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PY353 > Substance Misuse > Flashcards

Substance Misuse Flashcards

1
Q

Define drug

A

Any natural synthetic or natural chemical substance that is used in the treatment, prevention or diagnosis of disease.

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2
Q

Why do people take drugs?

A
  • For pleasure, to get a ‘rush’, euphoria –> positive reinforcement/ reward
  • As anxiolytics or to overcome withdrawal –> negative reinforcement
  • Because people are addicted and cannot control their use –> overwhelming urge
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3
Q

The ____ the onset of the drug effects, the better the ______

A

faster

rush

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4
Q

Finish the chain, from slow to fast:

  • Chewing tobacco, _____, ____
  • _____ _____, paste, _______, ____
  • ________, _________, snorted, __ ________
A
  • snuff, cigarettes
  • cocoa leaves, cocaine, crack
  • methadone, morphine, IV heroin
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5
Q

Explain the science of addiction.

A
  • Drugs of abuse increase DA in the nucleus accumbens of the mesolimbus
  • Increase in DA is key to +ve reinforcement
  • DA increased by cocaine, amphetamines, alcohol, opiates, nicotine and cannabinoids.
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6
Q

The nucleus accumbens has high levels of ____ receptors

A

D3

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7
Q

The nucleus accumbens:

A
  • high levels of D3 receptors
  • DA release here is involved in learning associations
  • Reduced DA is noted in withdrawal states and is likely to be associated with depression, irritability and dysphoria.
  • DA is modulated mu opioids
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8
Q

Opiates are ______ substances ; e.g. ______, ______

Opioids are ____- _______; e.g __________, _______
or ______; e.g. ______

A

natural
morphine, codeine

semi synthetic
dihydrocodeine,heroin

synthetic
methadone

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9
Q

What receptors do opioids act as agonists at?

A

delta
kappa
mu
nociceptin receptors

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10
Q

What effects are seen when opioids bind to delta receptors?

A

antidepressant, physical dependence, analgesia

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11
Q

What effects are seen when opioids bind to kappa receptors?

A

sedation, dysphoria, miosis, inhibition of ADH release

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12
Q

What effects are seen when opioids bind to mu receptors?

A

analgesia, euphoria, +ve reinforcement, respiratory depression

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13
Q

What effects are seen when opioids bind to nociceptin receptors?

A

anxiety, depression, appetite, tolerance to mu agonist

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14
Q

What are some chronic effects of opioids?

A

depression, insomnia, constipation, dependence, ahedonia

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15
Q

What are some acute affects of opioids?

A

itching, miosis, nausea, euphoria, drowsiness, tranquility

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16
Q

Mechanism of tolerance is?

A

not well understood

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17
Q

How are opioids taken?

A

smoked, swallowed, injected, inhaled

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18
Q

Opioid withdrawal:

A
  • may occur within hours of the last ‘fix’
  • may peak between 2 - 4 days
  • usually will not last beyond 7 days

THE ONSET, INTENSITY AND DURATION IS MULTIFACTORIAL. (e.g. previous experiences of withdrawal may be an important variable)

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19
Q

What are some symptoms of withdrawal?

A 
Depression
Diarrhoea
Shivering
Restlessness
Insomnia
Dilated eyes
Myalgia
Tachycardia
Piloerection
Rhinorrhoea
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20
Q

Opioid withdrawal is associated with

A

increased noradrenergic activity due to opioid affect on locus coeruleus… tachycardia, piloerection

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21
Q

short term opioid detoxification takes

A

30 days

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22
Q

long term opioid detoxification takes

A

180 days

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23
Q

what are some pharmacological aids for opioid detoxification?

A

In order to suppress all aspects of withdrawal:
methadone - full mu agonist
buprenorphine - partial mu agonist

In order to suppress autonomic signs - not subjective discomfort
clonidine - a2 adrenoceptor agonist

24
Q

rapid opioid detoxification takes

A

3-10 days

25
Q

ultra rapid opioid detoxification takes

A

1-2days

26
Q

ultra rapid opioid detoxification:

withdrawal is precipitated using?

A 
naloxone 
naltrexone
PLUS: -
clonidine
benzodiazepine
general anaesthesia
27
Q

What’s the risk of rapid/ ultra rapid opioid detoxification

A

respiratory distress, renal complications

28
Q

How does methadone work?

A

Attenuates withdrawal + craving but patient does not experience ‘rush’

29
Q

Why is methadone administration supervised?

A

to reduce risk of abuse (there is some evidence of a black market for methadone - addicts sell methadone to finance buying heroin)

30
Q

Maintenance therapy of methadone.

Talk about it’s half life

A

It can be v. effective but there is risk of dependence.

It has a long half life. One oral dose of methadone can suppress craving for heroin + withdrawal symptoms for 36 hours.

31
Q

Acute action of opioid is to _____ cAMP and _______ NA neuronal firing.

A

inhibit

reduce

32
Q

Chronic action of opioid is ________ __-_____ of cAMP. This results in an _______ in NA tone which is revealed on _________ symptoms

A

compensatory
up-regulation
increase
withdrawal

33
Q

Compare methadone and buprenorphine for maintenance/ detoxification

A

Methadone:

  • full mu opioid agonist
  • half life: 24hrs but on chronic dosing; 36hrs.

Buprenorphine

  • partial mu opioid agonist therefore reduced risk of respiratory depression
  • Antagonist at kappa therefore less likely to cause dysphoria
  • half life: 24hrs therefore withdrawal syndrome less
34
Q

If heroin is injected, buprenorphine is useful because it’s ______ property will prevent relapse

A

antagonist

35
Q

What is naltrexone?

A
  • oral
  • non-selective opioid antagonist (blocks acute opioid effects)
  • used to prevent relapse in drug-free subjects
  • most common adr’s are GI
36
Q

Most common ADR for Naltrexone is?

A

GI disturbance

37
Q

What are some acute affects of cocaine?

A 
formication
euphoria
increase heart rate and bp
confusion
psychosis
38
Q

What are some chronic affects of cocaine?

A 
paranoia 
depression
psychosis
anorexia
variable effects on D1 and D2 receptors
39
Q

What happens when cocaine use stops?

A

‘CRASH’

  • depression
  • anxiety
  • hypersomnia (sleepy throughout the day)
  • anergia (abnormal lack of energy)
40
Q

What is the current therapy for cocaine use?

A

Partial D3 agonist

41
Q

THC alters both ______ and ________ neuronal activity

A

hippocampal

cerebral

42
Q

Acute effects of THC?

A 
relaxation
confusion
distorted perceptions
anxiety
impaired memory, concentration and coordination
43
Q

The most commonly abuse drug in the UK is?

A

alcohol

44
Q

Alcohol misuse results in

A 
Psychological
Physiological
Psychiatric
and
Societal damage
45
Q

Alcohol misuse is when:

A

a patient drinks to the extent of causing harm to self or others

46
Q

EQUATION FOR ALCOHOL UNITS

A

Alcohol by Volume (%) x Litres = units

47
Q

IF <50 units/week;

A

May not be required

48
Q

IF 50-100 units/week;

A

Consider detox

49
Q

IF >100 units/week

A

Detox required

50
Q

What are some risk factors that have an increased need for alcohol detox

A
  • older patients
  • severe dependence
  • Hx of failed community detox
  • Psychiatric co-morbidities - Poor physical health e.g. Diabetes, Liver damage, HTN
  • Hx of DTs and alcohol withdrawal seizures
  • Poor social support
  • Cognitic impariment
51
Q

What are some pharmacological agents for alcohol detox

A
  • Benzodiazepines e.g. Diazepam
  • Thiamine; High Potency Parenteral; Pabrinex IV / IM; 1 pair ampoules daily for
    3-5 days.
  • Then; long-term Vit B Co.Strong; One Tab PO; OD.

ALSO BREAKTHROUGH DOSE OF:
Diazepam 10mg PO Max TDS should be prescribed for ‘breakthrough’ withdrawal symptoms, WHEN REQUIRED

ALSO, FOR SEIZURES:
Diazepam 5 – 10mg PR; PRN for seizures should also be prescribed. WHEN REQUIRED

52
Q

Alcohol:

Pharmacological ‘Tools’ to support continued abstinence include:

A
  • Disulfiram ~ Antabuse
  • Acamprosate
  • Naltrexone
  • Nalmefene
53
Q

MOA of Disulfiram

A

Irreversibly inhibits effects of ALDH. SO, acetaldehyde accumulates. Leads to:

  • N&V
  • Headache
  • Sweating
  • Palpitations/ Tachycardia
  • Flushing
54
Q

Large doses of alcohol + disulfiram =

A
  • hypotension
  • collapse
  • arrhythmias
55
Q

Adverse effects of Disulfiram?

A
  • N & V
  • Halitosis
  • Psychiatric reactions; paranoia , depression
  • Hepatic cell damage

PY353 (19 decks)

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