Pharm Skel Muscle Relaxants Part 2

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Pharm Skel Muscle Relaxants Part 2 - Quiz

In the second part of our pharmacology quiz series we’ll be looking at the topic of skeletal muscle relaxants, which are drugs taken in the effort to relax and reduce tension in the muscles. Why are these used, and how do they work? We’ll let you answer those questions and more below!


Questions and Answers
  • 1. 

    A 48-year-old man, who had been suffering from Crohn disease for several years, underwent abdominal surgery to remove an intestinal obstruction. General anesthesia was supplemented with tubocurarine. The blockade of which of the following postreceptor pathways most likely mediated the muscle relaxant effect of this drug?

    • A.

      CAMP

    • B.

      Na+ channels

    • C.

      K+ channels

    • D.

      Phospholipase A2

    • E.

      IP3/DAG

    • F.

      Cl- channels

    Correct Answer
    B. Na+ channels
    Explanation
    Learning objective: explain the mechanism of action of tubocurarine.
    Answer: B
    Tubocurarine blocks competitively Nm receptors. The activation of these ionotropic receptors
    opens Na+ channels, so initiating the cascade that ultimately leads to skeletal muscle
    contraction. By blocking Nm receptors the Na+ channels postreceptor pathway is blocked and
    muscle relaxations occurs.
    A, C, D, E, F) These postreceptor pathway are not involved in the mechanism of action of
    nondepolarizing neuromuscular blockers

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  • 2. 

    A 49-year-old man diagnosed with inguinal hernia was prepared for surgery. Shortly after the initiation of general anesthesia with halothane and succinylcholine the patient developed muscle rigidity, tachycardia, labile blood pressure, profuse diaphoresis and high fever. The anesthesia was discontinued at once and a drug was administered by rapid IV push. Which of the following was most likely the mechanism of action of the administered drug?

    • A.

      Activation of GABA B receptors in the spinal cord

    • B.

      Blockade of excitatory neurotransmitter release in the brain

    • C.

      Blockade of Ca++ channels in skeletal muscle membrane

    • D.

      Blockade of Ca++ channels in sarcoplasmic reticulum

    • E.

      Increased K+ conductance in skeletal muscle membrane

    Correct Answer
    D. Blockade of Ca++ channels in sarcoplasmic reticulum
    Explanation
    Learning objective: explain the mechanism of action of dantrolene
    Answer: D
    The clinical picture of the patient suggest the diagnosis of malignant hyperthermia, a rare but
    potentially life-threatening disorder that can be triggered by a variety of stimuli, including the
    administration of certain anesthetics and neuromuscular blocking agents. The disorder is
    related to an hereditary impairment in the ability of sarcoplasmic reticulum to sequester calcium
    and therefore a prolonged release of calcium occurs after the triggering event. This causes
    massive muscle contraction, hyperthermia and lactic acidosis. Dantrolene is a drug of choice in
    this disorder because it blocks Ca++ channels in sarcoplasmic reticulum of skeletal muscle.
    Cardiac and smooth muscle are minimally affected by dantrolene since they have a different
    type of Ca++ channel in their sarcoplasmic reticulum.
    A, B, C, E) (see explanation above)

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  • 3. 

    A 59-year-old woman was undergoing surgery to remove a breast cancer. The anesthesia was induced by thiopental, maintained by enflurane and supplemented with a nondepolarizing neuromuscular blocker which has a short duration of action and is metabolized by plasma pseudocholinesterase. Which of the following drugs was most likely administered?

    • A.

      Succinylcholine

    • B.

      Tubocurarine

    • C.

      Vecuronium

    • D.

      Mivacurium

    • E.

      Cisatracurium

    Correct Answer
    D. Mivacurium
    Explanation
    Learning objective: describe the biotransformation of mivacurium.
    Answer: D
    Mivacurium is the only nondepolarizing neuromuscular blocker that is metabolized by plasma
    pseudocholinesterase. Because of this rapid metabolism the action of the drug is quite short.
    A) succinylcholine is metabolized by plasma cholinesterase, but it is a depolarizing, not a
    nondepolarizing neuromuscular blocker.
    B, C, E) (see explanation above)

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  • 4. 

    A 34-year-old woman suffering from hemifacial spasms started a treatment with botulin toxin injected directly into the abnormally contracting muscles. Which of the following molecular actions most likely mediated the therapeutic effect of the drug in the patient’s disorder?

    • A.

      Long lasting activation of Nm receptors

    • B.

      Inhibition of acetylcholine storage into synaptic vesicles

    • C.

      Inhibition of choline acetyltransferase

    • D.

      Inhibition of acetylcholine exocytosis from cholinergic terminals

    • E.

      Stimulation of acetylcholinesterase

    • F.

      Opening of Ca++ channels in cholinergic terminals

    Correct Answer
    D. Inhibition of acetylcholine exocytosis from cholinergic terminals
    Explanation
    Learning objective: explain the mechanism of action of botulin toxin
    Answer: D
    Botulin toxin must get inside the axon terminals in order to cause paralysis. Following the
    attachment of the toxin to proteins on the surface of axon terminals, the toxin can be taken into
    neurons by endocytosis. There it is able to cleave endocytotic vesicles and reach the cytoplasm.
    The light chain of the toxin has protease activity and proteolytically degrades a specific protein
    that is required for vesicle fusion that releases acetylcholine from the axon endings. In this way
    it prevents neurosecretory vesicles from fusing with the nerve synapse plasma membrane and
    releasing the neurotransmitter.
    A, B, C, E, F) (see explanation above)

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  • 5. 

    A 61-year-old man underwent surgery to remove a prostate cancer. The anesthesia was induced by thiopental and maintained by halothane. Tubocurarine was also added to ensure adequate muscle relaxation. Which of the following was most likely the correct sequence of the paralysis of skeletal muscles induced by tubocurarine on this patient?

    • A.

      Eye extrinsic muscles, limb muscles, diaphragm

    • B.

      Limb muscles, diaphragm, eye extrinsic muscles

    • C.

      Diaphragm, eye extrinsic muscles, limb muscles

    • D.

      Diaphragm, limb muscles, eye extrinsic muscles

    • E.

      Limb muscles, eye extrinsic muscles, diaphragm

    Correct Answer
    A. Eye extrinsic muscles, limb muscles, diaphragm
    Explanation
    Learning objective: describe the sequence of muscle paralysis induced by tubocurarine.
    Answer: A
    The skeletal muscle paralysis induced by nondepolarizing neuromuscular blocking drugs follows
    a sequence that is related to the innervation of the skeletal muscles. Muscles that are small,
    rapidly moving and richly innervated (like extrinsic eye muscles, small muscles of the face and
    pharynx) are affected first. The paralysis of the extrinsic eye muscles causes a lack of
    parallelism of the visual axes of the eyes which leads to double vision. As a rule, large muscles
    (like limb muscles) are paralyzed after small muscles. Ultimately the intercostal muscles and
    finally the diaphragm are paralyzed
    B, C, D, E) (see explanation above)

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  • 6. 

    A 47-year-old woman recently diagnosed with spasmodic torticollis received multiple injections of a drug into the dystonic muscles of the neck. The therapy improved the position of the head and reduced painful muscle spasms for 3 months after the injections. Which of the following drugs was most likely administered?

    • A.

      Succinylcholine

    • B.

      Botulin toxin

    • C.

      Mivacurium

    • D.

      Tubocurarine

    • E.

      Dantrolene

    Correct Answer
    B. Botulin toxin
    Explanation
    Learning objective: describe the therapeutic uses of botulin toxin.
    Answer: B
    Spasmodic torticollis is an involuntary tonic contraction of the neck muscles causing painful
    spasm and abnormal head position. In severe cases the selective denervation of the neck
    muscle is the most successful surgical approach but injection of botulin toxin into the dystonic
    muscles of the neck can reduce the symptoms for 1 to 3 months in about 70% of patients .
    Botulin toxin inhibits acetylcholine release from cholinergic terminals, so weakening skeletal
    muscle contractions.
    A, B, C) Neuromuscular blocking drugs are of no value in this disease mainly because of their
    short duration of action.
    E) Spasmolytic drugs (dantrolene, benzodiazepines, tizanidine, etc.) are sometimes used but
    they decrease spasms in only about 25% of cases.

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  • 7. 

    A 48-year-old man presented to his physician complaining of intermittent spasms of limb muscles. The patient was referred to the neurologic clinic where the diagnosis of stiff-man syndrome was made. An appropriate therapy was ordered to improve the muscular spasms. Which of the following drug was most likely prescribed?

    • A.

      Phenobarbital

    • B.

      Baclofen

    • C.

      Tubocurarine

    • D.

      Succinylcholine

    • E.

      Chlorpromazine

    • F.

      Mivacurium

    Correct Answer
    B. Baclofen
    Explanation
    Learning objective: describe the therapeutic uses of baclofen.
    Answer: B
    The stiff-man syndrome is a disorder of neuromuscular transmission characterized by the
    insidious onset of progressive stiffness in the trunk, abdomen, legs and arms. The cause of the
    syndrome is unknown but an autoimmune pathogenesis is suspected. Only symptomatic therapy
    is available and central spasmolytic drugs (benzodiazepines, baclofen) consistently relieve the
    muscle stiffness.
    A, C, D, E; F) (see explanation above)

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  • 8. 

    A 41-year-old man suffering from amyotrophic lateral sclerosis presented to his physician with muscle fasciculations, spasticity of limbs, hyperactive deep tendon reflexes and extensor plantar reflexes. Baclofen was prescribed to reduce spasticity and cramps. Which of the following actions most likely mediated the therapeutic effect of the drug in the patient’s disease?

    • A.

      Activation of GABA B receptors in the spinal cord

    • B.

      Blockade of Nm receptors of motor end plate

    • C.

      Increased substance P release in the spinal cord

    • D.

      Blockade of Ca++ channels in the skeletal muscle membrane

    • E.

      Increased K+ conductance in the skeletal muscle membrane

    Correct Answer
    A. Activation of GABA B receptors in the spinal cord
    Explanation
    Learning objective: describe the mechanism of action of baclofen.
    Answer: A
    Baclofen is an agonist at GABA B receptors. Activation of these receptors by baclofen results in
    hyperpolarization of presynaptic terminals, probably by increased K+ conductance. This
    hyperpolarization reduces the release of excitatory transmitters in both the brain and the spinal
    cord. Baclofen is at least as effective as diazepam in reducing spasticity and is frequently used
    for this purpose.
    B) This would be the action of nondepolarizing neuromuscular blockers.
    C) Actually baclofen can cause blockade of substance P release from spinal cord and this seem
    one of the reasons of its analgesic activity in patients with spasticity.
    D, E) Baclofen can indirectly block Ca++ channels as a consequence of membrane
    hyperpolarization, and can increase k+ conductance, but these actions occur in neuronal, nor in
    skeletal muscle membrane.

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  • 9. 

    A 44-year-old man, brought to the emergency room after a car accident, required intubation and mechanical ventilation. Patient history was significant for a genetically deficient plasma cholinesterase. A muscle relaxant was administered IV. Which of the following muscle relaxants would be contraindicated in this patient?

    • A.

      Tubocurarine

    • B.

      Cisatracurium

    • C.

      Baclofen

    • D.

      Mivacurium

    • E.

      Vecuronium

    • F.

      Tizanidine

    Correct Answer
    D. Mivacurium
    Explanation
    Learning objective: describe the pharmacokinetics of mivacurium.
    Answer: D
    Mivacurium and succinylcholine are two neuromuscular blockers metabolized by plasma
    cholinesterase. In patients with a genetically induced deficiency of the normal plasma
    cholinesterase these drug can cause apnea of several hours and are therefore contraindicated.
    A, B, C ,E, F) (see explanation above)

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  • 10. 

    A 45-year-old man, who was given tubocurarine as a muscle relaxant during surgery, showed a significant drop in blood pressure. Which of the following pairs of actions most likely mediated the adverse effect of the drug in this patient?

    • A.

      Inhibition of vasomotor center and ganglionic blockade

    • B.

      Blockade of nicotinic receptors in the adrenal medulla and bradykinin release

    • C.

      Inhibition of vasomotor center and bradykinin release

    • D.

      Blockade of carotid sinus baroreceptors and histamine release

    • E.

      Histamine release and ganglionic blockade

    Correct Answer
    E. Histamine release and ganglionic blockade
    Explanation
    Learning objective: describe the actions which mediate the tubocurarine-induced
    hypotension.
    Answer: E
    Tubocurarine induced hypotension can be due either to histamine release or to blockade of
    nicotinic receptors of autonomic ganglia or, most likely, to both.
    A, B, C, D) (see explanation above)

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  • 11. 

    A 37-year-old woman, who had been suffering from multiple sclerosis for two years, complained of increased painful cramp in her legs. The neurologist prescribed baclofen, three tablets daily. Which of the following adverse effects might most likely occur in this patient?

    • A.

      Hallucinations

    • B.

      Ataxia

    • C.

      Dystonic reactions

    • D.

      Hypotension

    • E.

      Drowsiness

    Correct Answer
    E. Drowsiness
    Explanation
    Learning objective: describe the adverse effects of baclofen.
    Answer: E
    Baclofen is a GABA B receptor agonist that is currently used to treat various forms of spasticity.
    The drug causes hyperpolarization of neuron membrane, which in turn reduced the release of
    excitatory neurotransmitters in the brain as well as in the spinal cord. The most common
    adverse effects of baclofen are relate to this central inhibitory activity. Drowsiness is by far the
    most common, affecting about one half of patients.
    A, B, C, D) All these listed effects can occur with baclofen but they are very rare at standard
    therapeutic doses.

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  • 12. 

    A 54-year-old male, who had been suffering from amyotrophic lateral sclerosis for one year, complained of generalized muscle spasm. His physician prescribed diazepam to reduce spasticity. Which of the following statements best explain the mechanism of the spasmolytic effect of diazepam in this patient?

    • A.

      Blockade of calcium release from the sarcoplasmic reticulum

    • B.

      Blockade of acetylcholine release from motor nerve

    • C.

      Depolarization blockade of Nm receptors

    • D.

      Facilitation of GABA actions in the spinal cord

    • E.

      Activation of GABA B receptors in the spinal cord

    Correct Answer
    D. Facilitation of GABA actions in the spinal cord
    Explanation
    Learning objective: explain the mechanism of the spasmolytic action of benzodiazepines
    Answer: D
    Benzodiazepines facilitate the action of GABA in the CNS by increasing the affinity of GABAA
    receptors for GABA. Their action in reducing spasticity however seems at least partly mediated
    in the spinal cord because they are effective also in patients with cord transection.
    A) This would be the mechanism of action of dantrolene.
    B) This would be the mechanism of action of botulinum toxin.
    C) This would be the mechanism of action of succinylcholine.
    E) This would be the mechanism of action of baclofen.

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  • 13. 

    A 48-year-old patient underwent heart surgery to received an artificial valve. Anesthesia was induced by thiopental, then a muscle relaxant was given IV to facilitate intubation. Soon after the administration of the drug the patient exhibited transient muscle fasciculations which progressed to generalized paralysis within one minute. Which of the following muscle relaxant was most likely given?

    • A.

      Cisatracurium

    • B.

      Succinylcholine

    • C.

      Dantrolene

    • D.

      Vecuronium

    • E.

      Tubocurarine

    • F.

      Tizanidine

    Correct Answer
    B. Succinylcholine
    Explanation
    Learning objective: describe the adverse effects of succinylcholine.
    Answer: B
    Succinylcholine activates Nm receptors This can account for the involuntary contraction of
    group of muscle fibers (called fasciculations or twitching), that occurs before the muscle
    paralysis. Nondepolarizing neuromuscular blockers do not activate Nm receptors and so
    contractions cannot occur before paralysis.
    A, C, D, E, F) (see explanation above)

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  • 14. 

    A 40-year-old woman, admitted to the emergency hospital after a car collision, had multiple surgeries to repair her injuries and was placed on mechanical ventilation to assist respiration. On day 13 she was scheduled for a transesophageal ECG, and was given a muscle relaxant IV to facilitate the procedure. Soon afterwards the patient suffered a cardiac arrest and CPR was performed successfully. The potassium recorded during arrest peaked at 7.3 mEq/L. Which of the following muscle relaxant was most likely administered?

    • A.

      Cisatracurium

    • B.

      Vecuronium

    • C.

      Tubocurarine

    • D.

      Dantrolene

    • E.

      Succinylcholine

    Correct Answer
    E. Succinylcholine
    Explanation
    Learning objective: describe the adverse effects of succinylcholine.
    Answer: E
    Succinylcholine can release rapidly potassium from intracellular sites. In a normal patient this
    results in a small, transient hyperkalemia. In patients with extensive soft-tissue trauma or burns,
    cerebral vascular accident and prolonged stays in an intensive care unit, this hyperkalemia can
    be much more pronounced when succinylcholine is given at least several days after the
    underlying condition has become established. The hyperkalemia can be life threatening since it
    can lead to cardiac arrest like in the present case. The cause of succinylcholine-induced
    hyperkalemia in these patients seems related to up regulation of Nm receptors in the skeletal
    muscle. Patients with the aforementioned conditions are deprived of neural influence or activity
    because of the prolonged immobilization. Such deprivation stimulates the synthesis of new Nm
    receptors across the muscle membrane. When these receptors are activated by succinylcholine
    an action potential occurs, ion channels open allowing Na+ to flow inside and K+ to flow outside
    of the cell. Since succinylcholine is metabolized more slowly than acetylcholine the receptor
    activation is more prolonged, causing a larger influx of Na+ and a vigorous efflux of K+. When
    Nm receptors are increased in skeletal muscle this K+ efflux can cause a life-threatening
    hyperkalemia.
    A, B, C) Nondepolarizing neuromuscular blockers cause blockade, not activation, of Nm
    receptors. Therefore they do not induce hyperkalemia.
    D) Dantrolene has no effect on Nm receptors.

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    Quiz Edited by
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