Illicit and Recreational Drugs Flashcards
Uses of amphetamines?
several analogues are used for tx of ADD, obesity and narcolepsy in humans, also illegal amphetamine products
Name several amphetamine drugs.
benzphetamine CIII, dextroamphetamine CII, methylphenidate CII and lisdexamfetamine
Source of amphetamine toxicosis?
accidental ingestion
Street names for amphetamine?
amphetamine–>speed, dex, dexies, bennies
methamphetamine–>ice, glass, meth, crystal
Oral LD50 for amphetamine is _____mg/kg and for methamphetamine is _____ mg/kg in the dog.
20-27 mg/kg–9-11 mg/kg
ADME of amphetamine?
A=readily orally, highly lipid soluble
D=widely including CNS
M=in liver, some metabolites are active
E=in urine–pH dependent
Half life of amphetamine in dogs?
3.7-6 hrs
Half life is dependent on what?
pH of the urine
MOA of amphetamine toxicosis?
CNS stimulant, block reuptake of norepinephrine and dopamine, inhibit MAO, dopamine excitatory receptor agonist, peripherally–sympathomimetic effect by releasing norepinephrine and direct stimulant effect on alpha-adrenergic receptors and beta-adrenergic receptors
T/F Mechanism of action of amphetamines in the CNS is unknown.
TRUE!
Clinical signs of amphetamine toxicosis?
hyperactivity, restlessness, circling, tremors, ataxia, seizures, mydriasis, hypersalivation, hyperthermia–some show depression, weakness and bradycardia
Laboratory diagnosis of amphetamine toxicosis?
hypoglycemia, amphetamines can be detected in blood, urine and saliva, tremors result in metabolic acidosis and rhadomyolysis–may cause myoglobinuria and renal failure (rare)
Prognosis of amphetamine toxicosis?
depends on severity of condition
Treatment of amphetamine toxicosis?
emesis, activated charcoal, pentobarbital and propofol for seizures, phenothiazine derivatives IV as dopamine excitatory receptor antagonists, treat hyperthermia, tachyarrhythmias treated with beta-blockers or lidocaine, urinary acidifiers, IV fluids
What urinary acidifiers can be used in the treatment of amphetamine toxicosis?
ammonium chloride, ascorbic acid–contraindicated in acidotic patient
Use of IV fluids in treatment of amphetamine toxicosis?
dehydration, correct systemic acidosis, enhance renal excretion, prevent renal damage due to myoglobinuria
Uses of cocaine?
topical local anesthetic for the oral, laryngeal and nasal cavities, used to confirm the cause of miotic pupil in conditions such as horners syndrome, illicit drug
Sources of cocaine toxicosis?
accidental ingestion of illicit cocaine
Source of cocaine?
alkaloid from the leaves of the plant Erythroxylon coca or E. monogynum–grown in mexico, south america, indonesia and west indies
Properties of cocaine?
cocaine hydrochloride is a powder form which dissolves in water and is taken IV or intranasally–the free base is the pure cocaine alkaloid obtained from the hydrochloride form in the shape of crystals, flakes or rock which makes a cracking sound when heated and can be smoked or taken orally
Street names for cocaine?
coke, bernies, girl, white lady, snow, star dust
What animals are most susceptible to cocaine toxicosis?
dogs esp police dogs!
What is the LD50 for pure cocaine IV in the dog? cat?
dog=3 mg/kg
cat=7.5 mg/kg
What is the oral LD50 for cocaine in the dog?
6-12 mg/kg
ADME for cocaine?
A=absorbed by all MM–highly lipid soluble
D=crosses BBB and alveolar capillary
M=hydrolyzed by plasma and hepatic esterase and is methylated in liver
E=unchanged (10-20%) and metabolites in urine
MOA of cocaine?
CNS stimulant and sympathomimetic, blocks reuptake of norepinephrine, dopamine and serotonin, increases catecholamine release, sensitizes sympathetic effector cells to catecholamines, direct effect on myocardium
Clinical signs of cocaine toxicosis?
V+, hypersalivation, mydriasis, hyperactivity, tremors, convulsive seizures, hyperthermia, tachycardia, tachypnea
Lesions seen in cocaine toxicosis?
myocardial degeneration, subendocardial and epicardial hemorrhage, pericardial effusion, pulmonary hemorrhage
Laboratory diagnosis of cocaine toxicosis?
elevated CK, systemic acidosis, detected in serum, plasma, urine, stomach contents
Differential diagnosis for cocaine toxicosis?
CNS stimulants–> amphetamines, strychnine, metaldehyde, methylxanthines, pseudoephedrine, organophosphate and carbamate insecticides, chlorinated hydrocarbon insecticides, permethrin in cats
Treatment for cocaine toxicosis?
emesis in animals not showing clinical signs, gastric lavage w/ activated charcoal, diazepam IV for seizures–also barbiturates or phenothiazines, beta blockers to control tachyarrhythmias, sodium bicarb IV or LRS for metabolic acidosis, IV fluids, body temp should be monitored
Prognosis of cocaine toxicosis?
depends on severity of condition
Why is it important to not induce vomiting in an animal showing clinical signs due to cocaine toxicosis?
may precipitate seizures
Uses of marijuana?
treatment of nausea associated w/ anticancer chemotherapy in patients who fail to respond to conventional antiemetics, treatment of anorexia associated w/ weight loss in AIDS patients, glaucoma and MS, recreational drug
Sources of marijuana toxicosis?
ingestion of loose marijuana, cannibis plant, cookies, brownies or cigarettes containing marijuana–inhalation–secondhand smoke
Street names for marijuana?
weed, grass, pot, puff, hemp, MaryJane, MJ
Name of marijuana plant?
Cannabis sativa–contains THC (tetrahydrocannibinol) and CBD (cannabidiol).
Amount of THC is determined by?
amount of THC in a sample decreases w/ time–hashish refers to dried resin from flower tops and contains 10% THC–hashish oil contains up to 20% THC–sinsemilla is seedless marjiuana which contains about 5% THC
What animals are most frequently poisoned by marijuana?
dogs–cats are also susceptible
Oral MLD dose for THC in the dog is greater than ___kg/mg.
3 mg/kg–1000 times the behaviorally effective dose in dogs!
ADME of marijuana toxicosis?
A=readily orally (increased by fatty meal) and by inhalation–THC highly lipid soluble
D=binds to plasma proteins, widely including CNS and fatty tissue
M=to several metabolites including an active metabolite which is more potent than THC and cross the BBB
E=mainly in bile and feces–enterohepatic recirculation and also in urine (10-15%)
What percentage of THC is bound to plasma proteins?
97-99%
T/F Half life is prolonged to 25-30 hrs due to redistribution from the adipose tissue.
TRUE
T/F Elimination is complete within 2 days.
FALSE 5 days!
MOA of marijuana?
2 cannabinoid receptors have been identified–CB1 widely distributed in the brain and has the cannabinoid effects on memory, perception and the control of movement. both CB1 and CB2 are found in the immune cells.
Clinical signs of marijuana toxicosis?
V+, CNS depression, ataxia, incoordination, tremor, weakness, mydriasis and hypothermia, rare seizures, hyperexcitability, brady/tachycardia, hyperthermia, apprehension
Chemical analysis of marijuana toxicosis?
detected in urine for several days following acute exposure–stomach contents and other specimens can be used for analysis
Diagnosis of marijuana toxicosis?
mainly hx and clinical signs, chem analysis, human urine tests are not effective in dogs
Differential diagnosis for marijuana toxicosis?
CNS depressants–>opioids, LSD, PCP, tranquilizers, ethylene glycol, propylene glycol, alcohols, macrolide antiparasitics, muscle relaxants and hallucinogenic mushrooms (Psilocybin mushrooms)
Treatment for marijuana toxicosis?
emesis, repeated doses of activated charcoal and a cathartic, symptomatic/supportive tx–>fluids, O2, diazepam for CNS stimulation, monitor temp
T/F Signs of marijuana toxicosis usually resolve spontaneously without treatment.
TRUE
Why is induction of emesis usually not effective in animals with marijuana toxicosis?
bc of antiemetic effect of THC
Recovery from marijuana toxicosis can take how long?
24 hrs to several days
Prognosis for marijuana toxicosis?
Cannabinoids have a wide safety margin so unlikely to be fatal
