alcoholic liver disease Flashcards

1
Q

what is the stepwise progression of alcoholic liver disease?

A
  1. alcohol related fatty liver- build up of fat in the liver, which stops when drinking stops
  2. Alcoholic hepatitis- inflammation of the liver, mild alcoholic hepatitis can be reversible with permanent abstinence
  3. cirrhosis- liver becomes scared and this is ireversible- continued drinking makes it worse
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2
Q

what are the CAGE questions?

A

C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?

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3
Q

what will the bloods look like for alcoholic liver disease?

A
  • FBC – raised MCV
  • LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.
  • Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver
  • U+Es may be deranged in hepatorenal syndrome.
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4
Q

what types of imaging would you do for alcoholic liver disease?

A
  • fibro scan to check for liver elasticity
  • endoscopy to check for oesophageal varices
  • CT/MRI= to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
  • biopsy can be done to confirm cirrhosis or hepatitis and is usually given before starting steroid treatment
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5
Q

how does alcohol withdrawal progress?

A
  • 6-12 hours: tremor, sweating, headache, craving and anxiety
  • 12-24 hours: hallucinations
  • 24-48 hours: seizures
  • 24-72 hours: “delirium tremens”
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6
Q

what is the pathophysiology of delirium tremens?

A
  • alcohol activates GABA which relaxes the brain and inhibits glutamate- essentially inhibiting electrical activity in the brain
  • the brain responds by down regulating GABA and up regulating glutamate to balance the situation
  • when alcohol is suddenly taken away the under functioning of GABA and the over functioning of glutamate results in extreme excitability of the brain
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7
Q

what are symptoms of delirium tremens?

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
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8
Q

what’s the difference between wernickes and korsakoffs?

A

wernikes happens first and is a medical emergency which can be reversed. if wernickes is not treated it can lead to korsakoffs

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9
Q

what is the triad for wernikes?

A
  • confusion
  • ataxia
  • opthalmaplegia
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10
Q

what are features of korsikoffs?

A
  • memory impairment

- behavioural change

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11
Q

what is the cause of wernikes?

A

caused by B1 (thiamine deficiency)

treat with:
Intravenous high-dose B vitamins (pabrinex). This should be followed by regular lower dose oral thiamine.

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12
Q

what is maddreys discriminant function?

A

Suggests which patients with alcoholic hepatitis may have a poor prognosis and benefit from steroid administration.

uses prothrombin time and bilirubin conc

> 32 - likely to need steroids

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13
Q

what is the steroid regimin for alcoholic hepatitis?

A

prednisolone 40mg/day for 28 days.

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14
Q

what type of liver function tests would someone with acute alcoholic hepatitis have?

A

gamma-GT is characteristically elevated

the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly

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15
Q

why is pentoxyphylline not used as often as steroids for the treatment of acute hepatitis?

A

the STOPAH study compared pentoxyphylline and prednisolone.

It showed that prednisolone improved survival at 28 days and that pentoxyphylline did not improve outcomes

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