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Flashcards in Drug abuse Deck (53):
1

Dependence

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

2

Addiction

compulsive, relapsing drug use despite neagative consequences, triggered by cravings and contextual cues

3

3 stages of dependence

chronic exposure- adaptation, tolerance- need for increased dose, withdrawal- changes apparent when drug is terminated

4

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

5

Caffeine pharmacology

CNS-stimulant, cardiac, resp, and diuretic effect; therapeutic- asthma, narcolepsy, HA, resp depression in neonatal pop*, behavior effects- increased mental alertness

6

Caffeine dosing

effects seen with small oral dose- 100-200mg, 1-2 cups coffee, lethal dose- 10 grams/ 100 cups coffee

7

Caffeinism

clinical syndrome- central and peripheral sx, CNS: anxiety, insomnia, mood changes, peripheral: tachycardia, HTN, arrhythmias, GI disturbances; generally dose related

8

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

9

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

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Effects of nicotine on periphery

inc heart rate, blood pressure, cardiac contractility, vasodilates nom-atherosclerotic coronary arteries

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Nicotine tolerance and dependence

clearly induces both physiological and psychological dependence, w/drawal syndrome is not life threatening

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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

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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

14

Nicotine Pulmonary disease

smokers syndrome- diff breathing, wheezing, chest pain, lung congestion, inc susceptibility to RTI, impairs ventilitation, reduces immune effects of lungs

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Nicotine Cancer

major cause of lung ca, mouth, laryngeal, throat, bladder, pancreatic, uterine, cervical

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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

17

Approaches to smoking cessation

Gum, inhaler, lozenge, nasal spray, transdermal, drugs

18

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

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ADRs of bupropion

tachycardia, HA, insomnia, dizziness, wt loss, nausea, pharyngitis

20

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

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ADRs of varenicline (Chantix)

HA, insomnia, abnormal dreams, suicidal ideation, angina

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Cocaine Pharmacology

Inhibits DA tranporter- dec DA clearance from the synaptic cleft and causes an inc in extracellular DA concentration

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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

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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

25

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

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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

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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)

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CNS and peripheral effects of amphetamines

tremor, restlessness, increased motor activity, agitation, insomnia, and loss of appetite, vasoconstricion, HTN, tachy

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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

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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

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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

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Treatment of amphetamine

d/c drug, cautious clin observation, recognize depression, treat w/ antidepressants, antipsychotic drugs- risperidone, quetiapine may be necessary

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Treatment of psychosis of amphetamine

primarily supportive, haloperidol, olanzapine, psychotic relapse following d/c were common over 30 months, hallucinations, delusions, depression, suicidal ideation

34

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

35

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

36

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

37

Withdrawal of EtOH

sweating, N/V, tremors, anxiety, agitation, paranoia, hallucinations, DT, seizures

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Stage 1 of EtOH withdrawal

6-8 hrs- tremors, anxiety, HA, GI upset, sweating

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Stage 2 of EtOH withdrawal

10-30 hrs- insomnia, hallucinations, autonomic hyperactivity

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Stage 3 of EtOH withdrawal

first 3 days- grand mall seizures

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Stage 4 of EtOH withdrawal

3-5 days- delirium tremors, agitation, hallucinations, tachy, HTN, fever, diaphoresis

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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

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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

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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

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Anticonvulsants for EtOH withdrawal

carbamazepine, valproic acid, gabapentin, pregabalin, oxcarbazepine, lamotrigine, topiramate

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Drugs to prevent EtOH relapse

Disulfiram (Antabuse), Naltrexone (revia)- opioid antagonist, acamprosate (Campral)- GABA agonist/glutamate antagonist

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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

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Naltrexone (revia) dose and ADRs

50 mg PO, syncope, HA, insomnia, N/V?D dec appetitie

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Acamprosate (Campral) dose and ADRs

666mg PO TID, diarrhea, ch pain, HTN, insomnia, anxiety

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Cannabinoids Pharm

binds to cannabinoid rec and inhibit release of glutamate or GABA, THC is active substance and is powerfully psychoactive

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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

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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

53

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)