Abuse.Anesthetics Flashcards
physiological dependence
neuroadaptations-abnml behavior and physical sxs if withdrawn
psychological dependence
dysphoria and intense craving following withdrawal
withdrawal
adverse reactions caused by discontinuation of drug
tolerance
more drug is required to produce effect
pharmacokinetic tolerance
increased metabolism
pharmacodynamic tolerance
receptor downregulation
learned tolerance
adaptation to the degree of intoxication
conditioned tolerance
adaption to setting/environment
acute tolerance
may occur when a drug is used repeatedly over a short period of time
cross tolerance
one drug produces tolerance to another
sensitization
increase of responsiveness after repeated use
does sensitization cause dose-response curve L or R?
left
addiction definition
drug taken to alleviate craving/dysphoria
person is physiological dependendt, are they addicted?
not necessarily
properties of abused drugs
euphoria
easy to use
potency, purity
rapid onset/short action
reward pathway
VTA–>NAc–>prefrontal cortex
pharmacotherpaies for nicotine addiction
nicotine replacement therapy
buproprion
varenicline
all w/ behavioral tx
uses of amphetamines
narcolepsy
ADHD
amphetamine NT effect
increase release of DA–reverses DA transport throught DAT
peripheral effects of amphetamines
increased BP
cardiotoxicity
methamphetamine
may produce psychosis
rapid psychological and physical dependence
withdrawal
most life-threatening withdrawal
alcohol
mechanism of cocaine
inhibits DA reuptake
medical use of cocaine
local anesthetic
vasoconstrictor
cocaine dependence
physical and psychological
peripheral effects of cocaine
tachycardia vasoconstriction HTN bronchodilation hyperpyrexia
effects of chronic cocaine use
reduction in overall brain activity
nasal issues
cocaine bugs
cocaine overdose
vtach/fib
stroke
seizures
tx for cocaine addiction
bromocriptine-decrease craving
nicotine MOA
activates nicotinic receptors in CNS and periphery, increasing serotonin, DA
nicotine dependence
psych and phsical
pharmokinetics of nicotine
induces CYP450s
MDMA MOA
increases 5HT activity by blocking reuptake and stiulating 5HT receptors
SE of MDMA
hyperthermia
dehydration
kidney failure
short term effects of MDMA
during: elevated mood (increased 5HT)
after: depression-like, irritability (decreased 5HT)
marijuana dependence
psychological possible
no physical
marijuana MOA
stimulates presynaptic CB1 receptors to inhibit transmitter (ACh) release
SE of maijuana
amotivational syndrome cannabinoid hyperemesis (cyclic vomiting syndrome)
synthetic “cannabinoid” agonists
bath salts
LSD MOA
acts on 5-HT receptors in the brain
what is synesthesia associated with?
LSD
peripheral effects of LSD
increased BP/HR
flushing
dilated pupils
angel duust
PCP
PCP MOa
NMDA receptor antagonist
ketamine MOA
NMDA receptor antagonist
GHB MOA
GABA receptor weak agonist
analgesia aaccompanied aggression
PCP and ketamine
effects of PCP
psychosis–treat with haldol
used as date rape drugs
ketamine
GHB
general dissociative anesthetics
PCP
ketamine
GHB
inhalants MOA
unknown
peripheral neuropathy
nitrous oxide
amyl and butyl nitrite
SMM relaxants
dilated pupils
LSD
non-reactive pupils
PCP
ketamine
GHB
infiltration anesthesia
injection directly into tissue without consideration of cutaneous nerves
drugs used for infustion anesthesia
procaine
lidocaine
bupivicane
advantages and disadvantages of infusion anesthesia
a: anesthesia w/o sirupting normal function
d: large amounts necessary
field block
subq injection that anesthetizes distal to injection
nerve block
injection around individual nerves or nerve plexuses
drugs used for spinal anesthesia
lidocaine
bupivicaine
tetracaine
physiological properties of esters
shorter duration of action
increased degree of systemic toxicity
what form must the anesthetic be in to cross the membrane?
non-ionized
ionized to bind to receptor
what kind of base or acid are anesthetics?
weak base
EXCEPT benzocaine
how is benzocaine used?
topical only
what things can decrease the effect of a local anesthetic?
inflammation (infection)
acidification
why might you add bicarbonate to an anesthetic?
increase level of non-ionized LA=increased membrane transport=shortened onset of action
MOA of local anesthetics
block Na channels and inhibit neuronal firing and the propagation action potentials
what state are Na channels when local anesthetics bind?
activated or inactivated
not resting
how do increases in calcium or potassium affect local anesthetics?
calcium: decreased effect
potassium: enhanced effect
what determines potency of local anesthetics?
lipid solubility
what determines the duration of action of local anesthetics?
lipid solubility
degree of protein binding
site of location
short acting local anesthetics
procaine
intermediate acting local anesthetics
lidocaine
mepivicaine
long acting local anesthetics
bupivicaine
ropivicaine
tetracaine
what are toxic effects of local anesthetics dependent on?
half life
how do vasoconstrictors affect local anesthetics?
reduce diffusion
what are esters metabolized by?
butyrycholinesterase in plasma
what are amides metabolized by?
liver CYPs
local anesthetics: myelinated vs unmyelinated nerves
m: affected before unm.
larger and more myelinated=less sensitive
conduction velocity
the greater the velocity of the action potential the faster the onset and the less sensitive the nerve
firing frequency
increased firing rate the more sensitive the nerve
sensory or motor fibers more sensitive?
sensory
main SE of local anesthetics
CNS PNS CV hypersensitivty localized toxicity
amides or esters more likely to cause allergic rxn?
esters
CV SE of local anesthetics
arrhythmias
vasodilation–hypoTN
prilocaine uniqu
methemoglobinemia
highest rate of clearance
how can you reverse toxicity of lipid-soluble drugs?
administraiton of lipids
worst drug for CV SE
bupivicaine
procaine drug interactions
metabolic product PABA inhibits culfonamides
how do we measure potency of local anesthetics?
compared to procaine
procaine general
short acting
infiltration, diagnostic
tetracaine general
long but slow duration
ophtho, spinal
benzocaine general
topical–pruritus
lidocaine general
intermediate
infiltration, epidural
risk with lidocaine
TNS–no spinal anesthesia
ropivicaine general
long acting
enantiomer of bupivicaine
peripheral, epidural
ropivicaine vs bupivicaine
ropivicaine: less CV toxicity
less lipid soluble
prilocaine general
intermediate
dentistry
prilocaine CI
CVD
respiratory dz
etidocaine general
long duration
affects motor nerves
articaine general
amide-type but has ester group
dental
SE of articaine
persistent paresthesias
dibucaine general
used to test for butyrycholinesterase deficiency
who has low butyrycholinesterase levels?
elderly
pregnant
children
parturition
baclofen MOA
GABAa agonist–hyperpolarize neurons–inhibit excitatory NTs
baclofen use
chronic spasticity
route of baclofen
oral
intrathecal pump
SE of baclofen
drowsy
mm weakness
increase seizures in epilepsy
diazepam use for muscle relaxant
local muscle trauma
adjunct in chronic
*sedation
tizanidine MOA
clonidine analogue
alpha2 agonist
tizanidine use
chronic due to SC injury
acute mm spasms
SE of tizanidine
hypotension
sedatopm
mm weakness, falls-elderly
cyclobenazaprine MOA
sedative at level of brainstem w/ cholinergic activity
cyclobenazaprine use
temporary- trauma/sprain
SE of cyclobenazaprine
confusion
transient visual hallucinations
carisoprodol MOA
metabolized to meprobamate
sedating
carisoprodol issues
short-term tx for anxiety–abuse potential
SE of carisoprodol
chronic=induction of hepatic microsomal enzymes
dantrolene MOA
direct action on the muscle- interferes with release of Ca2+
dantrolene use
malignant hyperthermia (general anesthetics) neuroleptic malignant syndrome (antipsychotics)
botulinum toxin MOA
blocks release of ACh