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8. Liver & Co > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

Describe the effects of alcohol on the body - the normal physiology.

A
  • Ethanol is metabolised in the liver by 2 pathways, resulting in the increase in the NADH/NAD ratio.
  • The altered redox potential causes increased hepatic fatty acid synthesis with decreased fatty acid oxidation - this results in the hepatic accumulation of fatty acids, which are then esterified to glycerides.
  • The changes in oxidation-reduction also impair carbohydrate and protein metabolism and are the cause of the centrilobular necrosis of the heaptic acinus that is typical of alcohol damage.
  • TNF-alpha release from Kupffer cells causes the release of reactive oxygen species (ROS), leading to tissue injury and fibrosis.
  • Acetaldehyde is formed by the oxidation of ethanol, and its effect on heaptic proteins could be a factor in producing liver cell damage.
  • Alcohol can also enhance the effects of the toxic metabolites of drugs e.g. paracetamol on the liver.
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2
Q

Give 5 complications that can arise from alcohol abuse.

A
  • Alcoholic Liver Disease
  • Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
  • Alcohol Dependence and Withdrawal
  • Wernicke-Korsakoff Syndrome (WKS)
  • Pancreatitis
  • Alcoholic Cardiomyopathy
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3
Q

Define alcoholic liver disease.

A

Results from the effects of the long term excessive consumption of alcohol on the liver.

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4
Q

What are the 3 phases of alcoholic liver disease?

A
  1. Fatty change: hepatocytes contain triglycerides.
  2. Alcohol hepatitis.
  3. Alcoholic cirrhosis: destruction of liver architecture and fibrosis.
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5
Q

Describe the 1st stage of alcoholic liver disease: Fatty change.

A

Fatty liver:

  1. Metabolism of alcohol produces fat in the liver
  2. This is minimal with small amounts of alcohol, but with larger amounts, the cells become swollen with fat (steatosis)
  3. There is no liver cell damage
  4. The fat disappears on stopping alcohol
  5. In some cases, collagen is laid down around the central hepatic veins and this can sometimes progress to cirrhosis, without a preceding hepatitis.
  6. Alcohol directly affects stellate cells, transforming them into collagen-producing myofibroblast cells.
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6
Q

What are the clinical features of fatty change (stage 1)?

A

Often no symptoms or signs.

  • Vague abdominal symptoms of nausea, vomiting, diarrhoea are due to the more general effects of alcohol on the GI tract.
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7
Q

Describe the 2nd stage of alcoholic liver disease: alcoholic hepatitis.

A
  1. In addition to fatty change, there is infiltration by polymorphonuclear leucocytes and hepatocyte necrosis.
  2. Dense cytoplasmic inclusions called Mallory bodies are sometimes seen in hepatocytes.
  3. Giant mitochondria are also a feature.
  • If alcohol consumption continues, alcoholic hepatitis can progress to cirrhosis.
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8
Q

What are the clinical features of alcoholic hepatitis (stage 2)?

A
  • SPIDER NAEVI
  • Rapid onset mild jaundice
  • Signs of chronic liver disease - Ascites, Bruising, Clubbing
  • Tender hepatomegaly
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9
Q

Describe the 3rd stage of alcoholic liver disease: alcoholic cirrhosis.

A

This is where the liver is made up of scar tissue rather than healthy liver tissue.

Classically of the MICRONODULAR TYPE but mixed pattern is also seen accompanying fatty change.
Evidence of pre-existing alcoholic hepatitis may be present.

This is irreversible.

Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

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10
Q

What are the clinical features of alcoholic cirrhosis (stage 3)?

A

Patients can be very well with few symptoms.

On examination there are usually signs of chronic liver disease - ascites, bruising, clubbing and Dupuytren’s contracture.

Features of alcohol dependency.

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11
Q

What is the path of damage that the alcoholic liver follows?

A

Fatty change - alcoholic heptatitis - fibrosis - micronodular cirrhosis

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12
Q

Investigations for stage 1 - fatty liver.

A
  1. Bloods:
    - Elevated MCV indicates heavy drinking
    - Raised ALT and AST
    - Serum GGT particularly elevated
  2. Ultrasound or CT will demonstrate fatty infiltration
  3. Liver histology will also show any fatty infiltration
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13
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT (gamma-glutamyl transferase) will be elevated.

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14
Q

Investigations for stage 2 - alcoholic hepatitis.

A
  1. Bloods:
    * Leucocytosis
  • Elevated:
  • Serum bilirubin
  • Serum AST and ALT
  • Serum GGT (gamma-glutamyl transferase)
  • Serum alkaline phosphate
  • Prothrombin time
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15
Q

What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?

A

Mallory bodies.

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16
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes.

17
Q

What is the AUDIT questionnaire?

A

The Alcohol Use Disorders Identification Test (AUDIT) was developed by the World Health Organisation to screen people for harmful alcohol use.

It involves 10 questions with multiple choice answers and gives a score.

A score of 8 or more gives an indication of harmful use.

18
Q

What are the CAGE questions?

A

Ever felt you should Cut down on your drinking?
Have people Annoyed you by criticising your drinking?
Ever felt Guilty about your drinking?
Ever had an Eye opener to help you get up in the morning?

19
Q

Management for alcoholic liver disease.

A
  1. STOP DRINKING ALCOHOL permanently- alcohol cessation
  2. Consider a detoxication regime
  3. Diet and nutritional support - vitamins particularly thiamine and a high protein diet
  4. Steroids - improve short-term outcomes (>1 month)
  5. Treat complications of cirrhosis
    - Portal hypertension, varices, ascites and hepatic encephalopathy
  6. IV Thiamine
    - To prevent Wernicke-Korsakoff encephalopathy
  7. Diazepam -
    - To treat delirium tremens (withdrawal symptom)
  8. Referral for liver transplant in severe disease
    - Must abstain from alcohol for 3 months prior to referral
20
Q

What is alcohol withdrawal?

A

When someone is alcohol dependent, there is a risk of them developing withdrawal symptoms when they stop drinking.
These can range from mild and uncomfortable to delirium tremens, which is life-threatening.
Symptoms occur at different times after alcohol consumption ceases.

21
Q

At what different times after alcohol consumption cessation do symptoms start occurring and what are the symptoms?

A

Symptoms occur at different times after alcohol consumption ceases:

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

22
Q

What is delirium tremens?

A

Delirium tremens is a medical emergency associated with alcohol withdrawal with a mortality of 35% if left untreated.

23
Q

Explain the pathophysiology of delirium tremens.

A

Alcohol stimulates GABA receptors in the brain. GABA receptors have a “relaxing” effect on the rest of the brain. Alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.

Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity.

24
Q

Clinical presentation of delirium tremens.

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
25
Q

What is the CIWA-Ar tool?

A

The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

26
Q

Managing Alcohol Withdrawal

A

The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

Chlordiazepoxide (“Librium”) is a benzodiazepine used to combat the effects of alcohol withdrawal.
Diazepam is a less commonly used alternative.
It is given orally as a reducing regime titrated to the required dose based on the local alcohol withdrawal protocol (e.g. 10 – 40 mg every 1 – 4 hours).
This is continued for 5-7 days.

Intravenous high-dose B vitamins (pabrinex).

This should be followed by regular lower dose oral thiamine.

27
Q

What is Wernicke-Korsakoff Syndrome (WKS)?

A

Alcohol excess leads to thiamine (vitamin B1) deficiency.
Thiamine is poorly absorbed in the presence of alcohol and alcoholics tend to have poor diets and rely on the alcohol for their calories.

Wernicke’s encephalopathy comes before Korsakoff’s syndrome.
These result from thiamine deficiency.

28
Q

Which one of Wernicke’s encephalopathy or Korsakoff’s syndrome is an medical emergency?
Which one is often irreversible

A

Wernicke’s encephalopathy is a medical emergency and has a high mortality rate, if untreated.

Korsakoff’s syndrome is often irreversible and results in patients requiring full time institutional care.

Prevention and treatment involve thiamine supplementation and abstaining from alcohol.

29
Q

Give 3 features of Wernicke’s encephalopathy.

A

Features of Wernicke’s encephalopathy:

  1. Confusion
  2. Oculomotor disturbances (disturbances of eye movements)
  3. Ataxia (difficulties with coordinated movements)
30
Q

Give 2 features of Korsakoff’s syndrome.

A

Features of Korsakoff’s syndrome:

  1. Memory impairment (retrograde and anterograde)
  2. Behavioural changes
31
Q

What 3 symptoms make up the triad of Wernicke’s encephalopathy?

A
  1. Ataxia.
  2. Opthalmoplegia.
  3. Confusion.
32
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

8. Liver & Co (18 decks)

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