Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
88 Cards in this Set
- Front
- Back
|
LA definition
|
agents capable of producing a tranient loss of sensation in a regionalized area of the body WIHTOUT producing a loss of consciousness
|
|
|
cocaine plant scientific name
|
erythroxylin coca
|
|
|
person who observed cocaine subcuntanoeously caused insensitivity
|
von anrep 1880
|
|
|
who laid the foundation for clinical intro of cocaine for regoinal anesthesia?
|
Halstead 1884
|
|
|
what does a high octanol/buffer distrib coefficient mean? which LAs have high OB distrib
|
a higher octanol/buffer distirb coefff means it's more lipophilic, e.g. bupivacaine, etidocaine, and tetracaine
|
|
|
TF Procaine has a high lipophilicity.
|
FALSE
|
|
|
TF lidocaine is more lipophilic than bupivacaine
|
FALSE
|
|
|
TF lidocaine is more lipophilic than articaine
|
TRUE
|
|
|
TF A drug with a high octanol/buffer coefficient is more likely to have a toxic effect on the heart.
|
True - hearts have lots of ion channels, so a drug that can easily be incorporated into the cell membrane can cause toxicity, arrythmia.
|
|
|
only LA with low potency and short duration.
|
procaine
|
|
|
Describe the rate of onset and duration of the three highly lipophilic LAs - ropivacaine, bupivaciane, tetracaine
|
moderate rate of onset with a LONG duration [get stuck in membranes and dont do work till later, but then they work forever cuz they dont wanna leave cell!]
|
|
|
theories regarding LA mechanism
|
1. Membrane expansion theory; 2. Receptor mechanism; physical occlusion of Na+ channel (blockade); allosteric-mediated channel change; electric field distortion
|
|
|
what theory states that LA lipophilicity allows incorp. into membrane, prventing opening of pores and passage of electrolytes? is this accurate?
|
membrane expansion theory (this is wrong, the receptor mechanism is the actually true one)
|
|
|
Which theory regarding LA mode of action is correct?
|
Receptor mecanism - blockade of Na+ conductance; Base from anesthetic interacts with membrane, changes sodium flux
|
|
|
TF Postassium channels determine LA efficacy.
|
false - sodium channels actually iniitate the AP, so thats what LAs block
|
|
|
TF LAs alter the resting membrane potential to prevent action potential propagation.
|
False, just inhibit the depolarization
|
|
|
main rationale for vasoconstrictor in LA
|
loss of autonomic function via LA causes VASODILATION, so you have higher systemic absorption and toxicity and lower duration/effectiveness.
|
|
|
Name the 2 topical LA agents
|
benzocaine, lidocaine
|
|
|
Which type of nerve fibers are most susceptible to LA?
|
A-delta and C fibers [and B, dorsal root fibers too]
|
|
|
LAs cause loss of local autonomic influence, followed by a blockade of 4 sensations (in order)...
|
1. temp; 2. pain; 3. touch; 4. press; 5. motor function [TP,TP,M]
|
|
|
4 factors contributing to differential nerve block choice.
|
1. critical fiber length; 2. use-dependent block; 3. peripheral nerve organization; 4. LA selectivity
|
|
|
How does diameter of nerve fiber affect signal conduction and LA efficacy?
|
the smaller it is, the faster it conducts the signal and the more sensitive it is
|
|
|
What type of fibers are C fibers?
|
Postganglionic sympathetic fibers: vasomotor, visceromotor, sudomotor, pilomotor
|
|
|
Write out the equation for LA dissoc. Seriously.
|
Base + H+ <--> BH+
|
|
|
Which form of LA can traverse the membrane? What happens to this form once it's inside the cell?
|
Base; base becomes the BH+ version inside cell
|
|
|
TF Sympathomimetic agents (epi-like agents) are topically effective in delaying absorption of the LA.
|
false - topically ineffective
|
|
|
Factors of pharmacokinetics
|
absorption, distribution, metabolism, excretion
|
|
|
In terms of distribution, what happens to the LA once it has entered circulation?
|
1. bind plasma proteins (alpha acidic glycoproteins); 2. After distrib throughout intravascular space, it enters various tissues (incl CNS, fetus)
|
|
|
The FDA has classified many LAs as category B and C for pregnant women. Why?
|
True, because drugs readily cross placenta and cause fetal cardiac depression
|
|
|
What enzyme metabolizes ester LAs?
|
cholinesterase
|
|
|
What body system is used to metabolize amide LAs?
|
hepatic microsomal mixed funciton oxidase system; hepatic amidase (N-dealkylation of 3rd AA terminus to a secondary amine, then more dealkylation;
|
|
|
Liver disease pt have a harder time metabolizing esters or amides?
|
amides
|
|
|
Which LA has a shorter half life, Lidocaine or Articaine? Why?
|
Articaine t1/2 is only half an hour, because of metabolism of ester side chain
|
|
|
TF articaine has high toxicity risk.
|
false - rapidly hydroylezed (4% with 1:100,000 is reduced risk)
|
|
|
Metabolism of which LA can form methemoglobinemia?
|
prilocaine (and articaine, benzocaine)
|
|
|
Monoethylglycinexylidide and glycinexylidide are toxic, active metabolites of which LA?
|
lidocaine
|
|
|
We can get paresthesia from which LAs?
|
articaine and prilocaine (BOTH 4% SOLNS)
|
|
|
Which LA has a thiophene ring strucutre?
|
articaine
|
|
|
TF Renal clearance of the metabolized LA is directly related to its protein binding capacity
|
false - inversely related
|
|
|
TF The better the LA metabolite is at binding proteins, the faster it will be excreted.
|
False - the better the binding, the slower the excretion [dont want proteinuria!]
|
|
|
TF Renal clearance of the metabolized LA is inversely proportional to the pH of urine.
|
TRUE
|
|
|
TF The more acidic the piss, the faster it will be excreted.
|
TRUE
|
|
|
TF Due the BBB, it is difficult for LAs to enter the reach the brain.
|
FALSE - LAs readily pass from peripheral circulation to brain, so you gotta watch out for depressed CNS function
|
|
|
3 subtoxic effects of LA (not incl. anesth)
|
drowsiness, analgesia, anticonvulsion
|
|
|
at what microg/mL level does lidocaine start to have CNS effects
|
> 5 microg/mL
|
|
|
TF Lidocaine will continuously cause CNS depression.
|
False - initial CNS excitation, but then you get a delayed depression resposne
|
|
|
What 2 types of pt should you watch out use of VC in?
|
cardiac pt, hyperthyroid pt
|
|
|
TF Talkativeness is a SnS of a toxic reaction to LA
|
TRUE
|
|
|
TF Euphoria, Excitement, and Deprssion are all SnS of a toxic reaction to LA
|
TRUE
|
|
|
Allergic reactions occur more often to ester LA or amide LA?
|
esters
|
|
|
What is metabisulfite and why is it significant?
|
preservative that stabilizes VCs hat some pt are allergic to (dermatitis, asthma, anaphylactic)
|
|
|
TF Fainting is a common response to pharmacologic effects of LA
|
false - usually pt fear
|
|
|
TF LAs can cause malignant hyperthermia
|
nah, never seen it before
|
|
|
Clark's rule is based on...
|
child pt body weight [MAX Child Dose = (lbs*adult dose)/150]
|
|
|
Young's rule is based on...
|
child pt age [MAX Child Dose = (age*adult dose)/(age +12)]
|
|
|
What type of child complicates dosage?
|
obese children - can't follow weight formula, cuz then you'd be trt like an adult
|
|
|
Dosage problem calculation: 2 carpules of xylocaine (2% lidocaine, 1:100,000 epi. also 2 carpules of 2% mepivocaine with no epi. [1 carp = 1.7 mL]
|
20*1.7=34mg/carp * 2 carp = 68mg lido. Vaso = .01mg*1.7*2 carps= .034mg. ...68mg + 102 mepi = 170mg; .034mg (if pt has severe HT, you're approaching max. rec dose at .04!)
|
|
|
vasoconstrictor ratios
|
now for epi, 1:100,000 = 0.01 mg/mL; 1:200,000 = 0.005 mg/mL; 1:50,000 = 0.02 mg/mL
|
|
|
lido carpule conversions
|
2% means 20 mg/mL. So you have 20mg lido * 2 carps.
|
|
|
TF kiddos you gotta watch out for LA dose. In adults, you gotta watch out for epi dose
|
TRUE
|
|
|
What is the maximum dose for 2% lidocaine with epi 1:100,000? [xylocaine with epi]
|
7 mg/kg; 500 mg
|
|
|
What is the maximum dose for 2% lidocaine with no epi?
|
3 mg/kg; 300 mg
|
|
|
MRD 4% prilocaine
|
6 mg/kg
|
|
|
MRD 4% prilocaine with 1:200,000 epi
|
8 mg/kg
|
|
|
Which LA is more potent and potentially more toxic than lidocaine - bupivacaine or prilocaine?
|
bupivacaine - avoid in children, mental pt
|
|
|
TF in combo with other CNS agents, LAs can cause permanent neuro deficits and even death
|
TRUE
|
|
|
VC agent can potentially elevate BP in pt who use...
|
tricyclic antidepressants
|
|
|
TF There may be an interaction b/w exogenously administered epinepherine and MAOIs
|
FALSE - no interaction
|
|
|
TF Phentolamine mesylate (OraVerse) is sufficient for reversal of CNS anesthesia
|
false - only good to reverse soft tissue anesthesia
|
|
|
What type of agent is phentolamaine mesylate and what's it used for
|
alpha-adrenergic blocker; reverseal for soft tissue LA effect
|
|
|
where do we find alpha adrenergic receptors
|
blood vessels
|
|
|
where do we find beta1 adrenergic receptors
|
heart
|
|
|
where do we find beta2 adrenergic receptors
|
blood vessels, bronchiole
|
|
|
Epi effect on alpha
|
vasoconstriction, inc. BP
|
|
|
Epi effect on beta1
|
inc. HR, inc. contractility force
|
|
|
Epi effect on beta2
|
VASODILATION, bronchodilation
|
|
|
propranolol + epi causes
|
hypertension (blocks beta2,1)
|
|
|
prazosin + epi causes
|
hypotension (epi reversal)
|
|
|
Benzocaine topical up to what % is safe?
|
20%
|
|
|
Lidocaine topical SPRAY up to what % is safe?
|
10%
|
|
|
Lidocaine topical OINTMENT/SOLN up to what % is safe?
|
5%
|
|
|
What is an emla
|
eutetic mixture of LA
|
|
|
Typical emla formulatoin
|
2.5% lido + 2.5% prilocaine
|
|
|
Use for emla
|
skin
|
|
|
Use for oraqix
|
intraorla LA for perio scaling and root planing
|
|
|
TF EMLA and Oraqix are made up of the same LAs
|
true - lido and prilo
|
|
|
Which one is liquidy - EMLA or Oraqix
|
oraqix
|
|
|
Which one reduces pain by 50% - EMLA or Oraqix
|
oraqix
|
