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47 Cards in this Set

  • Front
  • Back
What are neuromuscular blocking agents (NMBA)used for?
--Relax skeletal muscle for surgical procedures and tracheal intubation
--prevent fractures and dislocations associated with ECT
--Control of muscle spasms of tetanus
--Sustained NM blockade in critically ill patients
What are the non-depolarizing (competitive antagonists) isoquinoline derivative agents?
What are the non-depolarizing (competitive antagonsits) steroid derivative agents?
What is the depolarizing (agonist) agent?
What are the muscle relaxant agents used for?
Provide relief of spasticity associated with cerebral palsy, MS, spinal cord lesions, head trauma, etc.
What are the muscle relaxant agents?
What does the NMBA have a structural relationship to?
NMBA have...
at least one quaternary N (charged)
All are highly polar and are inactive orally
NMBA Tubocurarine...
--non-depolarizing blocker
--Quarternary N
--Competitive antagonist to ACh at NMJ (nicotinic)--skeletal muscle endplates
--Autonomic ganglia (adrenal medulla (Nn)
--Little or no effect on muscarinics
NMBA Tubocurarine...
--no effect on excitability or conduction of nerve or muscle
Flaccid paralysis of muscles goes in what order?
Smaller rapid muscles first and progress to larger slow moving muscles:
Function is recovered in reverse order
Why do you see hypotensive effects in Tubocurarine?
Due to ganglia/adrenal effect and histamine release
What are the adverse effects of Tubocurarine?
Reflex tachycardia
Respiratory paralysis
Bronchospasm (esp. in asthmatics)
What is the onset of action of Tubocurarine?
5 minutes and duration ~ 90 minutes
What reverses effects of NMBA?
AChE such as neostigmine
NMBA Tubocurarine...
Doesn't cross BBB and is eliminated extensively by kidneys
NMBA Tubocurarine have interactions with...
--Several drugs have some NMB effects that augment those of NMB agents--some anesthetics and antibiotics
--Low K potentiates and high K opposes
--Newborns, aged, and myasthenics are sensitive
NMBA Succinylcholine Duration
~ 5 minutes
Elimination--plasma cholinesterase
NMBA Mivacurium Duration
~ 10-20 minutes
Elimination--plasma cholinesterase
NMBA Atracurium Duration
~ 30-60 minutes
Elimination--Spontaneous and plasma cholinesterase
NMBA Cistracurium Duration
~30-60 minutes
Elimination--Mostly spontaneous
NMBA Vecuronium Duration
~60-90 minutes
Elimination--Liver metabolism
NMBA Tubocurarine Duration
~80-120 minutes
NMBA Pancuronium Duration
~120-180 minutes
Depolarizing NMJ Blockers Succinylcholine...
--Depolarizing agonist
--short acting
--produces initial depolarization...then block
--muscle fasiculations may be seen
Depolarizing NMJ Blockers Succinylcholine...
--Phase 1-depolarizatio like that of ACh but longer
--non-reversible by AChE inhibitors
--Phase II-with high dose or continuous exposure (desensitization)
Depolarizing NMJ Blockers Succinylcholine...
--Stimulates histamine release (< tubo but > than pancuronium)
--hyperkalemia can be extensive (denervation)--can be life threatening in certain patients, be careful in CHF on dig or diuretics
--use on short term procedures
Depolarizing NMJ Blockers Succinylcholine...
--AChE agents may increase blockade
--Rapidly metabolized by plasma and liver pseudocholinesterase
--Post-op muscle pain
What causes malignant hyperthermia (MH)?
--Genetic disorder of skeletal muscle
--One of main causes of death due to anesthesia
--Triggered by anesthetics or succs
What do you see in MH?
--Rapid hyperthermia and metabolic acidosis
--accelerated muscle metabolism and contractures
--potentially fatal
How do you treat MH?
Symptomatically and with Dantrolene
Why is muscle relaxants used?
--Spasticity d/t loss of supraspinal control over spinal cord reflexes-results in "hyperreflexia" of spinal refexes
--spasticity with MS, CP, etc.
--used to reduce hyperactive reflex by decreasing activity of Ia fibers or enhancing of internuncial inhibitory neurons
What is Baclofen?
--Skeletal muscle relaxant
--GABA analog acts on GABAb pre and post synaptic receptors
--increased K conductance, decreased calcium influx
--decreased excitatory NT release, decreased motor neuron activity
--effective as diazepam with less sedation and little effect on muscle strength (unlike dantrolene)
What are the side effects of Baclofen?
--graduated doses minimizes
--drowsiness and dizziness
--hypotension (OD)
--elderly/MS--more senstive and need smaller doses
--abrupt withdrawal potentiate increases spasm
--sometimes given via infusion pump
What is the agent of choice for spinal spasticity?
What is diazepam?
--Skeletal muscle relaxants
--anxiolytic agent (benzodiazepine)
--acts at all GABAA synapses but reduces spasticity partly at spinal cord level
--Not a GABA agonist but enhances GABA effect
What is the primary problem with Diazepam?
What type of metabolism does diazepam have?
Complex hepatic
Does tolerance develop with diazepam?
Yes, both therapeutic as well as side-effects
What is diazepam used to control?
Flexor and extensor spasms, spinal spasticity and MS as well as treat anxiety D/O
What drugs are used to treat signs and symptoms of localized muscle spasm?
--most are sedative and muscle relaxant properties may be partly a result of sedatoin (Drowsiness a common side effect)
What is the most popular drug for localized muscle spasm?
cxyclobenzaprine (Flexeril)--has significant anticholinergic side effects
What are other agents used to treat localized muscls spasm?
What is a peripheral acting skeletal muscle relaxant?
How does dantrolene work?
Acts at level of muscle --> inhibits calcium release form SR and uncouples excitation-contraction --> doesnt alter membrane contraction
What is the biggest problem with dantrolene?
Dose-dependent muscle weakness is biggest
--hepatotoxicity (rare)
What is dantrolene used for?
Spinal cord lesions
DOC for MH