Drugs And Addiction Flashcards

1
Q

Stubstance use disorder DSM-V

A

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

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2
Q

Dopamine pathways

A

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)

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3
Q

Reward prediction error

A

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

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4
Q

Baseline dopamine

A

sleep and non-REM deep rest
exercise
sun
food - healthy fats

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5
Q

Basic concepts of drug effects: routes of drug administration

A

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

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6
Q

Basic concepts of drug effects: Factors influencing effect

A

individual differences
- body weight
- gender
- genetics
- age
- health
- etc

placebo effects = a physiological response following the administration of a pharmacologically inert ‘remedy’

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7
Q

Basic concepts of drug effects: Agonists and antagonists

A

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

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8
Q

Stimulants

A

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

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9
Q

Depressants

A

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)

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10
Q

Opiods

A

= 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

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11
Q

Hallucinogens

A
  • 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

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12
Q

Cannabis

A
  • 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)
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13
Q

Physical dependence

A

= state of an individual who has repeatedly taken a drug and experiences unpleasant physiological symptoms if they stop it –> physiological dependence

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14
Q

Tolerance

A

= 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

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15
Q

Withdrawal

A

= 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)

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16
Q

Rat park experiment

A

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

17
Q

Biopsychosocial model of addiction

A

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

18
Q

Reward system dysfunction

A
  • 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
19
Q

Risk of psychosis

A

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

20
Q

Link to other mental health issues

A
  • 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)
21
Q

Ketamine in mental health

A

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
22
Q

Challenges and considerations in Ketamine therapy

A

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

23
Q
A