Substance misuse Flashcards

1
Q

what is reinforcement and when is this likely to occur?

A

this is the addictive potential of a drug
drugs which act more rapidly are used more frequently and are subsequently more addictive, so a shorter half life drug e.g. lorazepam, is taken more often so is more reinforcing.

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2
Q

why is methadone less reinforcing?

A

longer t1/2 so taken less frequently

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3
Q

1st signs of opioid withdrawal?

A
sweating
akathisia
lacrimating
goosebumps
yawning
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4
Q

usual starting dose of methadone?

A

30mg

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5
Q

when would starting dose of methadone be lower?

A

anorexic patients

COPD patients

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6
Q

what is the dosing regimen for detoxification with methadone?

A

once stable on dose (usually around 60mg), can be reduced at a rate that will result in 0 in around 12 wks. usually reduction of 5mg every 1 or 2 weeks.

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7
Q

how is it decided whether methadone or buprenorphine should be used for opioid detoxification?

A

start with same medication as used for any maintenance treatment/what the patient has stabilised with.
consider preference of service user.
pts report being able to reduce buprenorphine doses more quickly than methadone.

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8
Q

length of time for opioid detoxification?

A

4 weeks inpatient

up to 12 weeks outpatient

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9
Q

when might lofexidine be considered in opioid withdrawal?

A

this is a non-opioid alpha-adrenergic agonist and is not a controlled drug
may be considered in those who have decided not to use methadone or buprenorphine, those who have decided to detoxify within a short time period or have mild or uncertain dependence, including young people.

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10
Q

disadvantages of lofexidine in opioid withdrawal?

A

additional ST meds may be needed to control other effects of opioid withdrawal e.g. stomach cramps-mebeverine and diarrhoea-loperamide.
pt should be advised to take part of dose at bedtime to offset insomnia assoc with opioid WD.

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11
Q

side effects of methadone WD?

A

myalgia

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12
Q

why are patients at increased risk of OD on illicit drugs following opioid withdrawal?

A

lose opioid tolerance so will take more of the drug to have the same therapeutic effect as before, so increased risk of OD and death, that may be potentiated by use of alcohol or BZDs.

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13
Q

what are the indications for service users to NOT have detoxification in a community setting, but as an inpatient?

A

previously not benefited from formal community based detoxification
need medical and nursing care as significant co-morbid physical or mental health problems
require complex polydrug detox, e.g. concurrent detox from alcohol or BZDs
are experiencing significant social problems that will limit benefit of community based detox.

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14
Q

what drug may be helpful following opioid detox to maintain abstinence?

A

naltrexone=opioid antagonist
blocks former opiate user from experiencing effects of opiates
LFTs to be done before and during tmetn as potentially hepatotoxic
usual 50mg maintenance

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15
Q

general measures in stimulant withdrawal e.g. cocaine?

A

giving preventive advice about safer injecting practice
treat psychiatric problems on a symptomatic basis
abstinence-based psychosocial tment linking counselling and social support has been shown to have greatest impact on cocaine misuse
focus on stress reduction procedures if pt exhibits persistent anxiety and agitation
if persistent and severe psychotic symptoms, may need psychiatric unit admission
monitor pt’s mood and assess risk of suicide as stimulant WD can be assoc with significant depression
substitute stimulant prescribing does not have demonstrated effectiveness, but there is evidence that if maintenance tments of methadone or buprenorphine prescribed to those with opioid dependence who also take cocaine, their cocaine use can be expected to decrease or stop and when persists, may respond positively to improvement of opioid maintenance tment.

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16
Q

use of antidepressants in pts who misuse stimulants?

A

antidepressants such as the SSRI fluoxetine can be effective in management of major depressive episodes assoc. with stimulant use
BUT care must be taken if SSRIs given while using cocaine or amphetamines as toxic reactions have been described.

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17
Q

how does LSD in terms of dosage differ from other drugs?

A

only micrograms required to be effective, compared to milligrams for other drugs.

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18
Q

3 prominent effects cocaine has on the body?

A

powerful local anaesthetic
powerful vasoconstrictor
powerful psychostimulant that has stong re-inforcing qualities

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19
Q

major mortality risk with cocaine use?

A

MIs and CVAs as poweful vasoconstrictor causing rapid increase in BP and heart strain

20
Q

how is crack cocaine taken?

A

smoked-effects produced most quickly-greater experience of euphoria so reinforcement and possibility of side effects greater.
effects in 6-8s

21
Q

effects of cocaine on peripheral organs?

A

increased HR and vasconstriction, causing BP increase
increased muscular activity and vasconstriction causing increased body temp.
dilation of pupils
tremor
sweating

22
Q

CNS effects of cocaine?

A

euphoria, excitement, restlessness, decreased appetite

23
Q

cocaine MOA?

A

inhibits reuptake of dopamine, NA and 5-HT in synapse, potentiating their actions.
increase in dopamine causes euphoria

24
Q

why does tolerance occur with cocaine?

A

chronic exposure of post-synaptic receptors to dopamine causes a decrease in the number of post synaptic receptors (downregulation) and an increase in presynaptic dopamine transporter protein, so reduced sensitivity of postsynaptic receptors to dopamine and increased sequestration by presynaptic neurones.

25
Q

MOA of amphetamines (whiz, speed, uppers)?

A

synthetic chemicals which structurally resemble dopamine, 5-HT and NA.
can displace dopamine from storage vesicles so dopamine diffuses into synaptic cleft
euphoria and arousal produced via dopamine effect
decreased appetite likely due to NA effect

26
Q

behavioural effects of amphetamines?

A

stereotyped behaviour

thought to be due to effects of dopamine in the nigrostriatal system

27
Q

what is methamphetamine?

A

Ice/crystal/crank/meth
more pronounced stimulatory CNS effects than amphetamine, and less peripheral actions
high doses can produce psychotic reactions characterised by hallucinations, paranoia and mania.

28
Q

examples of psychostimulants?

A

cocaine
amphetamines
caffeine
nicotine

29
Q

mainstay of tment to eliminate symptoms of WD from stimulants?

A

psychosocial interventions

30
Q

Features of wernicke’s encephalopathy?

A

truncal ataxia-wide based gait
ophthalmoplegia-nystagmus, lateral rectus or conjugate gaze palsies
mental confusion

31
Q

Pathophysiology of wernicke’s encephalopathy?

A

Thiamine deficiency due to alcoholism or poor diet results in midbrain haemorrhages which produces an acute syndrome requiring tment with parenteral thiamine (pabrinex) to stop the bleeding.
Repeat haemorrhages occur (multiple wernicke’s episodes) produces korsakoff syndrome characterised by amnesia and confabulation- patients will tell you an elaborate story and then after 40 mins or so will give a completely different answer to the same qn asked as they can’t remember what they prev said.

32
Q

How does alcohol cause thiamine deficiency?

A

Destroys small bowel uptake pump

May be assoc with poor diet so pt takes in less thiamine.

33
Q

Why can buprenorphine only be given to combat WD from opioids in those who are already in mild withdrawal?

A

It is a partial agonist so produces only half a response

34
Q

Safety of buprenorphine in opioid WD?

A

Unable to OD on buprenorphine alone, partial agonist

Methadone-synthetic mu agonist

35
Q

Biochemical response in opioid withdrawal?

A

Profound dopamine decrease in nucleus accumbens and reduction in dynophin
Large increase in release of noradrenaline in hippocampus, nucleus accumbens and locus coeruleus

36
Q

How is alcohol thought to have an amnesic effect?

A

Inhibits ACh release in the CNS

37
Q

How is alcohol thought to have a positive reinforcing effect?

A

By binding to GABA A receptor, it results in inhibition of inhibitory interneurones, mediating excitatory effects on dopamine neurones in the VTA.
May also act directly on dopamine neurones.

38
Q

How is alcohol tolerance mediated?

A

Liver increases its amount of metabolising enzyme (25%of tolerance.)
Tissue of functional tolerance where neurones in brain adapt to amount of drug present.

39
Q

If detoxing from alcohol but pt has liver failure, which BZD should be used?

A

Oxazepam as least liver toxic.

40
Q

Symptoms of alcohol withdrawal?

A
Sweating
Tremor
Tachycardia
Anxiety
Visual hallucinations
Increase BP
Delirium tremens-requires BZD tment.
41
Q

Interventions for mild alcohol dependence?

A

Offer a psychological intervention e.g. CBT, behavioural therapy or social network and environment based therapies
Behavioural couples therapy if regular partner who is willing to engage
If unsuccessful or if asked for, consider pharmacological therapy with acamprosate or oral naltrexone alongside psychological intervention
For assisted WD, offer BZD chlordiazepoxide or diazepam. Gradually reduces dose over 7 to 10 days to prevent alcohol withdrawal from recurring. Give higher doses if severe alcohol dependence.

42
Q

Management of moderate to severe alcohol dependence after WD?

A

So WD with high dose of chlordiazepoxide or diazepam, reduced gradually over 7 to 10 days.
Then offer acamprosate or oral naltrexone with an individual psychological intervention e.g. CBT
Offer disulfiram for abstinence if acamprosate and naltrexone unsuitable or patient would prefer this.

43
Q

Considerations given to wernicke-korsakoff encephalopathy in alcohol WD?

A

In planned assisted WD give parenteral thiamine followed by oral thiamine to reduce risk of encephalopathy if in special inpatient alcohol services or prison and malnourished or at risk of malnourishment or have decompensated liver failure.

44
Q

what is delirium tremens and how is it treated?

A

medical emergency in which a hyperadrenergic state is present
due to alcohol WD state where loss of GABA A receptor stimulation causes a reduction in chloride flux and is assoc with tremors, excessive sweating, tachycardia, anxiety and seizures. lack of glutamate NMDA receptor inhibition may cause seizures and delirium.
characterising features=altered mental status=confusion, delusion, severe agitation, hallucinations-auditory, visual-lilliputian or olfactory
usually begins 1-3 days post stopping alcohol

A to E approach to patient
sedate patients with BZDs e.g. diazepam-rapid action onset, addition of barbiturates may also be necessary in those refractory to BZD treatment and may reduce the need for mechanical ventilation in very unwell patients in ITU.
if also wernicke’s encephalopathy, need IV pabrinex (500mg thiamine) at least 2 pairs of ampolues TDS for 3 days, if response then continue with two ampoules of Pabrinex® once daily for five days or for as long as improvement continues.
Magnesium may also protect against seizures and arrhythmias.

45
Q

RFs for delirium tremens?

A

prev. delirium tremens
prev. hx of alcohol withdrawal seizures
older age
more severe WD symptoms of presentation
abnormal liver function
recent higher than normal levels of alcohol intake
co-existing infection or medical problems including hepatitis and pancreatitis