drug abuse: presentation and treatment Flashcards
cause constricted pupils
opoids, nicotine (usually), sympatholytic agents
cause dilated pupils
sympathomimetic agents, amphetamine and derivatives, cocaine, LSD
cause horizontal nystagmus
barbiturates, ethanol, carbamazepine, phenytoin, scorpion venom
causes horizontal and vertical nystagmus
PCP
alcohol effects
CV and respiratory depression, relaxation of smooth muscle (vasodilation, hypothermia, increased gastric flow); relaxes uterine smooth muscle
insomnia, tremor, anxiety; seizures, N/V, arrhythmia
alcohol withdrawal
cause disulfiram like effects
sulfonylureas, cefotetan, ketoconazole, procarbazine
alcohol interactions
increase tox of acetaminophen, increased risk of bleeding with NSAIDs and anticoagulants; increased risk of hypoglycemia with diabetic medicine; increased risk of teratogenicity via changes in metabolism
heroine effects
IV: after injection - rush; euphoria, dry mouth warm sensation
later: “on the nod” - drowsy state
acute opiate intoxication
shallow and slow respirations, pupillary mitosis, bradycardia, hypothermia, stupor or coma - death from CV or respiratory collapse
seizures with mixed intoxication
methodone unique effect
QT prolongation
goal of naloxone administration
reverse respiratory depression
marijuana intoxication
2 cardinal signs: increased HR, reddened eyes
cognitive dysfunction, changes in perception, and reaction time impairment;
panic and paranoia uncommon except in psychotic patients
marijuana mechanism
binds presynaptic CB1 receptors and prevents the release of GABA or glutamate; this leads to disinhibition of DA neurons in the VTA and to the feeling of euphoria
cause rhabdomyolysis
amphetamines and derivatives, clozapine, lithium, cocaine, MAOIs, PCP
rhabdomyolysis treatment
hydration to avoid renal failure, alkalinize urine with sodium bicarb to prevent myoglobin deposition in renal tubules
cocaine mechanism
inhibits the DAT, prevents reuptake of DA - decreasing DA clearance from the synaptic cleft and causing an increase in extracellular DA conc.
amphetamine mechanism
competitively inhibits VMAT causing the free concentration of DA in the presynaptic terminal to rise and the DAT reverses its pumping to expel the DA into the synaptic cleft
used to decrease cravings in alcoholics
naloxone
acts by increasing the non-vesicular release of DA from DA neurons
amphetamine
zero order kinetics
ethanol, phenytoin, high dose aspirin
heroin addiction detox
buprenorphine first then naltrexone
delirium tremens associated with
hyperadrenergic state - alcohol intoxication; also causes visual hallucinations
can be lethal when used with an opoid
alcohol