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35 Cards in this Set

  • Front
  • Back
Nicotinic agonist effects
days of the week: MTWThF
mydriasis
muscle cramps
tachycardia
weakness
twitching
hypertension
hyperglycemia
fasciculation
How do Nn receptors differ from Nm
Nn are blocked by C6
Nm are blocked by tubocurarine
Sequence of transmission at autonomic ganglia
ACh --> rapid EPSP (Nn) = main event- depolarization
ACh -> slow IPSP (M2)
ACh -> slower EPSP (M3)
peptide release --> late slow EPSP (peptidergic receptors)
two nicotinic agonists
nicotine- low conc
and DMPP
low conc nicotine effects
stimulate Nn --> inc BP, salivation, nausea, vomiting
high conc nicotine effect
depolarizing blocfk of ganglionic transmission (both parasympathetic and sympathetic!)
also stimulates sensory receptors
rapid onset of nausea, salivation, abdominal pain, vomiting, diarrhea, cold sweat, headache, dizziness, distrubed hearing and vision, mental confusion, weakness -->
prostration, dec BP, difficult breathing, weak rapid pulse, convulsions -->
death
acute nicotine poisoning = green tobacco sickness
action of hexamethonium
C6 is a non-depolarizing (as compared to nicotine which was depolarizing) ganglionic blocking drug- no longer used clinically, used to be used for HT
How many molecules of ACh are needed to activate Nm
2
mechanism of action of non-depolarizing Nm blockers

administered?
compete with (therefore may be overdcome by) ACh for receptor binding
cause weakness --> flaccid paralysis (muscle contraction can still be caused by direct stimulation)

IV administration
pancuronium
long acting
vecuronium
intermediate acting
rocuronium
intermediate acting
atracurium
intermediate acting
metabolized by plasma cholinesterase*
mivarurium
short acting
metabolized by plasma cholinesterase
tobucurarin
long acting
prototype non-depolarizing Nm blocker
*some ganglionic blockade*- hypotension and tachycardia
Mechanism of action of depolarizing Nm blockers
activate -> open -> desensitize channel
persist at NMJ because they are resistant to acetylcholinesterase
phase I of depolarizing Nm blockers
persistant depolarization
fasciculations --> flaccid paralysis
inactivate Na channels
muscle contraction cannot be elicited by direct stimulation

*enhanced by adding ACh
phase II of depolarizing Nm blockers
flaccid paralysis
end-plate depolarization decreases
muscle repolarizes
prototype drug of depolarizing Nm blockers:

administration
onset
duration
metabolism
succinylcholine

IV admin
<1 min onset
<5 min duration
metabolized by plasma cholinesterase
what may happen if you use succinylcholine in pt's with trauma, burns, nergve damage, renal failure, taking digitalis and diuretics
hyperkalemia- potentially life-threatening
what may happen if you use succinylcholine in pt's with homozygous mutation for atypical plasma cholinesterase gene?
prolonged apnea
can use a dibucaine number plasma cholinesterase test (not routinely used because of low prevalence)
what may happen if you use succinylcholine and halothane together or if the pt has a defect in the ryanodine receptor
malignant hyperthermia
tx malignant hyperthermia
dantrolene
(Ryan is the deficient Receptor and Dan is the antiDote)
cooling oxygen
control acidosis
5 common uses of succinylcholine
muscle relax for abdominal surgery
muscle relax for orthopedic procedures
muscle relax for intubation
muscle relax for bronchoscopy, laryngoscopy, esophagoscopy, etc
prevent trauma during EST
would you use more or less inhaled anesthetics while on a non-depolarizing Nm blocker
less
use more or less local anesthetic while useing non-depolarizing or depolarizing Nm blockers
less
use more or less Ca channel blockers while using non-depolarizing and depolarizing Nm blockers
less
what types of antibiotics can cause some neuromuscular blockade
aminoglycosides and tetracyclines
Two causes of Myasthenia gravis
autoimmune- most common
congenital- rare
MG sx
muscle weakness, abnormal fatiguability
cranial muscles most notable
limb muscles
myasthenic crisis- respiratory distress
dx of autoimmune form
decremental response of mm to repetitive stimulation of motor neuron
Tensilon test (edrophonium)
Nm antibodies
biopsy
tx of MG
pyridostigmine (AChE inhibitor)
immunosuppresion
plasmapharesis to remove Nm Ab's
thymectomy (up to 1/2 remission)
4 uses of botulinum toxin
ocular- strabismus
esophageal- achalasia
vocal cord- spasmodic dysphonia
reverse signs of aging

IRREVERSIBLE ACh release block but muscle reinnervates in 3-6 months so must repeat dose
non-depolarizing vs. Phase I vs. Phase II
end-plate potential
onset
dose-dependence
recovery
anticholinesterase
muscle response
no effect depolarized repolarized
--- immediate slow
--- low high
--- fast slow
reverse augment reverse
weak--> fascic--> flaccid
flaccid flaccid