Nicotinic cholinergic transmission, NMBA Flashcards
Excitation contraction coupling
Process by which an action potential in a motor neuron leads to contraction of a muscle
Polarized membrane
Positive charge on the outside, negative charge on the inside
Steps in muscle contraction
Action potential at NMJ release ACH, ACH binds to nicotinic m, end plates depolarize, depol over muscle membrane happens, release of calcium ions from SR, calcium permits actin/myosin to bump uglies and cause muscle contraction, ach quickly dissociates from receptors on motor end plate, calcium take into SR causing relaxation
Non depolarizing compete with
binding to nicotinic M receptors
Order of paralysis
Eyes face first, then limbs, abdo and glottis. Last is respiratory muscles
Hypotension
NMBA can cause hypotension due to blockade of nicotinic m receptors, also from histamine release. Can’t cross BBB
Succs paralysis
4-6 minutes (at 1.5mg/kg)
Succ degraded by
Pseudocholinesterase which is present in plasma
Succ peaks
1 minute after administration, lasts no longer than 10 minutes
Psuedocholinesterase
Can be deficient
MH
Rare, potentially fatal, triggered by succ, 1:25,000 Muscle rigidity, extremely high temp (up to 43C)
MH cause in a nutshell
Increased calcium from SR causing prolonged muscle rigidity
Succ hyperK+
Rarely can cause hyperk+ on its own Significant hyperK+ from burns, trauma (crush injuries) rhabdo
Succ trade name
Anectine
Succ contras
Hypersensitivity known or suspected hyperK+, family hx of MH or pseudocholinesterase deficiency, myopathies with elevated CK