Pharm - Lecture 9 - ganlionic blockers, Nero-muscular blockers Flashcards Preview

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Flashcards in Pharm - Lecture 9 - ganlionic blockers, Nero-muscular blockers Deck (16)
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1


What are the therapeutic uses of neuromuscular blocking agents (both competitive and non-competitive)?

1) Used as an adjuvant in surgical anesthesia to obtain relaxation of skeletal muscle (particularly the abdominal wall) to facilitate operative manipulations

2) used to facilitate intubation with a tracheal tube and to facilitate laryngoscopy/bronchoscopy

3) used to control severe muscle spasms

 

2

What is the mechanism for Competitive neuromuscular blocking agents? (non-depolorizing drugs)

Shared characteristics regarding absorption?

Shared characteristics regarding CNS penetration?

These drugs compete with Acetylcholine for unoccupied end-plate nicotinic receptors without activating the ion channel. 

Poorly absorbed by GI

Can't penetrate GI

3


What drugs are competitive neuromuscular blocking agents?

Rocuronium

Atracurium

Vecuronium

Pancuronium

4


What are the charactierstics of Rocuronium?

Duration and onset of action?

Elimination?

Cardiovascular effects?

Histamine release?

Duration of action: intermediate (30-60 minutes)

onset of action: rapid (1-2 minutes, can be used for tracheal intabation)

Elimination: liver metabolism

Cardiovascular effects: none

Histamine release: none

5

What are the charactierstics of Atracurium?

Duration of action? onset?

Elimination?

Cardiovascular effects?

Histamine release?

Duration of action: Intermediate (30-60)

Onset: 2-4 minutes

elimination: spontaniously degrades in plasma and by plasma esterase

Cardiovascular effects: minimal

Histamine release: slight

6



What are the charactierstics of Vecuronium?

Duration of action?

Elimination?

Cardiovascular effects?

Histamine release?

Duration of action: intermediate (60-90 minutes)

onset: 2-4 minutes

Elimination: liver metabolism

no cardiovascular or histamine response

 

7



What are the charactierstics of Pancuronium?

Duration of action?

Elimination?

Cardiovascular effects?

Histamine release?

Long duration of action (120-180 minutes)

Onset: 4-6 minutes

eliminated primarily by renal excretion

Slight increase in heart rate and blood pressure

slight histamine release

8


What is the mechanism of Depolorizing neuromuscular blockers?


Activate nicotinic receptors at the neuromuscular junction maintaining motor end plate depolorization and thus preventing transmision of another action potential

9


What drug is a depolarizing neuromuscular blocker?


Succinylcholine

10


What are the characteristics of succinylcholine? (split card up)

effects?

durration and onset of action?

mebaolization? (by pseydocholinsterase so genetic diferences means longer duration)

therapeutic use?

 

effects: muscle fasiculations followed by flaccid paralysis

Ultra short duration of action (5.8 minutes)

very rapid onset (1-1.5 minutes)

Metabolized by pseudocholinesterase

Used frequently to facilitate intubation with tracheal tube

11


What are the adverse effects and toxicty of Competitive neuromuscular blocking agents?

Prolonged apnea, cardiovascular collapse (rare, sometimes due to histamine release) and anaphylaxis

 

12



What are the adverse effects and toxicty of Depolarizing neuromuscular blocking agents?

1) prolonged apnea

2) malignant hyperthermia

3) post operative muscle pain

4) hyperkalemia

13


How can competitive antagonist toxicity/overdose be reversed?


acetylcholinesterase inhibitor (neostigmine or edrophonium)

can't do this with depolarizing agents!

 

14


Why do neostigmine and edrophonium reverse the effect/decrease the duration of competitive neuromuscular blockade?


These two drugs are acetylcholinesterase inhibitors.  By inhibiting acetylcholinesterase, you increase the concentration of acetylcholine and thus outcompete the competitive neuromuscular inhibitor

15


What drug must be used to conteract the effects of acetylcholinesterase inhibitors during surgery?


muscarinic receptor antagonist- usually glycopyrrolate (doesn't penetrate CNS)

Need to do this to block muscarinic receptor actvity (bradycardia, GI/GU secretions/motility)

16


What is malignant hyperthermia and what is the mechanism?

What patients are at risk?


Potentially life-threatening event triggered by depolarizing neuromuscular blocking agents

Caused by uncontrolled release of calsium from sarcoplasmic reticulum

Susceptibility based on mutatnios in the ryanodine receptor (L-type calcium channel)