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Flashcards in Drug abuse Deck (53):


withdrawal syndrome- signs/symptoms which occur when a drug is no longer available, drugs of abuse, nonpsychoactive drugs



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



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)