Test 3 Flashcards
What are some influences to drug taking? short answer question
- 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
What is the physical dependence model of addiction?
Once physically dependent, attempts at abstinence lead to withdrawal symptoms
Individuals relapse in order to reduce withdrawal symptoms
Positive reinforcement model of addiction?
Drugs act as positively reinforcing stimuli
-Self-administration paradigm
Incentive-sensitisation model of addiction?
Repeated exposure can persistently change brain cells and circuits that normally regulate the attribution of incentive salience of stimuli.
Opponent-process model of addiction?
Addiction is emotionally paired with pleasure and emotional symptoms are associated with withdrawal.
Disease model of addiction?
Addiction comes from an inherited susceptibility to drug use and abuse.
What are three influences of drug use?
- 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
What are the 4 phases of alcoholism? short answer question
- The prealcoholic phase
- drinks first for social reasons
- stress reduction
- seeks out drinking occasions - 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 - The crucial phase
- solitary drinking
- avoidance of family and friends
- increase in memory blackouts
- reverse tolerance develops due to liver damage
- may have cirrhosis - 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
Absorption of alcohol:
passes from stomach to small intestine for rapid absorption
-rate is affected by stomach content
Enzymes involved in oxidising alcohol:
Alcohol dehydrogenase - converts alcohol to acetaldehyde
Acetaldehyde dehydrogenase - converts acetaldehyde to acetic acid
Further oxidation yields carbon dioxide, water, and energy
Alcohol tolerance:
chronic use increases alcohol dehydrogenase and P450 liver enzymes causing a reduction in blood alcohol levels
3 phases of alcohol withdrawal:
- 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
Acute effects of alcohol:
- inhibits ADH
- reduces amount of fat in the body that is oxidised
- suppresses REM sleep
- impairs memory
Physical consequences to alcoholism:
- fatty liver-fat accumulation that is reversible with abstinence
- alcohol hepatitis-inflammation and death of liver cells; reversible with abstinence
- cirrhosis-cell death and formation of scar tissue
Fetal alcohol syndrome:
- small eyes
- underdeveloped midface
- small head circumference
- low to severe impairments of intellectual functioning
Alcohol’s effects on glutamate and dopamine:
- inhibits glutamate
- increases dopaminergic transmission in mesolimbic pathway
Treatments available for alcoholics (short answer question):
- detoxification
- provision of medical care
- changing long-term behaviour so that destructive thinking patterns are discontinued (CBT)
- prescribing vitamins
- Alcoholics Anonymous
- Aversion therapy (antabuse)
- Anti-craving medication (Naltrexone)
- Tricyclic antidepressants
- Family therapy (relationships among family members may have contributed to destructive drinking)
How are opioids classified?
- natural substances (opium, morphine, codeine)
- semisynthetic narcotics (heroin)
- synthetic products (Demerol)
- endogenous opioids (endorphins)
Opiate drugs are absorbed:
- GI tract
- nasal mucosa and lungs
- intramuscularly and subcutaneously
- intravenously
Heroin and the blood brain barrier:
passes more readily than morphine
once in brain it is converted to morphine
Three types of opioids:
- full agonist
- partial agonist
- antagonist
Opioid full agonist:
morphine-like effect (heroin, oxycontin, methadone)
Opioid partial agonist:
Weak morphine-like effects with strong receptor affinity (buprenorphine)
Opioid antagonist:
no effect in absence of an opiate or opiate dependence (naloxone, naltrexone)
Three different opiate receptors:
- Mu2
- Delta
- Kappa
Delta and Kappa opiate receptors are involved in:
spinal analgesia
Mu2 opiate receptors:
constipation, respiratory depression
What are the effects of opiates?
- analgesia
- euphoria
- sedation and anxiolysis
- depression of respiration
- suppression of cough
Two methods used to determine neurobiology of opiate reinforcement:
- self-administration microinjection studies - conditioned place preference
- cells in the VTA - increase dopaminergic cell firing
- selective lesions
What brain areas contribute to opioid withdrawal?
- locus coeruleus
- periaqueductual gray
- nucleus accumbens
Areas of the brain involved in environmental cues of tolerance, drug abuse, and relapse:
amygdala and anterior cingulate
Medical complications associated with opioid addiction:
- HIV
- endocarditis
- TB
- Impaired immune function
- Hepatitis B and C
Treatments of opiate abuse (short answer question):
- detoxification; methadone - comes in every day
- detoxification; LAAM - has a slow onset and long duration of action (72 hours), administered three times a week; individual can reintegrate into society
- 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 - counseling
helping addict identify environmental cues that trigger relapse
individual designs behavioural response to those cues to prevent relapse
-Narcotics Anonymous
family therapy
What are the different forms of amphetamine?
L-amphetamine
D-amphetamine
What is Khat?
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
What is ephedrine?
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
Mechanism of action of amphetamines:
- causes release of NE and DA
- activates DA receptors in mesolimbic system
- activates dopmamine neurons in basal ganglia
Therapeutic uses of amphetamines:
- treats narcolepsy
- obesity - suppresses appetite
- ADHD (Ritalin)
Tolerance to amphetamines:
tolerance to anorexic, hyperthermic, cardiovascular, and reinforcing effects
Withdrawal symptoms of amphetamines:
- increased appetite
- weight gain
- decreased energy
- increased need for sleep
Amphetamine psychosis:
- visual or auditory hallucinations
- behavioural disorganisation
- paranoia
- formication
Neurotoxicity of chronic amphetamine use:
- persistent psychosis
- loss of dopaminergic and serotonergic neurons
- dopamine transporter function reduced in basal ganglia; persistent motor slowing and memory impairments
Characteristics of cocaine dependent individuals:
- typically young; 12-39 years old
- dependent on at least 3 drugs
- typically male (75%)
- tend to have coexisting psychopathology
Pharmacokinetics of cocaine-absorption:
- inhalation and intravenous; high concentrations of circulating cocaine
- snorted intranasally; absorption slower yielding lower cocaine levels
Pharmacokinetics of cocaine-distribution:
- penetrates brain rapidly
- vasoconstrictor; crosses placental barrier, or cuts off distribution to fetus
Metabolism of alcohol and cocaine generates:
cocaethylene
Cocaine’s major metabolite is:
benzoylecgonine
Half-life of cocaine:
0.5 to 1.5 hours
What are the mechanisms of action for cocaine?
- potent local anesthetic
- vasoconstrictor-raises blood pressure
- psychostimulant-strong behavioural reinforcing qualities
Pharmacological effects of cocaine:
- euphoria
- heightened energy
- insomnia
- restlessness
- increased sexual interest
- aggression
- inflated self-esteem
Adverse effects of cocaine abuse:
- convulsions or seizures
- cardiac arrhythmias
- heart attack
- stroke
Consequences of cocaine use while pregnant:
- premature birth
- bowel infarctions
- cerebral infarctions
- respiratory problems
- increased risk of seizures
What are the 3 phases of cocaine withdrawal? (short answer question)
- Crash (1-14 days): intense craving and exhaustion
- Withdrawal (1-10 weeks): intense cravings, moderate to severe depression
- Extinction (months to years): cravings occur by exposure to environmental cues
Mechanism of action of cocaine abuse:
- blocks cell uptake of DA, NE, and 5-HT
- NT levels are increased in the synapse, prolonging their effects
High baseline DA levels:
higher levels of DA in the synaptic cleft, plays a large role in addiction and reinforcing effects
Treatment of cocaine abuse:
- CBT to prevent relapse and encourage regulation of behaviour
- Dopaminergic agonists to treat withdrawal symptoms, relapse, and craving
- Antidepressants
- Cocaine vaccine
