Anesthesia Flashcards
- What are the 2 general classes of local anesthetics?
- How to remember the names?
- all end in?
-
Amides
- Lidocaine
- Mepivacaine
- Bupivacaine
- All have 2 i’s in their name
-
Esters
- Procaine
- Cocaine
- Tetracaine
- Benzocaine
end in -caine
All local anesthetics are?
- weak bases!
- like to accept H+ molecule
- unprotonated form
- MOA of local anesthetics?
All are weak bases; like to accept H+
- Unprotonated (uncharged) form crosses cell membrane
- binds to a H+ molecule
- is stuck inside cell
- work inside cell membrane
- Protonated form of drug will bind to interior of Na+ channel and block Na+ from entering neuron
- needed for depolarization
- harder for neuron to send pain signals
What kind of environment makes it harder for local anesthetic drugs to work?
-
Acidic environment
- high H+ levels (i.e. infected tissue)
- Will drive local base to be protonated
- can’t cross cell membrane
- Need more drug to get an effect
Why would you add epinephrine with local anesthesia (i.e. Litacaine)?
-
Causes vasoconstriction
- less bleeding
- less washout of drug = more local effect
- Local anesthetics exhibit a property called differential blockade.
- What does this mean?
- Certain types of nerve fibers are blocked more effectively than others
- small fibers> large
-
myelinated> unmyelinated
- block Nodes of Ranvier because have Na+ channel
What is the order of blockade of local anesthesia?
- Small, myelinated
- Small, unmyelinated
- Large, myelinated
- Large, unmyelinated
- Because there is different effects of local anesthesia on nerve fibers there is different effects on different senses too.
- Order of block of senses?
Pain blocked first, pressure last
- Pain
- Temperature
- Touch
- Pressure
What are two general situations in which local anesthetics are used?
- Minor surgical procedure
- Epidural/ spinal anesthesia
- needle inserted in spinal canal (e.g. C- section)
- Local Anesthetic side effects: common or uncommon?
- Side effects on:
- CNS?
- Cardiovascular?
- which drug is an exception?
- Which LA is most cardiotoxic?
Uncommon, because local
CNS Stimulation:
- Initial (exicitation): talking alot, anxiety, confusion
- Later: drowsiness, coma
Cardiovascular: (block Na+ in heart)
- Hypotension, arrhytmia, bradycardia, heart block
-
cocaine is exception: hypertension, vasoconstriction
- blocks norepinephrine at nerve terminals
-
cocaine is exception: hypertension, vasoconstriction
- Bupivacaine is most cardiotoxic
Side effect of Local Anesthesia: Methemoglobinemia
- MOA?
- Treatment?
- High levels turn blood what color?
- Iron is normally bound to Hb in reduced Fe 2+
- some local anesthesia drugs can oxidize iron to Fe3+
-
Methemoglobin= Hb bound to Fe 3+
- Fe 3+ can’t bind O2
- Also modifies remaining Fe2+ iron so can’t release O2 to tissues
- Creates functional anemia
- Turn blood “chocolate brown”
Treatment:
- Methylene blue
- converts Fe3+ back to Fe 2+
Before opiod receptors are activated on the presynaptic membrane what is the status of:
- Ca2+ channels
- K+ channels
Before opioid receptors are activated on presynaptic membrane
- Ca2+ channels are open
- K+ channels are closed
What type of receptors are opiod receptors?
Transmembrane, G protein coupled
- mu
- kappa
- delta
What happens to Ca2+ and K+ channels when agonist (e.g. morphine) binds to opiod receptor on presynaptic neuron and activates it?
- Ca2+ channels close
- prevent entering of calcium
- K+ channels open
- allow exit of K+ from intracellular to extracellular
When agonist bind to presynaptic opiod receptor and causes Ca2+ channel to close and K+ channel to open, what effect does this have on:
- polarization of presynaptic membrane?
- subsequent release of NT?
- effect on neurotransmitter release;
- lead to membrane hyperpolarization—>
- presynaptic neuronal inhibition—>
-
less release of NT
- (Glutamine, Ach NE, 5-HT, Substance P)
