Guided learning: Addiction Flashcards

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1
Q

Define Addiction

A
  • Addiction is classed as a relapsing and remitting disorder comprising behaviours that are performed in a complusive manner despite the potential for self harm
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2
Q

Why is addiction particularly difficult to treat?

A
  • Difficult to treat as it is a relapsing remitting disorder that cycles through behavioural stages of anticipation, intoxication and withdrawal.
  • Both psychological and physiological components underpin the behaviours making it very hard to treat.
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3
Q

What is the difference between addiction and dependence?

What is dependence syndrome?

A
  • Addiction refers to the compulsive need for the substance
  • Dependence is characterised by a state of withdrawal when the substance of abuse (drugs/ gambling) is removed.
  • ICD 10 definition of dependence syndrome includes both elements of addiction and dependence
  • Note addiction has been removed from ICD 10/ DMS 5 as it is considered stigmatising.
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4
Q

What are the most common substances/ behaviours that lead to dependence?

A
  • analgesics and opiods
  • alcohol
  • tobacco
  • stimulants –> caffiene
  • sedatives/hypnotics –> solvents
  • psychoactive substances
  • gambling –> habit and impulse disorders
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5
Q

What is the main pathway associated with addiction?

A

The main pathway associated with addiction is the Reward pathway:

From the ventral tegmental area to the nucleus accumbens in the basal forebrain.

From here DA neurons project to the limbic system, (mesolimbic pathway) and the cortex (mesocortical pathway).

In the mesocortical pathway they project particularly to the prefrontal cortex where they are involved in higher cognitive function and personality.

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6
Q

The reward pathway is only part of a complex neural circuit involved in addictive behaviours. What are the three behaviours involved in addiction and dependence?

A
  • drug seeking/ craving behaviours : anticipation of obtaining or taking the drug prior to its use
  • Binging /Intoxication: taking the substance, the “highs”, tolerance and dependence
  • Withdrawal: negative effects of removal of the drug
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7
Q

What two main categories can dependence be divided into?

A
  • Psychological dependence – the need to keep performing compulsive behaviours, emotional distress on stopping these behaviours
  • Physical dependence –> the need for the functional effect of the drug on the body itself, characterised by physical symptoms on withdrawal of the drug.
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8
Q

What are some of the physiological signs of withdrawal from prescription drugs?

What are some of psychological signs of dependence on prescription drugs?

A
  • Legs throbbing –> muscles aches and cramps
  • emesis –> throwing up
  • hypothermia –> freezing all the time

Pyschological signs:

  • behavioural change
  • personality changes
  • postive reinforcement
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9
Q

What is dependence syndrome?

What is the ICD 10 definition?

What is this classified as in DSM V?

A
  • Dependence syndrome describes a group of behavioural, cognitive, and physiological phenomena that develop after repeated substance abuse. Typically includes:
    • strong desire to take drug
    • difficulty controlling its use
    • persisting in its use despite harmful effects
    • increased priority to drug use than other activities
    • tolerance
    • physical withdrawal
  • DSMV classes all these behaviours as substance abuse disorders.
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10
Q

What is tolerance?

How might a patient experiencing tolerance present?

A

Tolerance describes the requirement for increasing amount of the drug/ behaviour to elicit the same level of positive reinforcement “high” as experienced during previous exposures to the substance/ behaviour.

Presents with: request for higher dose, complaint drugs arent working as well as they used to, may attend multple sites to obtain additional substance

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11
Q

What occurs when a person is experiencing tolerance?

A
  • During tolerance the positve effects of the drug use is decreased with each use, whilst the negative effects are increased during the wear off.
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12
Q

What are the three types of tolerance?

A
  • Acute tolerance –> repeated use of the drug in a short time frame, e.g. cocaine use in 1 night, each high will be less than before
  • Chronic tolerance –> constant exposure to the drug over a longer period of time, e.g. opiod abuse
  • Learned –> frequent exposure to the substance that is integrated into normal behavioural routine, e.g. alcohol abuse and “high functioning”, individual learns to compensate for the effects of alcohol.
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13
Q

Does exhibiting tolerance mean a person has an addiction/ dependence?

What is the physiological basis for tolerance?

A
  • Exhibiting tolerance does not mean an individual has an addiction/ is dependent.
  • Tolerance simply means decreased sensitivity or increased resistance to a drug that can result from long term exposure to many substances.
  • May lead to alteration in receptor density/ conformation or circuitry affected.
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14
Q

What is withdrawal and how does it differ from the immediate crash that occurs after wear off of the drug/ behaviour?

A
  • Withdrawal describes the effects of the removal of the substance
  • It is often prolonged and painful, also termed detoxification.
  • “Crash” is the rebound dip in mood or behaviour occuring immediately after wear off of the drug/ behaviour.
  • Crash actually occurs before plasma levels of the drug wear off, due to a change in regional neuronal activation.
  • High in striatum/ thalamus/ nucleus accumbens/ cortex subsides other areas take over such as striatum/ amydala, negative aspects become more dominant.
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15
Q

Complete this table with the physical and psychological effects of withdrawal

A
  • Psychological: HIDe Away Feel Crap
    • headache
    • irritability
    • dysphoria–> unease and dissatisfaction with life
    • anxiety, anhedonia
    • fatigue
    • confusion
  • Physical: SWEATTTY
    • Tachycardia
    • Tachypnoea
    • Tremor
    • hyperhidrosis
    • lacrimation
    • rhinorrhea
    • confusion
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16
Q

Why are some of the psychological symptoms of withdrawal also classed as physiological?

A
  • Withdrawal leads to physiological changes
  • physiological changes affect neuronal cell function
  • leads to psycholigcal changes occuring
  • e.g. confusion due to altered neuronal metabolism
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17
Q

What is the difference between acute withdrawal and PAWS?

A
  • Acute withdrawal: matter of weeks
    • tremors and seizures
    • intense cravings
    • autonomic hyperreactivity
  • PAWS: Post acute withdrawal syndrome:
    • months after initial withdrawal
    • psychological changes: insomnia, mood swings, anxiety, anhedonia
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18
Q

Label the following diagram showing the brain regions involved in the three stages of dependence:

1) druk seeking behaviour
2) binging behaviour
3) withdrawal behaviour

A

Green circuit –> Orbitofrontal cortex, mPFC (Medial prefrontal cortex), hippocampus

Red circuit —> Amydala, BNST (Bed nucleus of stria terminalis), which is the centre of integration for the limbic system, and ventral striatum

Blue circuit –> dorsal striatum, globus pallidus

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19
Q

What behaviours are the circuits shown involved in?

A

Green circuit –> Drug seeking behaviour: preoccupation, anticipation, craving, conditioned cues

Blue circuit –> Binge behaviour: euphoria, binge, reward, intoxication and habit

Red circuit –> negative emotions, dysphoria (unease general dissatisfaction), malaise, withdrawal

20
Q

Fill out the picture

A

Salience = want/ desire

21
Q

What is the effect of withdrawal from alcohol?

A
  • during withdrawal from alcohol, may experience:
    • shakiness
    • sweating
    • anxiety
  • Due to overproduction of NA and Adrenaline to combat the depressant effects of alcohol, both are produced to increase output of symp NS to increase HR and BP.
  • When alcohol wears off left with excessive adrenaline/ NA
22
Q

What are the two key factors that alter whether someone is likely to become dependent?

A
  • Genetics
  • environment
23
Q

What type of inheritance pattern does dependence follow?

A
  • Polygenic inheritance pattern
  • most behaviours are moderate - highly heritable, but are triggered and reinforced by personal choice.
24
Q

How does the route of administration infuence the likelihood of dependence forming?

Rate the speed of administration and the concentration peak in the CNS

A
  • Route of administration determines the speed at which the drug hits the CNS, and therefore has an effect on the likelihood of the drug and positive effects forming.
  • Inhalation, fast, large peak
  • injection similar to inhalation, fast large peaks of conc in CNS
  • Snorting, slower peak
  • ingestion, slowest onset of peak conc in brain
25
Q

What is the transtheoretical model for behaviour change?

A
  • Its is a behavioural model for the stages through which an individual must go to alter a health related behaviour. Many rehabiliation clinics base their programmes around this model.
  • The stages are:
    • precontemplation
    • contemplation
    • preparation
    • action
    • maintenance
    • can also replapse –> expected individuals will have to go through the cycle a few times before the behaviour will stick, reflect why relapse occurred and put systems in place to prevent it.
26
Q

where does nictoine act?

Where is its primary site of action?

how can it act?

what is its main action?

what receptor does it bind to?

A
  • Nicotine acts both centrally and peripherally, in the ANS/autonomic ganglia where they have their main effects
  • Nicotine can act as both a depressor and stimulant
  • Nicotine main action is to act as a parasympathomimetic
  • Nicotine binds to the nicotinic AchR (nAchR).
27
Q

What substances are released by nicotine use and what are the effects of the release of these substances?

What is the physiological basis of nicotine addiction

A
  • Stimulant effects caused by the release of Ach, NA , adrenaline at low doses of nicotine
  • Positive/ addictive effects caused by release of NA/ 5HT/ DA
  • cognitive enhancement and fine tuning of movement thought to postively reinforce addiction
  • Tobacco also contains MAOI’s, increasing +ve effects and addictive effects even more.
28
Q

What treatments are involved in smoking cessation programmes?

A
  • Counselling and pharmacological treatment which includes:
    • nicotine replacement therapy
    • atypical antidepressant buproprion
    • varenicline - partial agonist at nicotine receptor (link between taking drug and increase suical ideation.)
29
Q

What is the equation for units?

A
  • Units = ABV (alcohol by volume) % x volume (ml) / 1000 = units
30
Q

What are the pharmacological considerations of alcohol?

A
  • Speed of onset and ease of administration
  • Rapid absorption via small intestine
  • lipid solubke and non tissue specific
  • absorption is slower with higher percentage as slows peristalisis
  • Absorption slower with food (fat and carbs).
31
Q

What is the effect of alcohol on the brain at neuronal level?

How does this change with chronic use?

What region of the brain does it affect?

A
  • Alcohol acts like an anaesthetic in the CNS, depressant. Thought to:
    • enhance GABA activity
    • Inhibit glutamatergic NMDA receptors
    • inhibit VG calcium channels
    • Note chronic alcohol use reverses these effects, linked to insomnia and anxiety.
  • Known to affect the cerebellum due to an increased number of cells in this brain region –> loss of fine tuning motor control and gait issues
  • frontal lobe –> cognition and bladder control (frontal micturition centre).
32
Q

What are two screening tools for alcohol misuse?

A
  • AUDIT and AUDIT C
  • alcohol use disorder identification test
  • 5 or more for +ve AUDIT C
33
Q

What is fetal alcohol syndrome?

How would an infant present?

How would a child or adolescent present?

A
  • Fetal alcohol syndrome describes a developmental disorder caused by alcohol consumption during pregnancy, mainly occurs during 1-3 months pregnancy. Associated with growth and cognitive retardation.
  • As alcohol rapidly diffuses across all membranes there is no safe amount that can be consumed during pregancy
  • Alcohol associated with miscarriage and amenorrhoea
  • Neonate presents with thip upper lip, absent philtrum, flat mid face, small nose, low nasal bridge, ear abnormalities, epicanthal fold (skin fold of upper eyelid covering inner corner of eye).
  • Child presents with irritability, slow development and hyperactivity
  • teens present with learning difficulties, poor impulse control and coordination, heart defects.
34
Q

What are the most common opiod receptors called?

What is the pattern of receptor expression associated with opiod dependence?

A
  • µ, κ, δ and NOP (nociceptin opiod receptor).
  • Dependence receptor expression:
  • decrease in mu R,
  • increase in Kappa R –> links to behavioural change addiction
  • psychoactive effects linked to Kappa activation and sigma R
35
Q

Do all opiods have the potential to become addictive?

What class of drugs are used to treat heroin addiction?

A
  • All opiods have the potential to become addictive, not just heroin
  • Heroin addiction is treated with Kappa - agonists as they reduce the “highs” and stimulate mu R production to replace those lost in addiction.
36
Q

what is maitenance therapy?

What two drugs are used in maitenance therapy?

A
  • Maintenance therapy/ substitution therapy = patient substitues heroin for another opiod and remains on stable dose to allow slow withdrawal
  • Opiods used in maintenance therapy:
    • methadone
    • buprenorphine
  • Methadone –> T 1/2 24 hrs, mu receptor agonist
  • Buprenorphine –> T1/2 12 hrs, partial agonist mu receptor, partial agonist/ antagonist at kappa receptor
37
Q

What drug can prevent relapse in alcohol and opiod dependence?

A

Naltrexone (mu, kappa and delta antagonist)

MOA: reduces the “highs” of alcohol and opiod use

38
Q

Stimulant drugs:

What are the effects of a stimulant?

What are they used to treat clinically?

What are the examples?

A
  • Increase activity of the CNS, increasing focus, energy, alertness
  • Clinically treat ADHD
  • Examples: Cocaine, caffiene, amphetamine
39
Q

Most commonly used stimulant is caffeine:

What can caffeine overuse lead to?

How is caffeine a stimulant?

A
  • Caffeine overuse linked to dependence and withdrawal symptoms
  • Caffeine headache, associated with withdrawal, linked to changes in cerebral blood flow
  • Caffeine thought to work in the following ways:
    • Adenosine A2A receptor antagonist (Adenosine = inhibitory NT) (Principal MOA)
    • Noradrenaline increase, increase arousal, vigilance, reduce fatigue
    • increase Ca2+ from IC stores
40
Q

What is cocaine?

What is its mechanism of action?

What is its main site of action?

A

Cocaine is a powerful stimulant and sympathomimetic.

MOA: inhibits the monoamine transporters (MAT). Inhibits reuptake of 5HT > DA > NA

5HT is dominant site of action.

Sympathomimetic –> modulates interaction between 5HT and NA, modulates autonomic regulation of thermoregulation centre in hypoT

41
Q

What are amphetamines?

What is their MOA?

Examples?

A

Amphetamines are stimulants that act by:

Blocking vesicular monoamine transporter (VMAT), meaning less MA’s taken up into vesicles, so more are released when channels open.

Amphetamines reverse MAT which dumps MA into synaptic cleft

Examples: MDMA, speed, crystal meth

42
Q

What are tranquilisers used for?

What are the two main groups of tranquilisers?

A
  • Tranquilisers used to sedate, relax and induce calm
  • Major tranquilisers –> antipsychotic (non addictive)
  • Minor –> relaxants (muscle and neuro) (addictive)
  • Examples: Benzodiazpines and Barbiturates
43
Q

What are psychotomimetics?

what are the main drugs included in this group?

What receptors do they act on?

A
  • Psychotomimetics cause a change in perception and sensory distortion –> hallucination hence term hallucinogenic/ psychedelic drugs
  • Two groups:
    • Drugs acting on 5HT –> MDMA, mescaline, LSD “Acid”
    • Drugs acting on glutamate receptors (NMDA) –> PCP and ketamine
44
Q

What is MDMA?

What is its MOA?

What are the adverse effects?

A
  • MDMA is an amphetamine analogue, inhibits 5HT monoamine transporter, but also DA and NA too (lesser extent).
  • Euphoria and high energy
  • Adverse effects: hyperthermia, acute electrolyte loss, dehydration
  • Death from acute hyperthermia, skeletal muscle and renal failure, changes in mitochondrial function
45
Q

What is PCP?

What was its original use?

When abused what are its effects?

what is its MOA?

A
  • PCP = angel dust
  • used as an anaesthetic and painkiller, side effects of hallucinations, and transient psychotic states led to its discontinuation
  • Drug of abuse –> numbness, detachment, increased positivity, panic and paranoia
  • MOA: Blocks NMDA glutamate receptor, binds on inside preventing influx of Na+ and Ca2+
  • NMDA receptors enhance long term potentiation
46
Q

What is ketamine?

A
  • Class B drug, originated as a horse tranquiliser, clinically used to induce and maintain anaesthesia
  • Similar actions to PCP but fewer tendencies towards positive states, associated with panic and agitation
  • paralysis and sensory distortion can also lead to out of body experience
  • Binds to the NMDA receptor at the PCP binding site, (inside of NMDA receptor) preventing passage of Na+ and Ca2+