Chapter 19: Drugs That Block Nicotinic Cholinergic Transmission Flashcards
Nueromuscular drugs mechanism of action
- prevent ACh for activating nicotinic receptors on skeletal muscles, which results in muscle relaxation
Neuromuscular drugs cannot cross
- the blood brain barrier
- placenta
polarization
positive changes cover the outer surface of the mebrane; negative charges cover the inner membrane
depolarization
- postive changes move from the outside to inside
- in response to the binding of ACh to the nicotinic receptors
repolarization
- positively charged ions are pumped out of the cell so that the original resting membrane state is restored
- follows unbinding of ACh from endplate of nicotinic receptors
competitive (nonpolarizing) neuromuscular blockers
- do not depolarize the motor endplate
all neuromuscular blocking agents contain at least one
quaternary nitrogen atom
nondepolarizing neuromuscular blockers mechanism of action
- competes with ACH for nicotonic receptors
- blocks receptor activation of acetlcholine
competetive neuromuscular blockers pharmacologic effects
- muscle relaxation: flaccid paralysis
- hypotension
- no effect on the CNS
when a competitive neuromuscular blocker is administered peak effects persist
20-45 mins and then decline
recovery for a cometitive neuromuscular blocker takes
1 hour
competetive neuromuscular blocker effect
rapid onset of paralysis
Competetive neuromuscular blocker therapeutic uses
muscle relaxation during surgery, mechanical ventilation, endotracheal intubation
Competetive neuromuscular blockers adverse effects
- respitory arrest
- hypotension
- atracurium
Pancuronium is used for
muscle relaxation during general anesthesia, itubation, and mechanical ventelation
does pancuronium cause histamine release, gangloinic blockade, or hyptension
no
Pancuronium dise effects
Vagolytic effects may produce tachycardia
Pancuronium should be used with caution in
patients with liver disease
Pancuronium excretion
primarily through the urine
Succinylcholine [Anectine] mechanism of action
depolarizing the neuromuscular blockade
Succinylcholine [Anectine] pharmacologic effects
- ultra-short acting (peaks at 1 minute)
- mucle relaxation; state of flaccid paralysis
- no effect on CNS
Succinylcholine [Anectine] is eliminated by
plasma cholinesterases
Succinylcholine [Anectine] therapeutic uses
- muscle relaxation during endotracheal intubation
Succinylcholine [Anectine] causes prolonged apnea in clients with
low pseudocholinesterase activity
- causes paralysis to persists for hours
Malignant hyperthermia can be triggered by
succinylcholine
Maliganant hyperthermia symptoms
- muscle rigidity, profound elevation of body tempurature, cardiac dysrhythmias, unstable blood pressure, electrolyte derangements, and metabolic acidosis
a malignant hyperthermia reaction is determined
genetically
between 10% to 70% of patients experience postoperative muscle pain after recieving what medication
succinylcholine
postoperative muscle pain after succinylcholine occurs
12-24 hours after surgery
pain after succinylcholine is most common in which areas
neck, shoulders, and back
hyperkalemia can be caused by
succinylcholine
- promotes the release of potassium from tissues
significant hyperkalemia is most likely to occur in clients with
major burns, multiple trauma, denervation of skeletal muscles, or upper motor neuron injury
hyperkalemia complication
cardiac arrest has resulted
treatment for toxicology of succinylcholine
no specific antidote
- administered IV
toxicology of succinylcholine symptoms
- overdose can cause prolonged apnea
- client is awake but paralyzed
- suppresses gag reflex
