drugs of abuse Flashcards
Opioids examples
heroin, oxycodone and hydrocodone
CNS depressants examples
barbiturates, benzodiazepines, alcohol
CNS stimulants examples
methamphetamines, cocaine,
hallucinogens examples
Indoleamines (LSD, DMT, mushrooms), Phenylethylamines (MDMA, mescaline)
dissociative anesthetics examples
Phencyclidine (PCP), ketamine, dextromethorphan
Pharmacologic property of drugs of abuse
enhance dopamine activity in the nucleus accumbens
levels of drug abuse
experimental (one-few trials), circumstantial-recreational (occasional use under certain circumstances), and compulsive (reliance)
pathway of addiction
Amygdala learns drug and cues cause pleasure–may signal relief from craving > Drug cues lead to DA release in Nucleus accumbens > triggers output to thalamus and cortex > In absence of activity from reflective reward system (prefrontal cortex) drug-seeking initiated
Opioids MOA
Agonists at μ-opioid receptors [Gi]
CNS depressants MOA
Enhance GABA - inhibit glutamate
CNS stimulants MOA
Block DA reuptake or enhance DA release
nicotine MOA
Agonist at nicotinic neuronal receptors
hallucinogens MOA
Partial agonist at 5HT2 receptors
dissociative anesthetics MOA
Antagonist at NMDA-Glu receptors
cannabinoids MOA
Agonist at cannabinoid (CB1-CB2) receptors
Opioids reinforcing effects
Opioids: Euphoria, sedation, anxiolytic
CNS depressants reinforcing effects
CNS Depressants: Euphoria, sedation, loss of inhibition
CNS stimulants reinforcing effects
CNS Stimulants: Euphoria, decreased fatigue, increased arousal
nicotine reinforcing effects
Nicotine: Increased alertness
hallucinogens reinforcing effects
Hallucinogens: Altered sensory perception, enhanced insight
dissociative anesthetics reinforcing effects
Dissociative Anesthetics: Euphoria, heightened emotionality
cannabinoids reinforcing effects
Cannabinoids: Euphoria, “mellowness”, changes in perception
Opioids acute toxicity and treatment
Respiratory depression-pinpoint pupils-coma. Treatment: naloxone
CNS depressants acute toxicity and treatment
Respiratory depression, coma (extremely rare with BDZs). Treatment- Ethanol: supportive plus fluids-electrolytes-thiamine. Benzodiazepines: flumazenil. Barbiturates: supportive
CNS stimulants acute toxicity and treatment
SNS overactivity, increased HR-BP-temp, chest pain-MI, psychosis. Treatment: CVS support, vasodilators for BP (phentolamine), BDZs (diazepam) for agitation-seizures, haloperidol for psychotic symptoms
nicotine acute toxicity and treatment
rare – ingestion of insecticide or cigarettes by children. Nausea-vomiting, diarrhea, CVP collapse, convulsions. Treatment: CVS support, emetics-gastric lavage-charcoal
hallucinogens acute toxicity and treatment
LSD-Psilocybin: “Bad trip”, severe anxiety. Treatment: “talking down”, BDZs for agitation. MDMA: Agitation, hyperthermia, ADH release causing hyponatremia
dissociative anesthetics acute toxicity and treatment
PCP and ketamine. Delirium, RR-HR-BP-temp, agitation, violent behavior. Treatment: supportive for BP-hyperthermia, agitation (BDZs)
cannabinoids acute toxicity and treatment
Minimal - possible anxiety, impaired coordination-tracking, acute psychosis
What is pharmacodynamic tolerance
Lessened response at active target site to the same drug concentration. Due to changes in receptor sensitivity or other adaptive changes
What is metabolic (dispositional) tolerance
Change in pharmacokinetics results in lowered drug Cp at active site, due to increased metabolism
What is cross tolerance and give examples
•Tolerance develops to one drug – then will be seen to other drugs of the same class - same target. Ie. Heroin and hydrocodone both work at mu opioid receptors, and can develop cross tolerance. Ethanol and benzos work at GABA receptors and can develop cross tolerance
What is learned tolerance
Reduction in effects of a drug due to learned compensatory mechanisms. Behavioral tolerance and conditioned tolerance
What is reverse tolerance
Sensitization (increased response) to drug following repeated doses. Sensitization in nucleus accumbens may play a role in drug craving properties
Opioids tolerance
Develops rapidly (up to 100-fold); not to constipation
CNS depressants tolerance
Rapid to barbiturates > ethanol, benzodiazepines. Significant to sedation-intoxication, less to lethal dose
CNS stimulants tolerance
: develops to euphoria-anorexia-hyperthermia, but can see supersensitivity to paranoia
nicotine tolerance
Develops to subjective effects and nausea
hallucinogens tolerance
Not common, since repeated use minimal
cannabinoids tolerance
Rapid to most effects, also disappears rapidly
Compare physical and psychological dependence
physical: stop use abruptly leads to withdrawal symptoms due to resetting of homeostatic mechanisms. Psychological: perceived need (craving), related to pathologic learning in reward pathway
What is cross dependence and give examples
- Ability of one drug to suppress the withdrawal associated with physical dependence on another drug. Related to pharmacological effects at target – not chemical similarities. Ie. Morphine and other opioids. Alcohol, barbiturates and other sedative hypnotics
- Ability of one drug to suppress the withdrawal associated with physical dependence on another drug. Related to pharmacological effects at target – not chemical similarities. Ie. Morphine and other opioids. Alcohol, barbiturates and other sedative hypnotics
opioids dependence
develops rapidly (within 1-2 weeks)
CNS Depressants dependence
Appears within weeks
CNS stimulants dependence
arguable- strong psychologic dependence
nicotine dependence
moderate development
hallucinogens dependence
does not develop
dissociative anesthetics dependence
probably none
cannabinoids dependence
accumulating evidence
What are the characteristics of withdrawal symptoms
•Effects generally opposite of the acute effects of the drug. Ie If a drug relieves fatigue and causes mood elevation, withdrawal is characterized by lethargy and depression
Opioids withdrawal symptoms and treatment
Rarely life-threatening - insomnia, diarrhea, irritability, cramps, muscle aches, increased BP. Treatment: clonidine (for SNS overactivity), methadone (works via cross tolerance), buprenorphine (partial mu agonist), or naltrexone (blocks reinforcing actions of heroin)
CNS depressants withdrawal symptoms and treatment
Significant risk of mortality due to seizures (monitor). Treatment: substitution with BDZs - loading dose - then taper to prevent seizures
CNS stimulants withdrawal symptoms and treatment
sleepiness, fatigue, depression, hyperphagie, craving.. Treatment: behavioral
nicotine withdrawal symptoms and treatment
Irritability, hostility, anxiety, increased appetite, weight gain. Treatment of relapse: nicotine replacement, bupropion, varenicline (partial nicotine receptor agonist)
hallucinogens withdrawal symptoms and treatment
Not known, “flashbacks” in some former users [HPPD - hallucinogen persisting perception disorder]
dissociative anesthetics withdrawal symptoms and treatment
None observed
cannabinoids withdrawal symptoms and treatment
not clinically significant, no treatment needed
