Pharm Flashcards
atracurium
non-depolarizing agent: isoquinolone
AE: histamine release, SEIZURE due to laudanosine
cisatracurium
non-depolarizing agent: isoquinolone
fewer AE than atracurium
HOFFMAN elimination: spontaneous breakdown (doesn’t change t1/2 in renal/hepatic problems)
D-tubocurarine
non-depolarizing agent: isoquinolone
pancuronium
non-depolarizing agent: steroid
AE: cardiac M receptor block
rocuronium
non-depolarizing agent: steroid
not as potent as other steroid derivatives
AE: slight cardiac M receptor block, allergic reaction
vecuronium
non-depolarizing agent: steroid
succinylcholine
depolarizing agent
binds and opens nACh receptor and prevents repolarization after initial depolarization by preventing Na channel closure
SHORT duration
muscle contraction, then flaccid paralysis: twitches
AE: histamine release, stimulate cardiac M receptor, stimulate ganglia, MALIGNANT HYPERTHERMIA, HYPERKALEMIA (in injury), HTN, arrhythmia, brady or tachycardia, ANAPHYLAXIS, muscle pain
broken down by pseudocholinesterase
genetic variants of plasma cholinesterase: increase risk for long duration
endophonium
reversal agent
AChE inhibitor
give ATROPINE
shorter onset and duration than other AChE inhibitors
pyridostigmine
reversal agent
AChE inhibitor
give GLYCOPYRROLATE
longer onset and action
neostigmine
reversal agent
AChE inhibitor
give GLYCOPYRROLATE
sugammedex
reversal agent
capsule that prevents STEROIDAL NMB from accessing binding site on Ach nicotinic receptor
malignant hyperthermia
SUCCINYLCHONLINE
uncontrolled Ca release from SR
brown urine, rise in body temp, muscle rigidity
Tx: DANTROLENE
glycopyrrolate
anticholinergic
give with AChE inhibitor to reduce consequences of off target activation
atropine
anticholinergic
non-sedating
give with endrophonium to reduce consequences of off target activation
scopolamine
anticholinergic
crosses BBB: sedating
duloxetine
serotonin-NE reuptake inhibitor (SER greater)
CYP metabolism; CYP2D6 inhibition
Tx: fibromyalgia
AE: increase HR and BP, SIADH (hyponatremia), suicidal ideation
CI: liver dysfunction, alcoholism, close angle glaucoma, MAOI
milnacipran
serotonin-NE reuptake inhibitor (NE greater)
Tx: fibromyalgia
AE: increase HR and BP, SIADH (hyponatremia), suicidal ideation
CI: liver dysfunction, alcoholism, closed angle glaucoma, MAOI,
pregabalin
inhibit glutamate presynaptically (inhibit L-type Ca channels)
Tx: fibromyalgia (off label)
CI: reduce in renal dysfunction
AE: rebound, dependence, suicidal thoughts, depression, dizzy, sedation, blurred vision, xerostomia
monitor: serum creatinine
amitriptyline
tricyclic antidepressant
Tx: fibromyalgia (off label)
AE: anticholinergic
cyclobenzaprine
skeletal muscle relaxer
related to TCA, central action at brain stem
CYP metabolism
Tx: fibromyalgia (off label)
AE: anticholinergic (GI most significant)
CI: anticholinergics, 1st gen antihistamine, tricyclics (prolong QT)
fluoxetine
SSRI (SER reuptake inhibitor)
Tx: fibromyalgia
skeletal muscle relaxers
AE: sedation
dantrolene
ryanodine receptor: block release of Ca from SR
Tx: spasticity, malignant hyperthermia
AE: thrombophlebitis (need slow infusion), liver, floppy child syndrome (C-section), muscle weakness
CI: Ca channel blocker
monitor: LFTs
botulinum toxin (botox)
block fusion of vesicles with end of presynaptic terminal
Tx: spasticity
baclofen
GABA(B) agonist: inhibitory signals or reduces excitatory glutamate pathways
inhibition of substance P: pain relief
AE: dependence
Tx: spasticity
AE: rebound neural activity results in seizure, confusion, hallucinations, increased spasticity (TAPER down), increase blood glucose; drowsy, dizzy, confusion
CI: adjust in diabetic agents, CNS toxicity in renal failure
tizanidine
skeletal muscle relaxer pre-synaptic alpha 2 agonist AE: decreased sympathetic outflow, liver, taper cessation, xerosomia, dizzy, sedation, hypotension monitor: LFTs Tx: spasticity
methocarbamol
skeletal muscle relaxer
sedation, altered pain perception
AE: irritable, blurred vision, dizzy
CI: hepatic/renal dysfunction increases toxicity
non-depolarizing agents
prevents any activation of muscle contraction by preventing opening of channel
reversal agents
given post procedure to reverse residual effects of paralytic agents
Nm
nicotinic M receptors
found on skeletal muscle
site of action of paralytics
phase I NM blockade by succinylcholine
- EPP
- onset
- dose-dependence
- recovery
- TOF
- AchE inhibition
- muscle response
EPP: -55mV onset: immediate dose-dependence: low recovery: rapid TOF: no fade AchE inhibition: augments muscle response: fasciculations, then flaccid paralysis
phase II NM blockade by succinylcholine
- EPP
- onset
- dose-dependence
- recovery
- TOF
- AchE inhibition
- muscle response
EPP: -80mV onset: slow dose-dependence: high recovery: long TOF: fade, PTP follows fade AchE inhibition: reverses muscle response: flaccid paralysis
laudanosine
product of atracurium
causes seizures
dibucaine test
enzyme inhibitor
identify genetic variants of plasma cholinesterase
important in succinylcholine use
steroid derivatives
more potent
hepatic and renal elimination
isoquinilone derivatives
spontaneous elimination
effect of blocking/stimulating cardiac M receptor
block: tachycardia
stimulate: bradycardia
effect of histamine release
hypotension
edema
Off target actions of AchE inhibitors
bradycardia bronchospasm increased secretions pupillary constriction increase peristalsis and bladder tone cerebral excitation
therapeutic use of NMBs
IV
adjuvant to surgical anesthesia (no pain relier or amnesia)
short orthopedic procedures
endotracheal intubation
What causes death with NMB overdose?
diaphragm paralysis
carisoprodol
skeletal muscle relaxer
sedation and altered pain perception by CNS action on reticular activating system and spinal cord
CYP2C19 metabolism
AE: drowsy, dizzy, CNS, vision loss, mydriasis, orthostatic hypotension
CI: renal/hepatic dysfunction increases toxicity
