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PNS/Cardiology > Nicotinic Agonists and Antagonists > Flashcards

Nicotinic Agonists and Antagonists Flashcards

1
Q

What are ways to modulate transmission of the neuromuscular junction at presynpatic sites?

A

Block Ca2+ transport (some aminoglycosides)
Block ACh secretion (Botulinum toxin)
Block choline uptake (hemicholinium)

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2
Q

What are ways to modulate transmission of the neuromuscular junction at postsynpatic sites?

A

Block nicotinic acetylcholine receptor (using nicotinic agonists and antagonists)

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3
Q

How does botulinum toxin prevent ACh secretion from the presynaptic site?

A

Enzymatically cleave the snare proteins (SNAP-25, syntaxin, synaptobrevin/VAMP)

Snare proteins are required for docking and release of ACh from synaptic vesicles

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4
Q

Which subunit of the nicotinic acetylcholine receptor does ACh bind to?

A

Alpha

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5
Q

How many molecules of ACh are needed to activate nicotinic receptor?

A

2

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6
Q

What are the two groups of neuromuscular blocking agents?

A

Nondepolarizing

Depolarizing

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7
Q

What drugs are in the non-depolarizing (antagonist) group?

A 
d-Turbocurarine
Pancuronium
Vecuronium
Cisatracurium
Rocuronium
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8
Q

What drugs are in the depolarizing (agonist) group?

A

Succinylcholine

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9
Q

Why non-depolarizing and depolarizing drugs are used for intubation and why?

A

Non-depolarizing: rocuronium
Depolarizing: succinylcholine

Have short onset and short duration

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10
Q

Which drugs increase histamine release?

A

d-Tubocurarine

Succinylcholine

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11
Q

What is unique about the elimination of cisatracurium?

A

Hoffman elimination (spontaneous cleavage)

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12
Q

What are potential side effects of succinylcholine?

A

Malignant hypothermia

Increased intraocular pressure

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13
Q

What is the mechanism of action of the nondepolarizing neuromuscular antagonists?

A

Binds nicotinic receptor and blocks it

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14
Q

Do the following characteristics increase, decrease, or stay the same when a nondepolarizing agent is used:

  • mini-EPP and EPP amplitude
  • Resting membrane potential
  • Action potential threshold
A

Decreased mini-EPP amplitude, decreased EPP amplitude
No change in RMP
No change in action potential threshold

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15
Q

How can an action potential be achieved in the presence of a nondepolarizing agent?

A

Temporal summation

Repetitive stimulation causes release of enough ACh to displace the blocker (changes the EPP enough to cause action potential)

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16
Q

What is the mechanism of action of the depolarizing neuromuscular agonists?

A

Binds nicotinic receptors and causes activation of these receptors below threshold, causing small local depolarization of the membrane

17
Q

Do the following characteristics increase, decrease, or stay the same when a depolarizing agent is used:

  • mini-EPP and EPP amplitude
  • Resting membrane potential
  • Action potential threshold
A

No change in mini-EPP and EPP amplitude
Increased (aka more positive) resting membrane potential (due to depolarization of membrane)
Increased action potential threshold (due to inactivation of Na+ channels with the increasing RMP)

18
Q

Can succinylcholine be inactivated by AChE?

A

No

19
Q

Can succinylcholine be inactived by butyryl-cholinesterase?

A

Yes

20
Q

What is a potential side effect if succinylcholine is applied quickly in a large dose?

A

Muscle contracture

Must apply slowly and in low doses

21
Q

What is ‘dual block’ and how does it occur?

A

Dual block = extended depolarization with succinylcholine leads to permanent desensitization of the ACh receptor

This happens because the ACh receptor changes conformation to a state where it cannot be activated

22
Q

How is the effectiveness of a neuromuscular block measured in the OR?

A

Train of 4 stimulation, measure response of adductor pollicis to stimulation of ulnar nerve

23
Q

How does AGE influence response to neuromuscular block?

A

Infants - more sensitive to non-depolarizing, less sensitive to depolarizing

Young infants have fewer receptors at neuromuscular junction, and this number increases with age

24
Q

How does TEMPERATURE influence response to neuromuscular block?

A

Hypothermia - more sensitive to depolarizing, less sensitive to non-depolarizing

Decreased temp = decreased efficiency of Na/K pump = reduced membrane potential (aka more positive) = more sensitive to depolarizing block that reduces membrane potential even more

25
Q

How do GENETIC VARIANTS influence response to neuromuscular block?

A

Genetic mutation can cause deficiency in butyrylcholinesterase

Cannot degrade succinylcholine (but would not affect anything else in life)

26
Q

How does HYPOKALEMIA influence response to neuromuscular block?

A

Reduced K+ = hyperpolarized membrane = enhanced effect of non-depolarizing blocker, decreased effect of depolarizing blocker

27
Q

How does HYPERKALEMIA influence response to neuromuscular block?

A

Increased K+ = depolarized membrane = decreased effect of non-depolarizing blocker, enhanced effect of depolarizing blocker

28
Q

Are myasthenia gravis patients particularly sensitive to depolarizing or nondepolarizing blocks?

A

Nondepolarizing

Decreased # of ACh receptors = extremely sensitive to nondepolarizing block

29
Q

Are bronchiogenic carcinoma patients particularly sensitive to depolarizing or nondepolarizing blocks?

A

Both! Sensitive to nondepolarizing and depolarizing

Reduced number of calcium channels (similar to Lamber Eaton autoimmune dx) = reduced ACh release

30
Q

How does liver disease influence response to neuromuscular block?

A

Liver metabolizes many of the blockers and produces plasma butyrylcholinesterase

Results in decreased succinylcholine, vecuronium ,and rocuronium metabolism

31
Q

How does succinylcholine induce malignant hyperthermia?

A

Inherited mutation in ryanodine receptor (calcium release in sarcoplasmic reticulum of muscle)

Succinylcholine binds mutated receptor and causes it to stay open = massive release of intracellular Ca2+ = rapid rise in body temp

PNS/Cardiology (33 decks)

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