Alcohol-related Liver Disease Flashcards

1
Q

Give a brief overview of the pathogenesis of alcohol related liver disease.

A

Spectrum of liver disease ranges from reversible fatty change to end stage cirrhosis.
The spectrum ranges from alcoholic fatty liver (steatosis) to alcoholic hepatitis and chronic cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the pathogenesis of Fatty Liver Disease.

A
  • Alcohol is converted to acetaldehyde by the mitochondrial enzyme alcohol dehydrogenase.
  • Acetaldehyde is converted in turn to acetate and then to fatty acids.
  • Alcohol is calorie rich, fat is deposited in the liver (steatosis) initially around the central veins (zone 3) and then later around parenchyma.

If alcohol consumption ceases the liver will return to normal.
•If not inflammation and fatty change occurs (steatohepatitis).

Fibrosis, initially around central veins, may occur leading to cirrhosis in some patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the pathogenesis of alcohol related cirrhosis.

A

Cirrhosis related to alcohol consumption is typically micron ocular with steatosis.

In some patients little evidence of steatosis is present.

If alcohol consumption ceases the cirrhosis may become macronodular with little inflammatory change.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the pathogenesis of acute alcoholic hepatitis.

A

In addition to fatty change, may be infiltration with polymorphonuclear leukocytes and hepatic necrosis.
⏩hepatomegaly, fever, abdo pain, jaundice and hepatic decompensation.

Acute alcoholic hepatitis.
May occur on a background of cirrhosis of in those without underlying cirrhosis.
Liver may return to normal with nutritional support and abstinence from alcohol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What would a patient with alcoholic liver disease describe in their history?

A

May remain asymptomatic and undetected unless they present for other reasons.

May be mild illness with nausea, malaise, epigastric or right hypochondrial pain and a low-grade fever.

May be more severe with jaundice, abdominal discomfort or swelling, swollen ankles or GI bleeding.

Women tend to present with more florid illness than men.

There is a history of heavy alcohol intake (~15–20 years of excessive intake necessary for development of alcoholic hepatitis).

There may be trigger events (e.g. aspiration pneumonia or injury).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What would be found on examination of a patient with excessive alcohol intake?

A
Signs of alcohol excess: 
•Malnourished, 
•palmar erythema, 
•Dupuytren’s contracture, 
•facial telangiectasia, 
•facial mooning
•parotid enlargement, 
•spider naevi, 
•gynaecomastia, 
•testicular atrophy, 
•hepatomegaly, 
•smell of alcohol
•easy bruising.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What would be found on examination of a patient with severe alcoholic hepatitis?

A
Signs of severe alcoholic hepatitis: 
•Febrile (50% of patients), 
•tachycardia, 
•jaundice (>50% of patients), 
•bruising, 
•encephalopathy (e.g. hepatic foetor, liver flap, drowsiness, unable to copy a five-pointed star, disoriented), 
•ascites (30–60% of patients), 
•hepatomegaly (liver is usually mild–moderately enlarged and may be tender on palpation), 
•splenomegaly.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the definition of alcoholic hepatitis?

A

Inflammatory liver injury caused by chronic heavy intake of alcohol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What investigations would you perform on a patient with suspected alcoholic hepatitis?

A

Blood:
•FBC: ⬇️ Hb, ⬆️ MCV, ⬆️ WCC, ⬇️ platelets.
•LFT (⬆️ transminases, ⬆️ bilirubin, ⬇️ albumin, ⬆️ AlkPhos, ⬆️ GGT).
•U&E: Urea and K+ levels tend to be low, unless significant renal impairment.
•Clotting: Prolonged PT is a sensitive marker of significant liver damage.

Ultrasound scan:
For other causes of liver impairment (e.g. malignancies).

Upper GI endoscopy:
To investigate for varices.

Liver biopsy:
Percutaneous or transjugular (in the presence of coagulopathy) may be helpful to distinguish from other causes of hepatitis.

Electroencephalogram:
For slow-wave activity indicative of encephalopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How would you manage a patient with alcoholic hepatitis?

A

Acute:
•Thiamine,
•Vitamin C and other multivitamins (initially parenterally).
•Monitor and correct K+ , Mg2+ and glucose abnormalities.
•Ensure adequate urine output.
•Treat encephalopathy with oral lactulose and phosphate enemas.
•Ascites is managed by diuretics (spironolactone with or without frusemide (furosemide)) or therapeutic paracentesis.
•Glypressin and N-acetylcysteine for hepatorenal syndrome.

Nutrition:
•Nutritional support with oral or nasogastric feeding is important with increased caloric intake.
•Protein restriction should be avoided unless the patient is encephalopathic.
•Total enteral nutrition may also be considered as this improves mortality rate.
•Nutritional supplementation and vitamins (B group, thiamine, folic acid) should be started parenterally initially and then continued orally after.

Steroid therapy:
•Meta-analyses show that steroids reduce short-term mortality for severe alcoholic hepatitis.

Long-term:
See Alcohol dependence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What complications are associated with alcoholic hepatitis?

A
  • Acute liver decompensation,
  • hepatorenal syndrome (renal failure secondary to advanced liver disease),
  • cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the prognosis for a patient with alcoholic hepatitis?

A

Mortality in first month is about 10%; 40% in first year.

If alcohol intake continues, most progress to cirrhosis within 1–3 years.

Various validated prognostic scores can be used:
•Maddrey’s discriminant function (MDF)
•Glasgow alcoholic hepatitis score (GAHS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the definition of alcohol dependence?

A

Alcohol dependence is characterized by three or more of:
•Withdrawal on cessation of alcohol.
•Tolerance.
•Compulsion to drink, difficulty controlling termination or the levels of use.
•Persistent desire to cut down or control use.
•Time is spent obtaining, using, or recovering from alcohol.
•Neglect of other interests (social, occupational, or recreational).
•Continued use despite physical and psychological problems.

Recommended limits for F and M are 14 and 21 units/week, respectively.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What questions should you ask if you are screening for alcohol dependence?

A

CAGE screening questions:
•Cut-down: ‘… felt that you should cut-down on intake?
•Annoyed: ‘… felt annoyed by criticism of your drinking?
•Guilt: ‘… felt guilty about how much you drink?
•Eye-opener:‘… feel that you need a drink when you wake up?

Evaluate for associated comorbidities including smoking, other substance abuse, depression, anxiety and panic attacks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What would a patient suffering with alcohol dependence describe in their history?
•acute intoxication
•symptoms of withdrawal?

A

Acute intoxication:
Amnesia, ataxia, dysarthria, disorientation, palpitations, flushing and
coma.

Symptoms of withdrawal:
Nausea, sweating and tremor, restlessness, agitation, visual
hallucination, confusion, seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What complications are associated with alcohol dependence?

A

GI:
Oesophagitis, Mallory–Weiss tears, varices, gastritis, peptic ulcers, acute or chronic pancreatitis.

Liver:
Fatty change, alcoholic hepatitis, cirrhosis.

Neurological:
Acute intoxication.

Withdrawal:
Fits, delirium tremens (48–72h after cessation – coarse tremor, agitation, fever, tachycardia, confusion, delusions and hallucinations). Chronic complications include cerebral atrophy and dementia, cerebellar degeneration, optic atrophy, peripheral neuropathy, myopathy. Indirect effects include hepatic encephalopathy, thiamine deficiency, causing Wernicke’s encephalopathy or Korsakoff’s psychosis.

Haematological:
Anaemia (vitamin B12 or folate deficiency, iron deficiency in patients with GI bleeding), thrombocytopaenia (due to enlarged spleen in patient with cirrhosis or direct toxic effect on megakaryocytes), abnormal platelet function.

Respiratory:
Depression, inhalation of vomitus.

Cardiac:
Hypertension, cardiomyopathy, arrhythmias.

Drug interactions:
E.g. oral contraceptive pills (alcohol is a liver enzyme-inhibitor acutely,
but chronic abuse induces liver enzymes.)

Teratogenicity:
Foetal alcohol syndrome.

Psychosocial:
Depression, anxiety, deliberate self-harm. Domestic, employment and financial problems.

17
Q

Describe Wernicke’s encephalopathy.

A

nystagmus, ophthalmoplaegia and ataxia, together with apathy, disorientation and disturbed memory.
Treat urgently with thiamine or may progress to Korsakoff’s psychosis.

18
Q

Describe Korsakoff’s psychosis.

A

characterized by profound impairment of retrograde and anterograde memory with confabulation, as a result of damage to the mammillary bodies and the hippocampus.

Irreversible.