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three common endings for NMJ blocker drugs?
What type of receptors are found at the NMJ of skeletal muscle?
Function fo succinylcholine at NMJ?
- **depolarizing blocker
- Starts off by depolarizing but eventually haults any repolarization and causes desensitization
What moves in and out of Ach receptors at the motor end plate?
T/F using an AchE inhibitor will slow down APs?
F, they will speed up b/c the mini potentials will enter summation faster due to non-inhibition of Ach on nicotinic receptors
Highlight drug for NMJ depolarizing blockers?
What happens to non-depolarizing blocks in the presence of anesthetics?
potentiation of block
T/F non-depolarizing NMJ blocks are competitive
T, therefore can be reversed w/ AchE inhibitors or excessive Ach release
What is the duration time of non-depolarizing drugs when metabolized through the kidney and liver?
Tubocurarine, pancuronium, doxacurium duration
Long 2-3 hrs
Vecuronium, atracurium, cisatracurium duration & onset?
Intermediate 30-90 min, 2-4 min onset
Rocuronium duration & onset
intermediate, 1-2 min onset
Non-depolarizing drug muscle paralysis order?
- small mm first (hand, eye, etc...)
- large mm (trunk)
- respiration mm
- ** recovers in opposite direction
Compare train-of-four & Posttetanic potentiation of NDep. block and Dep. block?
- NDep: fades
- Dep: constant
- Posttetanic potentiation (overshoot b.c of Ach buildup)
- NDep: present
- Dep: absent
What are the two complications that have removed Tubocurarine from common use?
- Histamine release
- Ganglion blockade in heart
Succinylcholine onset & duration?
- Onset: 1 min
- duration: 5-10 min = great drug for short procedures
What metabolizes succinylcholine?
Pseudocholinesterase in plasma
What test is used to measure cholinesterase effect on succinylcholine? Normal rate?
- Dibucaine number
- 80% = normal
T/F AchE inhibitors can reverse effects of Succinylcholine?
F, b/c succinylcholine is not a competitive antagonist of nicotinic receptors at the NMJ
describe the Phase I blockade of succinylcholine?
Continued depolarization until end plate no longer responds = flaccid paralysis
Describe Phase II block w/ succinylcholine
membrane repolarizes but receptor is desensitized to Ach = appears similar to non-depolarizing block
Why is succinylcholine dangerous for denervation and burn pts?
Hyperkalemia can be heightened b/c of depolarization of cells and excess K released
M2 response to Succinylcholine
N receptor response to succinylcholine
cardiac issue it two doses of succinylcholine given together?
Issue caused when S.choline and Halothane are mixed?
muscular side effects of succinylcholine?
- post-op pain
- intragastric pressure
- increased intraocular pressure
Two drugs that block calcium channels and enhance NMJ blocks?
- 1) Aminoglycosides: inhibit calcium channel
- 2) Tetracyclines: chelate calcium
- ** both stop release of Ach from presynaptic cleft = no stimulation
What type of antagonist is a ganglion blocker?
non-depolarizing competitive antagonist
Problem with ganglion blockers?
Block all autonomic ganglia ( inhibit a lot of PNS and SNS systems)
NM and NN drugs used as Ganglion blockers?
- NM= decamethonium
- NN = hexamethonium
Most common ganglion blocker?
What is required in a muscle to be affected by ganglion blockers?
high tone (eye, BVs, GI, etc...)
Ganglion blockade effect on eye, blood vessels, heart, urinary, sweat, BP, GI?
- eye: mydriasis bilaterally (cycloplegia), no tears
- blood vessels: vasodilation, hypotension, BP down (recovered via baro receptor)
- heart: contractility blocked, tachycardia (decreased vagal tone)
- urinary: urinary retention, ejaculation reduced
- sweat: gone = ward
- BP: normal
- GI: constipation, no hunger pain, no saliva, dry mouth