addictions Flashcards

1
Q

define tolerance

A

reduced responsiveness to a drug caused by previous administration

an example of homeostasis - body likes things the way they were

underlying mechanisms vary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when does tolerance develop

A

in response to many but not all drugs

e.g. opioids, ethanol, barbituates, benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

mechanisms of tolerance

A
  • drug metabolised faster (or if metabolite is the active form then it would be metabolised slower to produce a smaller effect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is dispositional tolerance

A

less drug reaches the active site:

  • decreased rate of absorption
  • increased rate of metabolism to inactive metabolites
  • decreased rate of metabolism to active metabolites
  • increased rate of excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is pharmacodynamic tolerance

A

aka tissue/functional tolerance

site of action is less affected by the drug:

  • down-regulation or internalisation of drug receptors
  • reduced signalling down stream of drug receptors
  • some other compensatory mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how is tolerance linked to dependence

A

development of tolerance may also lead to withdrawal symptoms

e.g. drug effect - reduced transmitter release (unbalanced state)
adaptive response - increased sensitivity to transmitter (balanced state)
drug removed - unbalanced state again and now the adaptive response remains; the development of tolerance will cause dependence on the drug to achieve the normal state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

withdrawal phenomena

A

the withdrawal effect of a drug is usually the reverse of the acute effect

development of tolerance may lead to physical dependence in order to avoid the (unwelcome) withdrawal effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the reward pathway

A

neurones project from the ventral tegmental area to the nucleus accumbens and prefrontal cortex

when VTA neurones are stimulated dopamine is released

this causes a sensation of pleasure/reward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why has the reward pathway evolved

A

the reward pathway is normally activated by eating, drinking and sex

it therefore encourages those ‘healthy’ behaviours that lead to propagation of your genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

drugs and reward centres

A

some drugs of abuse tap into the reward pathway and increase dopamine levels e.g.

  • heroin - increases firing rate of dopaminergic neurones
  • amphetamine - increases dopamine release
  • cocaine - inhibits dopamine uptake
  • alcohol - inhibits inhibitory synapse (?)

produces the psychological component of addiction - craving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

issues of risk re. drug use

A

type of drug and effect
purity, dose, strength, tolerance
route of administration + unsterile nature
legal status - different jurisdictions
comorbid health conditions
likelihood of dependency
method of purchase - legal, prescribed, OTC, black market, internet

drug related deaths - >1000 p/a in scotland and increasing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what substances have the biggest impact on local health services and communities

A

alcohol

heroin/opiate misuse
benzodiazepine misuse
cocaine/crack cocaine misuse

cannabis misuse - most widely abused but relatively lower risk profile than the above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

examples of stimulant drugs

A

cocaine
amphetamine (speed)
methamphetamine - much more common in US/australia
methylphenidate (prescribed for ADHD, mild stimulant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cocaine

  • historical use
  • forms
A
most potent natural stimulant
historical indigenous use
extracted from leaves of coca plant 
first isolated in 1880s
formerly used in ENT surgery
cocaine (powder), crack cocaine (smoked)
crack produced by mixing cocaine w/ base (sodium bicarbonate) and purified
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does cocaine work

A

monoamine reuptake inhibitor - dopamine, serotonin, noradrenaline increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

issues with cocaine abuse

A

settings for drug use - financial wealth to poverty

image issues - crack cocaine vs powder

significant issue in NE Scotland

can use a large amount w/o overdosing (huge financial issues and associated problems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

rate of onset of effects of cocaine

A

depends on dose and rate of entry to the brain

smoking - almost immediate
injecting (high risk) - 13-30s
snorting - 3-5mins

effects of crack smoking are very intense but short lived (15 mins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effects of cocaine

A

stimulant and euphoriant

anaesthetic effect

hypersensitive - noises, light

increased alertness and energy

increased confidence and impaired judgement

lessens appetite and desire for sleep

if mixed w/ alcohol –> cocaethylene (like cocaine but with longer 1/2 life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

medical problems w/ cocaine use

A

damage to nose and airways (from consistent vasoconstriction)

convulsions w/ resp failure

cardiac arrhythmias and MI - very cardiotoxic

HT and CVA

toxic confusion

paranoid psychosis

20
Q

cocaine withdrawal effects

A
depression 
irritability 
agitation
craving 
hyperphagia - want to eat lots
hypersomnia - want to sleep lots

broadly opposite of drug effect

21
Q

amphetamine

  • route of administration
  • effects
  • problems
A

generally amphetamine sulphate

sniffed, swallowed or injected

effects similar to cocaine but longer lasting

toxic confusion occasionally w/ convulsions and death
amphetamine psychosis in heavy chronic use

22
Q

how does amphetamine work

A

dopamine enhancer

23
Q

examples of opiates

A
opium 
morphine 
heroin (diamorphine)
methadone 
codeine and dihydrocodeine
24
Q

heroin

- history and forms

A

first synthesised from morphine in 1874

addictive potential unrecognised for yrs - marketed as treatment for morphine addiction and cough

available as diamorphine or diamorphine hydrochloride

may be presented as powder or tar like substance

25
Q

heroin

- route of administration

A

snorting (uncommon in UK)
smoking
injection (cultural or tolerance reasons)

smoking is safest, injecting is the most dangerous

26
Q

how does heroin work

effects from different receptors

A

opioid agonist
acts via mu receptors (principally)
- acts principally via mu, delta and kappa receptors

kappa and delta - analgesia
mu - mood effects, analgesia, euphoria

27
Q

heroin 1/2 life

A

30 mins

multiple administrations needed if dependent (increased risk)

subjective effect of ~4hrs

28
Q

heroin effects

A

analgesia
emotional analgesia - you know the problems are still there but you don’t care
nausea initially
euphoria
pin point pupils
itching/sweating
constipation
decreased libido/menstrual irregularities
reduced cough reflex - risk of resp infections

29
Q

heroin and overdose

treatment

A
resp depression 
snoring indicates risk 
bradycardia
hypotension 
death 

risk increased if mixed w/ other resp depressants - alcohol, benzodiazepines etc

naloxone - opiate antagonist (national naloxone programme)

30
Q

side effects of opiates

A

1st time - N+V, headache

medium term - phlebitis, endocarditis, injection injuries/consequences (BBVs), anorexia, constipation

longer term - tolerance, withdrawal, social and health problems

31
Q

opiate withdrawal syndrome

A
craving 
insomnia 
yawning
muscle pain and cramps
increased salivary, nasal and lacrimal secretions
dilated pupils
piloerection
32
Q

methadone maintenance

A

decriminalises drug use
allows normalisation of lifestyle
reduces IV misuse
leakage onto the illicit market

33
Q

examples of benzodiazepines

A
diazepam (valium)
nitrazepam 
temazepam 
alprazolam (xanax)
lorazepam 
etizolam
34
Q

benzodiazepines

what are they
how do they work

A

previously misused medical prescriptions

now easily accessible online - main route for misuse
can be abused in huge doses

GABA agonists

anxiolytics, sedatives

35
Q

ecstasy (MDMA)

what is it
route

A

3,4-methylenedioxymethamphetamine

almost always oral

relaxed euphoric state w/o hallucinations

majority of ecstasy tabs contain no MDMA

instead nil active, LSD, amphetamine, ketamine (?)

36
Q

ecstasy effects

A

likened to mixture of LSD and amphetamine

euphoria followed by feeling of calm

increased sociability

inability to distinguish between what is and isn’t desirable

effects after 20 mins lasting 2-4hrs

37
Q

ecstasy side effects

A
nausea and dry mouth 
increased BP and temp 
risk of dehydration in clubs
large doses can cause anxiety and panic 
drug induced psychosis 
? liver and brain cell damage
38
Q

cannabis

what is it
forms

A

most commonly used illicit drug

tetrahydrocannabinol is the psychoactive agent

presented as marijuana, hashish (cannabis resin), oil (extract cannabinoids from plant material w/ solvent)

sensimilla (skunk) has a high THC content

39
Q

effects of cannabis

A

THC - psychedelic, hallucinatory effect
CBD - anxiolytic and antipsychotic effect

important balance between THC and CBD

harm reduction advice
CBD products now legally available

40
Q

psychological effects of cannabis

A
relaxing or stimulating 
euphoriant 
increases sociability and hilarity 
increases appetite
changes in time perception
synaesthesia

higher dose - anxiety, panic, persecutory ideation, hallucinatory activity

41
Q

ill effects of cannabis

A

resp problems as w/ tobacco
toxic confusion
exacerbation of major mental illness
cannabis psychosis

42
Q

performance and image enhancing drugs

areas for risk

A

anabolic steroids
growth hormone
injectable tanning agents e.g. melotan

risk from drug effect, route of administration and route of access

43
Q

steroid side effects

A

CV - increased cholesterol, HT

growth deficits due to premature closure of epiphysis

liver disease - cholestatic jaundice, liver tumours

44
Q

how to decide on treatment for drug abuse

A
what drug 
what combinations 
is it harmful/hazardous use
dependency 
risk
45
Q

areas of treatment for drug abuse

A

biopsychosocial treatment packages

strong emphasis on risk reduction

abstinence vs harm reduction debates

treatment is effective

46
Q

how to manage drug related deaths

A

public health crisis

optimise treatment 
reduce barriers to treatment 
public health rather than criminal justice response
research 
national naloxone programme
47
Q

heroin 1/2 life

A

30 mins

multiple administrations needed if dependent (increased risk)

subjective effect of ~4hrs