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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
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24
Q

how many units can prompt alcohol withdrawal?

A

alcohol dependence starts at around 10 units daily

25
define alcohol withdrawal syndrome?
- Abrupt cessation or reduction in long term use produced well defined symptoms
26
what are early withdrawal symptoms?
: sweating, tachycardiac, nausea, vomiting, retching, tremor, agitation, confusion, anxiety, fever, headache (6-12hrs)
27
what symptoms are associated with alcohol withdrawal (12-24hrs post)
visual and auditory hallcinations, tactile disturbances (pins and needles, numbess) , diarrhoea, delusion
28
why does withdrawal seizures occur?
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
what is delirium tremens?
- 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
how is delrium tremens treated?
- >48hrs: benzodiazepines, B vitamins, fluids, dextrose (prevent hypo), infection/ head injury is common
31
what is GMAS?
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
what symptoms may be seen with wernickes thiamine deficiency?
- Ocular palsy – abducens nerve (days to weeks appear) - Ataxic gait - Nausea - Memory problems - Wernickes triad: eye signs, ataxic gait, confusion
33
how do you treat wernickes?
- 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
what is korsakovs?
chronic thiamine deficiency?
35
what are symptoms of chronic thiamine deficiency?
- 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
what medications are used in alcohol withdrawal?
disulfiram acamprosate naltrexone
37
what does disulfiram do?
nasty taste with alcohol –maintain abstinence
38
what does acamprosate do?
reduce cravings
39
what does naltrexone do?
alcohol and opioid abuse drug – stop narcotic users to stay drug/ drink free
40
how much does alcohol abuse cost society?
£21 billion
41
how many adults in england are drinking at levels that puts health a risk?
10.8 million
42
what % does alcohol account for liver disease cases?
1/3
43
what enzyme processes alcohol?
alcohol dehydrogenase - ADH
44
how can alcohol levels vary between people?
ADH is a polymorphic enzyme - hence differences in protein
45
what does more alcohol do tp the level of acetate?
more alcohol - more acetaldehyde - more acetate
46
how does alcohol effect fat metabolism?
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
how does alcohol cause oxidative stress?
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
how is HepB spread?
spread via unprotected sex, sharing needles, maternal to baby
49
what is the incubation period of HBV?
HBV incubation is between 30 and 180 days
50
what does HBV do to liver?
- 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
what can hep C lead to?
chronic infection can cause cirrhosis, portal hypertension, hepatic decompensation with encephalopathy and hepatocellular carcinoma
52
what is the pathophysiology of HepC?
- Persistent infection appears to be due to CD4+ and CD8+ T cell response – failed to control viral replication - Local inflammation response triggers fibrinogenesis
53
which hepatitis is Hep D linked to?
hep B
54
what is primary sclerosing cholangitis?
chronic cholestatic disease of liver and bile ducts – chronic stagnation or reduction in bile secretion or flow
55
how does inflammation contribute to PSC?
- 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
what is the histology of PSC present as?
- End stage – onion skin – degeneration and atrophy of biliary epithelial cells
57
what are signs of wernickes?
CAN OPEN C - confusion A- ataxia N-Nystagmus O- opthalomplegia P-PEripheral N-Neuropathy
58

GI (12 decks)

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