NMB Flashcards

1
Q

Isoquinoline Derivatives (6)

A
  • Tubocurarine
  • Atracurium
  • Mivacurium
  • Cisatracurium
  • Metocurine
  • Doxacurium

(MCAT MD)

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2
Q

Steroids (3)

A
  • Pancuronium
  • Vecuronium
  • Rocuronium

(PVR, all end in -ronium)

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3
Q

Short Acting Non-Depolarizing Agents (1)

A

-Mivacurium

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4
Q

Intermediate Acting Non-Depolarizing Agents (5)

A
  • Atracurium
  • Cisatracurium
  • Tubocurarine
  • Rocuronium
  • Vecuronium

(V-CART)

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5
Q

Long Acting Non-Depolarizing Agents (3)

A
  • Doxacurium
  • Metocurium
  • Pancuronium

(DPM)

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6
Q

Pancuronium
3 important things
2 ADRs

A
  • First steroidal
  • Onset 2-3 min, long DOA
  • Used in babies
  • ADRs: CV (increased HR and BP), bronchospasm
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7
Q

Vecuronium
2 important things
2 ADRs

A
  • Shorter DOA than pancuronium
  • Least histamine release than any NMB
  • ADRs: minimal CV, interaction with other steroids
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8
Q

Rocuronium
3 important things
1 ADR

A
  • Most rapid onset of all NMBs
  • Good for intubating
  • Minimal hepatic metabolism
  • ADRs: minimal CV
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9
Q

Atracurium
4 important things
1 ADR

A
  • No cumulative effect with dosing
  • Stereoisomers present (cisatracarium)
  • Inactivated by spontaneous breakdown (Hofman elimination; hydrolyzed by plasma cholinesterases)
  • Laudanosine: product of breakdown (crosses BBB causes seizure)
  • ADRs: histamine release (hypotension)
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10
Q

Cisatracium
2 important things
1 ADR

A

-Inactivated by spontaneous breakdown (Hofman elimination; hydrolyzed by plasma cholinesterases)
-Less histamine release and Laudanosine (than atracarium)
ADRs: minimal CV

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11
Q

Doxacurium

1 important thing

A

-No doss-related CV effects

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12
Q

Mivacurium
1 important thing
1 ADR

A
  • Shortest DOA of all NMBs

- ADRs: induces histamine release

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13
Q

Tubocurarine

1 ADR

A

-ADRs: histamine release (hypotension)

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14
Q

Metocurine

1 ADR

A

-ADRs: histamine release (hypotension)

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15
Q

Non-Depolarizing Agents

7 important things

A
  • Block ACh from receptor then block receptor channel
  • block presynaptic Na channels, preventing ACh from moving from synthesis sites to release sites
  • Characterized by rapid initial distribution followed by slower elimination
  • Do NOT cross membranes well
  • Excreted by kidney (longT1/2, long DOA), excreted by liver (shorter T1/2, shorter DOA), especially dependent with intermediate-acting drugs
  • Steroids are metabolized by 3-hydroxy, 17-hydroxy or 3,17-dihydroxy in liver
  • Reversal: cholinesterase inhibitors, neostigmine/physostigmine, edrophonium
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16
Q

Succinylcholine (SUX)
6 important things
5 ADRs

A

-Blocks transmission via excess depolarizing agonist (only depolarizing)
-Wears off quickly in patients with normal plasma cholinesterase (metabolizes it)
-Produces rapid, reliable paralysis
-Good for intubation
-Phase I: depolarizing, reacts with nicotinic receptors to cause opening of Na
-Phase II: desensitizing, continued exposure decreases endplate depolarization and repolarized membrane (membrane cannot be depolarized again by ACh)
ADRs: CV (tachycardia in adults, bradycardia in children), hyperkalemia, intra-occular pressure, intra-gastric pressure, muscle pain

17
Q

Reversal

A

Neostigmine, physostigmine, edrophonium

18
Q

Drugs that cause CV effects

3 main

A
  • Tubocurarine: hypotension, premedicate with antihistamine
  • Pancuronium: increase in HR independent of histamine release
  • Succinylcholine: bradycardia (children), tachycardia (adults), thiopental prevents bradycardia
  • Vecuronium, pipecuronium, doxacurium, cisatracurium, rocuronium have little or no CV effect
19
Q

Drug interactions with NMBs

6 main

A
  • Anesthetics (inhaled and local)
  • Antibiotics (especially aminoglycosides, clindamycin, tetracyclines)
  • Succinylcholine
  • Local antiarrhythmics
  • Corticosteroids (muscle weaknes and myopathy)
  • Metoclopramide, birth control, tacrine
20
Q

Effects of disease and aging on NMB response

A
  • MG: blockade amplified
  • Old age: increase DOA
  • Burned patients and UMN disease: may be resistant