Drug abuse Flashcards
Dependence
withdrawal syndrome- signs/symptoms which occur when a drug is no longer available, drugs of abuse, nonpsychoactive drugs
Addiction
compulsive, relapsing drug use despite neagative consequences, triggered by cravings and contextual cues
3 stages of dependence
chronic exposure- adaptation, tolerance- need for increased dose, withdrawal- changes apparent when drug is terminated
Dopamine hypothesis of addiction
physiologic condition- mesolimbic DA- learning and adaptation; addiction- mesolimbic dopamine- pleasure and rewards center, stimulus and rewards, result- behavior becomes compulsive
Caffeine pharmacology
CNS-stimulant, cardiac, resp, and diuretic effect; therapeutic- asthma, narcolepsy, HA, resp depression in neonatal pop*, behavior effects- increased mental alertness
Caffeine dosing
effects seen with small oral dose- 100-200mg, 1-2 cups coffee, lethal dose- 10 grams/ 100 cups coffee
Caffeinism
clinical syndrome- central and peripheral sx, CNS: anxiety, insomnia, mood changes, peripheral: tachycardia, HTN, arrhythmias, GI disturbances; generally dose related
Caffeine tolerance and dependence
chronic use associated w/ habituation/ tolerance, may produce low-grade withdrawal sx, HA, drowsiness, fatigue, neg mood state, maximaized after 1-2 days and cease withing few days
Nicotine pharmacology
selective agonist of nicotinic AcH receptor causing rewarding effect, effects= early- nausea/vomiting, stimulates hypothalamus to release antidiuretic hormone, reduce nerve fivers in muscle, reduce appetitie, alters taste buds, increases psychomotor activity, memory
Effects of nicotine on periphery
inc heart rate, blood pressure, cardiac contractility, vasodilates nom-atherosclerotic coronary arteries
Nicotine tolerance and dependence
clearly induces both physiological and psychological dependence, w/drawal syndrome is not life threatening
Nicotine toxicity
nicotine- responsible for acute pharm effects and withdrawal signs; tar- responsible for disease associated long term tobacco use, life is shortened by 14 mins for every cigarette smoked
Nicotine cardiovascular disease
CO- dec o2 delivery to heart muscle, nicotine- inc myocardial O2 demand d/t cardiac stimulation, both inc the incidence of atherosclerotic and thrombosis in coronary arteries, atherosclerosis also occurs elsewhere- strokes
Nicotine Pulmonary disease
smokers syndrome- diff breathing, wheezing, chest pain, lung congestion, inc susceptibility to RTI, impairs ventilitation, reduces immune effects of lungs
Nicotine Cancer
major cause of lung ca, mouth, laryngeal, throat, bladder, pancreatic, uterine, cervical
Nicotine pregnancy
adversely effects developiing fetus, low birth weight, preterm delivery, cig smoke reduces O2 delivery to developing fetus, cessation early in preg appears to reverse these effects
Approaches to smoking cessation
Gum, inhaler, lozenge, nasal spray, transdermal, drugs
Bupropion (Zyban)
antidepressant may mimic nicotinic effects on DA and norepinephrine, start 1-2 weeks prior to target wuit date, Day 1-3 150mg orally once daily, Day 4- 150 mg orally BID, continue 7-12 weeks
ADRs of bupropion
tachycardia, HA, insomnia, dizziness, wt loss, nausea, pharyngitis
Varenicline (Chantix)
a4B2 nAcHR partial agonist works on DA neurons of the VTA preventing nicotine from exerting action, start 1 week prior to quit date, day 1-3: .5 mg orally twice every day, D 4-7: .5 mg orally BID, Day >8: 1 mg orally BID for 11 weeks
ADRs of varenicline (Chantix)
HA, insomnia, abnormal dreams, suicidal ideation, angina
Cocaine Pharmacology
Inhibits DA tranporter- dec DA clearance from the synaptic cleft and causes an inc in extracellular DA concentration
Cocaine effects of moderate-dose use
as duration inc, effects are intensified followed by depression, anxiety, somnolence, progressive loss of coordination followed by tremors and eventually seizures, local depletion of O2, vascular thrombosis, brain hemorrhage, cardiac complications
Cocaine effects of long term- high dose
toxic paranoid psychosis, produces toxic sx- anxiety, sleep deprivation, hypervigilance, suspiciousness/ paranoia, interpersonal conflicts, depression, dysphoria, and bizarre violent psychotic disorders
Comorbities and cocaine
typically effect young (12-39 yom), generally reckless, rebellious, low tolerance for frustration, may have coexisting anxiety, depression, paranoia, bipolar, antisocial personality, PTSD, ADHD
Treatment of dependence of cocaine
cog- behavior therapy- contingency management strategies are usefule in preventing relapse, no FDA approved pharm therapy, disulfiram, suboxone, ritalin, wellbutrin, modafil (Provigil), gabapentin
Amphetamines pharmacology
competitively inhibits DA transport causing inc in extracellular DA concentration, interferes w/ vesicular monamine transporter and impedes filling of synaptic vesicles (cytoplasmic release of DA)
CNS and peripheral effects of amphetamines
tremor, restlessness, increased motor activity, agitation, insomnia, and loss of appetite, vasoconstricion, HTN, tachy
Chronic high dose users of amphetamines
contiual, purposeless, repetitive acts, sudden outbursts of aggression and violence, paranoid delusions, psychosis and abnormal mental conditions and severe anorexia
Amphetamines in pregnancy
may exhibit growth retardation and lower birth wt, inc incidence of intracerebral hemorrhage, evidence of psychometric deficits, poor academic performance, behavioral probs, cog slowing, and general maladjustment
Dependence and tolerance of amphetamines
potent psychomotor stimulant and behavior-reinforcing agen prone to compulsive abuse, physical dependence follow positive cond model, withdrawal sx, paranoia, wt gain, inc appetitie, fatigue
Treatment of amphetamine
d/c drug, cautious clin observation, recognize depression, treat w/ antidepressants, antipsychotic drugs- risperidone, quetiapine may be necessary
Treatment of psychosis of amphetamine
primarily supportive, haloperidol, olanzapine, psychotic relapse following d/c were common over 30 months, hallucinations, delusions, depression, suicidal ideation
Ethyl alcohol Pharmacology
alters GABA, Kir/GIRK, adenosine reuptake, glycine rec, NMDA, and 5HT3; reversible depr of behavior, mental functioning and cognition, resp is stimulated at low dose but dec w/ inc dose, CNS depression, high dose= heart disease
Blood EtOH levels
.02 (g/dL)= dec inhibition, slight buzz; .08+ dec in complex cog function and motor performance; .2= obvious slurred speech, motor incoordination, irritability, poor judgement; .3= light coma and depressed vitals; .4=death
Tolerance and dependence of EtOH
tolerance w/ reg use, metabolic tolerance- liver inc amt of drug metabolizing enzyme; tissue- neurons in brain adapt to amt present; association, contingent or homeostatic tolerance- environment manipulation can counter effects of etoh, counter response are possible mech of tolerance
Withdrawal of EtOH
sweating, N/V, tremors, anxiety, agitation, paranoia, hallucinations, DT, seizures
Stage 1 of EtOH withdrawal
6-8 hrs- tremors, anxiety, HA, GI upset, sweating
Stage 2 of EtOH withdrawal
10-30 hrs- insomnia, hallucinations, autonomic hyperactivity
Stage 3 of EtOH withdrawal
first 3 days- grand mall seizures
Stage 4 of EtOH withdrawal
3-5 days- delirium tremors, agitation, hallucinations, tachy, HTN, fever, diaphoresis
Pregnancy and EtOH
physical and behavioral teratogen, causes alterations in brain structure or function, FAS- development disorder in offspring of mothers w/ high BAL during critical stages of fetal development
Effects of FAS
CNS dysfunction- low intelligence and microcephaly, mental retardation, behavioral abnormalities, dec growth rate, facial abnormalities, congenital heart defects and malformed eyes and ears
Treatment of EtOH withdrawal
Benzos- inc GABA activity and ameliorate the sx, can prevent seizures and DT, lorazepam, diazepam, and chlordiazepoxide, multivitamins, thiamine, folic acid and fluids (banana bag), anticonvulsants
Anticonvulsants for EtOH withdrawal
carbamazepine, valproic acid, gabapentin, pregabalin, oxcarbazepine, lamotrigine, topiramate
Drugs to prevent EtOH relapse
Disulfiram (Antabuse), Naltrexone (revia)- opioid antagonist, acamprosate (Campral)- GABA agonist/glutamate antagonist
Dose?ADRs of Disulfiram (Antabuse)
500 mg PO daily for 1-2 weeks, then 250 mg PO daily until recovered, cause drowsiness, HA fatigue, rash taste disturbance
Naltrexone (revia) dose and ADRs
50 mg PO, syncope, HA, insomnia, N/V?D dec appetitie
Acamprosate (Campral) dose and ADRs
666mg PO TID, diarrhea, ch pain, HTN, insomnia, anxiety
Cannabinoids Pharm
binds to cannabinoid rec and inhibit release of glutamate or GABA, THC is active substance and is powerfully psychoactive
Physiological affects of cannabinoids
analgesia, cog alterations, euphoria, dec body temp, calms aggression, blocks convulsants, inc HR, HTN, may contain more tars, bronchial irritation, inc lung CA
Tolerance and dependence of Cannabinoids
down reg and desensitizationof brain cannabinoid receptors, behavioral tolerance, mild and short lived withdrawal syndrome, restlessness, irritability, agitation, anger, insomnia, strange dreams, nausea, depression
Treatment of cannaminoid withdrawal
psychotherapeutic strategies- cog behavior therapy, contingency management, family counseling, motivational enhancement interventions, mertezepine (Remeron), dronabinol (Marinol), Bupropion, buspirone (Buspar), naltrexone (revia)
