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167 Cards in this Set

  • Front
  • Back
what is the primary concentration gradient in a neuron?
3 Na out for 2 K in
what does the concentration gradient favor in neuron?
*extracellular diffusion of K
*intracellular diffusion of Na
what is the cell membrane more permeable to?
*relative excess of - ions accumulate intracellularly
what accounts for the - resting membrane potential
*excess accumuluation intracellularly
what is the resting membrane potential for neurons?
what is active transport?
Na/K/ATPase pump
what is passive diffusion?
concentration gradient
what types of channels do LAs have an affinity for?
active and inactive Na channels
what passes through the neuronal sheath more easily?
lipid soluble drugs
what are nerve fiber actions dependent on?
*axonal diameter
*degree of myelination
describe the cascade of the motor, sensory & ANS system in regards to LAs in spinal anesthesia?
ANS > sensory > motor
the initial response to LAs
ANS is 2 dermatomes higher
motor block @ T10
sensory block @ T8
ANS block @ T6
what are the relative measures of potency in LAs?
*type of neuron
*diameter of neuron
*sensitivity of neuron
what are the types of nerve fibers?
*A alpha
*A beta
*A gamma
*A delta
describe the A alpha nerve fibers?
*1 sensitivity
*proprioception/large motor
describe the A beta fibers?
*5-12 microns
*1 sensitivity
*sm motor/touch/pressure
describe the A gamma fibers?
*3-6 microns
*1 sensitivity
*muscle tone
describe the A delta fibers?
*2-5 microns
*slower conduction
*0.5 sensitivity
*temp/sharp pain
describe the B fibers?
*some myelination
*3 microns
*0.25 sensitivity
describe the C fibers?
*0.3-1.2 microns
*0.5 sensitivity
*dull pain/temp/touch
*blocked quickly
where are the C fibers located?
sympathetic > highly conductive
*dorsal horn > pain/temp/touch
what are the properties of LAs?
*affinity for Na channels
*action is voltage & time dependent
*may block Ca/K channels
*may block NMDA receptors
what is important about blocking Ca channels when using LA?
*can decrease myocardial contractility
*can decrease NT release from presynaptic terminals
What is the sequence of LA?
*sympathetic block
*loss of pain/temp(cold)/touch
*loss of touch and pressure
*motor paralysis
*loss of proprioception
what are the CV implications w/LAs?
*all are generally myocardial depressants
*rarely impact CV d/t small amt given
*don't usually get systemic effects
what are the properties of LAs?
*onset is r/t pKa
*potency is r/t lipid solubility
*DOA is r/t protein binding & lipid solubility
what two factors of LAs are determined by lipid solubility?
*duration of action
what happens w/decreased lipid solubility?
inc onset of action
what happens w/alkalinization and LAs?
*add bicarb 1cc 8.4%/10cc Lido
*speeds onset
*improves quality of block
*prolongs block (r/t inc amt of free base)
*dec pain durin SQ infil
what happens w/increased protein binding?
*inc elimination
what happens w/molecular size and LAs?
bigger the molecule, the longer it stays around
what is the pKa range of LAs?
8.0 - 9.0
*weak bases
if an LA pKa is closer to physiologic pH, what happens?
*higher concentration of nonionized base
what happens w/a larger nonionized base of LAs?
passes through nerve cell membranes
*faster onset of action
what is pKa?
the pH @ which 50% ionized and 50% nonionized
what is the physiologic norm of pH?
what happens w/a nonionized drug?
passes BBB/placenta
*has greater effect
what are weak acids of LAs?
Na + drug
Ca + drug
Mg + drug
what are weak bases of LAs?
Cl + drug
Sulfate + drug
what is more effective @ the receptor site?
cation form
where is the primary site of action of LAs?
intracellular side of Na channels
what is the predominant form for an active LA?
charged form
what does the uncharged form of an LA do?
important for rapid penetration of cell membranes
what happens to a LA in an acidic environment?
ECF cation is decreased
what is an acidic environment for an LA?
an infected site
what is the structure of lipophilic LA?
*benzene or aromatic ring
*physiochem properties r/t substitutions here
what is the structure of ester/amide linkage LA?
intermediate hydrocarbon chain
what is the structure of hydrophilic LA?
tertiary amine
what kind of charge is a/w a tertiary amine?
what are some lidocaine properties?
*gold standard (for comparison)
*neural blockade
*antiarrythmic (1 -1.5mg/kg)
*blocks SNS effect of intubation (inc HR/BP)
*blocks bronchospasms
what are important lido properties to consider during intubation?
*dec CBF
*attenuates inc ICP
*block SNS effects (inc HR/BP)
*dec hypoxic drive
what are lido properties in r/t coagulation?
*dec coag
*prevention of thrombosis
*dec plt aggreg
*enhance fibrinolysis
what are lido properties in r/t hepatic?
*dec clearance r/t dec blood flow
*cimetidine & propanolol dec hepatic blood flow
*any hepatic insult > dec hep BF --> dec clearance
how are LAs prepared commercially?
*H2O soluble
*pH 6-7
what happens when you add epi to a LA?
*prolongs block
what are the two classifications of LAs?
how do you know an LA is an amide?
I before aine in the name
(ie lidocaine, ropivacaine, etc)
What type of classification is lido?
Does lido vasoconstrict/dilate?
what is the OA/DOA of lido?
rapid onset
short-moderate DOA
what is the max dose of lido?
3-5 mg/kg
what is the max dose of lido w/epi?
what is the toxic dose of lido?
how long does epi prolong the effect of lido?
what are the uses of lidocaine?
*nerve block
how is lidocaine met?
rapidly by the liver
what can lidocaine be used for besides LA?
ventricular irritability
what is the pKa of lido?
what classification is bupivicaine?
what is the OA/DOA of bupi?
slow onset (15-20 min)
long DOA (1-2 hrs)
what is the max dose of bupi?
what is the max dose of bupi w/epi?
2.5 mg/kg
what is bupi used for?
*nerve block
describe the protein binding of bupi?
highly protein bound
what is the elimination time of bupi?
*210 min
*r/t protein binding
describe the potency of bupi?
what are the CV effects of bupi?
*very cardiotoxic
*protein affinity binds it to protein receptors in ion channels in heart
*pt resistant to resuscitative efforts
what is the contraindication for its use?
bier blocks (IV regional)
can bupi cause allergic rxn?
what is the pKa of bupi?
what is the classification of ropivicaine?
describe the protein binding of ropi?
highly protein bound
compare the systemic toxicity of ropi to bupi?
less toxic
what is the elimination half time?
108 min
what is the max dose of ropi?
in a 70kg pt it is 200mg
what are uses of ropi?
*useful in labor r/t good separation of sensory/motor
*nerve block
what is ropi an analogue of?
*less systemically toxic than bupi r/t dec protein binding
what is levo bupi?
*an amide stereoisomer of bupi
*similar to bupi
*less cardiotoxic
what is the classification of mepivacaine?
what is the pKa of mepi?
*close to physiologic pH, so large % is nonionized
why is mepi rarely used in OB?
*crosses placenta
*effects fetus
*fetal hep enzymes not developed, so unable to metabolize
what is the onset of mepi?
what are the uses of mepi?
*nerve blocks
what is the max dose of mepi?
*7mg/kg to a max of 400mg
what is the pKa of mepi?
what is mepi used for mostly?
nerve blocks
what is the class of procaine?
what is the OA/DOA of procaine?
*slow onset
*short DOA
what is procaine used for?
*nerve block
why do ester LA particularly inc allergic rxn?
formation of PABA
what is the pKa of procaine?
what class if prilocaine?
what are the uses of prilocaine?
dental anesthesia
what is EMLA?
1:1 ratio of 5% lido and 5% prilocaine in oil/water emulsi
*eutectic mixture of LA
what is the depth of penetration of EMLA?
how long should EMLA stay on under an occlusive dressing?
1 hr for effective analgesia
what is the DOA of EMLA?
what is the max dose of prilocaine?
400-600 mg for 70kg pt
what are the uses of prilocaine?
*nerve block
*IV regional
what is the OA/DOA of prilocaine?
slow onset
*DOA 60-120 min
what is the pKa of prilocaine?
what is the caveat regarding prilocaine?
exception to the pKa onset rule
what is a caution in prilocaine?
what are the uses for EMLA?
*IV start
*split thickness skin graft (STSG)
*laser removal of port wine stains
*circumcision (EMLA contraindicated < 1yoa)
what is the max area for EMLA applicatin in:
<10kg 100cm2
2000 cm2
what are the SE of EMLA?
*skin blanching
what class is etidocaine?
what is the OA/DOA of etidocaine?
fast onset
long DOA (4-8 hrs)
what is the pKa of etidocaine?
what class if chloroprocaine?
what is the OA/DOA of chloroprocaine?
*rapid onset
*short DOA
*what are the uses of chloroprocaine?
*nerve block
what is a SE of interthecal chlorprocaine?
what is the toxic dose of chloroprocaine?
compared to other LA, rate the toxicity of chloroprocaine?
lease toxic
how is chloroprocaine metabolized?
ester hydrolysis
what is the pKa of chloroprocaine?
what is chloroprocaine's profile w/the onset rule
it is an exception to pKa-onset rule
what is the class of tetracaine?
what is the DOA of tetracaine?
intermediate to long acting
what are the uses of tetracaine?
*what is the max dose of tetracaine?
what is the pKa of tetracaine?
what is the sole determinant of tetracaine termination?
vascular absorption
what is the class of cocaine?
what is unique about cocaine?
only LA that is a vasoconstrictor
*used on topically on mucous membranes
what are the SE of cocaine?
*highly addictive
*cardiotoxic chronic/acute use
what is the pKa of cocaine?
what is the class of benzocaine?
what are the uses for benzocaine?
what is the byproduct of benzocaine metabolism?
what is the tx for methemoglobinemia r/t benzocaine use?
methylene blue 1-2mg/kg
how is benzocaine usually administered?
describe the rate of absorption of LAs from least to greatest?
IV > tracheal > Intercostal > caudal > paracervical > epidural > brachial plexus > sciatic/femoral > SQ
what determines the rate of absorption in LAs?
how are ester LAs metabolized? 2 types
*ester hydrolysis
describe the ester hydrolysis of LAs?
ester hydrolysis
*water soluble metabolites excreted in urn
what are the two types of pseudocholinesterases that metabolize LAs?
*plasma cholinesterase
what other drugs can be metabolized by pseudocholinesterases?
what is PABA?
*breakdown of ester LA
*responsible for allergic rxn
name a pt @ risk for toxic SE when using ester LAs?
pts w/pseudocholinesterase
r/t slower metabolism of drug
what is methemoglobinemia in LA?
a metabolite of prilocaine
*accumulates after large dose
*converts heme to metheme
how are amide LAs metabolized?
*hydroxylation by CYP 450
is ester or amide LA metabolism quicker?
*route of metabolism is agent specific
list the LAs w/ rate of metabolism?
Prilocaine > lido > mepi > ropi > bupi
describe what happens w/LAs and hepatic fxn?
any dec in hepatic fxn/flow will dec metabolic rate and inc risk of toxicity
what happens in LA toxicity?
*block Na channels
*affect AP throughout body
*ability for systemic toxicity
*toxicity proportionate to potency
what are the s/s of LA toxicity?
*circumoral numbness
*metallic taste
*tongue parasthesia
*blurred vision
*slurred speech
*change of LOC
*muscle twitching
*resp arrest
*CV collapse (r/t K/Ca channels)
what is the tx for LA toxicity?
BZD (inc szr threshold)
(dec CBF & drug exposure)
what terminates szr activity in LA toxicity?
pentothal 1-2mg/kg
epidural vs subarachnoid blocks?
*epidural is a volume block
*subarachnoid is a concentration block
which produce allergic rxns?
what is the MOA of LAs?
block nerve conduction pathways by blocking Na channels
how can you tell if the pt has a successful block?
nerve fibers are blocked in a specific sequence
what is the onset of action r/t in LAs?
what is the DOA r/t in LAs?
protein binding
what is the potency r/t in LAs?
lipid solubility