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Addiction Flashcards

1
Q

what are the causes of addiction?

A
  • Genetic
  • Environmental – psychological stressors, ACEs
  • Age – adolescents
  • Comorbid – ADHD, PTSD
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2
Q

how is stress related to addiction?

A

acute stress triggers dopamine release, chronic stress causes downregulation of D receptors

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3
Q

which neuro pathway is the reward pathway?

A

mesolimbic pathway

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4
Q

what neurotransmitter is largely involved in addiction?

A

Dopamine

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5
Q

where is dopamine produced from?

A

VTA midbrain

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6
Q

what areas of the brain are involved in the mesolimbic pathway?

A

Amygdala
Nucleus Accumbens
Prefrontal cortex
Hippocampus

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7
Q

what is the role of dopamine?

A

DA is released when we experience pleasure and
removed from synaptic space into neuron by DA receptors triggering response and neuron activation
DA molecules are then removed from receptors and reabsorbed back via DA transporter

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8
Q

what are the dopamine levels in addiciton?

A

Initially elevated

As addiction continues brain limits amount - tolerance

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9
Q

what is the role of noradrenaline in addiction?

A

o NA and A released to put bodies in motion to complete addictive act
o Upregulation of ATP to allow for the increased production of noradrenaline
o Explains jitters in withdrawal and tolerance

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10
Q

what is the mechanism of tolerance development?

A

o Due to repeated dopamine release, dopamine receptors are down regulated
o Threshold for rewards during abstinence is increased.

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11
Q

what are the drivers of addiction?

A

Initially - reward (positive reinforcement)

Later - need (negative reinforcement)

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12
Q

what are the two ways that drugs can affect the brain pathway?

A

o Artificially mimic one of the naturally occurring NTs

o Alter availability of a NT

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13
Q

what are the common types of addiction?

A

Drugs, alcohol, gaming, extreme sports, social media, sexual

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14
Q

what are the different types of mimicking drugs?

A

Opiates
Nicotine
Alcohol

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15
Q

what is the mechanism of opiates?

A

similar structure to endorphin so binds to endorphin receptors - effect more powerful than natural substance

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16
Q

what is the mechanism of nicotine?

A

mimics ACh which triggers release of dopamine, glutamate and GABA (prevents inhibited response to dopamine)

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17
Q

what is the mechanism of alcohol?

A

binds to receptors for ACh and 5-HT causing sedative effects
Slower communication between neurons
Brain compensates by increasing production of NT

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18
Q

what are the examples of altering drugs?

A

Cocaine
Meth
Amphetamines

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19
Q

what is the mechanism of cocaine?

A

interrupts the reabsorption of DA and NA

High concentrations of DA and NA overstimulates the neurons and the person feels pleasure and energy

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20
Q

what is the effect of smoking meth?

A

causes excessive release of DA. Eventually the brain starts to produce an enzyme which will break down DA and reduce its ability to produce more

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21
Q

what are the CAGE features of addiction?

A

cut-down, annoyed, guilty, eye-opener

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22
Q

what is the ICD-10 criteria for addiciton?

A 
o	A strong desire to take the substance
o	Difficulties in controlling substance use
o	A physiological withdrawal state
o	Tolerance
o	Neglect of alternative pleasures
o	Persistence despite evidence of harm
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23
Q

what affect does alcohol have on the CNS?

A

depressant

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24
Q

what is the initial effect of alcohol in the brain?

A

depression of inhibitory neurons (feel relaxed + disinhibited)

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25
Q

what is the later effect of alcohol in the brain?

A

down-regulation of inhibitory neuronal gamma-aminobutyric acid receptors, up-regulation of excitatory glutamate receptors, and increased central norepinephrine activity

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26
Q

what parts of the brain are affected by alcohol?

A

Hypothalamus and Pituitary Glands, Medulla, nucleus accumbens, cerebral cortex, prefrontal cortex, cerebellum

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27
Q

what is the effect of alcohol on the hypothalamus and pituitary glands?

A

Increases sexual arousal, decreases ability to engage in sexual activity

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28
Q

what is the effect of alcohol on the medulla?

A

Increases sleepiness, Slows breathing, Lowers body temp

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29
Q

what is the effect of alcohol on the nucleus accumbens?

A

Pleasant or rewarding feelings

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30
Q

what is the effect of alcohol on the cerebral cortex?

A

difficulty thinking, difficult to speak clearly

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31
Q

what is the effect of alcohol on the prefrontal cortex?

A

More relaxed, Less self-conscious

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32
Q

what is the effect of alcohol on the cerebellum?

A

Affects coordination, Difficulty walking and driving

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33
Q

what neurotransmitter does alcohol largely affect?

A

GABA - enhances effect

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34
Q

what are the different factors that can contribute to alcohol misuse?

A 
Genetic
Psychological 
Occupational 
Cultural
Availability
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35
Q

what are the psychological factors that contribute to alcohol misuse?

A

children who are impulsive, aggressive and hyperactive, also anxiety

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36
Q

what occupations factors are implicated in alcohol misuse?

A

doctor, entertainer, wine merchant, bar staff, armed forces, publican, journalists

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37
Q

what are the cardiovascular consequences of alcohol misuse?

A

o moderate intake protective?

o high intake – increases BP – increases risk of IHD, CVA Stroke, arrhythmias

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38
Q

what are the hepatic consequences of alcohol misuse?

A

hypoglycaemia, lactic acidosis – leads to fatty liver, cirrhosis, oesophageal varices, hepatitis (reduced clotting factors, reduced albumin, asterixis, jaundice

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39
Q

what are the GI consequences of alcohol misuse?

A

gastritis, pancreatitis (nausea, vomiting, abdo pain, haematemesis), poor teeth

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40
Q

what are the blood consequences of alcohol misuse?

A

anaemia (macrocytic, megaloblastic)

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41
Q

what are the consequences of sexual function in alcohol misuse?

A

o short term increases

o long term damages leydig cells – causing decreased testosterone = loss of libido, infertility, loss of male body hair

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42
Q

what are the neuropsychiatric consequences of alcohol abuse?

A 
o	vitamin B peripheral neuropathy and dementia 
o	withdrawal =  seizures
o	sleep – decreases REM, poorer quality
o	impaired memory
o	depression/anxiety
o	Subdural hematoma
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43
Q

what are the dermatology consequences of alcohol abuse?

A

increased superficial cutaneous vasculature, urticarial reactions, porphyria cutanea tarda, flushing, cutaneous stigmata of cirrhosis, psoriasis, pruritus, seborrhoeic dermatitis, and rosacea

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44
Q

what is the ICD-10 criteria for alcohol abuse?

A

A pattern of psychoactive substance use that is causing damage to health. The damage may be physical or mental

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45
Q

what is the ICD-10 criteria for alcohol dependence syndrome?

A

o Strong desire or sense of compulsion to take drug
o Difficulty in controlling use of substance in terms of onset, termination or level of use
o Physiological withdrawal state
o Evidence of tolerance
o Progressive neglect of other pleasures/interests because of use or effects of substance
o Persistence with use despite clear evidence of harmful consequences

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46
Q

what are the 1st line investigations in alcohol abuse?

A 
diagnostic interview
alcohol level (breath + blood)
Withdrawal assessment
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47
Q

what are the different tools used for diagnostic interviewing in alcohol abuse?

A

AUDIT
CAGE
TACE
Also - TWEAK, MAST, PAT, FAST

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48
Q

what AUDIT score indicates low risk drinking?

A

0-7

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49
Q

what AUDIT score indicates hazardous drinking?

A

8-14

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50
Q

what AUDIT score indicates harmful drinking?

A

15-19

51
Q

what AUDIT score indicates dependent drinking?

A

20+

52
Q

which lab tests can be used in alcohol treatment monitoring?

A

GGT, ALT, AST Carbohydrate Deficient Transferrin
MCV
FBC
Urinary ethyl glucuronide

53
Q

what is the 1st line management of mild alcohol dependence?

A

Physician advice + brief intervention

54
Q

what is the 1st line management of moderate-severe alcohol dependence?

A

Psychosocial Interventions + Pharmacotherapy

55
Q

what Psychosocial Interventions are used in alcohol abuse management?

A

CBT, motivational therapy, 12 step facilitation therapy

56
Q

what drugs are used in the pharmacotherapy of alcohol abuse management?

A

Naltrexone
Acamprosate
Disulfiram
Nalmefene

57
Q

what is the pathophysiology of acute alcohol withdrawl?

A

extended alcohol use causes upregulation of excitatory NMDA-glutamate ion channels and downregulation of inhibitory GABA-A ion channels
Withdrawal causes excess glutamate and reduced GABA

58
Q

when do symptoms occur in in acute alcohol withdrawal?

A

occur within hours, peak at 24-48hrs

59
Q

what are the common symptoms of acute alcohol withdrawal?

A

o Restlessness, tremor, sweating, anxiety, n&v, loss of appetite, insomnia, depression, fatigue, clammy skin, dilated pupils, headaches, irritability
o Tachycardia and systolic hypertension
o Generalised seizures

60
Q

what is the management of acute alcohol withdrawal?

A

most resolved in 5-7days

1st Line = Detoxification + Supportive medical care

61
Q

what pharmacology is used in the 1st line management of acute alcohol withdrawal?

A

 Diazepam or Lorazepam or Oxazepam

 AND Thiamine

62
Q

where are the different places you can receive treatment for acute alcohol withdrawal?

A

Inpatient/residential speciality treatment

Outpatient/intensive outpatient speciality treatment

63
Q

what are the clinical features of delirium tremens?

A

restlessness, fear, paranoia, confusion / clouded consciousness, terror-stricken face, ataxia / tremor, sweaty / tachycardia / pyrexia / flushing / pallor, visual hallucinations, auditory hallucinations

64
Q

what is delirium tremens?

A

occurs in alcohol withdrawal

65
Q

What is the management of delirium tremens?

A

o Benzodiazepine – Diazepine
o B vitamins
o Fluid replacement, dextrose

66
Q

what is Wernicke’s encephalopathy?

A

acute and reversible syndrome caused by thiamine deficiency

67
Q

what is Korsakov’s syndrome?

A

chronic and irreversible condition also caused by thiamine deficiency

68
Q

what is the cause of WE and KS?

A

thiamine deficiency

69
Q

what are the causes of thiamine deficiency?

A
  • Alcohol
  • Decreased intake – malnutrition
  • Decreased absorption – pernicious anaemia
70
Q

how does thiamine become metabolically active?

A

• Enzyme thiamine pyrophosphate synthetase transfers pyrophosphate group from ATP to thiamine turning it into co-enzyme thiamine pyrophosphate

71
Q

where is thiamine stored?

A

liver

72
Q

where is thiamine absorbed?

A

duodenum

73
Q

what is the role of thiamine pyrophosphate?

A

assists other enzyme - particularly in glucose metabolism

74
Q

what is the role of thiamine in the brain?

A

o Helps metabolise lipids and carbohydrates
o Maintain normal amino acid & neurotransmitter levels
o Helps with propagation of neural impulse down axons

75
Q

what is the cellular consequence of thiamine deficiency?

A

Impairs glucose metabolism – reduced cellular energy

76
Q

how does alcohol abuse cause thiamine deficiency?

A

o Alcohol interferes with conversion of thiamine to active form
o Ethanol prevents absorption from duodenum (reduces expression for thiamine transporter 1)
o Cirrhosis – interferes with storage of thiamine

77
Q

what parts of the brain can be affected by impaired glucose?

A

o Affects the medial dorsal thalamic nucleus, mammillary bodies, the periaqueductal grey matter, and the floor of the fourth ventricle, which includes the ocular motor and vestibular nuclei and the cerebellar vermis.
o Lesions may also involve the fornixes, the hippocampus, the area round the third ventricle, the quadrigeminal bodies, and the cortex.

78
Q

what is the disease progression of WE and KS?

A

Wernicke’s first

Korsakoff if Wernicke’s untreated?

79
Q

what are the most common symptom of WE?

A

altered mental status – slowing, impaired concentration, apathy

80
Q

what are the symptoms in Wernicke’s Triad?

A

eye signs (nystagmus, ophthalmoplegia), ataxic gait, confusion

81
Q

what are the other common symptoms of WE?

A

irritability, delirium, acute psychosis

82
Q

what are the uncommon symptoms of WE?

A

coma, misois, anisocoria, light near dissociation, papilledema, retinal haemorrhage, tachycardia, hypotension, hypothermia, hyperthermia, hearing loss, seizures

83
Q

how is WE diagnosed?

A

o Trial of thiamine
o Glucose, FBC, electrolytes, renal function, LFTs, urinary and serum drug screen, serum ammonia, blood alcohol level, blood thiamine and metabolites, serum magnesium
o LP, MRI, CT

84
Q

what is the management of moderate/high suspicion WE?

A

stabilisation/resuscitation + thiamine + magnesium + multivitamins

85
Q

what is the management of low suspicion WE?

A

thiamine + magnesium + folic acid

86
Q

what is the role of glucose in WE?

A

Given but after thiamine

87
Q

what is the pathophysiology of KS?

A

targets limbic system

88
Q

what are the clinical features of KS?

A

Anterograde amnesia
Retrograde amnesia
Confabulation

89
Q

what is the management of KS?

A

no cure

90
Q

what is the process of making opiates?

A

opium (mixture of alkaloids esp codeine and morphine) → Morphine (morphine extracted though often codeine contaminants remain) → Diamorphine (addition of 2 acetyl rings to produce diacetylmorphine (diamorphine)

91
Q

what are the different ways opiates are taken?

A

IV, smoking, suppository, insufflation, ingestion

92
Q

how is morphine metabolised?

A

DIACETYLMORPHINE → 6-MONO-ACETYL MORPHINE → MORPHINE

93
Q

how are opiates classed?

A

Opioids are classed as agonists, partial agonist or agonist-antagonists

94
Q

what receptors do opiates act on?

A

mu, kappa, delta

95
Q

what effects to Mu receptors trigger?

A

analgesia, sedation, respiratory depression, euphoria, GI dysmotility, physical dependence

96
Q

what effects to Delta receptors trigger?

A

analgesia, inhibition of dopamine release, cough suppression

97
Q

what effects to Kappa receptors trigger?

A

analgesia, misois, diuresis, dysphoria

98
Q

what is the action of opiates?

A

Bind to GABA receptors, slowing down GABA production.

Normally GABA monitor levels of dopamine, so reduced GABA leads to increased dopamine

99
Q

what are the clinical features caused by taking opiates?

A

• Euphoria, analgesia, respiratory depression, constipation (alcohol causes diarrhoea), reduced conscious level, hypotension and bradycardia, pupillary constriction,

100
Q

what are the clinical features of opiate tolerance?

A

cold/shivery, flu-like symptoms, body pain

101
Q

what are the additional clinical features caused by opiates?

A

weight loss, n+v, sedation, restless sleep, memory impairment, sneezing, yawning, abdo cramps, backache, slurred speech, aggressive behaviour, excess perspiration, rhinorrhoea, piloerection,

102
Q

what is the criteria for opiate misuse?

A
  • Using larger amounts of opioids or over a longer period than was intended
  • Persistent desire to cut down or unsuccessful efforts to control use
  • Great deal of time spent obtaining, using, or recovering from use
  • Craving, or a strong desire or urge to use substance
  • Failure to fulfil major role obligations at work, school, or home due to recurrent opioid use
  • Continued use despite recurrent or persistent social or interpersonal problems caused or exacerbated by opioid use
  • Giving up or reducing social, occupational, or recreational activities due to opioid use
  • Recurrent opioid use in physically hazardous situations
  • Continued opioid use despite physical or psychological problems caused or exacerbated by its use
  • Tolerance (marked increase in amount; marked decrease in effect)
  • Withdrawal syndrome as manifested by cessation of opioids or use of opioids (or a closely related substance) to relieve or avoid withdrawal symptoms.
103
Q

what investigations are used to diagnose opiate misuse?

A

Urinary drug screen, GC-MS, serum electrolytes, FBC, urea/creatinine, LFTs rapid plasma reagent, hepatitis serology, HIV serology, PPD skin test, blood cultures, beta-hCG

104
Q

what is the 1st line management of opiate misuse?

A

maintenance therapy: buprenorphine +/- naloxone

105
Q

what is the 2nd line management of opiate misuse?

A

methadone

106
Q

what are the supportive therapies of opiate misuse?

A

o Urine drug screening
o Monitoring of physical health problems, HIV testing, Hep C screening
o Individual and group drug counselling, cognitive therapy, 12-step-orirnetated groups

107
Q

naloxone should be avoided in…

A

pregnancy

108
Q

what are the causes of opiate overdose?

A
  • Complications of substance abuse in regular users/abusers of illicit or prescription drugs
  • Unintentional overdose in patients prescribed opioids for pain by taking larger amounts that tolerated
  • Intententional
  • Therapeutic drug error
109
Q

what are the risk factors to opiate overdose?

A

own or friends home, recent non-fatal overdose, not in treatment, recent abstinence of reduction of use, witnesses present, polydrug use, longer history of drug use, depression, significant life events, poor physical/mental health, injecting homeless

110
Q

what are the clinical features of opiate overdose?

A
  • Miosis, bradypnea, altered mental state, response to naloxone
  • Fresh needle marks, drugs paraphernalia, reduced GI motility, old track marks
  • Pulmonary rales, frothy pink sputum, seizures, dysrhythmias, cyanosis
111
Q

what are the investigations of opiate overdose?

A
  • Therapeutic trial of naloxone
  • ECG
  • Also consider: chest xray, abdo xray, abdo CT, opioid urine screen, gas chromatography/mass spectrometry
112
Q

what is the management of opiate overdose when there is antidote available?

A

ventilation prior to naloxone + naloxone (do CPR first, sats 94-99%)

113
Q

what is the management of opiate overdose when there is antidote not available?

A

supportive ventilation

114
Q

what is the management of opiate overdose when there is retained drug packages + signs of opioid toxicity ?

A

ventilation prior to naloxone + naloxone

115
Q

what is the management of opiate overdose when there is retained drug packages + no signs of opioid toxicity ?

A

whole bowel irrigation

116
Q

what are the different ways naloxone can be administered?

A

standard syringe
autoinjector
nasal spray

117
Q

what are the dosage regime of naloxone standard syringe?

A

o Repeat dose every 2-3 mins

o Titrate dose by 0.2 to 0.4mg increments according to response, maximum 10mg/total dose

118
Q

where is the naloxone syringe administered?

A

lateral aspect of thigh

119
Q

what are the dosage regime of naloxone autoinjector?

A

o 0.4mg OM/SC initially

o May repeat in 2-3mins if no response

120
Q

what are the dosage regime of naloxone nasal spray?

A

o 2-4mg into one nostril as a single dose

o May repeat in alternate nostrils every 2-3mins if required

121
Q

how long does naloxone last?

A

30-90 mins

122
Q

what is the action of naloxone?

A

Lipophilic compound, temporarily displaces opioid from opioid receptors

123
Q

what type of drug is naloxone?

A

Non-selective and competitive receptor antagonist

124
Q

which receptor does naloxone act on best?

A

u-opioid receptor

Psychiatry (11 decks)

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