Neuromuscular Physiology And Pharmacology Flashcards
Spinal cord for motor nerves
Efferent nerves
Exit the ventral cord
Spinal cord for sensory nerves
Afferent
Enter the dorsal cord
Type of neurons for motor nerves
A alpha
Largest, most heavily myelinated
Fastest conduction velocity
Release of ACh from nerve terminal
AP moves into presynaptic nerve terminal Causes VgCaC to open Ca diffuses into the nerve terminal Ca causes vesicles to fuse with nerve cell membrane and opens to exterior This release ACH by exocytosis
Quantum
Each vesicle contains quantum of ACh (this process is quantal release)
125 quanta released per AP
10,000 Ach molecues released per quantum (vesicle)
Positive feedback of Ach
Presynaptic nicotine receptor responds to ACh in cleft
Causes synthesis of ACh and mobilization of ACh vesicles
Prevents depletion of ACh
Examples
- Fade with nondepolarizers
- Phase 2 with succ
Events at motor end plate
Ach binds to both alpha subunits of nicotinic receptor- takes 2 Ach molecules to bind to the 2 alpha subunits r
Na, Ca, and K diffuse through open channel
Na and Ca diffuse into cell, K diffuses out of cell
At a critical level, AP is initiated
Excitation contraction coupling
Process from presynaptic membrane to muscle fiber contraction
Termination of neurotransmitter action
AChe breaks ACh to choline and acetate by hydrolysis
Choline transported back into the cell to make more ACh
Ca problems
Hypocalcemia- decrease in ntm release
Hypercalcemia- increase in ntm release
Mg problems
Hypomagnesemia- increase in ntm release
Hypermagnesemia- decrease in ntm release
Ca and Mg at nerve terminal (presynaptically)
Act as antagonists
What does AChE degrade
Ach Ester local anesthetics Neostigmine Edrophonim Remifentanil Esmolol
Nondepolarizing block
Agents competitively inhibit the ACh binding site
Depolarizer block
Binds to nicotinic receptors and opens channels like ACh does
Holds it in inactivated state
Characteristics of nondepolarizing block
(Same as Phase II block) Competitive inhibition Fade follows high frequency stimulation Post tetanic facilitation Antagonized by anticholinesterases No fasiculations
Characteristics of depolarizing block
(Same as Phase I block) Decreased single twitch height Response to high frequency stimulation maintained Minimal or no fade Antagonized by nondepolarizers Potentiated by anticholinesterase Muscle fasiculations
Metabolism of succ
By plasma choloinesterase
Succ must diffuse back into the plasma from skeletal muscle to be metabolized
what does succ do at presynaptic receptors?
Acts as ACh and causes ACh release
Presynaptic action enhances post synaptic action
Aminosteroids
Curoniums
Benzylisoquinolines
Curium
Monoquaternary aminosteroids
Vercuronium
Rocuronium
Bisquaternary aminosteroid
Pan uranium
Bisquaternary benzylisoquinolines
Atracurium
Cisatracurium
Release of K with succ
0.5 in normal patient
5-10 in burn, trauma, and head injury
Metabolism primary route of elimination
Succ
Atracurium
Cisatracuriu
Mivacurium
Biliary excretion primary route of elimination
Vecuronium
Rocuronium
Renal excretion primary route of elimination
D-tubocurarine Metocurine Pancuronium Gallamine Doxacurium Pipecuronium
Metabolism of atracurium
Ester hydrolysis (non specific esterases, biologic elimination) Hofmann elimination (pH and temp dependent, chemical elimination)
Metabolism of cisatracurium
Hofmann elimination
Properties of neuromuscular relaxants
100% ionized at physiologic pH
-Don’t cross BBB
-Don’t cross placental barrier
-Trapped in renal tubule after filtration
Very highly protein bound
All can be excreted by kidney if other route unavailable
