pharm Flashcards
how is remifentanyl metabolized
ester hydrolysis
how is a bolus dose of thiopental terminated
redistribution from brain to periphery
this is the same for propofol, fentanyl, methohexital
doxyrubicin
does it have a dose dependnt effect on cardiotoxicity?
what are the EKG changes seen with acute toxicity
what are the other systems that it can effect?
- yes dose dependent effect during and mnths after therapy
- ST segment changes
- hepatic, renal, GI, plum, myelotoxicity can also occur
what local anesthetics can cause methemeglobinemia?
prilocaine and benzocaine
treated by methlylene blue
think i take PRIde when i roll up to the MET in my BENZ
which anticholinergic agents are best paired wth AcHesterase inhbiitors of neostigmine, pyridostigmine, edrophonium, when revering neuromuscular blockade
edrophonium –> atropine
neostigmine/pyridostigmine –> glyco
what procedure is methohexital usually used for and whalso what class of drugs is it
its a short acting barbituate
used for ECT, can trigger seizures
think you are HEXED with methohexital aka seizure activity
what is the preferred method to reverse INR
when patient needs surgery or if theres hella bleeding
prothrombin complex concentrate +vitamine K
relative contracindiations to ketamine use
ischemic heart disease (as sole agent)
vascular anuersym (as sole agent)
increased ICP / brain mass w spontaneous ventilation
open eye opthalmic injury (increased IOP)
schizophrenia
mostly bc ketamine will cause tachycardia and htn
what 2 benzos will not undergo phase 1 meabolism
lorazepam + oxazepam
phase 1 = dealkalation or alphatic hydoxylation
phase 2 = glucuronidatio + actylation
what drugs are metabolized by psuedocholinesterase in the plasma
succinylcholine
mivacurium
2 chloroprocaine
what drugs are metabolized by nonspecific ester in intestine and muscles
remifentanil
atracurium
what drug is metabolized by hoffman degrdation in the plasma
atracurium
cisatracurium
zero order vs first order kinetics
zero order is that the same amount of of drug is removed per a period of time, linear relationship
first order is dose dependent and removes a percentage of drug per unit time, this is dependent on liver blood flow
what drugs do NOT undergo anny lung metabolism
dopamine
isoproterenal
epinephrine
think if the lung touches these drugs u DIE
how to volatile anesthetics affect CBF and CMRO2
CMRO2 decreases CBF increases (vasodiation)
NO DOES NOT HAVE this uncoupling effect
from greatest to least wahts the vapor pressure of volatile anesthetics
desflurane > iso > sevo
DIS
whats the mechanism of milrinone
pde III inhibitor which decreases hydrolysis (breakdown) of cAMP
this drug will increse contractility, decrease afterload
how does introducing ccb to a patient that hasnt had it before affect paralytic agents
mild augmentation of both depolarizing and nondepolarizing agents
time of onset of oral vs IV famotadine
oral takes 1 hour
IV takes 30 min
what drugs will decrease the changes of K hole symptoms when using ketamine
benzos (versed) think u forget about the nightmates
barbituates
propofol
fluride ion production from greatest to least of the volatile gases
methoxyflurane > sevo > enflurane > isoflurane > desflurane
recurrence of hypoapnea can happen when narcan is given after what two opioids
morphine
dilaudid
think the longer acting ones because narcan only has a 30 min ish duration
narcan = nolaxone
testing for HIT
antiplatlet factor 4 has high sensitivity
serotonin release assay has high specficity
what are the hemodynamic effects of high doses of meperidine and why
hypotension bc histamine
tachycardia bc atropine like effect
If patient has hypercalcemia how should u change ur nondepolarization muscular blocking agent dose
increase dose of paralytic bc ca can antagonize it
how do paralytics affect MG patients
they are resistent to succ
and very sensitive to non depolarizating agents
chlorprocaine’s rapid onset of action is due to what property?
its high concentration
what is the mechanism of action of IV regional anesthesia
blockade of nerves with LA thorugh vasciualr beds reading peripheral nerves and nerve trunks
how does lithium affect depolarizing and non depolarizing muscle blockers
it prolongs the effects of depolarizing and non depolarizing muscle paralytics
what patients should you not use succ in
any pathology that causes an increase in ach receptors, denervating disorders etc.
you CAN use succ in MG and lambort eaton bc this will not cuase life threatening hyper k since there are less receptors available bc of the antibodies