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alcohol Flashcards

1
Q

what are safe limits weekly of alcohol?

A

<14 units

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2
Q

what are safe limits of daily alcohol?

A

<3 units

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3
Q

how many units does a shot equal to?

A

1 shot = 1 unit

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4
Q

how long does it take for the body to process 1 unit?

A

1 unit = 1 hr post stopped drinking

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5
Q

how does alcohol effect people process alcohol differently?

A

due to own alcohol dehydrogenase (ADH)

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6
Q

what % of people have an alcohol problem?

A

38% of men and 16% of men

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7
Q

what % of people are alcohol dependent?

A

: 6% men and 1.2% of women

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8
Q

what % of people binge drink?

A

21% men and 9% of women

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9
Q

who is high risk of having an alcohol problem?

A
  • Male, single, social isolation
  • Anxiety – alcohol is a CNS depressant
  • Occupation – high stress
  • Childhood trauma
  • Family history
  • Chronic pain – help to dull pain
  • Other substance misuse
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10
Q

what does alcohol do to neurotransmitters?

A
  • Neurotransmitters: GABA (inhib) is reduced and NMDA (excitatory) is heightened
  • Dopamine and serotonin releases – involved in addiction
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11
Q

what does chronic tolerance do to the neurotransmitters?

A

: though neuroadaptation of inhib and excitatory pathways

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12
Q

how does alcohol effect cerebral cortex?

A
  • Lower inhibitions – act without thinking or angry for no reason
  • May affect your sense: blurring vision, long term alcohol abuse can permanently damage this region
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13
Q

how does cerebellum get effected by alcohol?

A

important for coordinating many daily movements such as walking, grabbing
- lose balance

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14
Q

can the medulla get affected by alcohol?

A

involuntary processes such as breathing and maintaining body temp
can cause comas

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15
Q

how can CNS be affected by alcohol?

A

alcohol slows system
- Made up of brain, spinal cord, nerves
- Affects how signals flow through body
- Making you think, speak and move more slowly

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16
Q

how does alcohol affect hypothalamus?

A

many body processes eg heart rate and feeling of hunger and thirst
- Alcohol can slow heart rate and make you hungrier and thirsty
- Crave carbs

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17
Q

how is memory impacted by alcohol?

A

memory controlled here
- Drinking a lot at one time can cause blackout or forget a period of time
- Long term alcohol can permanently damage area – hard to learn

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18
Q

what questions need to be included in an alcohol history?

A
  • When did they notice an increase in drinking?
  • Ask alcohol intake – last 24hrs? last week?
  • Establish pattern of binge drinking/ constant drinking
  • Is first drink to stop withdrawal? Drink to get drunk?
  • Drink throughout the day? Specific times? First thing?
  • Falls/ blackouts? Previous withdrawl seizures
  • Where/ who drink with? – hiding it? Embarrassed?
  • Any previous attempts to reduce/ abstain?
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19
Q

are binge drinkers at risk of withdrawal?

A
  • Not at risk of withdrawal if they binge – could be several days
  • If a patient drinks for up to 10-14 days daily could be at risk of withdrawal look at previous history
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20
Q

what is the CAGE screening tool?

A

C: have you felt like you need to CUT DOWN on intake?
A: have people felt ANNOYED by your drinking?
G: have you ever felt GUILTY about drinking? – hiding it?
E: do you need to drink first thing in morning to function – EYE OPENER? – does this help with nerves/ get rid of hangover
Score of > 2 is clinically significant

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21
Q

what is the AUDIT score?

A

alcohol use identification test

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22
Q

what is the AUDIT - C score?

A

AUDIT – C – alcohol use disorders identification test for consumption

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23
Q

what is the warning shot before starting alcohol history taking?

A
  • Now I am going to ask some questions about your alcohol intake
24
Q

how many units can prompt alcohol withdrawal?

A

alcohol dependence starts at around 10 units daily

25
Q

define alcohol withdrawal syndrome?

A
  • Abrupt cessation or reduction in long term use produced well defined symptoms
26
Q

what are early withdrawal symptoms?

A

: sweating, tachycardiac, nausea, vomiting, retching, tremor, agitation, confusion, anxiety, fever, headache (6-12hrs)

27
Q

what symptoms are associated with alcohol withdrawal (12-24hrs post)

A

visual and auditory hallcinations, tactile disturbances (pins and needles, numbess) , diarrhoea, delusion

28
Q

why does withdrawal seizures occur?

A

these can occur as early as 2hrs after cessation of alcohol consumption and even blood alcohol level has fallen below zero
usually seen 12-48hrs

29
Q

what is delirium tremens?

A
  • Usual onset is 24-72hrs after alcohol cessation
  • Is fatal in 15-20% of inappropriately managed patients
  • Hypertension, fever, agitation, disorientation, tachycardiac, severe tremor, visual/ auditory and tactile hallucinations
  • Sensation of ants on legs
30
Q

how is delrium tremens treated?

A
  • > 48hrs: benzodiazepines, B vitamins, fluids, dextrose (prevent hypo), infection/ head injury is common
31
Q

what is GMAS?

A

Glasgow modified withdrawal scale
- Modified assessment tool developed in Glasgow to help decide whether a patient requires symptom triggered treatment with chlordiazepoxide and IV vitamin prophylaxis and treatment for wernicks encephalopathy
- But fixed dose may be easier and then modify when needed (20mg chlordiazepoxide or 10mg diazepam)

32
Q

what symptoms may be seen with wernickes thiamine deficiency?

A
  • Ocular palsy – abducens nerve (days to weeks appear)
  • Ataxic gait
  • Nausea
  • Memory problems
  • Wernickes triad: eye signs, ataxic gait, confusion
33
Q

how do you treat wernickes?

A
  • Pabrinex IV/ IM – high dose vit B
  • Thiamine administration – to prevent diminished thiamine stores and becoming exhausted and triggering onset
  • Parental thiamine as oral is poorly absorbed considered in all patients and definitely within wernicke’s
  • Oral thiamine:
34
Q

what is korsakovs?

A

chronic thiamine deficiency?

35
Q

what are symptoms of chronic thiamine deficiency?

A
  • Long term memory is normal
  • Unable to make new memories
  • Distorted sense of time
  • Making up events – ‘ I went to uni’ when in fact they were in bed doing nothing – confabulation ( limbic system effected – hence memory is impaired)
  • Peripheral neuropathy
  • Lifelong chronic illness
36
Q

what medications are used in alcohol withdrawal?

A

disulfiram
acamprosate
naltrexone

37
Q

what does disulfiram do?

A

nasty taste with alcohol –maintain abstinence

38
Q

what does acamprosate do?

A

reduce cravings

39
Q

what does naltrexone do?

A

alcohol and opioid abuse drug – stop narcotic users to stay drug/ drink free

40
Q

how much does alcohol abuse cost society?

A

£21 billion

41
Q

how many adults in england are drinking at levels that puts health a risk?

A

10.8 million

42
Q

what % does alcohol account for liver disease cases?

A

1/3

43
Q

what enzyme processes alcohol?

A

alcohol dehydrogenase - ADH

44
Q

how can alcohol levels vary between people?

A

ADH is a polymorphic enzyme - hence differences in protein

45
Q

what does more alcohol do tp the level of acetate?

A

more alcohol - more acetaldehyde - more acetate

46
Q

how does alcohol effect fat metabolism?

A

alcohol uses same oxidative pathway as fatty oxidation
inhibits fatty acid oxidation and gluconeogenesis - promotes fat accumulation
chronic alcohol use - has to use different pathways (MEOS) - more oxidation and stress

47
Q

how does alcohol cause oxidative stress?

A

using different pathways when alcohol in excess
All the oxidative stress and fatty build up causes more inflammation, cell death and fibrosis – vicious circle – causing hepatocyte death

48
Q

how is HepB spread?

A

spread via unprotected sex, sharing needles, maternal to baby

49
Q

what is the incubation period of HBV?

A

HBV incubation is between 30 and 180 days

50
Q

what does HBV do to liver?

A
  • Can directly cause cytotoxic injury to liver
  • Hepatitis antigens (HBsAg) promote T cell induced lysis of HBC cells – cytotoxic T cell response is relatively ineffective
    predominant portal inflammation with hepatitis and spotty lobular inflammation
51
Q

what can hep C lead to?

A

chronic infection can cause cirrhosis, portal hypertension, hepatic decompensation with encephalopathy and hepatocellular carcinoma

52
Q

what is the pathophysiology of HepC?

A
  • Persistent infection appears to be due to CD4+ and CD8+ T cell response – failed to control viral replication
  • Local inflammation response triggers fibrinogenesis
53
Q

which hepatitis is Hep D linked to?

A

hep B

54
Q

what is primary sclerosing cholangitis?

A

chronic cholestatic disease of liver and bile ducts – chronic stagnation or reduction in bile secretion or flow

55
Q

how does inflammation contribute to PSC?

A
  • Cellular response: mixed inflame cell infiltrate of lymphocytes, plasma cells, neutrophils and mainly focused around bile ducts – combination of portal fibrosis and oedema and progressive reduction of the number of bile ducts
56
Q

what is the histology of PSC present as?

A
  • End stage – onion skin – degeneration and atrophy of biliary epithelial cells

GI (12 decks)

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