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Psychopharmacology > Test 3 > Flashcards

Test 3 Flashcards

1
Q

What are some influences to drug taking? short answer question

A
  • Individual characteristics
    1. Risk-taking or novelty-seeking behaviour
    2. Lack of emotional control
  • Family factors
    1. parental substance abuse/dependence
    2. parent-offspring relationship
    3. sibling influences
  • Developmental influence
    1. peer influences
    2. marital partner relations
  • Contextual influence
    1. Low socioeconomic status
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2
Q

What is the physical dependence model of addiction?

A

Once physically dependent, attempts at abstinence lead to withdrawal symptoms
Individuals relapse in order to reduce withdrawal symptoms

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3
Q

Positive reinforcement model of addiction?

A

Drugs act as positively reinforcing stimuli

-Self-administration paradigm

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4
Q

Incentive-sensitisation model of addiction?

A

Repeated exposure can persistently change brain cells and circuits that normally regulate the attribution of incentive salience of stimuli.

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5
Q

Opponent-process model of addiction?

A

Addiction is emotionally paired with pleasure and emotional symptoms are associated with withdrawal.

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6
Q

Disease model of addiction?

A

Addiction comes from an inherited susceptibility to drug use and abuse.

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7
Q

What are three influences of drug use?

A
  • Predisposing factors (susceptibility)
    1. demographics and sociocultural influences
    2. adolescence
    3. heredity
  • Enabling influences (Facilitation)
    1. availability and accessibility to drugs
    2. inability to say no to experimentation
  • Reinforcing influences (encouragement)
    1. experience of pleasure
    2. social and peer-group pressure
    3. advertising
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8
Q

What are the 4 phases of alcoholism? short answer question

A
  1. The prealcoholic phase
    - drinks first for social reasons
    - stress reduction
    - seeks out drinking occasions
  2. The prodromal phase
    - develops feelings of guilt about drinking
    - lies about drinking
    - drinking before joining others in drinking situations
    - need for increased intake to produce desired effects
    - physical dependency; will experience withdrawal symptoms
  3. The crucial phase
    - solitary drinking
    - avoidance of family and friends
    - increase in memory blackouts
    - reverse tolerance develops due to liver damage
    - may have cirrhosis
  4. The chronic phase
    - develops after a number of years of excessive intake
    - drinking bouts last for several days at a time
    - person is drunk on important occasions
    - institutionalisation or death may occur due to complications
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9
Q

Absorption of alcohol:

A

passes from stomach to small intestine for rapid absorption

-rate is affected by stomach content

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10
Q

Enzymes involved in oxidising alcohol:

A

Alcohol dehydrogenase - converts alcohol to acetaldehyde

Acetaldehyde dehydrogenase - converts acetaldehyde to acetic acid

Further oxidation yields carbon dioxide, water, and energy

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11
Q

Alcohol tolerance:

A

chronic use increases alcohol dehydrogenase and P450 liver enzymes causing a reduction in blood alcohol levels

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12
Q

3 phases of alcohol withdrawal:

A
  • Phase 1
  • onset a few hours after drinking has stopped; shakes, headache, agitation
  • Phase 2
  • onset within 24 hours of drinking cessation; seizures
  • Phase 3
  • onset after 30+ hours of drinking cessation; may last 3-4 days; referred to as delirium tremens; severe agitation, hallucinations
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13
Q

Acute effects of alcohol:

A
  1. inhibits ADH
  2. reduces amount of fat in the body that is oxidised
  3. suppresses REM sleep
  4. impairs memory
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14
Q

Physical consequences to alcoholism:

A
  1. fatty liver-fat accumulation that is reversible with abstinence
  2. alcohol hepatitis-inflammation and death of liver cells; reversible with abstinence
  3. cirrhosis-cell death and formation of scar tissue
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15
Q

Fetal alcohol syndrome:

A
  1. small eyes
  2. underdeveloped midface
  3. small head circumference
  4. low to severe impairments of intellectual functioning
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16
Q

Alcohol’s effects on glutamate and dopamine:

A
  • inhibits glutamate

- increases dopaminergic transmission in mesolimbic pathway

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17
Q

Treatments available for alcoholics (short answer question):

A
  1. detoxification
  2. provision of medical care
  3. changing long-term behaviour so that destructive thinking patterns are discontinued (CBT)
  4. prescribing vitamins
  5. Alcoholics Anonymous
  6. Aversion therapy (antabuse)
  7. Anti-craving medication (Naltrexone)
  8. Tricyclic antidepressants
  9. Family therapy (relationships among family members may have contributed to destructive drinking)
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18
Q

How are opioids classified?

A
  1. natural substances (opium, morphine, codeine)
  2. semisynthetic narcotics (heroin)
  3. synthetic products (Demerol)
  4. endogenous opioids (endorphins)
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19
Q

Opiate drugs are absorbed:

A
  1. GI tract
  2. nasal mucosa and lungs
  3. intramuscularly and subcutaneously
  4. intravenously
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20
Q

Heroin and the blood brain barrier:

A

passes more readily than morphine

once in brain it is converted to morphine

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21
Q

Three types of opioids:

A
  1. full agonist
  2. partial agonist
  3. antagonist
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22
Q

Opioid full agonist:

A

morphine-like effect (heroin, oxycontin, methadone)

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23
Q

Opioid partial agonist:

A

Weak morphine-like effects with strong receptor affinity (buprenorphine)

24
Q

Opioid antagonist:

A

no effect in absence of an opiate or opiate dependence (naloxone, naltrexone)

25
Q

Three different opiate receptors:

A
  1. Mu2
  2. Delta
  3. Kappa
26
Q

Delta and Kappa opiate receptors are involved in:

A

spinal analgesia

27
Q

Mu2 opiate receptors:

A

constipation, respiratory depression

28
Q

What are the effects of opiates?

A
  1. analgesia
  2. euphoria
  3. sedation and anxiolysis
  4. depression of respiration
  5. suppression of cough
29
Q

Two methods used to determine neurobiology of opiate reinforcement:

A
  1. self-administration microinjection studies - conditioned place preference
  2. cells in the VTA - increase dopaminergic cell firing
  3. selective lesions
30
Q

What brain areas contribute to opioid withdrawal?

A
  1. locus coeruleus
  2. periaqueductual gray
  3. nucleus accumbens
31
Q

Areas of the brain involved in environmental cues of tolerance, drug abuse, and relapse:

A

amygdala and anterior cingulate

32
Q

Medical complications associated with opioid addiction:

A
  1. HIV
  2. endocarditis
  3. TB
  4. Impaired immune function
  5. Hepatitis B and C
33
Q

Treatments of opiate abuse (short answer question):

A
  1. detoxification; methadone - comes in every day
  2. detoxification; LAAM - has a slow onset and long duration of action (72 hours), administered three times a week; individual can reintegrate into society
  3. narcotic antagonists;
    naloxone-rapidly precipitates withdrawal; very brief duration
    naltrexone-is like naloxone but has a long duration of action and is well-absorbed orally
  4. counseling
    helping addict identify environmental cues that trigger relapse
    individual designs behavioural response to those cues to prevent relapse
    -Narcotics Anonymous
    family therapy
34
Q

What are the different forms of amphetamine?

A

L-amphetamine

D-amphetamine

35
Q

What is Khat?

A

Flowering shrub found in East Africa

  • can be chewed or brewed as a tea and has stimulant properties similar to those of amphetamine or cocaine
  • active components are cathinone and cathine
36
Q

What is ephedrine?

A

Only in use today in anesthesiology to transiently increase blood pressure

  • can be toxic or fatal when combined with other stimulants
  • pseudoephedrine used in cough and cold medicines
37
Q

Mechanism of action of amphetamines:

A
  • causes release of NE and DA
  • activates DA receptors in mesolimbic system
  • activates dopmamine neurons in basal ganglia
38
Q

Therapeutic uses of amphetamines:

A
  1. treats narcolepsy
  2. obesity - suppresses appetite
  3. ADHD (Ritalin)
39
Q

Tolerance to amphetamines:

A

tolerance to anorexic, hyperthermic, cardiovascular, and reinforcing effects

40
Q

Withdrawal symptoms of amphetamines:

A
  • increased appetite
  • weight gain
  • decreased energy
  • increased need for sleep
41
Q

Amphetamine psychosis:

A
  • visual or auditory hallucinations
  • behavioural disorganisation
  • paranoia
  • formication
42
Q

Neurotoxicity of chronic amphetamine use:

A
  1. persistent psychosis
  2. loss of dopaminergic and serotonergic neurons
  3. dopamine transporter function reduced in basal ganglia; persistent motor slowing and memory impairments
43
Q

Characteristics of cocaine dependent individuals:

A
  • typically young; 12-39 years old
  • dependent on at least 3 drugs
  • typically male (75%)
  • tend to have coexisting psychopathology
44
Q

Pharmacokinetics of cocaine-absorption:

A
  • inhalation and intravenous; high concentrations of circulating cocaine
  • snorted intranasally; absorption slower yielding lower cocaine levels
45
Q

Pharmacokinetics of cocaine-distribution:

A
  • penetrates brain rapidly

- vasoconstrictor; crosses placental barrier, or cuts off distribution to fetus

46
Q

Metabolism of alcohol and cocaine generates:

A

cocaethylene

47
Q

Cocaine’s major metabolite is:

A

benzoylecgonine

48
Q

Half-life of cocaine:

A

0.5 to 1.5 hours

49
Q

What are the mechanisms of action for cocaine?

A
  1. potent local anesthetic
  2. vasoconstrictor-raises blood pressure
  3. psychostimulant-strong behavioural reinforcing qualities
50
Q

Pharmacological effects of cocaine:

A
  • euphoria
  • heightened energy
  • insomnia
  • restlessness
  • increased sexual interest
  • aggression
  • inflated self-esteem
51
Q

Adverse effects of cocaine abuse:

A
  • convulsions or seizures
  • cardiac arrhythmias
  • heart attack
  • stroke
52
Q

Consequences of cocaine use while pregnant:

A
  • premature birth
  • bowel infarctions
  • cerebral infarctions
  • respiratory problems
  • increased risk of seizures
53
Q

What are the 3 phases of cocaine withdrawal? (short answer question)

A
  1. Crash (1-14 days): intense craving and exhaustion
  2. Withdrawal (1-10 weeks): intense cravings, moderate to severe depression
  3. Extinction (months to years): cravings occur by exposure to environmental cues
54
Q

Mechanism of action of cocaine abuse:

A
  • blocks cell uptake of DA, NE, and 5-HT

- NT levels are increased in the synapse, prolonging their effects

55
Q

High baseline DA levels:

A

higher levels of DA in the synaptic cleft, plays a large role in addiction and reinforcing effects

56
Q

Treatment of cocaine abuse:

A
  • CBT to prevent relapse and encourage regulation of behaviour
  • Dopaminergic agonists to treat withdrawal symptoms, relapse, and craving
  • Antidepressants
  • Cocaine vaccine

Psychopharmacology (2 decks)

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