Skeletal Muscle Relaxants Overview
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Questions and Answers

What is the primary mechanism of action of Dantrolene?

  • Increasing the activity of plasma cholinesterase
  • Interfering with calcium release from sarcoplasmic stores (correct)
  • Directly activating GABA A receptors
  • Inhibiting the reuptake of neurotransmitters

    • What is the half-life of Dantrolene?

  • 10-12 hours
  • 4-5 hours
  • 2-3 hours
  • 8-9 hours (correct)

    • Which of the following is an adverse effect associated with Succinyl Choline?

  • Hyperkalemia (correct)
  • Dry mouth
  • Elevated blood pressure
  • Dysphagia

    • What therapeutic use is Dantrolene primarily indicated for?

    <p>Managing malignant hyperthermia (C)</p> Signup and view all the answers

    How does Baclofen primarily act to reduce pain?

    <p>By inhibiting substance P in the spinal cord (A)</p> Signup and view all the answers

    What adverse effect is commonly associated with Botulinum toxin?

    <p>Blurred vision (C)</p> Signup and view all the answers

    What is the route of administration for Dantrolene?

    <p>Intravenously and orally (A)</p> Signup and view all the answers

    What type of drugs are Botulinum toxins considered?

    <p>Neuromuscular-blocking agents (D)</p> Signup and view all the answers

    What is the mechanism of action of Baclofen?

    <p>Enhances the activities of GABA and Glycine (D)</p> Signup and view all the answers

    What is the half-life of Baclofen?

    <p>3-4 hours (B)</p> Signup and view all the answers

    Which of the following is a potential adverse effect of Baclofen?

    <p>Sedation (D)</p> Signup and view all the answers

    What is a therapeutic use of Baclofen?

    <p>Preventing migraines (A)</p> Signup and view all the answers

    How should Baclofen dosage be initiated?

    <p>From the lowest possible dose gradually increasing (C)</p> Signup and view all the answers

    What side effect is potentially caused by sudden withdrawal from Baclofen?

    <p>Anxiety (D)</p> Signup and view all the answers

    What is the maximum daily dose of Baclofen?

    <p>80 mg (C)</p> Signup and view all the answers

    What is the mechanism of action of Tizanidine?

    <p>Agonist action at Alpha-2 adrenergic receptors (C)</p> Signup and view all the answers

    What is the mechanism of action of succinylcholine?

    <p>It mimics acetylcholine but acts for a longer duration. (B)</p> Signup and view all the answers

    Which of the following non-depolarizing agents is classified as safer due to its metabolism?

    <p>Cisatracurium (D)</p> Signup and view all the answers

    What adverse effect is commonly associated with tubocurarine?

    <p>Release of histamine causing bronchospasms (A)</p> Signup and view all the answers

    What effect do cholinesterase inhibitors have on non-depolarizing agents?

    <p>They decrease the effectiveness of non-depolarizing agents. (A)</p> Signup and view all the answers

    What is the primary therapeutic use of non-depolarizing agents?

    <p>As adjuvants in surgical anesthesia (D)</p> Signup and view all the answers

    Which class of drugs is known to decrease acetylcholine release, thereby increasing the action of non-depolarizing drugs?

    <p>Calcium channel blockers (A)</p> Signup and view all the answers

    What is a unique characteristic of acetylated non-depolarizing agents like vecuronium and rocuronium?

    <p>They cause prolonged clearance in hepatic impairment. (B)</p> Signup and view all the answers

    How are non-depolarizing agents typically administered?

    <p>By injection, due to poor oral absorption. (C)</p> Signup and view all the answers

    Flashcards

    Baclofen's action on neurotransmitters

    Baclofen increases the activity of GABA and Glycine (inhibitory neurotransmitters), and decreases the release of Glutamate and Aspartate (excitatory neurotransmitters).

    Baclofen absorption

    Baclofen is rapidly and completely absorbed when taken orally.

    Baclofen half-life

    Baclofen's half-life is 3-4 hours.

    Baclofen's effect on seizures

    Baclofen may increase seizures in people with epilepsy.

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    Baclofen dosage start

    Start Baclofen therapy with the lowest possible dose and gradually increase it.

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    Baclofen maximum daily dose

    The maximum daily dose of Baclofen is 80 mg.

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    Tizanidine mechanism of action

    Tizanidine reduces spasticity by inhibiting the release of excitatory neurotransmitters (like Glutamate) at Alpha-2 adrenergic receptors.

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    Tizanidine initial dose

    The initial dose of Tizanidine is 4 mg every 6-8 hours (maximum of 3 doses in 24 hours), and it can be increased based on response.

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    Atracurium & Histamine

    Atracurium, when broken down in the body, releases histamine, which can cause a drop in blood pressure, flushing, and narrowed airways (bronchoconstriction).

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    Atracurium & Seizures

    Atracurium breaks down into a substance called laudanosine, which can lead to seizures.

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    Cisatracurium & Atracurium

    Cisatracurium is a safer alternative to Atracurium because it has similar effects but fewer side effects.

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    Non-Depolarizing Drug Excretion

    Non-depolarizing muscle relaxants that are excreted by the kidneys have a longer duration of action than those excreted by the liver.

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    Vecuronium & Rocuronium

    Vecuronium and rocuronium are muscle relaxants broken down by the liver.

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    Non-Depolarizing Drug Absorption

    Non-depolarizing muscle relaxants are usually given by injection because they are poorly absorbed by the digestive system (oral route).

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    Non-Depolarizing & Blood Brain Barrier

    Non-depolarizing muscle relaxants do not cross the blood-brain barrier, meaning they don't affect brain function directly.

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    Tubocurarine & Histamine

    Tubocurarine, an older non-depolarizing drug, can cause histamine release, leading to low blood pressure, airway narrowing, and skin reactions.

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    Prolonged Paralysis Cause: Genetic Variants

    A genetic abnormality in the gene coding for cholinesterase, the enzyme that breaks down acetylcholine, reducing its activity and leading to prolonged paralysis.

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    Prolonged Paralysis Cause: Anticholinesterase Drugs

    Drugs that inhibit the enzyme cholinesterase prevent the breakdown of acetylcholine, leading to prolonged muscle contraction and paralysis.

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    Prolonged Paralysis Cause: Neonates

    Newborns have low levels of cholinesterase, making them more susceptible to prolonged paralysis caused by medications that affect acetylcholine breakdown.

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    Dantrolene's Action

    Dantrolene directly interferes with the release of calcium from the sarcoplasmic reticulum, preventing muscle contraction.

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    Dantrolene's Use

    Dantrolene is very effective in treating malignant hyperthermia, a life-threatening condition caused by certain anesthetic agents.

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    Tubocurarine Side Effects

    Tubocurarine can release histamine, leading to a drop in blood pressure, flushing, and narrowing of the airways.

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    Succinylcholine Side Effects

    Succinylcholine can cause an increase in potassium levels in the blood, breakdown of muscle tissue (myoglobinuria), increased eye pressure, and increased pressure in the stomach.

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    Botulinum Toxin Side Effects

    Botulinum toxin can cause dry mouth, blurred vision, difficulty swallowing, and eventually even breathing problems, leading to paralysis.

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    Study Notes

    Skeletal Muscle Relaxants

    • Skeletal Muscle Relaxants are categorized into CNS Muscle Relaxants and Neuromuscular Blocking Drugs.
    • CNS Muscle Relaxants include Diazepam, Baclofen, Carisoprodol, Cyclobenzaprine, and Tizanidine.
    • Neuromuscular Blocking Drugs include non-depolarizing blockers (like Tubocurarine, Benzylisoquinolines, aminosteroids) and depolarizing blockers (like Succinylcholine).
    • Neurotoxins, like botulinum toxin, interfere with calcium influx, impacting acetylcholine release.

    Neuromuscular Junction

    • The neuromuscular junction involves a cholinergic motor neuron, motor end-plate, vesicles, and mitochondria.
    • Acetylcholine vesicles are crucial for signal transmission.

    Non-Depolarizing Agents

    • At low doses, these drugs bind to nicotinic receptors, competing with acetylcholine.
    • Approximately 70% of acetylcholine receptors must be blocked for a clinical effect.
    • This prevents depolarization at the end-plate, inhibiting muscle contraction.

    Non-Depolarizing Agents: Mechanism of Action

    • Non-depolarizing agents at lower doses block acetylcholine binding to receptors, competing with it.
    • They directly inhibit muscle contraction leading to relaxation.
    • To achieve a clinical effect, around 70% of ACh receptors are blocked.

    Overcoming Non-Depolarizing Agent Action

    • Increasing acetylcholine in the synaptic cleft can overcome the blockade.
    • This is achieved by inhibiting the breakdown of acetylcholine (e.g., Neostigmine, Physostigmine, Edrophonium).
    • Anesthesiologists utilize this to shorten blockade or manage overdoses.

    Non-Depolarizing Agents: High Doses

    • At high doses, the drugs block ion channels at the end-plate.
    • This further weakens transmission and reduces the effectiveness of acetylcholine esterase inhibitors.

    Skeletal Muscle Actions

    • Different muscles display varying sensitivity to blockade.
    • Small, fast-contracting muscles are paralyzed initially.
    • Respiratory muscles are the last to be affected and first to recover.

    Pharmacokinetics

    • Skeletal muscle relaxants are often administered intravenously.
    • Many cross the blood-brain barrier poorly. They are often not metabolized in the liver.
    • They are eliminated in the urine, either unchanged or after some metabolism.

    Atracurium

    • Atracurium undergoes spontaneous degradation, releasing histamine and potentially causing a drop in blood pressure, flushing, and bronchoconstriction.
    • It's metabolized to laudanosine, potentially leading to seizures in some cases.
    • Cisatracurium is a safer alternative with similar pharmacokinetics because of reduced histamine release.

    Vecuronium and Rocuronium

    • Vecuronium and Rocuronium are acetylated in the liver.
    • Clearance can be prolonged in liver impairment.
    • They can be excreted unchanged in bile.
    • They differ in onset, duration, and recovery time.

    Non-Depolarizing Agents: Summary

    • Therapeutic Use: Adjuvant drugs in surgical anesthesia.
    • Pharmacology: Given via injection, not orally absorbed, doesn't cross the blood brain barrier, often not metabolized.
    • Adverse effects: Tubocurarine can release histamine, potentially causing blood pressure drops, wheezing, and skin reactions.

    Drug Interactions

    • Cholinesterase inhibitors decrease the efficacy of non-depolarizing agents.
    • Aminoglycoside antibiotics can diminish acetylcholine release, potentially amplifying non-depolarizing action.
    • Calcium channel blockers can enhance non-depolarizing responses by reducing acetylcholine release.
    • Halogenated anesthetics can strengthen neuromuscular blockage and increase the effectiveness of non-depolarizing agents.

    Depolarizing Agents

    • Succinylcholine is the primary depolarizing agent.
    • Its mechanism of action is similar to acetylcholine, acting by depolarizing the muscle membrane.
    • Two distinct phases:
      • Phase 1: Brief depolarization causing muscle twitching
      • Phase 2: Continued occupation of the receptors after depolarization, causing prolonged block.

    Depolarizing Agents: Additional

    • It's insensitive to potassium (K+) and electrical stimulation.
    • The effect is amplified by acetylcholine esterase inhibitors.
    • It paralyzes skeletal muscles initially more than respiratory muscles.

    Depolarizing Agents: Therapeutic Use

    • Depolarizing agents are used as adjuvants in surgical anesthesia.
    • They act quickly, meaning they can be given by infusion in short bursts.
    • Malignant hyperthermia: Some patients exhibit this syndrome when these agents are administered with halothane.

    Succinylcholine

    • Induces skeletal muscle paralysis.
    • The paralysis sequence differs from non-depolarizing drugs; respiratory muscles are paralyzed later than others.
    • It causes a transient muscle twitching before muscle blockage.
    • It continuously maintains depolarization at the end-plate, leading to a loss of electrical excitability.
    • It has a shorter duration of action than non-depolarizing agents.
    • It mimics acetylcholine in action but diffuses at a slower rate which leads to prolonged depolarization.

    Succinylcholine: Additional

    • Low doses have negative ionotropic/chronotropic effects (weakening).
    • High doses produce opposite effects (strengthening).

    Unwanted Effects:

    • Bradycardia is preventable with atropine.
    • Hyperkalemia can arise in patients with burns or trauma, potentially causing arrhythmias and cardiac arrest.
    • Intraocular and intragastric pressure can increase due to skeletal muscle contraction.
    • Malignant hyperthermia: rare, inherited condition, caused by Ca++ channel defects resulting in muscle spasms and fever. Treated by cooling the body and using dantrolene.
    • Prolonged paralysis can occur due to factors affecting cholinesterase activity (genetic variants, anticholinesterase drugs, and liver dysfunction).

    Dantrolene

    • Dantrolene acts directly on skeletal muscles, reducing the activity of excitation-contraction coupling.
    • It's helpful in treating malignant hyperthermia induced during use of depolarizing agents.
    • Administered orally, but absorption is limited to around one-third of the intravenous dose.
    • Half-life is roughly 6–8 hours.
    • Repeated dosing after 10 minutes.

    Baclofen: Overview

    • Baclofen acts through GABA B receptors in the spinal cord.
    • It increases potassium conductance, reducing calcium influx, and reducing activity of excitatory neurotransmitters (like aspartate and glutamate).
    • Baclofen also acts by reducing substance P in the spinal cord.
    • It is considered a less sedative agent.

    Baclofen: Additional Information

    • It inhibits monosynaptic and polysynaptic reflexes.
    • Hyperpolarization of afferent terminals may occur when it is used.
    • Speeds nerve activity within the spinal cord.
    • It acts on excitatory transmitters.

    Baclofen: Characteristics

    • Rapid and complete oral absorption.
    • Half-life of 3-4 hours.
    • May worsen seizures in epileptics.

    Baclofen: Dosage

    • Optimal dose is determined by titration, starting at low doses (e.g. 5mg tid) and gradually increasing.
    • Maximum daily dose of 80 mg is generally recommended.
    • Titration schedules are often used in patients.

    Baclofen: Side Effects

    • Potential side-effects include sedation, drowsiness, muscle weakness, ataxia, anxiety, tachycardia, hallucinations.
    • It may cause increased seizures in some patients.
      • Pregnancy risk, including possible teratogenicity.
      • Side effects like blurred vision or double vision, convulsions, shortness of breath, slow or troubled breathing, and vomiting.

    Tizanidine: Overview

    • Tizanidine is an alpha-2 adrenergic receptor stimulator.
    • It's used for treating skeletal muscle spasticity, acting by reducing presynaptic activity of motor neurons, via reduction in excitatory neurotransmitters (e.g., glutamate, aspartate).

    Tizanidine: Dosage

    • Initial dose: 4 mg orally every 6 to 8 hours (maximum three doses in 24 hours).
    • Dose may be increased by 2 to 4 mg steps to optimize effect and tolerance.
    • Maintenance dose: 8 mg orally every 6 to 8 hours (maximum three doses in 24 hours).
    • Maximum dose: Up to 36mg per day.

    Tizanidine Presentations:

    • Available in 2mg and 4mg tablets.

    Individual Drug Presentations

    • Specific tablet strengths and dosing schedules are provided for each drug mentioned.

    Other topics

    • This document also includes details of elimination mechanisms, clearance rates, potency, and pharmacodynamic characteristics for a variety of muscle relaxants.

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    Description

    Explore the classification of skeletal muscle relaxants, including CNS muscle relaxants and neuromuscular blocking drugs. Learn about their mechanisms, particularly the role of acetylcholine at the neuromuscular junction. This quiz will enhance your understanding of muscle relaxation and pharmacological effects.

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