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Questions and Answers
What is a potential complication that can occur due to the use of succinylcholine?
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?
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?
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?
In which condition is succinylcholine use particularly risky due to increased potassium release?
What is a characteristic of malignant hyperthermia?
What is a characteristic of malignant hyperthermia?
Which of the following describes a symptom associated with succinylcholine apnoea?
Which of the following describes a symptom associated with succinylcholine apnoea?
What is the primary action of neuromuscular blockers like succinylcholine?
What is the primary action of neuromuscular blockers like succinylcholine?
How does succinylcholine affect intraocular pressure?
How does succinylcholine affect intraocular pressure?
Which type of skeletal muscle relaxant is primarily used in surgical procedures?
Which type of skeletal muscle relaxant is primarily used in surgical procedures?
What distinguishes spasmolytics from neuromuscular blockers?
What distinguishes spasmolytics from neuromuscular blockers?
Which of the following drugs acts directly on muscle rather than centrally?
Which of the following drugs acts directly on muscle rather than centrally?
Which agent is an example of a non-depolarizing neuromuscular blocker?
Which agent is an example of a non-depolarizing neuromuscular blocker?
Which mechanism do presynaptic neuromuscular blockers utilize?
Which mechanism do presynaptic neuromuscular blockers utilize?
Which of the following statements about botulinum toxin is correct?
Which of the following statements about botulinum toxin is correct?
What is a common side effect of botulinum toxin poisoning?
What is a common side effect of botulinum toxin poisoning?
Which of the following statements correctly describes spasmolytics?
Which of the following statements correctly describes spasmolytics?
What is the primary mechanism by which non-depolarizing neuromuscular blockers exert their effects?
What is the primary mechanism by which non-depolarizing neuromuscular blockers exert their effects?
Which of the following neuromuscular blockers is considered long-acting?
Which of the following neuromuscular blockers is considered long-acting?
What effect does increasing acetylcholine concentration have on non-depolarizing neuromuscular blockers?
What effect does increasing acetylcholine concentration have on non-depolarizing neuromuscular blockers?
Which of the following statements about depolarizing neuromuscular blockers is true?
Which of the following statements about depolarizing neuromuscular blockers is true?
What is the role of neostigmine in the context of neuromuscular blockers?
What is the role of neostigmine in the context of neuromuscular blockers?
What is one potential complication when using neuromuscular blockers that is related to autonomic effects?
What is one potential complication when using neuromuscular blockers that is related to autonomic effects?
Which muscles are the most sensitive to non-depolarizing neuromuscular blockers?
Which muscles are the most sensitive to non-depolarizing neuromuscular blockers?
Which neuromuscular blocker is known for having the most rapid onset?
Which neuromuscular blocker is known for having the most rapid onset?
What is the mechanism of action of succinylcholine at the neuromuscular junction?
What is the mechanism of action of succinylcholine at the neuromuscular junction?
Which phase of succinylcholine action involves depolarization and initial muscle twitches?
Which phase of succinylcholine action involves depolarization and initial muscle twitches?
What is the expected order of muscle paralysis upon administration of succinylcholine?
What is the expected order of muscle paralysis upon administration of succinylcholine?
What is a potential adverse effect associated with succinylcholine use?
What is a potential adverse effect associated with succinylcholine use?
What effect do aminoglycosides like gentamicin have when used with succinylcholine?
What effect do aminoglycosides like gentamicin have when used with succinylcholine?
Which of the following is NOT a therapeutic use of depolarizing neuromuscular blockers?
Which of the following is NOT a therapeutic use of depolarizing neuromuscular blockers?
What factor influences the duration of action of succinylcholine?
What factor influences the duration of action of succinylcholine?
What is a consequence of prolonged or repeated administration of succinylcholine?
What is a consequence of prolonged or repeated administration of succinylcholine?
What is the primary characteristic of recovery from neuromuscular blockers?
What is the primary characteristic of recovery from neuromuscular blockers?
Which of the following is NOT an effect of neuromuscular blockers?
Which of the following is NOT an effect of neuromuscular blockers?
What advantage do synthetic competitive blockers have over traditional blockers?
What advantage do synthetic competitive blockers have over traditional blockers?
What is a key therapeutic use of neuromuscular blockers during surgery?
What is a key therapeutic use of neuromuscular blockers during surgery?
Which neuromuscular blocker is preferred for its rapid onset of action?
Which neuromuscular blocker is preferred for its rapid onset of action?
Which of the following is an adverse effect associated with tubocurarine?
Which of the following is an adverse effect associated with tubocurarine?
What is the mechanism by which atracurium is metabolized?
What is the mechanism by which atracurium is metabolized?
Why is mivacurium considered a short-acting neuromuscular blocker?
Why is mivacurium considered a short-acting neuromuscular blocker?
What is a primary reason for infusing fresh frozen plasma in treatment?
What is a primary reason for infusing fresh frozen plasma in treatment?
Which of the following accurately describes the action of non depolarizing blockers?
Which of the following accurately describes the action of non depolarizing blockers?
What is a common side effect of the spasmolytic drug baclofen?
What is a common side effect of the spasmolytic drug baclofen?
Which of the following is true regarding the drug dantrolene?
Which of the following is true regarding the drug dantrolene?
How does tizanidine relate to clonidine?
How does tizanidine relate to clonidine?
Which of the following medications can enhance neuromuscular blockade?
Which of the following medications can enhance neuromuscular blockade?
What distinguishes succinyl choline from competitive blocking agents?
What distinguishes succinyl choline from competitive blocking agents?
What is a notable effect of hyperkalemia in patients with extensive tissue damage?
What is a notable effect of hyperkalemia in patients with extensive tissue damage?
Flashcards
Skeletal Muscle Relaxants
Skeletal Muscle Relaxants
Drugs that reduce muscle contractions, divided into neuromuscular blockers and spasmolytics.
Neuromuscular Blockers
Neuromuscular Blockers
Drugs that block the transmission of nerve impulses at the neuromuscular junction, used in surgery and for ventilation assistance.
Spasmolytics
Spasmolytics
Drugs that reduce muscle spasticity by acting directly on the muscles or within the central nervous system.
Non-depolarizing Blockers
Non-depolarizing Blockers
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Depolarizing Blockers
Depolarizing Blockers
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Botulinum Toxin
Botulinum Toxin
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Acetylcholine
Acetylcholine
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Neuromuscular Junction
Neuromuscular Junction
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Neuromuscular Blockers
Neuromuscular Blockers
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Non-depolarizing Blockers
Non-depolarizing Blockers
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Competitive Antagonism
Competitive Antagonism
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Depolarizing Blockers
Depolarizing Blockers
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Succinylcholine
Succinylcholine
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Reversal of Neuromuscular Blockers
Reversal of Neuromuscular Blockers
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Cholinesterase Inhibitors
Cholinesterase Inhibitors
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Flaccid Paralysis
Flaccid Paralysis
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Neuromuscular Blockers: Recovery Order
Neuromuscular Blockers: Recovery Order
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Non-Depolarizing Blockers: Cardiovascular Effects
Non-Depolarizing Blockers: Cardiovascular Effects
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Atracurium: Degradation
Atracurium: Degradation
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Synthetic Blockers: Advantages
Synthetic Blockers: Advantages
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Neuromuscular Blockers: Therapeutic Uses
Neuromuscular Blockers: Therapeutic Uses
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Neuromuscular Blockers: Administration
Neuromuscular Blockers: Administration
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Tubocurarine: Side Effects
Tubocurarine: Side Effects
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Adverse Effects of NM Blockers
Adverse Effects of NM Blockers
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Succinylcholine
Succinylcholine
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Depolarizing Blocker
Depolarizing Blocker
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Phase 1 of Succinylcholine
Phase 1 of Succinylcholine
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Phase 2 of Succinylcholine
Phase 2 of Succinylcholine
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Malignant Hyperthermia
Malignant Hyperthermia
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Neuromuscular Blockers
Neuromuscular Blockers
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Rapid Onset and Short Duration
Rapid Onset and Short Duration
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Drug Interactions
Drug Interactions
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Succinylcholine
Succinylcholine
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Malignant Hyperthermia
Malignant Hyperthermia
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Hyperkalemia (Succinylcholine)
Hyperkalemia (Succinylcholine)
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Treatment for MH
Treatment for MH
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Neuromuscular Blockers
Neuromuscular Blockers
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Depolarizing NMBs
Depolarizing NMBs
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Adverse effects of Succinylcholine
Adverse effects of Succinylcholine
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Apnea (due to NMB)
Apnea (due to NMB)
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Hyperkalemia Cause
Hyperkalemia Cause
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Competitive Blocker
Competitive Blocker
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Depolarizing Blocker Action
Depolarizing Blocker Action
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Drug Interactions- Non-depolarizers
Drug Interactions- Non-depolarizers
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Hyperkalemia Danger
Hyperkalemia Danger
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Spasmolytic Mechanism (Diazepam)
Spasmolytic Mechanism (Diazepam)
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Spasmolytic Mechanism (Baclofen)
Spasmolytic Mechanism (Baclofen)
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Dantrolene's Action
Dantrolene's Action
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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.
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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.
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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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Description
This quiz covers the key concepts related to skeletal muscle relaxants, including neuromuscular blockers and spasmolytics. You'll learn about their classifications, mechanisms of action, and specific agents used in medical practice. Come test your knowledge on these important pharmacological agents!