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24 Cards in this Set

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Used in ICU to induce muscle paralysis
Interfere with transmission at NMJ
Lack CNS activity
Mainly used as adjuncts during general anesthesia
Neuromuscular Blockers
Reduce spasticity
Used to treat chronic pain and fibromyalgic conditions
Spasmolytics
non-depolarizing NM blockers block action of ? at Nm receptors

depolarizing blockers block by using an ?
ACh

agonist (succinyl choline)
Both nondepolarizing and depolarizing have 2 ?
quaternary nitrogens
depolarizing NM have ? structure similar to ?
linear ; ACh
Non depol. NM blockers conceal double ACh structures in ?
a ring system
All steriodal muscle relaxants are metabolized to ?
3, 17 hydroxy products
Intermediate acting
Hepatic and spontaneous degradation (laudanosine, long half life, crosses bbb, may cause seizures)
Causes transient hypotension (histamine release)
Atracurium (generic, Tracrium):
Potent isomer of atracurium
Produces less laudanosine and is less likely to release histamine
Has replaced atracurium
Cisatracurium (Nimbex):
Shortest acting (duration 15 min)
Rapidly inactivated by plasma cholinesterases (liver disease patients or genetic deficiency of cholinesterase, renal impairment)
Onset is slower than succinylcholine, histamine release
Mivacurium (Mivacron):
Short duration of action (5-10 min)
Highly metabolized by cholinesterases (plasma, liver)
Metabolite (succinylmonocholine) is rapidly degraded
Plasma esterases (prolonged duration in patients with abnormal variant of cholinesterase)
Succinylcholine (generic, Anectine)
measure of the ability of the patient to metabolize succinylcholine
Normally, dibucaine inhibits normal enzyme activity by 80% and abnormal enzyme by 20%
dibucaine number
act competitive antagonists at the nicotinic muscle receptors at the NMJ
Effect of neostigmine, edrophonium, and pyridostigmine
In larger doses, can block the pore
Can also block prejunctional sodium channels
Non Depolarizing blockers
succinlycholine, are agonists on the Nm receptors, stimulate rec at low conc, block the pore at high conc
depolarizing blockers
Depolarization, prolonged flickering, unresponsive to stimuli
Flaccid paralysis
Augmented by ChEI

which phase I or II?
phase I
Membrane repolarization
Similar to nondepolarizing block
Reversible by ChEI

Which phase I or II?
phase II
Adverse affects of depolarizing blockade
hyperkalemia, increased intraocular pressure, increased intragastric pressure, muscle pain
Submitted for FDA approval as a reversal drug
Rapidly inactivates steroidal NMN blockers by forming an inactive complex
Sugammadex
antagonize NM blockade by nondepolarizing blockers
ChEI (Neostigmine, pyridostigmine)
Mechanism
Used in patients with almost any type of muscle spasm

spasmolytic
Diazepam (Valium)
GABAB agonist
Reduce release of
Excitatory nt in brain, spinal cord
Reduce pain, inhibit release
of substance P
Start at 15 mg dose 2x daily
Increase as tolerated to 100
Adverse effects:
Drowsiness
Increased seizures in epileptic patients
Baclofen (Lioresal)
spasmolytic
a2 agonist
Both pre and postsynaptic inhibition in spinal cord
Inhibits nociceptive transmission in spinal cord dorsal horn
Adverse effects:
Drowsiness, hypotension, dry mouth, asthenia
Tizanidine (Zanaflex):
Progabide (GABAA and GABAB agonist)
Glycine, inhibitory neurotransmission

spasmolytic
gabapentin (neurontin)
Blocks excitation-contraction coupling
Doses start at 25 mg daily, may increase up to 100 mg daily
Used in malignant hyperthermia (1 mg/kg IV)

spasmolytic
dantrolene