Pharm 1 - Local Anesthetics Q&As

isabellepjk's version from 2017-05-06 22:52

Q & A

Question Answer
Who is Eutectic?EMLI
What can you treat bupivacaine toxicity w/?Lidocaine
Which is a pure S-Enantiomer?Ropivacaine
Which is a racemic mix OR S-enantiomer?Bupivacaine
Most potent LA?Bupivacaine
Which drug for IVRA/cat endotracheal tube?Lidocaine (dogs "lupis" hate cats--so tube them, or tourniquet them like you have to in IVRA)
Which drug for intraplural & infiltration?Bupivacaine ( i-i dont like dysrhythmia)
What is the ion channel that local anesthetics affect?Na+ (2 kinds, Na (v1) & Na (x) )
What is light sensitive that is often used w/ LAs?Epinephrine
If I say Dysrhythmia, you think?Toxicity of BUPIVACAINE. (Your heart w/ go bupbupbupbupbupbupbup)
*What are defining characteristics of a LA drug?Applied locally,
block conduction of sensory impulses from periphery to CNS,
w/o causing unconsciousness they block sensation in a specified region of the body.
At higher doses can affect motor function
How do LAs work?Local anesthetics prevent voltage dependent increase in sodium conductance by blocking the initiation & propagation of APs
What are the 2 types of Na+ channels? What are their mode of actions?(1) Nav1 = transmembrane voltage gated Na+ channel
(2) Nax = passive channel, Na+ moves across membrane in response to conc. gradient
*What is meant by freq-dep block?A nerve cell that is being stimulated repetitively will have increased opportunity to be blocked
What are the steps in the combined membrane expansion theory & specific receptor theory?(1) Local anesthetic drugs in form of uncharged base (B) pass through cell memb
(2) Once inside the cell the uncharged base form of the drug is protonated, thus becoming a charged cation (BH+)
(3) Charged cation attaches to receptor & blocks the Na+ channel
Where do local anesthetic drugs have contact w/ myelinated nerves?Nodes of Ranvier
*What are the 3 structural parts for all LAs? What is each part doing?(1) Lipophilic end: responsible for blocking the Na+ channel (membrane is made of lipids, of course it wants to be here)
(2) Intermediate linking chain: assists in placing the lipophilic end of the LA into the Na+ channel (part which varies from amide-linked to amino-ester linked)
(3) Hydrophilic end: attracts the LA to the axoplasmic (cytoplasm in the axon) side of Na+ channel in the nerve memb
*The 3 structural parts of LA drugs have different roles in blocking Na+ channels, what are they?(1) Lipophilic end: responsible for blocking the Na+ channel
(2) Intermediate linking chain: assists in placing the lipophilic end of the LA into the Na+ channel (also variable region between amide linked & amino-ester linked)
(3) Hydrophilic end: attracts the LA to the axoplasmic side of Na+ channel in the nerve memb
*What are the 2 types of intermediate linking chains? How do they differ in their half-lives & metabolism?(1) Amino ester linked: short ½ lives, unstable, metabolism=cholinesterase break ester link
(2) Amine linked: longer ½ lives, metabolism=liver conjugation, stable & heat resistant link
*Which type of local anesthetic drugs have increased risk of toxicity?Amide linked (don't break down as fast as esters so can build up to toxic levels)
Which LA drugs have stereoisomer potential? What are they derived from? Stereoisomers of amide linked LA have distinct characteristics; derived from ppx (pipexolyl xylidide)
What factors can influence clinical char of LA drugs? (5)Potency of drug, duration of action, onset of action, which nerve or nerves are being blocked, pp binding of drug
Which type of LA drugs will not be metabolized in the CNS? Why? Amino ester b/c no cholinesterase
*Which LA drug has potential of causing an allergy?Procaine
What are factors that can influence amide linked LA drug metabolism?Liver disorders reducing liver function, other drugs increasing or decreasing liver enzyme function (AMIDE NEEDS LIVER TO METABOLIZE, the amino-ester linked have the cholinesterase enzymes which are ubiquitous)
List some different forms of applying LA drugs? (4)Parenteral (sterile injectable form), topical (gel/ointment), airway use (aerosol), transdermal (patch)
*Are local anesthetic drugs bases or acids? How does this change when LA drugs are formulated?LA are bases; but when formulating them, their salt forms are used. This LOWERS their pH (more acidic). (Epi lowers their pH even more, so they sting when they're injected)
If a patient was given an injection of a LA drug containing epinephrine would he or she feel it?Yes would feel it b/c sting when injected (epi lowers the pH of the LA more, which is stingy)
*What are 2 considerations when selecting a LA drug for spinal (epidural) anesthesia?Want to limit spread to have it remain local (Inc specific gravity...formulate w/ glucose to make use of osmosis) & can have NO preservatives (preservative-free to avoid neuronal damage)
What are benefits of using vasoconstricting agent w/ LA drugs? Prolong duration of action, limit systemic diffusion
*Why would an α-2 sympathomimetic drug be used in conjunction w/ a LA?Depth & duration of LA can increase (synergism) via α-2 sympathomimetic
opioids: morphine/buprenorphine
xyazine, dexmed in humans
Would a drug w/ a higher pKa be more likely to cross the nerve membrane compared to a drug w/ a lower pKa?Lower pKa more likely to cross (the higher the pKa, the lower the membrane permeability)
*Why do LA drugs have less of an effect in inflamed tissue?The pH of the tissue drops (more acidic) which would ionize the drugs before they could diffuse into the membrane/nerve to block the Na channel.
*In which 2 body systems are LA drugs toxicity seen?CNS & CVS (cardiovas sys)
*T/F - toxicity 1st occurs in CNS then CVSTrue - CNS toxicity seen (first) at lower plasma conc than CVS toxicity
*What is 1st CNS sign of LA drug toxicity? Why does this occur?Muscle twitching & tremors around the head & face followed by convulsions, because the preferential blocking of inhibitory pathways
What signs do LA drug toxicity progress to? Severe CNS depression, possibly resulting in rep depression & death
The degree of LA drugs toxicity depends on the conc of ______ that has entered the CNSFree drug
*list 4 factors that limit LA drugs entry into CNS:(1) BBB (blood brain barrier)
(2) Lipid solubility of drug
(3) Conc of free drug in circ (pp binding) (4) rate at which local anesthetic is metabolized
*Drugs w/ which char would influence the decision to use LA drug? (Other drugs which would affect the LAs functionality should be watched if they have these 3 characteristics) (3)Drugs changing seizure threshold, competing w/ pp binding sites, inducing/inhibit microsomal enzyme function
*What are 2 cardiovas signs of LA drug toxicity?Hypotension, dysrhythmia
What actions of LA drugs may be responsible for hypotension?Depression of myocardial contractility, relaxation of sm mm surrounding blood vessels, loss of vasomotor sympathetic tone
*Do all LA drugs cause dysrhythmia?No, only 1 (bupivacaine)
Does bupivacaine toxicity worsen/improve as HR increased?Toxicity = DYSRHYTHMA. It is worsened; increased HR increases bupivacaine's toxicity (If you Inc HR, the Na+ channels are open more, b/c they're open during systole, which inc the toxicity)
*What may be admin to potentially Tx bupivacaine toxicity? (Not another LA)"Intralipid' for lipid emulsion
Toxicity to LA drugs occurs when drug plasma conc are _________Elevated
What steps can be followed in order to prevent elevated drug plasma conc?Low conc of drugs, use drugs that incorporate a vasoconstricting agent in order to localize drug action, minimize possibility of drugs going systemic-avoid injection into vascular areas ( low conc, low dose, incorporate vasoconstrictor agent to localize drug, avoid injection into vascular areas)
*Which form of LA drugs can be autoclaved? What is an exception to this (if they contain what)?Autoclaved= Amide linked (tougher than the esters). The exception if they contain epi, then you can't autoclave them.
Why is epinephrine dispensed in amber colored bottles? It is light sensitive
*How do LA drugs given in cri (constant rate infusion) influence the amt of inhalant anesthetic drugs req by patient?Reduces the amt of req inhalant
*Describe the PROCAINE slide's details (lipid solubility? describe its interaction w/ mucous membranes, what can you combine it w/, & why? what is the most important thing to know about this drug, as a potential side effect? what was its original trade name?)1st synthetic LA, amino-ester linked, low lipid solubility, poor penetration of mucous membranes, used in conjunction w/ PENICILLIN G to SLOW penicillin's release into systemic circ; PABA is a metabolite(has allergy potential can cause urticaria (hives) in animals), originally sold as novocaine (Procaine, Penicillin G, PABA, Poor lipid solubility & muc.mem. Penetration ) (making me sick w/ PABA isnt very professional)
*Describe the lidocaine slide's details (how common? How do you apply? How fast does it work/last? How toxic? What else can it be used as? USES as an LA?)Most commonly used LA drug, \rapid onset of action, less than 5 mins, duration of action 20-40 mins, less toxicity potential than bupivacaine, also used as an anti-arrhythmia drug, uses as a LA: nerve blocks, IVRA(Intravenous regional anesthesia), spinal anesthesia, cat endotracheal intubation (dogs=lupo like to see cats get tubes in their throat)
*Describe the mepivacaine slide's detailsUsed in equine limb blocks, parent drug of bupivacaine (butyl substituted w/ methyl) (the horse & me share parents)
*Describe the bupivacaine slide's details (potency? what are the diff formulations? Toxicity? Onset? Duration? Doesnt affect where? Uses? (4) )Most potent long acting anesthetic drug, sold in 2 forms: racemic 50:50, S/Enantiomer form (LEVOBUPIVACAINE): LEVOBUPIVACINE is LESS toxic than the racemic form: onset of action: 20-30 mins; duration of action 5-8 hrs, has NO topical effect, application include= infiltration, NERVE BLOCK, intra-pleural, & spinal anesthesia
*Describe the ropivacaine slide's details (duration? unique about its structure? toxicity? What is its unique property? )Long acting LA, a pure S [-] enantiomer, slightly less potent than bupivacaine, lower toxicity than bupivacaine, vascular effect of ropivacaine: diphasic effect: *vasoconstrictor at conc below 0.5% w/v *vasodilator at conc greater than 1% w/v (weight/volume) (when you climb the long S-shaped rope, you change sides)
*Describe the benzocaine slide's details (solubility? how is it administered? What is it used for? )Very LOW solubility, used TOPICALLY & for FISH anesthesia (Ben the fish)
*Describe the EMLI slide's details (What is it composed of? How is it administered? What is a unique property of it?)Eutectic mixture of LAs. Mixture of lidocaine & prilocaine. (Emily loves prying lids off & touching skin) Used topically. eutectic mixture: a mix where the mp (melting point) of mixture is lower than melting point of indiv components (melts faster)
Describe the cocaine slide's detailsOriginal local anesthetic
Controlled drug
No vet therapeutic use