psych of addictions exam 2 (chapters 5-8)

biological factors influencing drug effects

inherited differences in reaction to drugs- initial sensitivity, gender, weight, age

Initial sensitivity

the effect of a drug on someone using it for the first time

psychological factors influencing drug effects

Personality (sensation seeking), like addictive personalities, drug expectancies and beliefs. The more sensation-seeking an individual is, the more likely they are to become addicted. Also show the stress reduction strategies people are more likely to take.

Drug expectancy

a person’s anticipation of of belief of what they will experience upon taking a drug

setting

influences the effects of alcohol, marijuana, hallucinogenic drugs, whether using alone or with others

dispositional tolerance

increase in the rate of metabolizing a drug with regular use AKA- your body metabolizes the drug faster so you need to consume more to receive desired effects (common for drugs consumed orally and alcohol)

functional tolerance

your brain’s way of compensating for the behavioral changes that typically come with drinking large amounts of alcohol. People can consume a lot of alcohol without appearing to be intoxicated. Biological response.

Acute tolerance

a decrease in response to a drug within a single exposure to the drug (Common for alcohol)

protracted tolerance

occurs over 2 or more drug administrations

behavioral tolerance

adjust behavior, mannerisms and behavior in order to mask drug use (learned response)

cross-tolerance

tolerance to a drugs never taken resulting from protracted tolerance to another drugs

consequence

a response to an action/outcome an action

reinforcer

a consequence of a behavior that increases its future likelihood that the behavior will continue

punisher

a consequence of a behavior that suppresses or decreases its future likelihood of a behavior continuing

snorting cocaine

• How it's done: Cocaine powder (cocaine hydrochloride) is inhaled through the nose using a straw or rolled-up paper.

• Onset: 3-5 minutes.

• Duration: 20-30 minutes.

• Effects: The drug is absorbed through the nasal mucous membranes into the bloodstream. Users experience increased energy, alertness, and euphoria.

• Risks: Damage to nasal tissues, chronic nosebleeds, and risk of infections. Over time, snorting can lead to a perforated septum (hole in the nasal partition).

smoking crack cocaine

• How it's done: Cocaine is turned into crack (a solid, smokable form) by mixing it with baking soda and heating it. The smoke is inhaled through a pipe or other device.

• Onset: Immediate (within seconds).

• Duration: 5-15 minutes.

• Effects: Crack produces an intense, rapid onset of euphoria, increased heart rate, and a feeling of invincibility. The high is short-lived but powerful.

• Risks: Severe respiratory issues, lung damage, and high addiction potential due to the rapid onset of effects.

injection of cocaine

• How it's done: Cocaine powder is dissolved in water, and the solution is injected into the bloodstream.

• Onset: Immediate (within seconds).

• Duration: 5-10 minutes.

• Effects: The drug quickly enters the bloodstream, leading to an intense rush of euphoria, heightened energy, and alertness.

• Risks: Needle use carries significant risks, including HIV, Hepatitis C, and other infections. There is also a high risk of overdose due to the rapid, concentrated effect.

oral (ingesting cocaine)

• How it's done: Cocaine is swallowed, often in a pill or dissolved in a liquid.

• Onset: 20-60 minutes.

• Duration: 1-2 hours.

• Effects: The drug is absorbed through the digestive system, leading to a slower, less intense high. It may produce feelings of euphoria, increased alertness, and confidence, though less powerful than other routes.

• Risks: Stomach and gastrointestinal issues, and the drug's effects are delayed compared to other methods, leading to possible overconsumption.

Mucous membrane absorption (buccal, sublingual) consumption of cocaine

• How it's done: The cocaine is absorbed through the mucous membranes of the mouth, either by holding it against the gums or under the tongue.

• Onset: 15-30 minutes.

• Duration: 1-2 hours.

• Effects: Similar to oral ingestion but with a quicker onset and a longer duration than snorting.

• Risks: Less common, but it still carries risks of addiction and potential harm to the mucous membranes.

cocaine

became popular in the 1970s- intranasal consumption. Low rate of injection/IV use. Cocaine psychosis causes hallucinations and delusions.

Therapeutic use of cocaine

• rarely used today but it has medical applications as a local anesthetic in certain surgeries (e.g., nasal, throat, and eye procedures)

• blocking nerve signals, numbing the area, and reducing bleeding due to vasoconstriction

• not prescribed for general use due to high potential for abuse and addiction

recreational use of cocaine

• Typically smoked as crack or injected for its powerful stimulant and euphoric effects

• produces intense energy, confidence, talkativeness, and pleasure, but the effects are short-lived

• can lead to compulsive redosing, as users chase the high

excessive or chronic use of cocaine

• Leads to severe physical and psychological effects, including paranoia, anxiety, aggression, insomnia and loss of appetite

• heart problems like high blood pressure and heart attacks

• nasal damage from snorting or lung damage from smoking

amphetamines (speed)

• first of these drugs were synthesized in the late 19th century

• used to treat symptoms of colds, sinus, obesity, narcolepsy, and ADHD

• high potential for harmful use

• WWII soldiers used them but became a major US problem when physicians began prescribing them to treat heroin dependence, which backfired

intravenous (injected)- amphetamines

• possible but dangerous

• some people dissolve crushed tablets or powdered amphetamines in water and inject them, but this is extremely risky due to fillers, contaminants, and injection risks

• prescriptions are not designed for injection and meth os more commonly injected

Oral consumption of amphetamines

• common and safe for prescriptions

• •Most prescription amphetamines (e.g., Adderall, Vyvanse, Dexedrine) are designed for oral use.

• •Vyvanse is a prodrug, meaning it must be metabolized in the body to become active, so it doesn’t work effectively if snorted or injected

intranasal (snorted) consumption of amphetamines

• possible with certain forms

• •Crushed immediate-release tablets (like Adderall IR) can be snorted, leading to a faster onset and stronger effects.

• •However, extended-release formulations contain binders and fillers that don’t break down well and can damage nasal passages.

smoking amphetamines

• rare but possible

• Prescription amphetamines are not designed to be smoked, and they often contain additives that burn poorly.

• •Methamphetamine, a powerful amphetamine derivative, is commonly smoked in crystal form.

amphetamine feeling

• intense rush

therapeutic use of amphetamines

• Increased focus and alertness – Feels like a sharpening of attention, making tasks easier to complete.

• Mild euphoria or well-being – A subtle boost in mood, often described as motivation rather than intense pleasure.

• Increased energy – Less fatigue, but without a jittery feeling when taken as prescribed.

• Suppressed appetite – Less desire to eat, which can lead to unintended weight loss.

• Mild increase in heart rate and blood pressure – Usually not noticeable unless taken in high doses.

Recreational use of amphetamines

• higher doses or non-prescribed use

• Intense euphoria – A rush of pleasure, confidence, and well-being, sometimes described as a "high.”

• Hyperfocus and Talkativeness – Feeling extremely engaged in tasks or conversations, sometimes to the point of obsession.

• Increased physical activity – Restlessness, pacing, or an urge to keep moving.

• Decreased need for sleep – Users may stay awake for long periods without feeling tired.

• Heightened sensitivity to music or sensations – Sounds and touch may feel more intense or pleasurable.

• Compulsive redosing – A strong urge to take more as the effects wear off, especially with snorting or injecting

Excessive or chronic use

• Anxiety, paranoia, or agitation – Feeling restless, jittery, or suspicious of others.

• Hallucinations or delusions – Seeing or hearing things that aren’t there, especially after prolonged use.

• Severe insomnia – Staying awake for days can lead to a "crash" with extreme fatigue and depression.

• Twitching, repetitive behaviors (stereotype) – Fidgeting, picking at the skin, or grinding teeth (bruxism).

amphetamine psychosis

• symptoms resembling schizophrenia, including paranoia and delusional thinking

• paranoia more common than death with amphetamine overdose

• often led to acts of violence

• depression = common withdrawal symptom after heavy use of amphetamine or cocaine

recreational use

• Euphoria & Confidence – Users feel powerful, motivated, and socially engaged.

• Increased Energy & Focus – Less need for sleep, heightened alertness.

• Suppressed Appetite – Reduced hunger, sometimes leading to weight loss.

• Elevated Heart Rate & Blood Pressure – Mild to moderate physical stimulation.

• Compulsive Redosing – Because the high fades quickly (especially when smoked or injected), users may take more to prolong the effects.

excessive or chronic use

• Severe Insomnia – Users may stay awake for several days ("runs"), leading to exhaustion.

• Extreme Weight Loss & Malnutrition – Due to prolonged appetite suppression.

• Paranoia, Anxiety, & Psychosis – Chronic use can cause hallucinations and delusions (e.g., "meth bugs" sensation, believing insects are crawling under the skin).

• Severe Dental Damage ("Meth Mouth") – Caused by dry mouth, teeth grinding, and poor hygiene.

• Skin Sores & Deterioration – Repetitive skin picking due to hallucinations or obsessive behaviors.

• Heart & Organ Damage – Chronic meth use increases the risk of heart attacks, strokes, and organ failure.

• Intense Addiction & Withdrawal – Users experience severe depression, fatigue, and cravings when stopping.

physiological effects of cocaine, amphetamines, and meth

• impact autonomic nervous system

• anorectic effects: appetite suppression, weight loss (typically regained after drug use stops)

behavioral effects of cocaine, amphetamines, and meth

• mood elevation, increased talkativeness/sociability, increased alertness and sexual arousal, insomnia

• state-dependent learning: information learned while under the influence is best recalled while under the influence

stimulant psychosis

• can be produced in normal volunteers in lab settings by amphetamines, cocaine, methcathinones, or methylphenidate

• serious problem with high doses of meth or crack cocaine

• paranoid delusions = most common symptom

• compulsive stereotyped behaviors = rocking, hair-pulling, chain-smoking, fiddling

hallucinations/formication

• Stimulant psychosis may be successfully treated with Thorazine, other antipsychotic drugs used to treat schizophrenia

overdose death

• convulsions or seizures causing respiratory collapse; myocardial infarction (heart attack) due to coronary artery spasm; stroke

• further complication: stimulant users often combine drugs: unpredictable reactions

nicotine stimulates acetylcholine sensitive receptors

a cholinergic agonist drug

effects of nicotine on nervous system and behavior

• increases dopamine levels in the mesocortical limbic system, increases blood pressure, increases heart rate, stimulates adrenal glands to release adrenaline, increases tone and activity of the gastrointestinal tract, facilitates release of dopamine and serotonin, affects CNS functions of arousal, attention, learning, memory storage and retrieval, mood, and rapid eye movement during sleep

nicotine as a biphasic drug

stimulates ACH receptors at low doses, but slows down neural transmission at higher doses- partly explains complex effects perceived

reinforcing effects of nicotine

alertness, learning, memory: reversal or prevention of cognitive impairment could play a part in maintaining cigarette use

autonomic effects of nicotine

heart stimulation and resulting increased demands for oxygen underlie association of nicotine and heart disease- inadequate oxygen may lead to angina or a heart attack

biphasic action

acts as a depressant at higher doses

powerful reinforcers to humans

• CNS-stimulating effects of nicotine

• Frequent perception that it is sedating

• Highly accessible drug, despite taxation

• Social Support

• Rapid rise and fall of nicotine blood levels demand many reinforcements per day

• Many social and environmental associations with nicotine use strengthen psychological dependence

• Physical dependence = strong incentive to continue use, to avoid or escape withdrawal symptoms (negative reinforcement)

• Pharmacological, psychological, and social/environmental variables combine to make nicotine a drug with high dependence liability

mechanisms of action for caffeine

• antagonism of adenosine receptors

• adenosine leads to: behavioral sedation, regulation of oxygen delivery to cells, dilation of cerebral and coronary blood vessels, and production of asthma

• occupies adenosine receptors and then block the action of adenosine

caffeine withdrawal

headache and fatigue, depression, less alertness, less contentment, less relaxed mood, less activity, less energy, more sleepiness and irritability

• 2013 DSM includes caffeine use disorder endorsing caffeine withdrawal as a clinical phenomenon

caffeine and mood

Elevates mood, feeling energized, creative, efficient, confident, and alert. Accounts for popularity of coffee and tea as morning wake-up beverages

caffeine and performance

complicated. Caffeine decreases fatigue, increases vigilance, improves motor parts, impairs decision-making in some tasks. Enhances athletic performance, including perceived exertion endurance.

caffeinism

An abnormal condition caused by the consumption of large amounts of caffeine and marked by restlessness, nervousness, irritability, insomnia, diuresis, tremors, and tachycardia

Adult lethal dose of caffeine

75 cups of coffee, 125 cups of tea, 200 colas, 100 NoDoz tablets

alcohol withdrawal timelines

• 6-12 hours: minor withdrawal

• 12-24 hours: alcoholic hallucinosis

• 24-28 hours: seizures

• 48+ hours: delirium tremens

physiological effects of alcohol

• inhibits secretion of vasopressin, causing increased urination

• reduced body fat oxidation, which results in increased body fat and weight gain when used with food intake

• peripheral dilator

• increases gastric secretion, stimulating appetite

• disrupts sleep patterns: suppresses REM sleep when most dreaming occurs

• impairs memory

• hangovers

peripheral dilator

makes skin turn red, feel warm

alcohol impairing memory

Acute effects are on short-term memory; blackouts=amnesia about events when drinking, despite no loss of consciousness; thought to be a failure of transfer of short-term or long-term memory. Grayouts are partial recall of events. These are not consistent and determining factors are unidentified

Hangovers

Begin to appear about 4-12 hours after reaching peak BAC. Headache, dizziness, nausea, vomiting, increased heart rate, fatigue, thirst. Associated with a reduced ability to perform complex skills for driving a car. Nothing relieves symptoms as well as preventing one by drinking in moderation or not at all.

Mixture of alcohol and other depressants

• mixing alcohol and barbiturates can cause death

• Mixing alcohol and benzodiazepines can impair performance needed to survive

alcohol affecting emotion and mood

• changes with BAC and person

• situational and cognitive variables, and the person’s mood state before starting to drink are all factors

• when BAC is lower and starts to rise, it causes elation, expansiveness, friendliness, relaxation, joviality, and self-confidence. Others feels hostile or depressed.

• When BAC falls, many people feel angry or tired

• Can cause emotional lability and lower tolerance for frustration

• effects on thinking and perception are more influenced on BAC than other factors such as short-term memory, ability to estimate passage of time, depth perception, attention, and concentration

• at higher BAC, cognitive effects are intensified and compounded disorganized thinking

wenicke-korsakoff syndrome

• severe CNS disorder from combination of extreme nutritional deficiency and chronic heavy drinking; the symptom is a combination of two diseases: wernicke’s disease and korsakoff syndrome

wernicke’s disease

• symptoms include confusion, memory loss, staggering gait, inability to focus the eye; absent permanent brain damage, it is reversible by vitamin B

korsakoff’s syndrome

primarily due to alcohol; symptoms include damage to brain structure, affecting memory, serious impairments in short-term memory, learning; often causes considerable confusion and confabulation (fabrication in answer to questions due to inability to recall things about oneself)

fatty liver

• earliest, most benign effect of alcohol; reversible with abstinence

alcohol hepatitis

• more serious; involves inflammation and death of liver cells; jaundice often occurs due to accumulation of bile; reversible with abstinence and medical treatment, but can cause death if severe enough and not treated

cirrohosis

• most serious, life-threatening- chronic inflammatory disease of the liver involving cell death, formation of scar tissue; liver becomes unable to metabolize various toxins (ammonia); and toxins accumulate in the body, causing death

Fetal alcohol syndrome

• mental and physical defects such as a small head and flat face occur

• small eyes, short nose, low nasal bridge, underdeveloped jaw, smooth philtrum, thin upper lip, epicanthal folds

single-factor explanations for etiology (alcohol use disorder)

• biological, psychological, or sociological

biological approaches explanations for etiology (alcohol use disorder)

• metabolic, glandular, body chemistry, allergic condition; many US treatment providers consider alcohol use disorder a physical disease

• suggestion of genetic predisposition to some types of more severe alcohol use disorder- evidence from family, twin, adoption studies

psychological explanations for etiology (alcohol use disorder)

• identifying specific personality traits that may be linked to alcohol use disorder- not been able to pin point specific ones as of yet

sociological models for etiology (alcohol use disorder)

• partly a response to failure to find a unique alcoholic personality; supported by cross-cultural differences in drinking patterns and demographic factors

• studies consistently show sociological factors help to explain development of alcohol use disorder

biopsychosocial approaches to etiology

• combined biological, psychological, and sociological factors= biopsychosocial

• each single-factor explanation alone ultimately fails to explain how alcohol use disorder develops so all types have to be considered together

pioneered the cocaine epidemic

Freud

anhedonia

prolonged period of sadness and lack of motivation. Loss of enjoyment of things.

receptor that nicotine acts on

dopamine