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CNS I > NM Blocking agents > Flashcards

NM Blocking agents Flashcards

1. Describe the neuromuscular junction, the motor endplate, nicotinic acetylcholine receptors, and how non-depolarizing muscle blockers cause paralysis. 2. Distinguish the prototype non-depolarizing blocking drugs based upon the clinical pharmacology. 3. Describe the mechanism of action of succinylcholine, list its primary clinical uses, and its contraindications. 4. List the prototype agents used to reverse neuromuscular blockade and to describe the physical signs of inadequate and ina

1
Q

primary NT at the NMJ

A

ACh

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2
Q

ACh must bind to _______ at the motor end plate to open the Na+ channel

A

BOTH a alpha subunits

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3
Q

size and ionization of NMBs

A

large molecules, highly ionized

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4
Q

effect of size of NMB molecules on CNS

A

large molecules cannot pass through BBB, therefore cannot act on CNS. Therefore can result in awake, paralyzed pt

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5
Q

onset of action of NMB

A

slow (2-5 minutes)

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6
Q

how to decrease onset time of NMBs

A

multiple ED95 dose

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7
Q

how to prolong the duration of NMB

A

multiple ED95 dose

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8
Q

can effect kinetics of NMBs

A

age, other drugs, hepatic/renal disease

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9
Q

prototype non-depolarizing locking drug (NDBD)

A

d-tubocurare (d-TC)

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10
Q

MOA of d-TC

A

reversible (competitive) binding to ACh receptor on a subunit (only needs to bind to 1)

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11
Q

prototype sterolidal NMB

A

vecuronium and rocuronium

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12
Q

advantages of sterodial NMB

A

stable hemodynamics, duration not affected by renal dysfunction

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13
Q

SE of vercuronium

A

associated with prolonged blockage in ICU pts

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14
Q

SE rocuronium

A

associated with occasional prolonged duration

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15
Q

longest acting, least expensive NMB

A

pancuronium

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16
Q

pancuronium shows prolonged action in ___ pts

A

renal

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17
Q

pancuronium has profound dependance on:

A

renal metabolism

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18
Q

NDBD that is sympathonimetic

A

pancuronium

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19
Q

prototype Benzylisoquinolinium (BQ) drugs

A

cis-atracurium, mivacurium

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20
Q

NDBD safe for renal/hepatic failure

A

BQ (cis-atracurium, mivacurium)

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21
Q

NMB that can be inactivated by high ambient temps

A

BQs

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22
Q

side effect of Mivacurium

A

can cause histamine release

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23
Q

NMB that may not require reversal

A

mivacurium

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24
Q

can cause prolonged blockade in mivacurium and/or Sch

A

plasma cholinesterase insufficiency

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25
Q

prototype depolarizing agent

A

Succinylcholine (Sch)

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26
Q

MOA of Sch

A

depolarizes membrane by opening Na+ channels by binding both a - subunits

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27
Q

drug that causes fasciculations

A

Sch

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28
Q

drug that causes flaccid paralysis

A

Sch

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29
Q

cause of Sch termination of action

A

redistribution away from motor end plate, and/or matabolized by plasma cholinesterase

30
Q

NMD metabolized by plasma cholinesterases

A

Sch

31
Q

effect of deficiency of plasma cholinesterases on Sch

A

prolonged blockade

32
Q

advantages of Sch

A

rapid onset (30 seconds)

33
Q

clincal use of Sch

A

rapid intubation/ intubation of trauma pts with full stomachs

34
Q

NMD with shortest duration of action

A

Sch

35
Q

NMD that causes hyperkalemia

A

Sch

36
Q

drug that can cause post op myalgia, increased IOP/ICP/IGP

A

Sch

37
Q

drug that can cause malignant hyperthermia

A

Sch

38
Q

drug not reversiable with anticholesterase drugs

A

Sch

39
Q

NMB drug that can cause cardiac arrythmias

A

Sch

40
Q

how Sch can cause arrythmias

A

Sch mimics ACh at cardiac muscarinic receptors

41
Q

why is NMB montoring essential?

A

clinical accumen not always accurate

42
Q

method for monitoring NM blockade

A

evoked stimulatory response

43
Q

areas for testing NM blockade stimulation

A

ulnar nerve, facial nerve, posterior tibial nerve

44
Q

drug causing phase 1 blockade

A

Sch

45
Q

drug(s) causing phase 2 blockade

A

all of them

46
Q

phase of blockade with an antidote

A

phase 1

47
Q

type of blockade in phase 1

A

prolonged blockade

48
Q

type of blockade in phase 2

A

repolarized, but blocked

49
Q

antidote for phase 2 blockade

A

cholinesterase inhibitors

50
Q

ways to measure blockade

A

subjective/objective/ assement of evoked responses and clinical assesment of muscle strenght

51
Q

signs of residual blockade/inadequate reversal

A

strong hand grip that weakens, and jerky movement

52
Q

NMB only anethetic drugs that are:_____

A

routinely antagonized with pharmacologic reversal agents

53
Q

common (3) NMB reversal agents

A

neostigmine, edrophonium, pyridostigmine

54
Q

MOA of blockade reversal agents

A

inhibition of ACh-esterase, increases synaptic ACh concentrations

55
Q

short onset blocking reversal agent

A

edrophonium

56
Q

longest onset blocking reversal agents

A

pyridostigmine

57
Q

side effects of NMB reversal agents

A

bradycardia, icnreased secretions, post-op N/V

58
Q

drug given with NMB reversal agents to attenuate side effects

A

atrooine (edro) or glycopyrrolate (___stigmines)

59
Q

when are anticholinesterase drugs contraindicated

A

absence of measurable responses to muscle stimulation

60
Q

inadequate reversal can lead to:

A

residual neuromuscular blockade (RNMB)

61
Q

signs of RNMB

A

ventilatory insufficiency, insufficient airway protection, visual disturbances, inability to sit without assistance, facial weakness, systemic fatigue

62
Q

inappropriate reversal of NMB results in

A

postop N/V, tachycardia or bradycardia, bronchial/nasal secretions, excess sweating (can mimic MI diaphoresis)

63
Q

NDBD antagonist drug

A

sugammadex

64
Q

MOA of sugammadex

A

binds rocuroum or vecurinium with high affinity in bloodstream

65
Q

signs of malignant hyperthermia

A

rapid onset of tachycardia, hypercarbia, hypertension, rigidity, hyperthermia, acidosis

66
Q

results of malignant hyperthmia if untreated

A

rhabdo, organ failure, death

67
Q

triggers of malignant hyperthermia

A

inhaled anesthetics and Sch

68
Q

pathophys of malignant hyperthermia

A

hypermetabolism due to exagerated release of Ca++ from sarcoplasmic reticulum

69
Q

only drug treatment for malignant hyperthermia

A

dantrolene

70
Q

MOA of dantrolene

A

binds ryanodine receptor, inhibiting release of Ca++ from SR

CNS I (36 decks)

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