Exam 3-Local Anesthetics Flashcards
Voltage gated Na Channels open in response to
inside of the cell becoming more positive via depolarization
Na channel pore is made of
one subunit protein (alpha)
alpha unit protein positive areas
sense the change in the voltage state of the cell and repulsive forces between inside of cell and pore cause channel to open
Closed state
no ion flow, cell resting state or negative membrane potential. after repolarization the cell ends here
Open state
due to the movement of the four positive charge areas in the pore. only open to Na ions!
Inactive state
structurally different than closed, found when cell is at higher depolarization. second gate (inactivation gate) closed.
AP begins with
Na or Ca entering cell to cause depolarization
Three features of APs
- threshold depolarization 2. all or none 3. ends with brief resting period, during which cell cannot be triggered for another AP
Refractory period
channels will not respond while in the inactive state. cannot move to closed states until the cell has repolarized
Endogenous ligands for VG channels
there are none. only exogenous and are usually toxins.
Local anesthetics are what type of ligand
antagonist, they do not change the pore
Local anesthetics bind where
to the inactivation conformation most tightly. slow the channels return to the closed state. prolongs refractory period
Local anesthetics and threshold
increase threshold requiring more stimulus to trigger AP. Think about spare receptors….when there are more receptors available, cell is less responsive to ligand.
Local anesthetics and AP speed
AP is slowed, fewer channels are available. ability of pumps to move Na out will pass ability of channels to let Na in, so AP slows to zero
Local anesthetics and amplitude of AP
fewer channels respond and let in Na, not enough to reach threshold
LA targets
more in nerves that are very active or have high firing rate
Cells with higher membrane potential
more likely to have inactive channels and therefore will be more receptors the ligand likes. more sensitive to LA
Nerve size
small nerves are more senstive
Nerve function lost in this order (onset order)
pain, temp, touch, motor
Nerve bundles
admin of LA at bundle, motor neurons will see higher concentration than sensory nerve effects on the inside
Toxicity
high concentration of LA will bind nAch receptor cause actions at the NM junx and autonomic ganglia ex: convulsions d/t blocking inhibitory NT
Cocaine
original. vasoconstriction. primary use limited to respiratory mucosa
Procaine (novacaine)
first synthetic local. low potency, slow onset, short-acting
Lidocaine (xylocaine)
rapid onset, stronger effect than procaine, intermediate DOA. used as antiarrythmic
Bupivicaine (marcaine)
long duration (slow dissociation), more effect on sensory than motor, popular for labor and post-op
Etidocaine (duranest)
fast onset like lidocaine, long DOA like bupivicaine and strong effect on motor neurons
Mepivacaine (carbocaine)
poor topically, more toxic in newborns d/t pka
Tetracaine (pontocaine)
longer duration, slower metabolism-higher toxicity risk, more for spinal
Injectable
lidocaine, bupivacaine, procaine, mepivacaine, tetracaine
Topical
dibucaine, dyclonine HCL, pramoxine HCP, benzocaine
Opthalmic
proparacaine, tertracaine
Infiltration
inject into local tissues at nerve ends (dental). larger area=larger dose. duration lengthened with epi. allows normal muscle function.
Field block
block nerves farther away from where you are injecting. inject SQ to block further up nerve chain. larger affected for larger dose
Nerve block
plexus. usually highly vascularized at center-so there is continuous removal of LA from the area. increased likelihood of systemic effects. goal to produce anesthesia. DO NOT INJECT INTO NERVE BUNDLE
Spinal
more dense drug will affect areas further down from administration site. problems due to sympathetic inhibition
A. Closed, nothing happening
B. Na Channels are open
C. Inactive
D. Closed. K channels are closing, K going out and cell becoming slightly more negative.
