Skeletal Muscle Relaxants Overview
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Questions and Answers

What is a potential complication that can occur due to the use of succinylcholine?

  • Increased intraocular pressure (correct)
  • Prolonged sedation
  • Severe hypotension
  • Bradycardia

Which of the following is a treatment for malignant hyperthermia?

  • Ephedrine
  • Atropine
  • Midazolam
  • Dantrolene (correct)

What effect does succinylcholine have on potassium levels in the body?

  • Transient hyperkalemia followed by hypokalemia
  • No effect on potassium levels
  • Hypokalemia due to muscle relaxation
  • Hyperkalemia due to fasciculations (correct)

In which condition is succinylcholine use particularly risky due to increased potassium release?

<p>Burn injuries (B)</p> Signup and view all the answers

What is a characteristic of malignant hyperthermia?

<p>Skeletal muscle rigidity (A)</p> Signup and view all the answers

Which of the following describes a symptom associated with succinylcholine apnoea?

<p>Prolonged respiratory muscle paralysis (D)</p> Signup and view all the answers

What is the primary action of neuromuscular blockers like succinylcholine?

<p>Skeletal muscle paralysis (D)</p> Signup and view all the answers

How does succinylcholine affect intraocular pressure?

<p>Increases it due to compressive muscle contractions (A)</p> Signup and view all the answers

Which type of skeletal muscle relaxant is primarily used in surgical procedures?

<p>Depolarizing neuromuscular blockers (C), Non-depolarizing neuromuscular blockers (D)</p> Signup and view all the answers

What distinguishes spasmolytics from neuromuscular blockers?

<p>Spasmolytics reduce spasticity while neuromuscular blockers relax normal muscles. (D)</p> Signup and view all the answers

Which of the following drugs acts directly on muscle rather than centrally?

<p>Dantrolene (B)</p> Signup and view all the answers

Which agent is an example of a non-depolarizing neuromuscular blocker?

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

Which mechanism do presynaptic neuromuscular blockers utilize?

<p>Prevent synthesis or release of acetylcholine. (A)</p> Signup and view all the answers

Which of the following statements about botulinum toxin is correct?

<p>It inhibits acetylcholine release. (B)</p> Signup and view all the answers

What is a common side effect of botulinum toxin poisoning?

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

Which of the following statements correctly describes spasmolytics?

<p>They can be classified as either centrally or directly acting. (A)</p> Signup and view all the answers

What is the primary mechanism by which non-depolarizing neuromuscular blockers exert their effects?

<p>Competitive antagonism at nicotinic receptors (D)</p> Signup and view all the answers

Which of the following neuromuscular blockers is considered long-acting?

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

What effect does increasing acetylcholine concentration have on non-depolarizing neuromuscular blockers?

<p>Reverses the blocking effect (D)</p> Signup and view all the answers

Which of the following statements about depolarizing neuromuscular blockers is true?

<p>They lead to persistent depolarization followed by relaxation. (C)</p> Signup and view all the answers

What is the role of neostigmine in the context of neuromuscular blockers?

<p>To reverse the effects of competitive antagonism (A)</p> Signup and view all the answers

What is one potential complication when using neuromuscular blockers that is related to autonomic effects?

<p>Bradycardia during reversal (A)</p> Signup and view all the answers

Which muscles are the most sensitive to non-depolarizing neuromuscular blockers?

<p>Rapidly contracting facial and ocular muscles (D)</p> Signup and view all the answers

Which neuromuscular blocker is known for having the most rapid onset?

<p>Atracurium (B)</p> Signup and view all the answers

What is the mechanism of action of succinylcholine at the neuromuscular junction?

<p>It overstimulates nicotinic receptors, leading to desensitization. (D)</p> Signup and view all the answers

Which phase of succinylcholine action involves depolarization and initial muscle twitches?

<p>Phase 1 (B)</p> Signup and view all the answers

What is the expected order of muscle paralysis upon administration of succinylcholine?

<p>Eye, jaw, limbs, intercostals, diaphragm (B)</p> Signup and view all the answers

What is a potential adverse effect associated with succinylcholine use?

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

What effect do aminoglycosides like gentamicin have when used with succinylcholine?

<p>Enhance NM blocking activity (C)</p> Signup and view all the answers

Which of the following is NOT a therapeutic use of depolarizing neuromuscular blockers?

<p>Epidural anesthesia induction (D)</p> Signup and view all the answers

What factor influences the duration of action of succinylcholine?

<p>Patient's metabolic rate (D)</p> Signup and view all the answers

What is a consequence of prolonged or repeated administration of succinylcholine?

<p>Desensitization of nicotinic receptors (A)</p> Signup and view all the answers

What is the primary characteristic of recovery from neuromuscular blockers?

<p>It occurs in a reverse order with the diaphragm recovering first. (A)</p> Signup and view all the answers

Which of the following is NOT an effect of neuromuscular blockers?

<p>Improvement in respiratory function. (D)</p> Signup and view all the answers

What advantage do synthetic competitive blockers have over traditional blockers?

<p>They have negligible effects on blood pressure and heart rate. (A)</p> Signup and view all the answers

What is a key therapeutic use of neuromuscular blockers during surgery?

<p>To facilitate endotracheal intubation. (A)</p> Signup and view all the answers

Which neuromuscular blocker is preferred for its rapid onset of action?

<p>Rocuronium (B)</p> Signup and view all the answers

Which of the following is an adverse effect associated with tubocurarine?

<p>Bronchoconstriction. (A)</p> Signup and view all the answers

What is the mechanism by which atracurium is metabolized?

<p>Hofmann elimination and plasma esterases. (D)</p> Signup and view all the answers

Why is mivacurium considered a short-acting neuromuscular blocker?

<p>It has a rapid onset and quick recovery. (B)</p> Signup and view all the answers

What is a primary reason for infusing fresh frozen plasma in treatment?

<p>To supply enzymes (C)</p> Signup and view all the answers

Which of the following accurately describes the action of non depolarizing blockers?

<p>Can be reversed with anticholinesterases (C)</p> Signup and view all the answers

What is a common side effect of the spasmolytic drug baclofen?

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

Which of the following is true regarding the drug dantrolene?

<p>It can cause muscle weakness (B)</p> Signup and view all the answers

How does tizanidine relate to clonidine?

<p>Tizanidine is related but has different action mechanisms. (A)</p> Signup and view all the answers

Which of the following medications can enhance neuromuscular blockade?

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

What distinguishes succinyl choline from competitive blocking agents?

<p>It produces persistent depolarization. (D)</p> Signup and view all the answers

What is a notable effect of hyperkalemia in patients with extensive tissue damage?

<p>It increases potassium release from cells. (B)</p> Signup and view all the answers

Flashcards

Skeletal Muscle Relaxants

Drugs that reduce muscle contractions, divided into neuromuscular blockers and spasmolytics.

Neuromuscular Blockers

Drugs that block the transmission of nerve impulses at the neuromuscular junction, used in surgery and for ventilation assistance.

Spasmolytics

Drugs that reduce muscle spasticity by acting directly on the muscles or within the central nervous system.

Non-depolarizing Blockers

Neuromuscular blockers that compete with acetylcholine for receptor sites, preventing muscle contraction.

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Depolarizing Blockers

Neuromuscular blockers that cause prolonged muscle stimulation, leading to muscle weakness or paralysis.

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Botulinum Toxin

A toxin produced by bacteria that inhibits acetylcholine release, used for cosmetic and medical purposes.

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Acetylcholine

A neurotransmitter that transmits nerve impulses to muscles.

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Neuromuscular Junction

The site where nerve impulses meet muscle fibers to trigger contraction.

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Neuromuscular Blockers

Drugs that block the transmission of nerve impulses at the neuromuscular junction, causing muscle relaxation or paralysis.

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Non-depolarizing Blockers

Neuromuscular blockers that act by competing with acetylcholine for the receptor sites, preventing the initiation of muscle contraction.

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Competitive Antagonism

A type of antagonism where a drug competes with a natural neurotransmitter (like acetylcholine) for the same receptor site.

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Depolarizing Blockers

Neuromuscular blockers that initially cause muscle depolarization and contraction, followed by prolonged depolarization and relaxation (paralysis).

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Succinylcholine

A depolarizing neuromuscular blocker that causes persistent depolarization of the motor end plate resulting in muscle relaxation and paralysis.

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Reversal of Neuromuscular Blockers

The process of counteracting the effects of neuromuscular blockade. Usually achieved with cholinesterase inhibitors.

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Cholinesterase Inhibitors

Drugs that inhibit the activity of cholinesterase, an enzyme that breaks down acetylcholine. Used reverse neuromuscular blockade.

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Flaccid Paralysis

A state of muscle weakness and loss of tone due to neuromuscular blockade.

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Neuromuscular Blockers: Recovery Order

Recovery from neuromuscular blockade happens in the reverse order of administration, starting with the diaphragm.

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Non-Depolarizing Blockers: Cardiovascular Effects

Non-depolarizing neuromuscular blockers can cause significant blood pressure drops and increased heart rate due to autonomic ganglion blocking effects and histamine release.

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Atracurium: Degradation

Atracurium is broken down in the body by a special enzyme (Hoffmann elimination) in addition to liver metabolism.

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Synthetic Blockers: Advantages

Newer, synthetic neuromuscular blockers typically cause less histamine release and do not block autonomic ganglia, reducing some side effects.

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Neuromuscular Blockers: Therapeutic Uses

Used during surgery to facilitate incisions, intubation, reducing anesthesia doses, and calming patients.

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Neuromuscular Blockers: Administration

Neuromuscular blockers are administered intravenously (IV) as they are highly polar, limiting CNS penetration, and are poorly absorbed orally.

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Tubocurarine: Side Effects

Tubocurarine can cause hypotension, flushing, bronchoconstriction, and allergic reactions due to histamine release and ganglia blocking.

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Adverse Effects of NM Blockers

NM Blockers can cause hypotension, tachycardia, respiratory paralysis, bronchospasm, and aspiration of gastric contents.

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Succinylcholine

A depolarizing neuromuscular blocker used to rapidly induce muscle relaxation, particularly for intubation and electroconvulsive therapy.

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Depolarizing Blocker

A type of neuromuscular blocker that produces prolonged depolarization at the neuromuscular junction, leading to muscle paralysis.

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Phase 1 of Succinylcholine

The initial phase of succinylcholine's action, marked by depolarization of the postsynaptic membrane, causing muscle fasciculations.

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Phase 2 of Succinylcholine

The second phase of succinylcholine's action, characterized by receptor desensitization, resulting in sustained flaccid paralysis.

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Malignant Hyperthermia

A potentially life-threatening complication associated with succinylcholine, leading to uncontrolled muscle rigidity and potentially fatal hyperthermia.

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Neuromuscular Blockers

Drugs that block nerve signals to muscles, used for surgery and other procedures.

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Rapid Onset and Short Duration

A characteristic of depolarizing neuromuscular blockers, enabling quick intubation and a controlled duration of muscle relaxation.

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Drug Interactions

Certain medications can affect the efficacy and/or safety of Neuromuscular Blockers

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Succinylcholine

A depolarizing neuromuscular blocker, causing muscle paralysis.

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Malignant Hyperthermia

Rare genetic disorder triggered by anesthetics; causes muscle rigidity and high body temperature.

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Hyperkalemia (Succinylcholine)

Elevated blood potassium levels; a potential adverse effect with succinylcholine due to muscle fiber breakdown

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Treatment for MH

Rapid cooling, acidosis correction, and dantrolene administration.

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Neuromuscular Blockers

Drugs that paralyze muscles by blocking nerve signals at the junction.

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Depolarizing NMBs

Cause prolonged muscle stimulation initially.

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Adverse effects of Succinylcholine

Increased intraocular tension, hyperkalemia, apnea, malignant hyperthermia, and postoperative muscle pain.

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Apnea (due to NMB)

Prolonged or complete cessation of breathing due to lack of respiratory muscle contraction after use of NMBs.

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Hyperkalemia Cause

Increased potassium release from cells, especially dangerous in severe injuries (like burns) where potassium quickly leaves cells.

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Competitive Blocker

A neuromuscular blocker that acts by competing with acetylcholine for receptor sites, preventing the initiation of muscle contraction.

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Depolarizing Blocker Action

A neuromuscular blocker that first stimulates, then results in prolonged muscle stimulation and eventually paralysis.

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Drug Interactions- Non-depolarizers

Anticholinesterase drugs reverse (opposite of) the action of non-depolarizers. Other drugs (like halothane, aminoglycosides, and calcium channel blockers) enhance the neuromuscular blockade.

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Hyperkalemia Danger

An increase in potassium in the blood that can harm cells by causing a sudden and extreme shift in potassium levels.

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Spasmolytic Mechanism (Diazepam)

Diazepam acts on GABA receptors in the central nervous system to cause sedation and reduce spasms.

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Spasmolytic Mechanism (Baclofen)

Baclofen reduces spasticity by reducing calcium influx and substance P release (chemical messengers) in the spinal cord.

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Dantrolene's Action

Dantrolene prevents calcium release, stopping muscle contractions from being further triggered.

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Study Notes

Skeletal Muscle Relaxants

  • Two main groups: neuromuscular blockers and spasmolytics
  • Neuromuscular blockers relax muscles, used in surgery and aiding ventilation
  • Neuromuscular blockers have no central nervous system activity and are used primarily in general anesthesia
  • Spasmolytics reduce spasticity, centrally acting exceptdantrolene, used in various neurological conditions
  • Neuromuscular blockers are further categorized into non-depolarizing (competitive) and depolarizing (non-competitive) types
  • Non-depolarizing blockers include d-tubocurarine, pancuronium, vecuronium, atracurium, and mivacurium
  • Depolarizing blockers include succinylcholine and decamethonium
  • Spasmolytics include centrally acting (diazepam, chlorzoxazone, tizanidine, baclofen) and directly acting (dantrolene) types
  • Pre-synaptic drugs interfere with acetylcholine (ACh) synthesis and/or release

Mechanism of Action of Post-synaptically Neuromuscular Blockers

  • Non-depolarizing blockers (competitive) act reversibly, competing with ACh at nicotinic receptors
  • High doses of non-depolarizing blockers can block sodium channels, further weakening neuromuscular transmission
  • Neostigmine, a choline esterase inhibitor, is used to counteract the effects of these blockers
  • Depolarizing blockers (succinylcholine) initially cause depolarization, then desensitization of the receptor to ACh, leading to flaccid paralysis

Actions of Non-depolarizing Blockers

  • Cause muscle weakness progressing to flaccid paralysis
  • Small, rapidly contracting muscles (eyes, face) are affected first
  • Muscle paralysis progresses to limbs, neck, and trunk, ultimately reaching the diaphragm, causing respiratory paralysis
  • Recovery follows the reverse sequence of paralysis
  • Consciousness and pain perception remain unaffected

Actions of Depolarizing Blockers (Succinylcholine)

  • Muscle relaxation begins rapidly (within one minute), peaks at two minutes, and lasts for about five minutes.

  • Can cause small, rapid muscle contractions called fasciculations, followed by paralysis

  • Paralysis starts in small muscles (eye, jaw, larynx) moving to larger muscles (intercostals, diaphragm) leading to respiratory paralysis.

  • Recovery occurs in the reverse order that the paralysis started in.

Therapeutic Uses of Non-depolarizing Blockers

  • Used as adjuvants to anesthesia to decrease anesthetic dose, facilitate incision and intubation, and decrease cough and laryngospasm.
  • Help assess mechanical ventilation by paralyzing respiratory muscles to prevent interference.
  • Are used to facilitate endotracheal intubation using drugs like Rocuronium (rapid onset) over Succinylcholine (short duration).

Pharmacokinetics of Non-depolarizing Blockers

  • Non-depolarizing NM blockers are administered intravenously (IV) due to their poor lipid solubility and lack of oral absorption
  • Many are not metabolized and are excreted unchanged in urine or bile
  • Atracurium is degraded spontaneously in blood plasma by esterases or the Hofmann elimination pathway.

Adverse Effects of Neuromuscular Blockers

  • Non-depolarizing Blockers cause hypotension, flushing, bronchoconstriction, allergy due to histamine release; and ganglionic blockade (nicotinic receptors).
  • Generally, non-depolarizing blockers are safe. However, they are contraindicated in renal disease.
  • Depolarizing Blockers (succinylcholine) causes transient intraocular tension increase, and hyperkalemia.
  • Also, succinylcholine can cause malignant hyperthermia when used with halothane, in general anesthesia.
  • Post-operative muscle pain and increased intraocular or gastric pressure.

Interactions With Other Drugs

  • Cholinesterase inhibitors decrease the effects of non-depolarizing blockers
  • Calcium channel blockers increase the effects on non-depolarizing blockers.
  • Halogenated hydrocarbons (i.e., halothane) enhance the effects of non-depolarizing blockers by stabilizing neuromuscular junctions.
  • Aminoglycosides (i.e., gentamicin) enhance the effects of non-depolarizing blockers by competing with calcium ions, inhibiting acetylcholine (ACh) release.

Spasmolytic Drugs

  • Diazepam acts on GABA receptors in the central nervous system (CNS) and has sedative properties.
  • Baclofen acts on GABA-B receptors, reducing calcium influx and inhibiting substance P release in the spinal cord
  • Tizanidine is related to clonidine, a known drug for high blood pressure
  • Gabapentin is an antiepileptic that reduces muscle spasms.

Directly Acting Drug: Dantrolene

  • Dantrolene is a drug related to phenytoin, an antiepileptic
  • It interferes with excitation-contraction coupling by binding to the ryanodine receptor (RyR) channel in the sarcoplasmic reticulum to reduce activator calcium release
  • Dantrolene can lead to weakness, drowsiness and hepatitis as side effects
  • Inhibits depolarization induced calcium release from the sarcoplasmic reticulum
  • Drug of choice in severe cases of malignant hyperthermia

Myasthenia Gravis

  • Autoimmune disorder
  • Myoneural junction dysfunction causing varying degrees of voluntary muscle weakness
  • Muscle receptors are destroyed or deformed by antibodies in this disease.
  • Some genetic links and female gender or older age are possible factors
  • Symptoms include fatigue, illness, stress, extreme heat and some medications
  • Signs and symptoms include double vision (diplopia), drooping eyelids (ptosis) weak facial muscles and laryngeal issues causing difficulty to swallow.

Diagnosis and Medical Management

  • Diagnosis involves Edrophonium or Tensilon administration
  • Blood tests might detect antibodies
  • Treatment targets reducing antibody production or increasing ACh activity
  • Cholinesterase inhibitors, corticosteroids, immunosuppressants are standard medical treatments
  • Surgical interventions might include thymectomy to remove or improve thymus gland's role in autoimmune progression
  • Nursing management focuses on breathing issues, communication problems, physical mobility issues or aspiration risk related to muscle problems.

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