Pharm 1 - Local Anesthetics Q&As

hpaul2's version from 2017-04-06 23:02

Q & A

Question Answer
Who is Eutectic?EMLI
What can you treat bupivacaine toxicity w/?Lidocaine
Which is a pure S-Enantiomer?Ropivacaine (& levobupivacain)
Which is a racemic mix OR S-enantiomer?Bupivacaine
Most potent LA?Bupivacaine
Which drug for IVRA/cat endotracheal tube?Lidocaine
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
What are defining characteristics of a LA drug?Applied locally, block conduction of sensory impulses from periphery to CNS, w/o causing unconsciousness
How do LAs work?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) Uncharged base (B) pass through cell memb
(2) Uncharged base is protonated --> 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
(2) Intermediate linking chain: assists in placing the lipophilic end of the LA into the Na+ channel
(3) Hydrophilic end: attracts the LA to the axoplasmic 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: blocking the Na+ channel
(2) Intermediate linking chain: assists in placing the lipophilic end of the LA into the Na+ channel
(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 (forms PABA as metabolite)
What are factors that can influence amide linked LA drug metabolism?Liver disorders reducing liver function, other drugs increasing or decreasing liver enzyme function
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?Bases; salt forms used in formulation --> LOWERS pH (Epi lowers pH even more)
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?formulate w/ glucose to make use of osmosis & 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
Would a drug w/ a higher pKa be more likely to cross the nerve membrane compared to a drug w/ a lower pKa?No (the higher the pKa, the lower the membrane permeability)
Why do LA drugs have less of an effect in inflamed tissue?decreased pH (drugs ionized before crossing membrane)
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 of metabolism
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?Worsen (Na+ channels open more, during systole)
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?Cow conc, low dose, incorporate vasoconstrictor agent, avoid 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 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, low lipid solubility, poor penetration of mucous membranes, used w/ PENICILLIN G to SLOW penicillin's release; PABA is a metabolite, originally novocaine (Procaine, Penicillin G, PABA, Poor lipid solubility & muc.mem. Penetration )
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, poor penetration of skin when used alone, rapid onset (< 5 mins), duration: 20-40 mins, used as an anti-arrhythmia drug,
Uses: nerve blocks, IVRA, spinal anesthesia, cat endotracheal intubation
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, less potent/lower toxicity than bupivacaine
diphasic effect: *vasoconstrictor at conc below 0.5% *vasodilator at conc greater than 1%
Describe the benzocaine slide's details (solubility? how is it administered? What is it used for? )Very LOW solubility, used TOPICALLY & for FISH anesthesia
Describe the EMLI slide's details (What is it composed of? How is it administered? What is a unique property of it?)Mixture of lidocaine & prilocaine. 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

Recent badges