Flashcards in Neuromuscular Physiology and Pharmacology Deck (117)
Where do motor neurons to skeletal muscle originate?
anterior (ventral) horn of the spinal cord (DAVE--- ventral efferent)
The sensory neurons from the skeletal muscle carry action potentials to the spinal cord via the _______ _______.
dorsal horn (DAVE--- dorsal afferent)
The motor and sensory nerves of the skeletal muscle are ______ nerves.
Explain the role of calcium in the pre-synaptic junction?
when an action potential is generated and reaches the pre-synaptic junction--> stimulates Ca channel to open--> Ca causes vesicles to open--> release AcH into synaptic cleft--> pre-synaptic nicotinic receptor response to AcH--> produce more and release more AcH
What is the positive feedback system that is associated with AcH?
the pre-synaptic nicotinic receptor responds to AcH by increasing the synthesis and release of AcH... this is a positive feedback system that prevents depletion of AcH at the NMJ.
Explain the events that occur when AcH leaves the pre-synaptic membrane.
AcH diffuses down concentration gradient from pre-synaptic membrane to motor end plate of postsynaptic membrane--> combines with nicotinic receptors of protein channel--> when BOTH alpha subunits of nicotinic receptor channel are occupied by AcH, the channel snaps open= Na and Ca into the cell, K ions diffuse out into extracellular space--> contraction of muscle cell
How is the neurotransmitter action impulse at the neuromuscular junction terminated?
acetylcholinesterase, aka true cholinesterase, breaks down acetylcholine into choline and acetate--> as AcH is metabolized, the motor end plate repolarizes and the muscle cell becomes ready for another squirt of AcH from the nerve terminal--> choline is transported back into the nerve terminal where it is used to re-synthesize AcH
Acetylcholinesterase breaks acetylcholine down into _____ and ______.
choline (reabsorbed by nerve terminal to re-synthesize AcH) and acetate
The release of the neurotransmitter (AcH) from all nerve terminals, including the motor nerve terminals, depends on the entry into the terminal of ______ ions.
calcium ions; calcium comes in, neurotransmitter goes out
How does calcium relate to hyporeflexia and hyper-reflexia?
hypocalcemia is associated with a decrease in amount of neurotransmitter released (hyporeflexia), and hypercalcemia is associated with an increase in amount released (hyperreflexia)
Magnesium will be the OPPOSITE of calcium
Calcium and magnesium are ______ (agonists or antagonists) at nerve terminals (pre-synaptically).
The channel operated by the nicotinic receptor has _____ subunits. _____ AcH molecules are needed to open each nicotinic AcH receptor channel.
5 subunits (2 are identical-- 40k); 2 AcH molecules are needed
It takes ___ (#) acetylcholine molecules to open the ______-gated channel of the skeletal muscle motor end plate.
2; acetylcholine gated channels
Non-depolarizers are _______ (competitive or non-competitive).
competitive inhibitors; when non-depolarizers bind to either AcH binding site on a nicotinic receptor, AcH CANNOT attach to that receptor, so the channel CANNOT open.
Succinylcholine binds to the nicotinic receptors and _____ (opens or closes) the channels. ________ is maintained for an extended amount of time because Sux is not metabolized by true acetylcholinesterase.
What neuromuscular blocking agent mimics acetylcholine at the NMJ?
Succinylcholine; results in opening of the channel and remains open d\t slower metabolism by plasma cholinesterase---> depolarization is prolonged
What type of neuromuscular blocking agent produces the following effect: IV administration--> diffuses from vascular department into synaptic cleft of NMJ--> combines with nicotinic receptors of motor end plate--> exerts no direct effect on the channel--> channels stay closed, the post-synaptic membrane remains polarized.
What NMB agent is associated with the following: action potentials cannot be initiated in skeletal muscle until the cell repolarizes because the Na channels are in the inactivated state.
depolarizing neuromuscular blocker
How is succinylcholine metabolized?
by an enzyme in the plasma called plasma cholinesterase... also called pseudocholinesterase and butyrocholinesterase; as circulating Sux is metabolized, a gradient is created for Sux to diffuse from the skeletal muscle motor end plate back into the plasma to be quickly metabolized
How is succinylcholine terminated?
At the NMJ, does the pre-synaptic action of Sux enhance or antagonize its postsynaptic action?
Sux, by stimulating the presynaptic nicotinic receptor, augments the release of AcH--> since the released AcH opens channels and depolarizes the motor end-plate like Sux, the presynaptic action of Sux enhances its post-synaptic action.
What are some of the physiological properties of neuromuscular relaxants?
1- 100% ionized at physiologic pH
2- very highly protein bound
3- do not cross the BBB (ions do not cross lipid bilayers)
4- do not cross the placental barrier (same reason)
5- trapped in renal tubule after filtration because of high degree of ionization (all muscle relaxants can be excreted by the kidney if other routes are unavailable)
What is the trade name for succinylcholine?
Anectine (very short)
What is the trade name for vecuronium?
What is the trade name for rocuronium?
What is the trade name for pancuronium?
What is the trade name for cisatracurium?
What is the trade name for mivacurium?
What is the trade name for atracurium?