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Year 3 > Block 33 Week 7 > Flashcards

Block 33 Week 7 Flashcards

1
Q

what is binge drinking?

A
  • Heavy dinking in a single session
  • Twice the daily limit
  • Above 4-6 units for women
  • Above 6-8 units for men
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2
Q

what is harmful use of alcohol?

A
  • pattern of psychoactive substance use that damages health
  • harmful patterns of use often criticized by others
    Harmful use should not be diagnosed if dependence syndrome, a psychotic disorder or another specific form of drug- or alcohol-related disorder is present.
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3
Q

what is dependence syndrome?

A
  • A cluster of physiological, behavioural, and cognitive phenomena in which the use of a substance or a class of substances takes on a much higher priority for a given individual than other behaviours that once had greater value.
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4
Q

central characteristic of dependence syndrome?

A

desire (often strong, sometimes overpowering) to take alcohol.

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5
Q

diagnostic guidelines for dependence syndrome?

A
  • 3 of more of the following have been present together at some time during the past year:
  • (a) a strong desire or sense of compulsion to take the substance;
  • (b) difficulties in controlling substance-taking behaviour in terms of its onset, termination, or levels of use;
  • (c) a physiological withdrawal state when substance use has ceased or been reduced, as evidenced by: the characteristic withdrawal syndrome for the substance; or use of the same substance with the intention of relieving or avoiding withdrawal symptoms;
  • (d) evidence of tolerance, such that increased doses of the psychoactive substances are required in order to achieve effects originally produced by lower doses
  • (e) progressive neglect of alternative pleasures or interests because of psychoactive substance use, increased amount of time necessary to obtain or take the substance or to recover from its effects
  • (f) persisting with substance use despite clear evidence of overtly harmful consequence.
  • (g) Narrowing of the personal repertoire of patterns of drinking e.g. a tendency to drink alcoholic drinks in the same way regardless of social constraints that determine appropriate drinking behaviour.
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6
Q

tolerance?

A
  • either a need for markedly increased amounts of a substance to achieve intoxication or desired effect.
  • Or marked diminished affect with continued use of same amount of a substance.
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7
Q

withdrawal?

A
  • Characteristic withdrawal syndrome for substance used or closely related or same substance taken to relieve or avoid withdrawal symptoms.
  • A great deal of time is spent in activities necessary to obtain or use the substance or to recover from its effects.
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8
Q

7 fold inc in risk of alcoholism in?

A

first degree relatives of alcoholics

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9
Q

P300?

A
  • abnormalities in P300 event-related potential associated with familial alcoholism > P300 predicts alcohol abuse
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10
Q

FH in alcoholism?

A
  • family history
  • sons of alcoholics 4x more likely to be an alcoholic than sons of non-alcoholics regardless of drinking patterns of adoptive parents
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11
Q

receptor involved in alcoholism?

A

D2 dopamine receptor

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12
Q

variations in ? composition leads to?

A
  • variations in allele compositions for alcohol dehydrogenase and aldehyde dehydrogenase may contribute to risk patterns of alcoholism among oriental populations
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13
Q

reinforcement of alcohols effects via?

A
  • Alcohol’s reinforcing effects are modulated by dopamine, serotonin, and GABA systems
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14
Q

in alc dependence

dopamine

A
  • alcohol stimulates DA release in nucleus accumbens
  • increased DA may underlie ‘craving’
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15
Q

5HT?

A

*alcohol potentiates effects of serotonin at 5-HT3 receptors
*some reports of 5-HT agonists in reducing alcohol craving

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16
Q

psychodynamic theories of alcoholism?

A
  • intoxication is a gain to the patient, with disinhibition allowing the expression of aggression
  • maternal overprotection is described among some alcohol problems clinic attendees
  • childhood sexual abuse is more commonly reported in women alcoholics than in the general population
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17
Q

behavioural theory of alcoholism?

A
  • models include drinking becoming a conditioned response to a wide range of circumstances
  • modelling from parents, relatives, peers, etc. is clearly demonstrated
  • The euphoriant effect - important reinforcer
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18
Q

other behaviour factors linked to alcoholism?

A
  • Stress and negative life events – bereavement; separation; impending court case
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19
Q

type 1 alcoholic?

A

more dependent, anxious, rigid, less aggressive, more guilty, with either the mother or father an alcoholic

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20
Q

type 2 alcoholic?

A

early onset, severe problems, socially detached, distractible, confident, and whose behaviour is linked to a similar pattern in the biological father - can be seen as alcoholism secondary to antisocial personality disorder

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21
Q

epidemiology of alcohol disorders?

A
  • rise in females; rise in adolescents
  • 35 % of homeless have alcohol disorders
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22
Q

?% of MCP abuse alcohol

A

4-6%

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23
Q

age of onset for alcoholism?

A
  • age of onset in late teens or 20s for males
  • onset later in females, who are more likely to:
  • drink alone
  • delay seeking help
  • have co-morbid depression
  • have a stronger genetic predisposition
  • develop physical complications, especially cirrhosis
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24
Q

higher rates of alcoholism in:

A
  • urban areas
  • divorced/ separated
  • those who manufacture, or sell alcohol
  • commercial travellers, frequent overseas travellers
  • entertainers, doctors, journalists
  • North American, Afro-Caribbean, Irish
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25
Q

lower rates of alcoholism in:

A
  • ‘middle’ social groups
  • Jewish, Chinese
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26
Q

hepatic alcohol related consequences?

A
  • may be due to toxic effects of acetaldehyde / damage to immune system by alcohol
  • women are more susceptible than men
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27
Q

fatty liver?

A

*may be present in 90 % of drinkers
*reversible with abstinence

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28
Q

alcoholic hep?

A

*abstinence aids resolution, but cirrhosis may follow

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29
Q

cirrhosis?

A

*10 % of chronic alcoholics
*vulnerability may be due to HLA-B8 antigen, found in 25 % of population

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30
Q

HLA that has a protective effect on cirrhosis?

A

HLA-A28

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31
Q

hepatic carcinoma?

A

*15 % of patients with cirrhosis go on to develop hepato-cellular carcinoma

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32
Q

GI alcohol related consequences?

A
  • Baretts Oesophagus
  • MW tears
  • oesophageal varices
  • Peptic ulceration – 20 % of alcoholics; bleeding may be exacerbated by Vitamin K deficiency secondary to cirrhosis
  • Pancreatitis – both acute and chronic
  • DM
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33
Q

Haemtological alcohol related consequences?

A
  • alcoholism is the commonest cause of macrocytosis
  • Thrombocytopenia and anaemia
  • Zieve’s syndrome is a rare form of alcoholic haemolysis
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34
Q

neurological consequences of alcoholism?

A
  • delirium tremens
  • Alcoholic Hallucinosis
  • Trauma, alcohol withdrawal, brain damage
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35
Q

alcoholic hallucinosis?

A
  • rare conditions in which auditory hallucinations occur alone in clear consciousness
  • usually clears in a few days, but may be followed by secondary delusional misinterpretation
  • up to 50 % go on to develop symptoms of schizophrenia
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36
Q

what is the most common complication of neurological complication of alcoholism?

A
  • Epilepsy of late onset (> 25 yrs) is the most common neurological complication
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37
Q

peripheraly neuropathy from alcoholism?

A

most likely from b1 deficiency

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38
Q

optic atrophy?

A
  • loss of visual acuity
  • blindness associated with methanol poisoning, thiamine and B12 deficiency, and heavy tobacco smoking
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39
Q

CV comps of alcoholism?

A
  • increase in blood pressure
  • weakened contraction of myocardium, leading to heart failure
  • cardiac arrhythmia
  • cardiomyopathy
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40
Q

comps of alcohol use in pregnancy

A
  • stillbirth
  • neonatal mortality
  • low birth weight
  • later issues w distractibiltiy and attention
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41
Q

FAS?

A
  • microcephaly, mental retardation, low birth weight, cleft palate, ptosis, scoliosis, abnormal dermatoglyphics, congenital heart disease, congenital renal disease
  • may occur at alcohol intake of 4-5 units per day
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42
Q

social effects of alcohol - inc rates of?

A
  • physical / sexual abuse of partner
  • divorce
  • child abuse
  • later alcoholism in children
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43
Q

social effects of alcohol - emp?

A
  • 2 ½ times as many days off work
  • decreased productivity
  • increased accidents at work
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44
Q

social effects of alc - accidents?

A
  • 80 % of fatal car accidents involve alcohol
  • 40 % of casualty trauma involves alcohol
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45
Q

psychiatric complications of alc?

A
  • almost half of alcoholics meet criteria for another psychiatric disorder
  • affective disorders - depressive symptoms, contemplation of suicide
  • alcoholics have 7x the expected suicide rate
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46
Q

anxiolytic effects of alcohol?

A
  • Anxiety - the anxiolytic effects of alcohol wear off as tolerance develops
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47
Q

schiz and alc?

A
  • Schizophrenia - schizophrenic symptoms can occasionally be triggered by heavy drinking, which remit when the patient is detoxed
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48
Q

morbid jealousy?

A

may be associated with an alcoholic paranoid state

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49
Q

Delirium tremens?

A
  • risk develops when intake is 12 units per day
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50
Q

Triad of DT?

A
  • clouding of consciousness and confusion, patient is disorientated
  • vivid hallucinations - usually visual (rats, insects, Lilliputian) or tactile
  • marked tremor
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51
Q

Marchiafava-Bignami disease presents w?

A

Ataxia, dysarthria, epilepsy, severe impairment of consciousness due to extensive demyelination of the corpus callosum, the optic tracts, and the cerebellar peduncles

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52
Q

Central Pontine Myelinolysis consist of?

A
  • consists of demyelination involving the pyramidal tracts within the pons
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53
Q

Central Pontine Myelinolysis presents w rapid onset of?

A
  • pseudobulbar palsy, quadriplegia, loss of pain sensation in the limbs and trunk, vomiting, confusion, and coma are common
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54
Q

alc dementia

A
  • mild cognitive deficits frequent, but reversible with abstinence
  • dementia rarely occurs before 40 years
  • associated with CT and MRI evidence of ‘atrophy’
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55
Q

alcohols impact on actions?

A
  • causes us to act on impulse
  • sexually acting out
  • displaying behaviours and saying things they wouldn’t normally say
  • expressions of anger, happiness, violence
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56
Q

alc impact on semi volunatry actions?

A
  • dry mouth - stops body salivating
  • Red eyes; stop blinking and then eyes start to dry out
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57
Q

alcohols impact on involuntary systems?

A
  • Alcohol sedates this level so can cause nausea/ vomiting as food fails to be properly digested.
  • Libido affected & ability to perform the sexual act is lost.
  • The body can stop involuntary system actions in order to maintain vital functions-too much alcohol
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58
Q

Alc and vital systems?

A
  • In event of surge in alcohol the body creates a period of unconsciousness/ coma to protect vital functions.
  • Inexperienced drinkers pass out.
  • Acute alcohol poisoning is where the vitals start to shut down and can result in death.
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59
Q

assessment of alcohol/ drug misuse?

A
  • longitudinal and cross sectional history
  • Basic Investigations : Blood test, Urine drug test
  • Diagnosis: Evidence of dependence
  • Complications. (Physical, Mental, social)
  • RISK
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60
Q

blood tests for alc?

A

GGT, MCV, ALT

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61
Q

questionnaires for alc?

A

CAGE and AUDIT-C

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62
Q

CAGE?

A

score >2

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63
Q

AUDIT-C?

A
  • AUDIT-C: score of 5+ indicates higher risk drinking
  • overall total score of 5+ is AUDIT-C positive
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64
Q

Physical withdrawal symptoms?

A
  • hand tremors (‘the shakes’)
  • sweating
  • nausea
  • visual hallucinations (seeing things that are not actually real)
  • seizures (fits) in the most serious cases
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65
Q

Psychological alcohol withdrawal symptoms include:

A
  • depression
  • anxiety
  • irritability
  • restlessness
  • insomnia(difficulty sleeping)
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66
Q

Longitudinal and cross-sectional history ?

A
  • Age of onset.
  • Type of substance/s
  • Progression of Substance/s use.
  • Possible precipitating and perpetuating factors.
  • Current pattern of use
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67
Q

1 unit = ? of pure alc

A

10ml

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68
Q

most sensitive screening tool for alc?

A

GGT

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69
Q

Tx of det

A
  • benzos
  • fixed dose schedule best - acamprostate can be added
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70
Q

acamprostate?

A
  • antagonises glutamate function
  • Repeated ethanol withdrawal leads to greater levels of glutamate and increased mortality but acamprosate blocks this.
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71
Q

preventing alc related complications?

A
  • thiamine replacement
  • Must assess for signs of Wernicke’s encephalopathy
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72
Q

naltrexone?

A
  • opiod antagonist
  • not good for abstinence it seems to prevent people who relapse from going back to a full blown dependence
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73
Q

relapse preventing therapies?

A
  • naltrexone
  • acamprostate
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74
Q

acamprostate?

A
  • increases cumulative abstinence
  • reduces endogenous excitatory NTs and enhancing GABA transmission
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75
Q

what is the benefit of acamprosate?

A
  • Few contraindications – can “safely” drink
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76
Q

busipirone?

A

1.is a 5-HT1A agonist
2.can improve outcome in anxious alcoholics

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77
Q

what does disulfiram work?

A
  • Works by preventing the breakdown of acetaldehyde to acetate so if alcohol is drunk will lead to facial flushing, headaches, palpitations, nausea, vomiting headache, increased temp, increased pulse, decreased BP
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78
Q

what else does disulfiram do?

A
  • Increases dopamine in the nucleus accumbens by reducing conversion to noradrenaline by dopamine B hydroxylase
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79
Q

what can disulfiram precipitate?

A
  • Can precipitate anxiety, mania, psychosis and depression
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80
Q

side effects of disulfiram?

A
  • Patients must have capacity and many contraindications and cautions (eg PD, suicidal risk, cardiovascular….).
  • Rarely can cause fulminant hepatitis
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81
Q

NICE recommends disulfiram only after?

A

a trial of naltrexone or acamprosate

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82
Q

what is MI?

A

A directive, patient-centred counselling style that aims to help patients explore and resolve their ambivalence about behaviour change.

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83
Q

4 principles of MI?

A
  • empathy
  • discrepency
  • address resistance
  • support self efficacy
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84
Q

MI - empathy?

A
  • Express empathy by using reflective listening to convey understanding of the patient’s point of view and underlying drives
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85
Q

MI - discrepency?

A
  • Develop the discrepancy between the patient’s most deeply held values and their current behaviour (i.e. tease out ways in which current unhealthy behaviours conflict with the wish to ‘be good’ – or to be viewed to be good)
86
Q

MI - resistance?

A
  • Sidestep resistance by responding with empathy and understanding rather than confrontation
87
Q

MI - self -efficacy?

A
  • Support self-efficacy by building the patient’s confidence that change is possible
88
Q

stages of change in the cycle of change model?

A

PCPAML

89
Q

pre-contemplation?

A
  • doesn’t recognise the problem
  • no reason to change
90
Q

contemplation stage?

A

*Ambivalence
*“I might have a problem”
*Apprehension, fear of change.

91
Q

preparation stage?

A

ppt ready to engage in change process

92
Q

action stage?

A
  • noticable change in beh
  • re-inforcement and support
  • understand factors and strategies supporting the new behaviour
93
Q

maintenance stage?

A
  • consolidation of change
  • skills development
94
Q

what can be done during the maintenance stage?

A
  • Support and encouragement
  • Provision of support systems
  • Design of relapse prevention plans
95
Q

What can be done during the lapse/relapse stage?

A
  • Re-engagement with services and supports available.
  • Exploration of reasons for relapse and learn from lapse experience
  • Review of relapse prevention plan.
96
Q

what do psychoactive drugs do?

A
  • alter, mood, cognition, behaviour
97
Q

stimulants?

A
  • Euphoria
  • Increase energy/activity
  • Reduced need for sleep & food
98
Q

examples of stimulants?

A
  • e.g. cocaine, amphetamine, caffeine, ephedrine, methylphenidate
99
Q

what do depressants do?

A
  • Impair consciousness
  • Impair co-ordination
  • Disinhibition
  • Analgesia
  • Amnesia
100
Q

examples of depressants?

A
  • e.g. benzodiazepines
  • zimovane (“z” drugs)
  • chloral hydrate
  • barbiturates
  • chlormethiazole
  • alcohol
101
Q

opiods?

A
  • Dreamy/detached/euphoria
  • Sedation
  • Analgesia
  • Constipation
102
Q

examples of opiods?

A
  • e.g. heroin, morhine, codeine
  • tramadol
  • fentanyl
  • pethidine
103
Q

hallucinogens?

A
  • Visual illusions/hallucinations
  • Euphoria/emotional liability
  • Time distortion
104
Q

examples of hallucinogens?

A
  • LSD, psilcybin, fly agaric
105
Q

cannabis?

A

–depressant & hallucinogenic

106
Q

solvents?

A

–depressant & hallucinogenic & anaesthetic

107
Q

MDMA?

A

–stimulant & hallucinogenic

108
Q

Pharmakokinetics of psychoactive drugs?

A

*rapid absorption esp i.v. (rush with opiate buzz with amphetamines)
*rapid distribution, high affinity for CNS, lipophilic e.g. cannabis
*slow elimination

109
Q

plasticity?

A
  • = extent to which drug effects are shaped by
  • internal cues (anxiety, depression, relief etc)
  • external cues (friends,work etc)
110
Q

low plasticity drugs?

A
  • low plasticity → predicable results from use
  • low plasticity: heroin. amphetamines
111
Q

high plasticity drugs?

A
  • high plasticity: LSD, cannabis, solvents
112
Q

tolerance?

A
  • ↓effect of same dose of a drug on repeated exposure
  • need to ↑ dose to maintain same level of effect
113
Q

Tolerance is from a combination of?

A
  • pharmacokinetics: e.g. alcohol and enzyme induction and neuroadaptation
  • psychosocial - –tolerance may develop faster to behaviours important to the individual)
114
Q

alcohol duration of effects?

A

Duration - 5 – 10 minutes, lasts several hours

115
Q

amphetamines duration?

A

Duration - 15 minutes – effects may last 2 days

116
Q

barbituates duration

A

Duration - begins in 10 minutes – lasts 3 – 5 hours

117
Q

caffiene duration

A

Duration - begins within minutes – can last several hours

118
Q

cannabis duration

A

Duration - begins after a few minutes, lasts up to an hour

119
Q

cocaine duration

A

Duration works within minutes – peaks 15 – 30 minutes, dies quickly

120
Q

opiates duration

A

Duration immediate, last 10 – 30 minutes

121
Q

tobacco duration

A

Duration effects 5 – 10 minutes, lasts 10 – 30 minutes

122
Q

NS effects of opiods

A
  • euphoria
  • analgesia (mind & body)
  • drowsy detached state
  • sleep disturbance (â REM & stage 4)
  • pin point pupils
123
Q

hormonal effects of opiods

A
  • dec sperm motility
  • amenorrhoea
124
Q

GI effects of opiods

A
  • nausea/ vomiting
  • constipation
  • anorexia
  • dec secretions
125
Q

Genitourinary effects of opiods?

A

urgency & retention of urine

126
Q

CV effects of opiods?

A
  • dilated BVs, dec BP
  • sweating
  • itching
127
Q
A
128
Q

resp effects of opiods?

A
  • reduced resp rate
  • reducted cough reflex
129
Q

tolerance to opiods?

A
  • Develops rapidly (within days of continuous use) to euphoria, analgesic, respiratory depressant and emetic effects
  • Constipation may persist
  • Pin point pupils remain despite prolonged use
130
Q

drug effects of opiods - intoxication vs toxicity?

A
131
Q

dependence involves?

A

– tolerance
– characteristic withdrawal effects
– Psychosocial changes

132
Q

NS effects of amphetamines?

A
  • euphoria
  • alerting
  • inc self confidence
  • dec fatigue & need for sleep
  • inc activity
  • tremor
  • dilated pupils
133
Q

CV effects of amphetamines?

A
  • inc pulse - palpitations
  • inc BP - headaches
134
Q

GI effects of amphetamines

A
  • anorexia
  • abd cramps
135
Q

endocrinological effects of amphetamines?

A
  • sweating
  • inc body temp
  • dry mouth
136
Q

amphetamine - withdrawal symptoms

A
  • hypersomnia + vivid dreams
  • hunger & hyperphagia
  • fatigue/lethargy
  • depressed mood + suicidal thoughts (variable)
137
Q

amphetamine overdose?

A
  • Overdose–confusion inc BP, inc pulse, chest pain, palpo
  • inc temp, convulsions, myocardial infaret, CVA
  • Bruxism
  • Sterotyped behaviour
  • Suspiciousness à paranoid psychosis
  • Acute schizophroniform psychosis
138
Q

stimulant effects of LSD?

A
  • dilated pupils
  • inc pulseinc BP
  • tremor
  • piloerection
  • weakness
  • nausea
139
Q

Amphetamine overdose?

A
  • acute overdosage (convulsions, hyperthermia etc)
  • bad trips
  • accidents
  • flashbacks
  • acute psychosis
140
Q

paraxodical reactions from benzodiazepines?

A
  • aggressiveness (in some individuals violent behaviour),
  • depression (with or without suicidal thoughts or intentions),
  • personality changes.
  • Rarely reactions such as hallucinations, depersonalisation, derealisation and other psychiatric symptoms occur.
141
Q

which 2 benzos are more likely to produce dissociation and psychiatric symptoms?

A
  • Lorazepam and triazolam in particular may produce dissociation and other psychiatric symptoms.
142
Q

risk of paradoxical reactions?

A
  • 5%
  • ↑risk with short-acting compounds, may occur with all benzodiazepines
  • can occur in short-term use and rarely following first use
143
Q

tolerance to benzos - ? within a few weeks

A

sedation

144
Q

tolerance - ? effects within a few months

A

anxiolytic

145
Q

tolerance - anticonvulsant effects

A

after several months

146
Q

benzos - dependnce?

A
  • Can develop within weeks of regular use
  • More likely with the short acting potent benzodiazepines e.g. lorazepam, alprazolam
147
Q

brain disabiling effects of benzodiazepines

A
  • sedation or hyponsis
  • cognitive dysfunction - ST memory impairment, confusion, delirium
  • disinhibition and other behavioural aberrations
  • extreme agitation
  • psychosis
  • paranoia
  • depression
  • sometimes with violence toward self or others
148
Q

Benzos withdrawal?

A
  • anxiety and insomnia after routine use to
  • psychosis and seizures after the abrupt termination of long-term high doses
149
Q

screening tool for alcoholism?

A
  • CAGE questionnaire: .
  • AUDIT-C: a shortened version of the AUDIT screening tool, consisting of three questions.
  • score of 3+ requires use of a full AUDIT questionnaire
150
Q

questions to ask abt alcohol intake?

A
  • origin of the drinking problem - what was going on?
  • current drinking pattern
  • quantify
  • drinking behaviours - where and who with
  • previous attempts to stop
151
Q

asking abt biological signs of dependence?

A
  • If you stop drinking, do you…get the shakes/sweat a lot/feel sick/notice any physical changes?”
  • “Do you have to drink more than you used to, to get the same effects?”
152
Q

psych signs of dependence?

A
  • compulsion
  • how imp is drinking
  • on stopping - feel down, angry, anxious?
153
Q

effects on life of drinking?

A
  • relationships
  • occupation
  • do they currently drive? for work? driving under the influence
154
Q

impacts of addiction on society

A
  • child neglect
  • loss of productivity - days off associated w ill health
  • increased crime rates
  • substance related conditions e.g. liver disease -> increased healthcare cost
  • increased risk of homelessness and provery
155
Q

impact of addiction on family

A
  • distressing for the family
  • child neglect/ abuse
  • children may develop addiction at an early age
  • increased domestic disputes
156
Q

envir damage from drugs?

A
  • environmental damage from drugs e.g. methamphetamine or cannabis
157
Q

impacts of addiction on the indiv?

A
  • health conditions - MH, lung, cardiac etc
  • side effects - depression, psychosis
  • loss of job
  • loss of relationships
  • finances - cost of alcohol/ drugs, inability to work
158
Q

RF for drug taking

A
  • early aggressive factors
  • lack of parental supervision
  • academic problem
  • peer substance use
  • drug availability
  • child abuse/ neglect
  • poverty
159
Q

indiv RF for taking drugs

A
  • genetic disposition
  • prenatal alcohol exposure
  • difficult temperament
  • poor impulse control
  • low harm avoidance
  • lack of self regulation
  • ADHD/ anxiety/ depression/ antisocial behaviour
  • rebelliousness
  • Personality traits: including disinhibition, poor impulse control, novelty or sensation seeking may increase the risk of substance misuse.
  • Psychiatric co-morbidities(depression, anxiety, PTSD, psychosis): illicit drugs may be used in an attempt to self-medicate.
160
Q

social RF for taking drugs?

A
  • peer pressure
  • lack of family involvement
  • attitudes towards drugs/ alcohol
161
Q

social and environmental factors for taking drugs?

A
  • poor school achievement, unemployment, social deprivation, history of criminal activity, peer influence, and normalisation of substance misuse in the individual’s culture or peer group.
162
Q

psych theories of dependence - classical conditoning?

A
  • drinking alcohol is associated with a pleasurable feeling
  • triggering craving for the drug
  • craving may be triggered by familiar internal states (like anxiety, depression, loneliness) that were previously alleviated by taking drugs.
163
Q

psych theories of dependence - operant conditioning?

A
  • A person might use a drug for the first time and enjoy the feelings it creates, which is apositive reinforcementfor the behavior.
  • negative reinforcement - relief of pain, low, mood, anxiety
164
Q

psych theories - SLT?

A
  • watching others engaging in the behaviour - modelling
165
Q

Psych theories of dependence - self medictaion theories?

A
  • The underlying basis for the pain that is being medicated is usually attributed to trauma—adverse childhood experiences (ACES), sexual or violence trauma as an adult, or other experiences associated with post-traumatic stress.
166
Q

biological theories - dopamine?

A
  • positive reinforcing effect of alcohol comes from the dopaminergic reward pathway in the limbic system
  • dopamine is released in the VTA and projects to the NA where it is involved in motivation and reinforcement behaviours - mesolimbic pathway
167
Q

how do endogenous opiods influence drinking behaviour?

A
  • endogenus opiods influence drinking behaviour via interaction w the mesolimbic system
168
Q

GABA in alcohol dependence?

A
  • GABA - alcohol acts presynaptically at the GABA neuron, increasing GABA release and post-synaptically enhancing GABA action
169
Q

glutamate in alcohol dependence?

A
  • glutamate - alcohol reduces glutamate levels in the NA and supresses glutamate mediated signal transmission in the central nucleus of the amygdala
170
Q

genetics involved in alc dependence?

A
  • alcohol dehydrogenase 1B(ADH1B)and aldehyde dehydrogenase 2(ALDH2)
171
Q

Psych management of alcohol dependence?

A
  • MI in the initial assessment
  • psychological interventions - CBT, behavioural therapies or social network therapies focused on alcohol-related cognitions, behaviour, problems and social networks
172
Q

when should pharm interventions be used in alc dependence?

A
  • harmful drinkers/ mild alc dependence who haven’t responded to psych interventions alone
  • or who spec request ot
  • offer oral naltrexone in combination with an individual psychological intervention
173
Q

assisted withdrawal?

A
  • fixed dose regimens
  • benzodiazepines - chlordiazepoxide or diazepam
174
Q

when should acamprosate be used?

A
  • start treatment as soon as possible after assisted withdrawal
175
Q

side effects of acamprosate?

A
  • abd pain
  • sexual dysfunction
  • nausea
  • skin reactions
176
Q

naltrexone CI?

A

opiod dependence

177
Q

side effects of naltrexone?

A

palpitations, sexual dysfunction, tachycardia, constopation, hyperhydrosis

178
Q

when should disulfiram be started?

A
  • start at least 24 hrs after the last alcoholic drink consumed
  • need to stay under supervision for at least every 2 weeks for the first 2 months, then monthly for 4 months
179
Q

interaction between disulfiram and alc?

A

flushing, nausea, palpitations and, more seriously, arrhythmias, hypotension and collapse

180
Q

amount of alcohol needed to trigger a reaction w disufiram?

A
  • reactions may occur following exposure to small amounts of alcohol found in perfume, aerosol sprays, or low alcohol and “non-alcohol” beers and wines
181
Q

risk of ? w disulfiram that requires urgent medical attention

A
  • the rapid and unpredictable onset of the rare complication of hepatotoxicity; advise service users that if they feel unwell or develop a fever or jaundice that they should stop taking disulfiram and seek urgent medical attention.
182
Q

contra-indications of disulfiram?

A

psychosis, suicide risk, severe personality disorder

183
Q

SE of disulfiram?

A

hepatocellular injury, encephalopathy, psychotic disorder, paranoia, depression

184
Q

signs of opiod intoxication?

A
  • constriction of pupils, itching and scratching
  • sedation and somloence
  • lower BP
  • slower pulse
  • hypoventilation
185
Q

opiod withdrawal signs?

A
  • Watering eyes, rhinorrhoea, yawning, sneezing, cool and clammy skin,dilated pupils, cough.
  • Abdominal cramps, nausea, vomiting, diarrhoea.
  • Tremor, sleep disorder,restlessness, anxiety, irritability, hypertension.
186
Q

methadone vs buprenorphine for opiod dependence?

A
  • Methadone andbuprenorphine are equally effective as substitution therapy for opioid dependence
  • buprenoprhine is available with naloxone in a combined sublingual tablet
187
Q

opiod dependence -? is more effective in retaining ppl in Tx?

A

methadone

188
Q

what might be preferrred for ppl that use large amounts of heroin?

A
  • low dose methadone
189
Q

clouding can occur w ? use

A
  • buprenorphine - clear head
  • clouding can occur with methadone or heroin use
190
Q

what is preferred in ppl on LT treatment with drugs that affect liver enzymes?

A
  • buprenorphine preferred in people who are on long-term treatment with drugs that either induce or inhibit liver enzymes (such as anticonvulsants, rifampicin, ribavirin), as it is less affected by these liver enzymes than methadone.
191
Q

CI for methadone (and all opiods)

A
  • ARD
  • comatose patients
  • raised ICP
  • risk of paralytic ileus
192
Q

CI for methadone specifically?

A
  • Phaeochromocytoma
193
Q

side effects of methadone?

A
  • arrhythmias
  • dizziness
  • hallucinations
  • resp distress
  • vomiting - common on initiation
194
Q

when can methadone overdose occur?

A
  • can occur if methadone is taken with certain painkillers like oxycontin, hydrocodone, morphine
195
Q

methadone overdose signs?

A
  • pinpoint pupils
  • constipation
  • low BP/ weak pulse
  • slow, labored, shallow breathing
  • coma
  • cyanosis
196
Q

CI of buprenorphine?

A
  • resp distress
  • comatose patients
  • head injury
  • risk of paralytic ileus
197
Q

side effects of buprenorphine?

A
  • anxiety, depression, diarrhoea, tremor
198
Q

benzodiazepine withdrawal?

A
  • The two potential approaches for withdrawal are slow dose reduction of the person’s current benzodiazepine or z-drug, or switching to an approximately equivalent dose of diazepam, which is then tapered down.
199
Q

what should MI include?

A
  • helping people to recognise problems or potential problems related to their drinking
  • helping to resolve ambivalence and encourage positive change and belief in the ability to change
  • adopting a persuasive and supportive rather than an argumentative and confrontational position.
200
Q

how does co-working with other NHS specialities maintain high qual patient care?

A
  • collaborative approach - combined expertise
  • seamless care
  • improvement in decision making
  • working with local authorities - supported employment
  • better targeting of resources
  • better prevention
201
Q

symptoms of acute alc withdrawal

A
  • autonomic hyperactivity such as agitation,
  • tremors,
  • irritability,
  • anxiety,
  • hyperreflexia,
  • confusion,
  • hypertension,
  • tachycardia,
  • fever
  • diaphoresis:
202
Q

when does alc withdrawal usually occur?

A
  • usually develops 6-24 hrs after abrupt discontinuation or decrease in alcohol consumption
203
Q

mild alc withdrawal?

A

characterized by tremors, nausea, anxiety, and depression

204
Q

severe forms of alc withdrawal?

A
  • severe forms characterized by hallucinations, seizures, delirium tremens (DT) and coma
205
Q

management of AAW?

A
  • benzodiazepine or carbamazepine
  • Clomethiazole may be offered as an alternative to a benzodiazepine or carbamazepine.
206
Q

First line in delirium tremens?

A

lorazapam - oral

207
Q

if lorezapam doesn’t work in DT, use…

A
  • If symptoms persist or oral medication is declined, offer parenteral lorazepam or haloperidol.
208
Q

peak incidence of DT?

A

48-72 HRS

209
Q

signs of DT?

A
  • coarse tremor,
  • confusion,
  • delusions,
  • auditory
  • visual hallucinations
  • fever
  • tachycardia
210
Q

triad in WE?

A
  1. oculmotor abn - lateral rectus palsy, nystagmus, opthalmoplegia
  2. cerebellar dysfunction - ataxia
  3. altered mental state - confusion
211
Q

KS symptoms?

A

*** anterograde amnesia - impaired ability to acquire new episodic memories
* * confabulation **
* retrograde amnesia
* lack of insight
* disorientation in time and place
* executive dysfunction
* sequelae of WE

212
Q
A

Year 3 (45 decks)

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