2023-12-01T04:04:43+03:00[Europe/Moscow] en true <p>AP reaches the end of the motor neuron; Ca influxes; vesicle exocytosis; ACh is released</p>, <p>upon binding to a nicotinic receptor, sodium comes into the cell and stimulates a motor end plate potential; if large, AP is propagated along the entire muscle fiber causing contraction</p>, <p>surgical relaxation, endotracheal intubation, ventilation control, epileptic patients</p>, <p>diaphragm; first</p>, <p>look-alike packaging/labeling, look-alike drug names, unsafe mnemonics, orders entered wrong, knowledge deficit </p>, <p>antagonists that mimic ACh; depolarizing blocker- receptor desensitization</p>, <p>cisatracurium, vecuronium, rocuronium </p>, <p>pancuronium </p>, <p>succinylcholine </p>, <p>neostigmine, pyridostigmine, edrophonium </p>, <p>competitive AChR antagonist; compete for nAChR binding at muscle membrane in NMJ end plate</p>, <p>large doses can enter the pore of ion channel causing a more intense blockade that weakens NM transmission; can block pre-synaptic Na+ channels interfering with ACh release</p>, <p>elimination half-life</p>, <p>c</p>, <p>c</p>, <p>a</p>, <p>laudanosine </p>, <p>a</p>, <p>b</p>, <p>b</p>, <p>inhibit AChE and directly increase ACh release</p>, <p>more rapid onset than other reversals; less effective in presence of potent NM blockade</p>, <p>rapidly encapsulates and inactivates the NM blockers; forms a complex that is excreted in the urine</p>, <p>rocuronium, vecuronium </p>, <p>hypersensitivity reaction, anaphylaxis, encapsulates progesterone </p>, <p>AChR agonist; depolarizes membrane in the same manner as ACh; causes transient contractions/fasciculations and persistent stimulation that results in closure/inactivation of Na+ channels-flaccid paralysis </p>, <p>the membrane will gradually repolarize, but neurotransmission will remain blocked; resulting in receptor desensitization </p>, <p>quick; short</p>, <p>short procedures; emergencies when immediate airway reopening is required</p>, <p>false; most is metabolized by plasma cholinesterase </p>, <p>hyperkalemia, muscle pain, bradycardia</p>, <p>volatile anesthetics (halothane); malignant hyperthermia; due to abnormal release of calcium</p>, <p>malignant hyperthermia</p>, <p>dantrolene </p>, <p>massive muscle contraction, lactic acid production/metabolic acidosis, tachycardia, increased body temp</p> flashcards
Pharmacology of NM blockers

Pharmacology of NM blockers

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  • AP reaches the end of the motor neuron; Ca influxes; vesicle exocytosis; ACh is released

    Describe the role of the Action Potential in the NMJ.

  • upon binding to a nicotinic receptor, sodium comes into the cell and stimulates a motor end plate potential; if large, AP is propagated along the entire muscle fiber causing contraction

    Describe what happens when ACh binds to Nicotinic Receptors (nAChR).

  • surgical relaxation, endotracheal intubation, ventilation control, epileptic patients

    What are the clinical applications of NMBs? (4)

  • diaphragm; first

    The _______ is the last muscle to be paralyzed and the _______ to recover.

  • look-alike packaging/labeling, look-alike drug names, unsafe mnemonics, orders entered wrong, knowledge deficit

    What are common dispensing errors involved with NM blockers? (5)

  • antagonists that mimic ACh; depolarizing blocker- receptor desensitization

    How is muscle contraction blocked? (2)

  • cisatracurium, vecuronium, rocuronium

    What are the Non-depolarizing, short/intermediate-acting NM blockers? (3)

  • pancuronium

    What is the Non-depolarizing, Long-acting NM blocker?

  • succinylcholine

    What is the Depolarizing NM blocker?

  • neostigmine, pyridostigmine, edrophonium

    What are the ACh esterase inhibitors? (3)

  • competitive AChR antagonist; compete for nAChR binding at muscle membrane in NMJ end plate

    Non-depolarizing NM blocker MOA? (3)

  • large doses can enter the pore of ion channel causing a more intense blockade that weakens NM transmission; can block pre-synaptic Na+ channels interfering with ACh release

    What are the additional MOA's of Non-depolarizing NM blockers? (2)

  • elimination half-life

    The DoA of NM blockers strongly correlates with ___________.

  • c

    Which is the least potent?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • c

    Which has the quickest onset?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • a

    Which is a potent stereoisomer of Atracurium?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • laudanosine

    What is the active, toxic metabolite of Cisatracurium?

  • a

    Which is the most commonly used?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • b

    Which has a duration of action of 1 hour?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • b

    Which can cause tachycardia?

    a) Cisatracurium

    b) Pancuronium

    c) Rocuronium

    d) Vecuronium

  • inhibit AChE and directly increase ACh release

    Neostigmine/Pyridostigmine MOA?

  • more rapid onset than other reversals; less effective in presence of potent NM blockade

    Edrophonium characteristics? (2)

  • rapidly encapsulates and inactivates the NM blockers; forms a complex that is excreted in the urine

    Sugammadex MOA?

  • rocuronium, vecuronium

    Which NM blockers is Sugammadex approved for? (2)

  • hypersensitivity reaction, anaphylaxis, encapsulates progesterone

    Sugammadex AE's? (3)

  • AChR agonist; depolarizes membrane in the same manner as ACh; causes transient contractions/fasciculations and persistent stimulation that results in closure/inactivation of Na+ channels-flaccid paralysis

    Succinylcholine MOA?

  • the membrane will gradually repolarize, but neurotransmission will remain blocked; resulting in receptor desensitization

    If a patient receives multiple boluses of Succinylcholine, what will occur?

  • quick; short

    Succinylcholine has ______ onset of action and a ______ duration of action.

  • short procedures; emergencies when immediate airway reopening is required

    When is Succinylcholine best used? (2)

  • false; most is metabolized by plasma cholinesterase

    A large amount of Succinylcholine reaches the NMJ. T/F?

  • hyperkalemia, muscle pain, bradycardia

    AE's of Succinylcholine? (3)

  • volatile anesthetics (halothane); malignant hyperthermia; due to abnormal release of calcium

    Succinylcholine + _______ = ?

  • malignant hyperthermia

    -rare autosomal dominant disorder that leads to life-threatening

    hypercatabolic state

  • dantrolene

    What is given to treat Malignant Hyperthermia?

  • massive muscle contraction, lactic acid production/metabolic acidosis, tachycardia, increased body temp

    Malignant Hyperthermia symptoms? (4)