SUBSTANCE MISUSE AND DEPENDENCE Flashcards
substance misuse
defined in ICD-10 as a disorder of regulation of substance use arising from repeated or continuous use of that substance and consisting of a strong internal drive to use that substance
dependence
physical need the body develops towards a particular substance
addiction
the altered behaviour as a result of an overwhelming psychological need for a substance
associated components with substance misuse
- behavioural aspects
- physical aspects
- psychological and associative aspects
- socioeconomic/environmental aspects
behavioural pattern of drug use
- overwhelming involvement with the use of a drug (compulsive use)
- the securing of its supply (compulsive drug-seeking)
- a high tendency to relapse after withdrawal
theories of dependence - negative reinforcement model
physical dependence (withdrawal theory)
- relates mostly to opiates, barbiturates, alcohol
- based largely on increased tolerance and physical dependence
theories of dependence - positive reinforcement models
positive incentive (reward) theory
- relates mostly to cocaine, amphetamine, nicotine
- based largely on reward and reinforcement
theories on dependence - problems with the negative model
- amphetamine, cocaine, nicotine form strong dependency but have relatively little withdrawal effect
- alcohol and barbiturates have greater withdrawal but cause less dependence than heroin
what is a critical incentive during addiction
speed of effect
- heroin is biochemically converted to morphine in the body
- heroin enters the brain faster than morphine
injection > inhalation > absorption
cocaine speed into the bloodstream
IV > smoked > intranasal > oral
key dependence/reward pathways in the brain that operate via dopamine transmission
- dopamine signalling from the ventral tegmental area (VTA) to the nucleus accumbens (NA) is increased by drug action
- glutamate projections from the NA cause the prefrontal cortex to remember the environments and behaviours which leads to the reward
- excess signalling of glutamate neurons in the prefrontal cortex stimulates the NA, triggering drug-seeking behaviours at the expense of normal behaviours
environment/cues and relapse
dopamine release and sensitization creates a form of memory that cues (drug paraphernalia, social situation etc.) can induce dopamine release… even in the absence of drug
this could be a driver of relapse
how do different drugs of misuse act
- stimulants (cocaine, nicotine)
- depressants (tranquilisers, alcohol)
- opioids (heroin, methadone)
- marijuana/cannabis (clear dependence or reduced drive, memory problems etc.)
actions of stimulants
- cocaine inhibits the dopamine reuptake transporter
- amphetamines reverse the same transporter
- nicotine stimulates Ach receptor neurons but these in turn stimulate dopaminergic neurons
net effect of stimulants and risks
net effect: chronic dopamine flood into synapses and stimulation of dopamine receptors on target neurons
risk: unlike most drug-receptor interactions, those directly involving the dopamine system sensitize over time (contrast with tolerance) leading to greater desire
dependence of depressants: baributates and benzodiazepines
- patient failure to adhere to prescribed doses can cause dependence
- CNS develops tolerance to BZs sedation over a few months - leads to withdrawal (esp. short-acting/high potency forms) pt escalates dose beyond the prescribed amount
action of depressants
alcohol and barbiturate depressant actions are mediated by hyperexcitability of the inhibitory GABA receptors
be aware that both indirectly trigger the dopaminergic system
receptors for endogenous opioids
- mu receptor prefers B-endorphin
- delta receptor prefers enkephalins
- kappa receptor prefers dynorphins
drugs that act on the mu receptor
morphine
heroin
methadone
action and onset of morphine withdrawal
morphine blocks cAMP secondary messenger production, neurons try to redress cAMP balance
when morphine absent, too much cAMP generated… this ‘sensitization’ induces withdrawal symptoms
pharmacologically active components of marijuana/cannabis
- tetrahydrocannabinol (THC: main psychoactive ingredient)
- cannabidiol (CBD: relaxant/anti-inflammatory action)
- cannabinol (CBN: small psychoactive effect)
marijuana/cannabis mode of action
act on cannabinoid receptors CB1 and CB2 which are located throughout the brain and peripherally and bind the endogenous signalling molecules ‘anandamide’ and ‘2-arachidonoylglycerol’
action via dopamine release
experimental use of drugs
few occasions, curiosity, anticipation (short-lived)
recreational use of drugs
variable pattern of use, compliments users social activities
no adverse social or medical consequences
largely confined to weekend use - perception of harm associated with use is variable and at times contraindicatory
psychiatric co-morbidity
pharmacy services are geared towards substitution therapies (treatment of substance misuse) OR treatment of psychiatric morbidity (psychosis, depression)
1st-degree psychiatric diagnosis
- enjoyment/relaxation
- self-medication/escape
- peer group acceptance
- psychosis and cannabis, stimulants
- affective disorders and alcohol, stimulants
- PTSD, anxiety disorders and alcohol
1st degree substance misuse diagnosis
- genetic vulnerability/predisposition to psych illness
- dependent/chaotic lifestyle may act as precursor for mental health problems
- alcohol and depression, anxiety
- opiates and depression
- stimulants and depression, psychosis
- cannabis and depression, psychosis
gender-specific issues
- women more likely to have experienced trauma/abuse (physical, sexual and emotional) leading to SM/co-morbidity - can lead to re-victimisation (fund habit through prostitution, further risk of trauma)
- women tend to seek help from services for psychological problems then substance misuse
