Drugs And Addiction Flashcards
Stubstance use disorder DSM-V
risky substance use = quantity/frequency of consumption
SUD is defined by criteria
- biological
- psychological
- behavioural
- social
Addiction = most severe stage of SUD
- significant loss of control and the presence of compulsive behaviours despite the desire to stop
Dopamine pathways
Cognition
- mesocortical pathway (VTA to PFC)
Motivation
- mesolimbic pathway (VTA to NAc)
Motor function
- nigrostriatal pathway (SN to striatum)
Hormonal regulation
- tuberoinfundibulnar pathway (hypothalamus to pituitary)
Reward prediction error
1) no predictions - spike in dopamine signalling when reward occurs
2) after conditioning: reward predictions - spike in dopamine signalling when conditioned stimulus (cue) occurs, baseline activity during actual reward
3) no reward: reward predictions - spike in dopamine signalling when conditioned stimulus (cue) occurs, decrease in dopamine signalling at time when reward was supposed to occur
Baseline dopamine
sleep and non-REM deep rest
exercise
sun
food - healthy fats
Basic concepts of drug effects: routes of drug administration
enteral route = drugs are administered via the human gastrointestinal tract
topical route = application of drugs to the skin or an orifice
parenteral route = drugs given by routes other than enteral and topical
Basic concepts of drug effects: Factors influencing effect
individual differences
- body weight
- gender
- genetics
- age
- health
- etc
placebo effects = a physiological response following the administration of a pharmacologically inert ‘remedy’
Basic concepts of drug effects: Agonists and antagonists
agonists = drugs that enhance the activity if neurochemical
- L-dopa, cocaine, amphetamine, methylphenidate (Ritalin), apomorphine
- increase release and production of dopamine
- inhibit reuptake and stimulate dopamine receptors
antagonists = drugs that reduce the activity of a neurochemical
- reserpine, traditional medications used to treat schizophrenia
- storage of dopamine, blocking dopamine receptors
≠postsynaptic or behavioural excitation/inhibition
Stimulants
Caffeine
- effects: increases altertness and attentional performance
- side effects: may create dependence
Nicotine
- effects: improves alerting, orienting attention and epsiodic working memory
- side effects: major negative health effects if smoked or chewed
Amphetamine
- effects: improved cognitive functions, inhibitory control, episodic and working memory, aspects of attention, performance on effortful tasks
- side effects: possible dependence accompanied by severe ‘crash’ with depression as drug effects wear off, particularly if smoked or injected
Cocaine
- effects: leads to increased alertness, feelings of well-being and euphoria, increased energy and motor activity, feelings of competence and enhanced sexual vigour
- side effects: decreased appetite, headache
Depressants
Alcohol
- effects: slow brain function, impairs memory, attention and judgment
- side effects: long-term use raises risks for liver disease, cardiovascular problems, and dementia in older adults
Benzodiazepines
- Valium, Xanax
- effects: reduced anxiety, but impairs memory and concentration (especially with extended use)
- side effects: high risk of dependency, tolerance and withdrawal, (long term use) cognitive decline and possibly dementia
Barbiturates
- Phenobarbital
- effects: deep sedations, reduction of memory, attention and coordination
- side effects: high overdose risk, long-term use leads to dependency and potentially dangerous withdrawal
Inhalants
- effects: induce euphoria and disorientation by slowing brain function
- side effects: long-term use can cause memory loss, motor issues, and brain cell damage (particularly in areas controlling movement and cognition)
Opiods
= a class of drugs that bind to opioid receptors in the brain and spinal cord, reducing the percpetion of pain
- can be natural, semi-synthetic or fully synthetic
Symptoms
- slowing of many body functions
- constipation
- respiratory and cardiac depression
- rapid development of tolerance
Side effects
- restlessness
- irritability
- headache
- tremors (heroin and morphine)
- nausea and vomiting
- severe abdominal pain
Common opioids
- morphine
- heroin
- fentanyl
- oxycodone
Hallucinogens
- chemical compositions are similar to the neurotransmitters serotonin and epinephrine (adrenaline)
- act primarily by mimicking them
Effects
- euphoria , therapeutic insight and mystical experiences, anxiety and panic
Common hallucinogens
- LSD
- Mescaline (Peyote)
- PCP
Cannabis
- alterations in percpetion, cognition, motor behaviour, memory, and learning, also psychotic episodes (long-term use)
- activates cannabinoid receptors and leads to a decrease in adenylate
- increases GABA release, which leads to an increase in synaptic dopamine levels (similar to opioids)
Physical dependence
= state of an individual who has repeatedly taken a drug and experiences unpleasant physiological symptoms if they stop it –> physiological dependence
Tolerance
= a condition, resulting from persistent use of drug
characterised by:
1) a markedly diminished effect with regular use of the same dose of the drug
2) a need to increase the dose markeldy over time to achieve the same desired effect
Withdrawal
= a syndrome that develops after cessation of prolonged, heavy consumption of a substance
Symptoms vary but generally include:
- physiological, behavioural and cognitive manifestations (nausea, vomiting, insomnia, mood alterations and anxiety)
Rat park experiment
Overview
- examined the role of environment in addiction
- divided rats into two groups: one housing in isolated cages and the other in a large, social environment known as ‘Rat Park’
- both rat groups were given continuous access to plain water and a morphine solution
Findings
- rats in social settings with stimulating environments were less likely to develop a preference for drugs
Implications
- suggests that addiction is influenced not only by chemical dependency but also by social factors, such as isolation or lack of engagement, emphasizing the role of environment
Biopsychosocial model of addiction
Biological
- genetics and brain chemistry (eg dopamine release) increase susceptibility to addiction, impacting tolerance and withdrawal
Psychological
- mental health, personality traits, coping skills play key roles in how individuals respond to drugs
Social
- environmental influences (peer groups, family, socioeconomic status) affect vulnerability to addiction
= addiction is a complex condition shaped by an interplay of internal and external factors
BUT –> model was intended to be a more complete account of healthcase and illness behaviour NOT intended to replace biomedical matters
Reward system dysfunction
- long-term exposure to drugs is theorised to cause permanent changes in the substance reward circuit –> VTA, basal forebrain (amygdala), dopaminergic connections between VTA and basal forebrain, OFC
- chronic drug use causes the PFC damage that underlies impaired response inhibition and salience attribution (iRISA)
- changes with abstinence and recovery with treatment suggest plasticity of these same brain regions and functions
Risk of psychosis
Cannabinoids
- induce psychotic symptoms
Synthetic cannabinoids
- severe psychotic syndromes
Synthetic cathinones
- delirium-like symptoms and impulsivity
Cocaine and amphetamines
- associated with psychotic episodes
Hallucinogens
- induce transient psychotic symptoms
Link to other mental health issues
- multiple national population surveys –> found about half of those who experience a mental illness during their lives will also experience a SUD and vice versa
- SUD can also co-occur at high prevalence with mental disorders (depression and bipolar disorder, ADHD, psychotic illness, borderline personality disorder, antisocial personality disorder)
Ketamine in mental health
Ketamine
- originally developed as both an anesthetic and a potent painkiller
- produces dissociated analgesia, providing pain relief for brief medical procedures
- more recently, powerful tool in treating treatment-resistant depression (TRD)
- intravenous ketamine: significantly improving depression measures during the first 24 hours, subsequent decrease in its effect in the following 7 days
- ketamine as prototype for an enitrely new class of antidepressant medications
- particularly esketamine can be viewed as a long-term treatment
Challenges and considerations in Ketamine therapy
Potential for dependency
- psychoactive properties pose a risk of dependency
- necessitating strict medical oversight
Side effects
- dissociation and perceptual disturbances
- may complicate treatment
Long-term efficiacy
- durability effects is uncertain
- benefits often fading, requiring ongoing infusions to maintain relief
ethical and regulatory concerns
- using it clinically despite its recreational misuse –> ethical and regulatory challenges
