NMJ blockers Flashcards Preview

Pharm > NMJ blockers > Flashcards

Flashcards in NMJ blockers Deck (15):
1

Atracurium (Tracrium®)

non-depolarizing NMJ blocker
Benzylisoquinolines
Time to onset of action 2-4 min
-degraded by temp/pH-dependent Hofmann reaction.
-not metabolized by enzymes and may be useful for patients with liver and/or renal failure.

2

Mivacurium (Mivacron®)

non-depolarizing NMJ blocker
Short duration of action (12-18 min)
Benzylisoquinoline, Time to onset of action: 2-4 min
*metabolized by plasma
cholinesterase (why short duration)*
-Problems if given when decreased plasma cholinesterase activity
Pts with liver disease or nutritional deficiencies may have abnormal plasma cholinesterase activity. Flushing of the face and neck is common.

3

Rocuronium (Zemuron®)

non-depolarizing NMJ blocker
Intermediate Duration of action (30-60 min)
Steroidal structure, Liver metabolism
*Time to onset of action: very rapid (1-2 min) similar to succinylcholine and used to rapidly relax laryngeal and jaw muscles for tracheal intubation*

4

Succinylcholine (Anectine®)

depolarizing NMJ blocker
Duration (5-8 min); Time to onset; 1-1.5 min – very fast
*Used for very short procedures (e.g. intubation)
*initial fasciculations mostly in the chest and abdomen,
occur immediately after drug admin
-no antidote, (like non-depol NMJ blockers)

5

NMJ blocker uses

GA adjuncts in sx: Cause the complete relaxation of skeletal muscle
-no CNS effects; only given IV

6

1st muscles to be blocked/affected ??

small rapid moving muscles → limb trunk muscles → intercostal muscles → lastly, the diaphragm
*recovery in reverse order, diaphragm is 1st to regain function

7

Botox is used to treat ??

blephorospasm (involuntary eyelid closing), strabismus (eye spasms) and wrinkle treatment

8

Non-depolarizing (competitive) NMJ blockers characteristics

Not metabolized by AChE
-Competitive inhibitors of ACh binding to ACh receptor at NMJ
-antiAChE agents (e.g. neostigmine) reverse NMJ block by non-depolarizing NMJ blockers

9

general non-depolarizing (competitive) NMJ blocker SEs

Prolonged apnea, histamine release (bronchospasm, hypotension)


10

Benzylisoquinonlines ( “___curium” name) SEs

Histamine release, few vagal/ganglionic blocking effects

11

Steroidal compounds (“___curonium” name) SEs

-Block of ganglionic muscarinic receptors can occur resulting in tachycardia due to effects on vagus
-Vecuronium and rocuronium are newer agents with little or no associated tachycardia or histamine release

12

succinylcholine metabolism

Degraded by plasma choline esterase (e.g. butyrylcholinesterase)
Problems with decreased butyrylcholineesterase: atypical or deficient plasma cholinesterase, hepatic or liver disease, nutritional deficiencies

13

succinylcholine MOA

alters electro-chemical driving forces: excessive opening of nicotinic ACh receptors by SCh results in decreased electro- chemical driving forces and therefore less positive ion entry in presence of ACh resulting in less muscle response to motor neuron activity.
-this is phase I: single dose, fast onset; neostigmine augments blocking action of SCh

14

Phase II SCh

after prolonged infusion or dosing 10X of normal dose (5 mg/kg); slow onset
-MP: -80mV
-Neostigmine antagonizes SCh block

15

botulinum toxin

besides wrinkles, for
blephorospasm – involuntary closing of eyelid and strabismus – deviation of eye position that cannot be overcome
MOA: prevent release of presynaptic ACh at NMJ
SEs: upregulation of post-synaptic nicotinic ACh receptors at previous injection site(s) resulting in increased wrinkles and ptosis - eyelid droop