The Neuromuscular Junction (Nmj)

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  • 1. 
    The Neuromuscular Junction (NMJ) A synapse between a motor neuron axon and the motor end plate (consists of excitable muscle fibers) Uses ___ as a transmitter
    • A. 

      AChE

    • B. 

      5-HT

    • C. 

      NE

    • D. 

      ACh

  • 2. 
    Mediate NMJ and autonomic ganglia function Are found on muscle endplates and peripheral ganglia Distinct subtypes exist at NMJ and autonomic ganglia pentameric ionotropic receptors (Similar to GABAA) Gate Na+ and K+ ions, and in some forms, Ca++ ions Net effect of activation is depolarization OF POSTSYNAPTIC CELL
    • A. 

      Muscarinic receptors

    • B. 

      Nicotinic receptors

    • C. 

      Dopamine receptors

    • D. 

      Serotonin receptors

  • 3. 
    ____________was the first widely used Neuromuscular Blocking Agents
  • 4. 
    Two types of neuroblockin agents which one work by over-stimulating nicotinic receptors, causing muscle fiber membrane depolarization
    • A. 

      Polarizing agents

    • B. 

      Depolarizing agents

    • C. 

      Competitive agents

    • D. 

      Noncompetitive agents

  • 5. 
    Two types of neuroblockin agents which one work by antagonizing ACh receptors
    • A. 

      Polarizing agents

    • B. 

      Depolarizing agents

    • C. 

      Competitive agents

    • D. 

      Noncompetitive agents

  • 6. 
    Neuromuscular blocking agents currently in use typically have a slow onset, and long duration of action
    • A. 

      True

    • B. 

      False

  • 7. 
    Currently only ____________ is used as a depolarizing neuromuscular blocking agent
    • A. 

      Pancuronium

    • B. 

      Succinylcholine

    • C. 

      Vecuronium

    • D. 

      Rocuronium

  • 8. 
    Chemical makeup of neuromuscular blocking agents include:
    • A. 

      Natural alkaloids and congeners

    • B. 

      Ammonio steroids

    • C. 

      Benzylisquinolones

  • 9. 
    Competitive agents tend to be ____, ____ molecules, ______ bottom
  • 10. 
    Natural or synthetic alkaloids are not often used because lots of ‘side effects’, including causing _________release_______ also have a relatively ______duration of action
    • A. 

      Histamine, long

    • B. 

      5-HT, long

    • C. 

      Histamine, short

    • D. 

      5-HT, short

  • 11. 
    Pancuronium
    • A. 

      Prototype ammonio steroid

    • B. 

      No histamine release

    • C. 

      Block muscarinic receptors, and causes tachycardia

    • D. 

      Don’t have ganglionic blocking actions, don’t alter vagus nerve function

    • E. 

      Prototype benzylisquinolone

  • 12. 
    Atracurium
    • A. 

      Prototype ammonio steroid

    • B. 

      No histamine release

    • C. 

      Block muscarinic receptors, and causes tachycardia

    • D. 

      Don’t have ganglionic blocking actions, don’t alter vagus nerve function

    • E. 

      Prototype benzylisquinolone

  • 13. 
    Benzylisquinolones
    • A. 

      Prototype ammonio steroid

    • B. 

      No histamine release

    • C. 

      Block muscarinic receptors, and causes tachycardia

    • D. 

      Don’t have ganglionic blocking actions, don’t alter vagus nerve function

    • E. 

      Prototype benzylisquinolone

  • 14. 
    Neuromuscular Blocking Competitive Antagonists When applied directly to skeletal muscle, nicotinic agonists cause a localized _________
  • 15. 
    Neuromuscular Blocking Agent MOA: Depolarizing Agents
    • A. 

      Depolarization effect on the postsynaptic muscle is long lasting

    • B. 

      A short period of repetitive excitation and muscle twitching followed by…Blockade of neurotransmission and paralysis

    • C. 

      Initial action of depolarizing agents is to cause opening of ion channels

    • D. 

      All are true

  • 16. 
    Depolarization is achieved when muscle fibers are no longer responsive to ACh at With prolonged depolarization, muscle ____________, and Na+, Cl- and Ca++ are gained Depolarizing blockers are hydrolyzed by _____________
    • A. 

      Postsynaptic cell

    • B. 

      K+ is depleted

    • C. 

      Butyrylcholinesterases

    • D. 

      Presynaptic cell

    • E. 

      K+ is increased

  • 17. 
    What is true about NMJ Blocker Toxicity
    • A. 

      Results in bronchospasm, hypotension, increased secretory activity

    • B. 

      Can cause histamine release

    • C. 

      Dangerous in patients with CHF who are taking diuretics, digoxin

    • D. 

      Life threatening in individuals with ion regulation dysfunction

    • E. 

      Dangerous in patients withsignificant burns, soft tissue damage, and in children

    • F. 

      Cause a significant release of K+ from intracellular sites

  • 18. 
    Overdoses can be treated by AChE inhibitors like
    • A. 

      Edrophonium

    • B. 

      Neostigmine

    • C. 

      Pyridostigmine

    • D. 

      Atropine

    • E. 

      Trimethaphan

  • 19. 
    Step 1: activation of nAChRs, rapid depolarization of postsynaptic sites            Due to inward Na+ current (Ca++ current when neuronal nAChRs involved) Step 2: an action potential is caused in postganglionic neuron when threshold reached (mediated by nAChRs) Step 3: the action potential is followed by a slow IPSP, then a slow EPSP (mediated by mAChRs; does not occur in all ganglia) Step 4: a second late, slow EPSP follows (mediated by peptidergic release)  
    • A. 

      Nicotinic Neurotransmission

    • B. 

      Muscarinic Neurotransmission

    • C. 

      Ganglionic Neurotransmission

    • D. 

      Cholinergic Neurotransmission

  • 20. 
    Nicotine
    • A. 

      Has actions on both effector and chemosensory sites

    • B. 

      Can rapidly cause receptor desensitization

    • C. 

      Causes a transient stimulation of all autonomic ganglia

    • D. 

      Ultimate response is due to summation of all nicotine’s effects on an organ/system

    • E. 

      Pharmacological actions are complex, unpredictable

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