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템 > Pharmacology Of NMJ + NMJ CIS > Flashcards

Pharmacology Of NMJ + NMJ CIS Flashcards

1
Q

_________ is a drug/primary neurotransmitter at cholinergic nerve endings (preganglionic ANS, postganglionic parasympathetic, postganglionic sympathetic to thermoregulatory sweat glands, and somatic neuromuscular end plates

A

Acetylcholine

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2
Q

__________ = sympathomimetic drug that facilitates the release of catecholamines from adrenergic nerve endings

A

Amphetamine

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3
Q

_______ _______ is a bacterial toxin that enzymatically disables release of acetylcholine from cholinergic nerve endings

A

Botulinum toxin

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4
Q

What early neuromuscular blocking agent was one of the first used for muscular relaxation in general anesthesia and later led to the development of compounds like gallamine and pancuronium?

A

Curare

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5
Q

What are some of the ways that neuromuscular blockers are classified?

A 
Mechanism of action
Duration of action
Speed of onset and offset of action
Selectivity of action and safety margin
Adverse effects
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6
Q

What type of NMJ blocking agent is curare?

A

Competitive (non-depolarizing)

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7
Q

Competitive (non-depolarizing) agents like curare operate by competing with ACh for binding to the receptor.

What type of paralysis do they cause?

A

Flaccid, relaxed paralysis

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8
Q

Competitive (non-depolarizing) agents like curare operate by competing with ACh for binding to the receptor.

What are some non-NMJ effects caused by these agents?

A

Ganglia, muscarinic blocking, histamine release

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9
Q

Competitive (non-depolarizing) agents like curare operate by competing with ACh for binding to the receptor.

How is this type of NMJ block reversed?

A

Acetylcholinesterase inhibitors

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10
Q

What type of NMJ blocking agent is succinylcholine?

A

Non-competitive (depolarizing)

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11
Q

What are the 2 phases associated with the MOA of non-competitive (depolarizing) NMJ blocking agents like succinylcholine?

A

Phase 1 block: membrane depolarization; transient fasciculations followed by paralysis

Phase 2 block: desensitization; membrane repolarizes, hyposensitive to ACh

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12
Q

T/F: Both competitive and non-competitive NMJ blocking agents can be reversed by administering acetylcholinesterase inhibitors

A

False; competitive inhibitors CAN be reversed by AChE inhibitors, but non-competitive CANNOT

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13
Q

What is the progression of paralysis due to blocking the NMJ? In what order do these muscles recover?

A

Small rapidly moving muscles (eyes, fingers), then limbs, the last is respiratory muscles

These are recovered in reverse order

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14
Q

General poisoning due to ________ occurs after ingestion of various species of puffer fish. It is lethal even in small doses

A

Tetradotoxin

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15
Q

What is the MOA of tetradotoxin?

A

Tetradotoxin blocks diffusion of sodium through sodium channels, thus preventing depolarization and propagation of action potentials in nerve cells

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16
Q

All of the observed toxicity of tetradotoxin is secondary to blockade of the _______ _________. It acts on the central and peripheral nervous systmes.

In recent studies using tetradotoxin therapeutically in conjunction with __________, local anesthetic effect can be prolonged.

However, clinical use of tetradotoxin may increase the incidence of toxicity

A

Action potential

Bupivacaine

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17
Q

What agent affecting the action nerve potential produces COMPLETE sensory block, and its effect on motor function differs with varying concentrations?

A

Bupivacaine

18
Q

Which of the following would you use to provide motor blockade for caudal, epidural, or nerve block, but muscle relaxation may be inadequate for operations in which complete muscle relaxation is ESSENTIAL?

A. 0.25% Bupivacaine
B. 0.5% Bupivacaine
C. 0.75% Bupivacaine
D. 0.5% Tetradotoxin
E. 0.75% Tetradotoxin
A

B. 0.5% Bupivacaine

19
Q

Which of the following agents would you use for caudal, epidural, or peripheral nerve block to produce incomplete motor block in which muscule relaxation is not important?

A. 0.25% Bupivacaine
B. 0.5% Bupivacaine
C. 0.75% Bupivacaine
D. 0.5% Tetradotoxin
E. 0.75% Tetradotoxin
A

A. 0.25% Bupivacaine

20
Q

Which of the following would you use to produce complete motor block, especially when performing epidural block in abdominal operations requiring complete muscle relaxation?

A. 0.25% Bupivacaine
B. 0.5% Bupivacaine
C. 0.75% Bupivacaine
D. 0.5% Tetradotoxin
E. 0.75% Tetradotoxin
A

C. 0.75% Bupivacaine

[note that you would NOT use this for epidural anesthesia for obstetrical procedures]

21
Q

A major cause of adverse reactions to ________ include excessive plasma levels, overdose, unintentional intravascular injection, or slow metabolic degradation

A

Bupivacaine

22
Q

What are some drug interactions associated with bupivacaine?

A

Patients taking MAOIs or TCAs may produce severe, prolonged hypertension

Concurrent use of these agents should generally be avoided and careful patient monitoring is essential

23
Q

What are the 2 agents discussed in class that affect vesicular acetylcholine release?

A

Botulinum toxin

Tetanus toxin

24
Q

What produces botulinum toxin?

A

Clostridium botulinum, a gram-positive anaerobic bacteria

25
Q

The clinical syndrome of botulism can occur following ingestion of contaminated food. What is its mechanism of action?

A

BTX prevents the release of acetylcholine from axon endings at the NMJ and thus causes flaccid paralysis

[BTX is endocytosed, its light chain cleaves specific SNARE proteins necessary for ACh vesicle to fuse with membrane, so it cannot be released]

26
Q

What makes botulism toxin a good weapon?

A

Extreme potency and lethality
Ease of production
Difficult to distinguish intential exposures
Expensive, long-term care needed for recovery

27
Q

What produces tetanus toxin?

A

Tetanus toxin is an extremely potent neurotoxin produced by the vegetative cell of Clostridium tetani in anaerobic conditions, causing tetanus

28
Q

Tetanus toxin is the neurotoxin that causes ________; it travels through nerve cells to the ____ ______ and causes severe muscle cramps

A

Lockjaw

Spinal cord

29
Q

_______ _______ are non-depolarizing agents that compete with acetylcholine, a chemical that carries info between nerve and muscle cells, and blocks transmission of that information

A

Curare alkaloids

30
Q

___________ is a competitive, non-depolarizing blocking agent that is 5x more potent than tubocurarine but with reduced histamine release as well as a lack of ganglionic blockade

A

Pancuronium

31
Q

________ is a competitive, non-depolarizing blocking agent that also has some muscarinic blocking activity

A

Gallamine

32
Q

_________ is a competitive non-depolarizing blocking agent that is short-acting and undergoes hydrolysis by acetylcholinesterase

A

Mivacurium

33
Q

_________ is a competitive non-depolarizing blocking agent other than Mivacurium that undergoes hydrolysis by AChE

A

Atracurium

34
Q

What drug acts as a depolarizing muscle relaxant and may be used to induce anesthesia or when a tube must be inserted in the trachea?

A

Succinylcholine

35
Q

What is the mechanism of action of succinylcholine?

A

Affects depolarization; keeps muscles from contracting, leading to paralysis of muscles of the face and those used to breathe and move

36
Q

Succinylcholine keeps muscles from contracting, leading to paralysis of muscles of the face and those used to breathe and move. What are some adverse effects associated with succinylcholine?

A 
Postoperative pain
Jaw rigidity
Excessive salivation
Hypotension
Rash

[there are also many drugs known to interact with succinylcholine; risk of acute rhabdomyolosis with hyperkalemia followed by ventricular arrhythmias, cardiac arrest, and death in those found to have undiagnosed muscle myopathies like DMD]

37
Q

What are the clinical uses for agents that inhibit acetylcholinesterase?

A

Dementia associated with Alzheimer or Parkinson’s

Myasthenia gravis

Nerve gas and organophosphate pesticide exposure

Reversal of neuromuscular blockade during anesthesia

38
Q

What are some agents known to inhibit acetylcholinesterase?

A

Short acting (alcohol): edrophonium

Intermediate acting (carbamates): Neostigmine, pyridostigmine, physostigmine

Long acting (organophosphates): echothiophate, malathion, parathion, sarin

39
Q

What agent is used in the treatment of severe high body temperature (malignant hyperthermia), and clinical spasticity resulting from upper motor neuron disorders like spinal cord injury, stroke, cerebral palsy, or MS?

A

Dantrolene (aka Dantrium or Revonto)

40
Q

Dantrolene is an agent characterized by its ability to affect muscle contraction. What is its mechanism of action?

A

Muscle relaxant - restores a normal level of calcium in the muscles which helps to prevent or reduce severe high body temperature

41
Q

Dantrolene is a muscle relaxant that restores a normal level of calcium in the muscles which helps to prevent or reduce severe high body temperature. What are some adverse effects associated with Dantrolene?

A

Drowsiness, bloody/black tarry stool, dark urine, confusion, constipation

[many drugs are known to interact with Dantrolene as well]

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