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RB Y3 2 Psychiatry > Alcohol > Flashcards

Alcohol Flashcards

1
Q

which pathways are switched on to metabolise alcohol in heavy drinkers

A

MEOS pathways and CP450

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2
Q

what are the consequences of the MEOS pathway

A
  • citric acid cycle inhibition - switch to anaerboic metabolism - lactic acid build up
  • inhibits hepatic gluconeogenesis - makes you hungry, can push diabetics into hypo
  • impaired fatty acid oxidation - trigylceride accumulation in the liver
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3
Q

what effect does alcohol have on the heart

A

negative inotrope - tachycardia to compensate

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4
Q

how do you calculate alcohol units

A

(ABV x vol) / 1000

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5
Q

what is high risk drinking

A

>35 units a weel

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6
Q

what is low risk drinking

A

Men and women should not regularly drink more than 14 units of alcohol a week. Ideally, this should be spread evenly over three days or more

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7
Q

what is no risk drinking

A

there is no such thing!

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8
Q

what is TWEAK used for

A

screen for alcohol problems in pregnant women

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9
Q

which alcohol questionnaires are used in A and E

A

PAT and FAST

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10
Q

what is the purpose of CAGE screening tool

A

detect alcohol abuse and dependence

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11
Q

what lab tests can be done if chronic drinking is suspected

A

GGT, MCV, triglycerides

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12
Q

what is the science underlying the carbohydrate deficient transferrin test

A
  • Transferrin transports iron in blood, normally has 3-5 carbohydrate side chains attached. Misuse of alcohol gives higher proportion of transferrin to less carbohydrate side chains, hence the term ‘deficient’
  • Misuse of alcohol gives higher proportion of transferrin to less carbohydrate side chains, hence the term ‘deficient’
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13
Q

what is CDT used for

A

to detect heavy alcohol consumption, it is raised proportionally to alcohol intake and reflects the chronicity of drinking

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14
Q

how is CDT performed

A

blood tets

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15
Q

who uses teh CDT test

A

DVLA - to identify men drinking ≥5units/day for ≥2 weeks

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16
Q

is FRAMES used in dependent or non dependent people

A

non dependent - used to reduce alcohol consumption

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17
Q

outline FRAMES

A
  • Feedback - review problems experienced because of alcohol.
  • Responsibility – patient is responsible for change.
  • Advice – advise reduction or abstinence.
  • Menu – provide options for changing behaviour.
  • Empathy – use empathic approach.
  • Self-efficacy –encourage optimism about changing behaviour.
18
Q

what does alcohol do to GABA and glutamate receptors

A
  • Alcohol inhibits the action of excitatory NMDA-glutamate controlled ion channels (chronic use leads to upregulation of receptors)
  • Alcohol potentiates the actions of inhibitory GABA type A controlled ion channels (chronic use leads to downregulation of receptors).
19
Q

with this in mind, what happens when alcohol is withdrawn acutely

A

excess glutamate activity and decreased GABA activity - excitatory effect

CNS excitability and neurotoxicity

20
Q

when do alcohol withdrawal symptoms peak

A

24-48 hours after

21
Q

mild withdrawal symptoms

A
  • Fine tremor, sweating, anxiety, hyperactivity, inc. HR, inc. BP, fever, anorexia, nausea, retching
22
Q

moderate withdrawal symptoms

A
  • Coarse tremor, sharking, agitation, confusion, disorientation, paranoia, seizures, hallucinations
23
Q

severe withdrawal symptoms

A
  • Risk of DT (medical emergency) around 48 hours, severe agitation, anxiety, confusion, delusions, hallucinations
  • Circulatory collapse and death can occur
24
Q

when does delirium tremens usually occur

A

3 days into withdrawal symtoms

25
Q

what is delirium tremens

A

rapid onset of confusion

Confusion, disorientation, agitation, hypertension, fever, visual and auditory hallucinations, paranoid ideation.

26
Q

is there a morbidity associated with delirium tremens

A

mortality 2-5% - CV collapse and infection

27
Q

pharmacological management of alcohol withdrawal symptoms in the detoxifying period

A

benzodiazpines, usually diazepam or chlordiazepoxide as theya re long acting

28
Q

why do benzodiazepines work

A

they are cross tolerant with alcohol as both potentiate GABA A receptors

29
Q

how long are benzodiazepines given for

A

around 7 days, reduce dose gradually

30
Q

name a withdrawal rating scale that can be usd as a guideline for prescribing

A

CIWA-Ar

31
Q

complication sof benzodiazepines

A

over sedation and sometimes respiratory depression

32
Q

why is vitamin supplementation considered

A

alcohol depletes thiamine stores inthe body, this may be a problem in chronic drinkers

given as prophylaxis against Wernickes Korsakoff syndrome

33
Q

which vitamin is given

A

Thiamine (Pabrinex - B and C)

34
Q

how is pabrinex adminstered

A

parenterally (IV or IM) as chronic alcohol consumption results in reduced absorption of thiamine

35
Q

how does disulfiram work

A
  • Inhibits aldehyde dehydrogenase, leading to accumulation of acetaldehyde if alcohol is ingested – flushed skin, tachycardia, nausea and vomiting, arrhythmias and hypotension (depending on volume congested)
  • transient symptoms
36
Q

what is the major problem with prescribing disulfiram and how can this be managed

A

patinet compliance - efficacy requires compliance

supervision of adminstration increases treatment success

37
Q

what is Acamprosate used for

A

reduce ongoing symptoms associated with abstinence and cravings - relapse prevention

38
Q

how does Acamprosate work

A

acts centrally on glutamate and GABA systems to normalise levels

39
Q

AE of acamprosate

A

headache, diarrhoea and nausea

40
Q

how does Naltrexone work

A

it reduces the rewarding and reinforcing effects of alcohol

  • blocks stimulation of opioid receptors by endogenous opioids
  • decreases dopamine release in VTA of midbrain (first step in reward pathway)
41
Q

are brief interventions worth doing?

A

yes, very effective

average reduction in alcohol consumption of 45% at 12 months

42
Q

who is the minimum unit price of 50p likely to benefit most

A

harmful drinkers and those living in poverty

RB Y3 2 Psychiatry (12 decks)

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