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Pharmacology Block 1 > Cholinergics - Neuromuscular Blocking Agents > Flashcards

Cholinergics - Neuromuscular Blocking Agents Flashcards

1
Q

What are the two mechanisms for neuromuscular blocking agents?

A

1) Competitive neuromuscular blocking agents (non-depolarizing) -> bind unoccupied ACh nicotinic receptors without activating them ->paralysis of skeletal muscle
2) Depolarizing neuromuscular blockers -> agonist of nicotinic receptors, cause continuous opening of cation channel -> muscle fasciculations followed by flaccid paralysis

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2
Q

What is the ultimate effect of a neuromuscular blocking agent?

A

Paralysis of skeletal muscle

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3
Q

What are the main clinical uses of neuromuscular blocking agents? (5)

A
  1. adjuvant in surgical anesthesia, relax skeletal muscle for operative manipulation
  2. allows for higher level anesthesia
  3. facilitate indubation with tracheal tube, faciliate laryngoscopy, bronchoscopy
  4. reduce trauma during electroshock therapy
  5. control of muscle spasms
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4
Q

Why is the structure significant about competitive neuromuscular blocking agents?

A

Quaternary amine so cannot penetrate CNS -> also cannot be absorbed orally

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5
Q

What is the specificity of competitive neuromuscular blocking agents?

A

Targeting Nm receptors, but there are some effects of other ACh receptors too

  1. decreased blood pressure
  2. tachycardia
  3. stimulation of mast cells -> histamines
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6
Q

What needs to be considered when selecting a neuromuscular blocking agent?

A
  1. Duration of action
  2. Side effects
  3. Route of elimination
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7
Q

Rocuronium

  1. Chemical Class
  2. Duration of action
  3. Onset
  4. Metabolism
  5. Side Effects
A
  1. aminosteroid
  2. intermediate (30-60min)
  3. rapid (1-2 min)
  4. liver metabolism
  5. Unremarkable
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8
Q

Atracurium

  1. Chemical Class
  2. Duration of action
  3. Onset
  4. Metabolism
  5. Side effects
A
  1. benzylisoquinoline
  2. Intermediate (30-60 min)
  3. fast (2-4 min)
  4. spontaneous degradation in plasma to inactive metabolites (NOT DEPENDENT ON KIDNEY OR LIVER)
  5. Minimal CV effects, but slight histamine release
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9
Q

Vecuronium

  1. Chemical Class
  2. Duration of action
  3. Onset
  4. Metabolism
  5. Side effects
A
  1. aminosteriod
  2. intermediate (60-90 min)
  3. fast (2-4 min)
  4. liver metabolism
  5. no CV or histamine-releasing effects
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10
Q

Pancurinium

  1. Chemical Class
  2. Duration of action
  3. Onset
  4. Metabolism
  5. Side Effects
A
  1. aminosteroid
  2. long (120-180 min)
  3. fast onset (2-4 min)
  4. eliminted primarily by renal excretion -> avoid use in pts with renal failure
  5. slight increase in BP and HR, and slight histamine release
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11
Q

What is the only depolarizing neuromuscular blocking drug?

A

Succinylcholine

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12
Q

Succinylcholine

  1. Structure & Significance
  2. Metabolism
  3. Duration of action and onset
  4. Clinical uses
A
  1. dimer of 2 ACh molecules together, does not enter CNS
  2. metabolized by pseudocholinesterase (which is made in the liver)
  3. Very rapid onset 1-1.5min, short duration 6-8min
  4. assist with tracheal intubation
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13
Q

What are genetic variations and other considerations to have when using Succinylcholine?

A
  1. genetic variation in pseduocholinesterase activity (could last up to 2 hours in person with deficiency/defective enzyme)
  2. any pt with liver dysfunction -> b/c pseudocholinesterase made in liver (means prolonged duration of action)
    3
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14
Q

What are the major side effects (toxicity) of competitive neuromuscular blocking agents.

A

cardiovascular collapse

anaphylaxis

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15
Q

How can you reverse toxicity or overdose with competitive meuromuscular antagonists?

A

AChE Inhibitor such as neostigmine or edrophonium

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16
Q

How else are AChE inhibitors used in surgical procedures?

A

To reverse the effects or decrease duration of competitive neuromuscular blocking agents. Use neostigmine or edrophonium

17
Q

When treating with AChE inhibitor for reversal of neuromuscular blocking activity what else should also be co-administered and why?

A

Also give a muscarinic receptor antagonist -> do this to prevent muscarinic side effects (too much parasympathetic activity such as bradycardia, and hypotension, GI secretions) -> use glycopyrrolate b/c it does not penetrate into CNS (reduce CNS side effects from muscarinic antagonists such as sedation)

18
Q

What are the side effects (toxicity) of depolarizing agents?

A

prolonged apnea
malignant hyperthermia
post-operative muscle pain due to muscle fascilculation
hyperkalemia

19
Q

What is malignant hyperthermia and what can be done to treat it? Who is must susceptible?

A

pot. life threatening -> triggered by depolarizing agents b/c of uncontrolled release of Ca++ from sarcoplasmic reticulum -> results in contracture, rigidity, metabolic acidosis, tachycarida

treatment -> discontinue depolarizing agent, physical cooling, treat with dantrolene (blocks Ca++ release)

Susceptibility -> genetiv basis, autosomal dominant due to mutation in ryanodine receptor or L-type Ca++ channel

20
Q

How can depolarizing agents cause kyperkalemia and what types of pts is it most important to watch for?

A

Cause release of K+ from intracellular sites

pts with electrolyte imbalance, heart failure receiving digoxin or diuretics

Pharmacology Block 1 (8 decks)

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