Nicotinic antagonists Flashcards
nondepolarizing competitive antagonists MOA
hold the Nm receptor closed, preventing Na+ flow and depolarization–> no muscle contraction
effect of nondepolarizing blockers can be overcome with
ACh, as they are competitive antagonists
the only depolarizing blocker
succinylcholine
succinylcholine MOA
holds Nm open, continual flow of Na+ causes continual, longer than normal depolarization, which causes Nm to desensitize to subsequent ACh stimulation
neuromuscular blocking agents DO NOT
produce unconsciousness or anesthesia because they do not enter the brain
due to their high degree of ionization
neuromuscular blocking agents are NOT absorbed orally and do NOT enter CNS. IV ONLY.
nondepolarzing blockers interfere with the mobilization of ACh from the nerve terminal by
blocking pre-junctional sodium channels
endplate potential _______ when a nondepolarizing blocker is taken
decreases, an action potential can no longer be generated –> lack of muscle contraction (paralysis)
pharmacologic reversal for nondepolarizing blockers
cholinesterase inhibitors (increase ACh which can outcompete blockers)
muscles that are affected first by nondepolarizing blockers
small muscles followed by larger muscles
muscles that are affected last by nondepolarizing blockers
diaphragm, intercostal muscles
onset of action and recovery from succinylcholine are ________, so it’s used for
rapid
short procedures
succinylcholine’s action is terminated by
plama pseudocholinesterase
dibucaine
a local anesthetic that causes inhibition of AChE
abnormal dibucaine number
20%: abnormal cholinesterase acitivity, succinylcholine with last way too long
normal dibucaine number
80%: cholinesterase functions normally and succinylcholine will be short acting
delay recover from succinylcholine
cholinesterase inhibitors
succinycholine contraindications
soft tissue damage, burns, non-traumatic rhabdomyolisis, spinal cord injuries, muscular dystrophy, <8 years old
inhaled anesthetic
halothane
halothane is notorious for
malignant hyperthermia (also succ can cause)
malignant hyperthermia from succinylcholine/halothane treatment
dantrolene
patients who are at higher risk of too much K+ released by succinylcholine
burns, nerve degeneration, head trauma, peritoneal infection, kidney disease
prolonged release of potassium by succinylcholine + risk factor can cause
cardiac arrest, life threatening esp in CHF
malignant hyperthermia by succinylcholine/halothan MOA
uncontrolled release of Ca++ from sarcoplasmic reticulum –> muscle rigidity and high temperature
ventilation use of neuromuscular blocking agents
paralyze diaphragm so a ventilator can be used. intubation, bronchoscopy.
surgery use of neuromuscular blocking agents
paralysis, relax muscles for surgery
orthopedic use of neuromuscular blocking agents
allow manipulation of bones
other random ass use of neuromuscular blocking agents
decrease convulsions/muscle spasms (fine) in ECT (idk).
ganglion blockers are considered
nondepolarizing competitivie antagonists
2 ganglion blockers
hexamethonium
mecamylamine
(not used clinically)
effects of ganglion blockers
fire PNS and SNS so it depends on the dominant tone of the organ
ganglion blocker effects in eye
PNS blocked: cycloplegia, mydriasis
ganglion blocker effects on blood vessels
SNS blocked: vasodilation causes drop in BP, orthostatic hypotension
ganglion blocker effects on heart
SNS blocked: contractility reduced
PNS blocked: decrease in vagal tone causes tachycardia
GU ganglion blocker effects
PNS blocked: urinary retention, esp. BPH
sex ganglion blocker effects
PNS blocked: erectile dysfunction
SNS blocked: reduced ejaculation
ganglion blocker effects on body temp
SNS blocked: can’t sweat
maintain body heat through vasodilation
ganglion blocker effects if combined with autonomic drugs
normal/exaggerated effects on target organ receptors which are not blocked
Feedback and reflexes are decreased/abolished
