of plasma cholinesterase activity so some of them have high activity of Cholinesterase and others have low activity of Cholinesterase. We can determine the activity of Cholinesterase by giving the patient a drug called Dibucaine which is an inhibitor of cholinesterase and depending on that we shouldn t give the same dose of Succinylcholine for rapid and slow metabolizers. Slide#19: This is another picture that shows how succinylcholine works with the same explanation by the doctor!! Slide#20: Don t worry about this table, just read it for your knowledge. Slide#21: Slide#22: This is a picture about Tubocurarine and we have covered it in slide#8. Slide#23: P a g e 5
6 *Blockade lasts less than 10 minutes so if you have a patient in emergency room, we can use succinylcholine. Slide#24: *Both sympathetic and parasympathetic ganglia and muscarinic receptors in the heart can be stimulated there are muscarinic receptors in the heart, If we give exogenous Ach we are going to have an effect on the heart by these receptors but there is no direct innervations by Parasympathetic to release ach in the heart. *Usually causes hypotension, which can be attenuated by antihistamines that, happens because the Sympathetic nervous system increases the contraction and as a consequence increases hypertension. ((Actually, the doctor herself was confused when she was explaining this part!!!)) Slide#25: Hyperkalemia: In patients with burns, nerve damage, or neuromuscular disease, head injury, and other trauma hyperkalemia occurs because the prolonged depolarization state keeps the potassium channels open which is very important especially with patients having burns, nerve damage or history of neuromuscular disease because it will affect the heart,that is why succinylcholine is contraindicated in these cases. Slide#26: The doctor just read the slide in brief. Slide#27:.((من هون بل شت الشلفقة)) the doctor just read the slide Slide#28: Slide#29: *Diazepam ((Valium)): -Acts at GABA receptors ((receptors in the brain)) in the CNS. -Sedative we give this drug for patients before operations because it P a g e 6
7 causes muscle relaxation and reduces the anxiety of the patient. Slide#30: Slide#31; *Tizanidine: -Related to clonidine((alpha2 receptor blocker, antihypertensive drug)) Slide#32 : Slide#33; Slide#34: Botulinium Toxin used in cosmetics as Botox. ع ش كل ل حظات ي و م ك ق ب ل الفوات واعد نفسك للخرى قبل الممات وال ت ح زن لماض ف ات وال ت غ تم ل م ستق ب ل ات ل ي س لنا من الماضي س وى االعتبار ول ي س ع لي نا ا ن نكون للم ست ق بل بانتظار فإن الق د ر م حتوم. P a g e 7
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