Drugs of Abuse Flashcards
DEA Schedule I
High Potential for Abuse
No acceptable use as a therapeutic in the US
Examples: LSD, Heroin, Marijuana
DEA Schedule II
High Potential for Abuse
Abuse may lead to sever psychological (addiction) or physical dependence
These drugs have accepted medical uses in the US
Examples: morphine, codeine, amphetamine, cocaine, barbituates
DEA Schedule III
Potential for abuse less than drugs in Schedules I and II
Abuse may lead to moderate or low physical dependence or high psychological dependence
Examples: codeine+acetaminophen, anabolic steroids
DEA Schedule IV
Low potential for abuse compared to the drugs in Schedule III
Abuse may lead to limited physical or psychological dependence relative to the drugs in Schedule III
Examples: benzodiazepines, tramadol
DEA Schedule V
Low potential for abuse relative to the drugs in Schedule IV
Examples: OTC cough medicines w/codeine
Cellular Tolerance
Adaptive response of cells to drug exposure
Major Mechanism: Occurs within seconds, hours, or days
Changes in receptors or cell signaling proteins
Receptors can be removed from the cell surface or trafficked to the cell surface
Synthesis of new receptors can be inhibited
Metabolic Tolerance
Enhanced elimination rate of drug
Minor mechanism
Induction of drug metabolizing enzymes
Biological Theory of Addiction
Stimulation of the brain’s reward system
Main Component of the Reward System
Mesocorticolimbic pathway: dopaminergic neurons from midbrain (ventral tegmental area) to the forebrain (nucleus accumbens and prefrontal cortex)
Physiological Dependence
Appearance of withdrawal symptoms when drug intake is stopped
Occurs with repeated/chronic use of the drug
Impaired Control Over Substance Use Criteria
- Individual uses a substance in larger amounts or for longer period of time than intended
- Wants to cut down or quit but not able to
- Spends a lot of time obtaining and using a substance
- Craving: intense desire or urge to obtain the substance
Social Impairment Criteria
- Failure to fulfill obligations at work, school, or home due to substance use
- Continues substance use despite negative social or interpersonal consequences
- Important social, occupational, or recreational activities are given up or reduced due to substance abuse
Risk Use Criteria
- Recurrent substance use in situations that are physically hazardous
- Continues substance use despite known negative physical/psychological effects
Pharmacological Criteria
- Appearance of tolerance: use requires markedly increased doses of substance to achieve the desired effect
- Appearance of withdrawal symptoms: Individual is likely to consume the substance to relieve the symptoms
Opioids: Drug Effect
Activation of mu opioid receptors in medullary respiratory center, spinal and supraspinal sites mediating analgesia, enteric nerves
Opioids: Acute Effects
Histamine release resulting in vasodilation, bronchoconstriction, hypotension
Potentially life-threatening respiratory depression
Opioids: Tolerance/Withdrawal
Uncomfortable but not life-threatening symptoms: hyperalgesia, diarrhea, dilated pupils, hypertension, sweating, dysphoria, craving
Opioids: Mechanism of Reward Pathway Activation
Activation of mu opioid receptors in reward pathway
CNS Depressants: Drug Effects
Ethanol: enhances GABA binding to GABA-A receptors, inhibits glutamate binding to NMDA receptor
Benzodiazepines: enhance GABA binding to GABA-A receptor
Barbituates: enhance GABA binding and directly activate GABA-A receptor
CNS Depressants: Mechanism of Reward Pathway
Ethanol: inhibits glutamate binding to NMDA receptor, facilitates release of endogenous opioids in VTA
CNS Depressants: Acute Effects/Toxicity
Potentially life-threatening respiratory depression with ethanol and barbiturates
CNS Depressants: Tolerance/Withdrawal
Sympathetically driven tremors, tachycardia, hypertension, sweating
Stimulants: Drug Effect
Amphetamine and methamphetamine enhance synaptic release of DA
Cocaine blocks reuptake of DA
Stimulants: Acute Effects
Acute Effects: arousal, alertness, euphoria, increased HR and BP
Chronic Use can lead to hallucinations, violent behavior, psychosis
Stimulants: Tolerance/Withdrawal
Reverse tolerance can be seen in some patients
Withdrawal may be mild: dysphoria, sleepiness, bradycardia, craving and depression
Nicotine: Drug Effects
Activation of central and peripheral acetylcholine receptors in reward pathway
Nicotine: Acute Effects/Toxicity
Stimulant effects: increased arousal, concentration
Depressant effects: decreased anxiety
Nicotine: Tolerance/Withdrawal
Irritability, anxiety, dysphoria, difficulty concentrating, restlessness, increased appetite/weight gain
Cannabinoids: Drug Effect
Activation of cannabinoid receptors in brain and spinal cord
Cannabinoids: Acute Effects/Toxicity
Relaxation, increased appetite, psychedelic-like effects, sympathomimetic effects
Cannabinoids: Tolerance Withdrawal
Tolerance to acute effects develops quickly
Withdrawal: restlessness, irritability, depression, insomnia
Psychedelics: Drug Effect
Related to serotonin: agonists at 5HT, DA and adrenergic receptors
Related to dopamine and amphetamines: induce 5HT and DA release; agonist 5HT, DA, and adrenergic receptors
Psychedelics: Acute Effects/Toxicity
Altered perception, hallucinations (mostly visual), altered mood
Psychedelics: Tolerance/Withdrawal
Minimal tolerance
Withdrawal: craving, confusion, anxiety, depression
Dissociatives: Drug Effects
Inhibits NMDA receptors
Dissociatives: Acute Effects/Toxicities
Analgesia, anesthesia, feelings of detachment, increased HR and BP
Toxicities: hallucinations, delusions, psychosis, violent behavior
High doses: seizures, coma, death
Disulfram: Clinical App and Mechanism
Alcohol aversion therapy
Inhibits ALDH, leading to accumulation of acetaldehyde upon consumption
Disulfram: Adverse Reactions
Hepatotoxic
Can lead to respiratory depression, cardiovascular collapse, convulsions
Acamprosate, Topiramate: Clinical App and Mechanism
Alcohol addiction
known to increase the activity of GABA-A receptors and inhibit glutamatergic NMDA receptor activity
Naloxone: Clinical App and Mechanism
Used in opioid overdose
Inhibits mu opioid receptors in VTA of brain; SHORT ACTING
Naloxone: Side Effects
Cardiac arrhythmias, hepatotoxic, pulmonary edema, opioid withdrawal
Naltrexone: Clinical App
Anti-craving therapy for alcohol addiction
Limited success in treating opioid dependency
Naltrexone: Mechanism of Action
Inhibits mu opioid receptors in VTA; LONG ACTING
Methadone: Clinical App
Used for detoxification and maintenance of opioid addiction
Methadone: Mechanism of Action
Agonist at mu opioid receptor; suppresses symptoms of craving and withdrawal
Methadone: Adverse Effects
Cardiac arrest due to long QT syndrome, respiratory arrest, constipation, nausea
LAAM: Clinical App
Maintenance therapy and detox for opioid addiction
LAAM: Mechanism of Action
Same as methadone but longer lasting so delivered 2-3/week
LAAM: Adverse Effects
Same as methadone
Buprenorphine: Clinical App
Maintenance and detox for opioid addiction
Buprenorphine: Mechanism of Action
Partial agonist at mu opioid receptor and antagonist at kappa opioid receptor; LONG ACTING
Buprenorphine: Adverse Effects
Respiratory depression, hypotension, dizziness, sedation, bradyarrythmias, tachyarrhytmias
Nicotine Replacement Therapy (NRT): Clinical App
Smoking cessation aid; multiple forms available
NRT: Mechanism of Action
Slower absorption and longer nicotine plasma levels, less rewarding and alleviating cravings
Bupropion: Clinical App
Smoking cessation aid
Buproprion: Mechanism of Action
Non-competitive antagonist of nicotinic acetylcholine receptors in reward pathway
Buproprion: Adverse Effects
Suicidal thoughts, erratic behavior, exacerbation of underlying psych illness
Varenicline: Clinical App
Smoking cessation aid, reduces cravings, prevents withdrawal
Varenicline: Mechanism of Action
Partial agonist at nicotinic acetylcholine receptors in VTA and nucleus accumbens
Varenicline: Adverse Effects
Suicidal thoughts, erratic/aggressive behavior, exacerbation of underlying psych illness
