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Pharmacology > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

The NMJ Nicotinic AChR

slide 4

A

• Found on the muscle cell
• ligand gated channel Na+/Ca2+ enter when its
activated by the binding of 2 ACh molecules
• pentameric structure
• Na+/Ca2+ enters and K+ leaves the cell
◦ leads to depolarization and muscular contraction

  1. Unlike the nicotinic receptors in the NS (only a and B subunits), the NMJ Nic. AChR has 5 subunits (2alpha, 1 beta, 1 delta, 1 gamma)
    a) Hydrogen binding sites on the gamma and delta sites
    b) N+ binds to a neg (-) binding
    site on the alpha units
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2
Q

Tubocurarine History and its derivatives

A
  1. 1st NMJ Blocker
  2. Has benzylisoquinolone moiety which all curare based drugs have
    - things are attached to the N+
  3. Derivatives: mivacurium, atracurium, cisatracurium

“-urium”

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3
Q

Tubocurarine:

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 4-6 min
  2. 60+ min
  3. Kidney (80%)
    - think kidney tubes
  4. Weak
  5. N/A
  6. Moderate
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4
Q

Mivacurium

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 2-4 min
  2. 10-20 min
  3. Plasma ChE
  4. N/A
  5. N/A
  6. some
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5
Q

Atracurium

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autonomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 2-4 min
  2. 20-30 min
  3. Spontaneous (Hoffman Elimination-independent of any organ)
  4. N/A
  5. N/A
  6. some
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6
Q

Cisatracurium

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 2-5 min
  2. 30-45 min
  3. Spontaneous (Hoffman Elimination-independent of any organ)
  4. N/A
  5. N/A
  6. N/A
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7
Q

Pancuronium:

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 4-6 min
  2. 60+ min
  3. Kidney (80%)
  4. weak block
  5. Some block
  6. N/A
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8
Q

Rocuronium

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 1-2 min
    “1 rock 2” rule them all
  2. 20-30 min
  3. Liver (80%)
  4. N/A
  5. weak block
  6. N/A
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9
Q

Vercuronium

  1. Onset
  2. DoA
  3. Termination of Action:
  4. Effect-autnomic ganglia
  5. Effect-muscarinic receptors
  6. Histamine release
A
  1. 2-4 min
  2. 20-30 min
  3. Liver (80%)

N/A to the rest

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10
Q

Cons about tubocurarine and pancuronium

A

• Tubocurarine and Pancuronium had more S/E and lasted longer (pts under too long) and take longer too work
◦ both rely on renal excretion; can’t give to those with renal insufficiency; also for normal pts. this is bad b/c post-op their kidneys are not fully functioning
◦ wk block on autonomic ganglia (nic. R): little bit of hypotension

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11
Q

What are adverse effects seen only with succinlycholine and not with nondepolarizing blockers

A
  1. myalgias due to fasciculations
  2. Increased ICP and IOP
  3. Hyperkalemia
    - Because it opens the nAChRs: Ca2+/Na+ flow into cell and K+ flows out of the cell into the blood for normal patients and even worse for others

Precautions with Hyperkalemia:

a) Proliferation of extrajunctional nAChRs (5-10d)

b) Denervation (e.g. spinal cord injury, stroke)

c) Burns, trauma, prolonged immobility

d)Myopathies (esp. Duchenne muscular dystrophy)

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12
Q

How to get stronger/get unblocked?

A 
1) Wait for the
NMB to be metabolized and/or excreted . . .

• Succinylcholine ✔ 
-good choice, because lasts only 10 min
can take hours 
•Nondepolarizers
-can take hours

•Muscle strength may appear adequate even when up to
75% of nAChR are still occupied by a NMB!
—This is not okay! They’re really at risk! They can have opioids and get a little acidosis and then nAChR don’t work as well anymore
• the other nAChRs take up the slack but so many still blocked
• very severe problems: paralysis of respiratory system

2) You can chemically “reverse” the block
-Not succinlycholine





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13
Q

Reversal of the NM Blockade via chemicals

*only works against the nondepolarizing agents

A

1) Competitive antagonism is overcome with excess agonist (ACh)

2) Increase the concentration of ACh by inhibiting AChE at the NMJ
–Neostigmine, Edrophonium, Pyridostigmine

3) Prevent unwanted muscarinic side effects of excess ACh: SLUDGE
-give anti-muscarunics: atropine and glycopyrrolate to prevent

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Pharmacology (12 decks)

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