Condition - Alcoholic Liver Disease Flashcards

1
Q

Clinical features - history

A

Alcoholism!!

Symptoms:
Fever (associated with liver necrosis)
RUQ pain
Jaundice
Abdominal distension (ascites)
Easy bruising
GI bleeding (varices)
Poor concentration/drowsiness
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2
Q

Clinical features - examination

A
Jaundice - bilirubin conjugation
Fetor (bad smell)
Hepatic flap - nitrogen metabolism
Ascites - liver proteins
Oedema - liver proteins
Impaired consciousness - nitrogen metabolism

Fatty liver / hepatitis - enlarged liver
Cirrhosis - small nodular liver

Decompensation:

Dupuytren's contracture
Palmar erythema - oestrogen
Spider naevi - oestrogen
Gynaecomastia - oestrogen
Hepatosplenomegaly (portal hypertension)
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3
Q

Investigations

A

Raised GGT indicative of alcohol consumption.
Serum albumin and prothrombin (clotting) time are best indicators of liver function.

FBC
LFT
Ultrasound abdomen.
Viral (hepatitis) serology.
Autoimmune profile.
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4
Q

Treatment (general)

A

Stop drinking, fatty liver is reversible.

If cirrhosis and not decompensated - treat symptoms.

If decompensated - transplant is the only option.

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5
Q

Ascites / Oedema

A

This is due to decreased oncotic pressure and portal hypertension.
Treat with fluid restriction and loop diuretic (furosemide) or potassium sparing diuretic (spironolactone).
Severe/resistant ascites may require draining and IV albumin.

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6
Q

Hepatic encephalopathy

A

Bacteria in your gut produce nitrates.
They are absorbed and enter the hepatic portal system where they are metabolised in your liver (urea cycle).
If this does not occur, ammonia may accumulate and enter the CNS.
This results in cerebral oedema.

Treatment is with lactulose (osmotic laxative).
Ensures regular stools are passed to minimise nitrate absorption.

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7
Q

Wernicke-Korsakoff

A

Caused by thiamine (vitamin B1) deficiency, so give thiamine prophylactically.

Wernicke’s encephalopathy:

Vision disturbance
Dementia
Ataxia

Korsakoff’s syndrome:

Amnesia (loss of memory)
Aphasia (loss of speech/comprehension)
Apraxia (loss of motor control)
Agnosia (loss of sensation)

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8
Q

Aetiology.

A

Fatty liver - Hepatitis - Cirrhosis

Ethanol is metabolised in the liver.
Increased NADH/NAD ratio.
Increased fatty acid synthesis.
Decreased fatty acid oxidation.
Metabolites are also hepatotoxic, leads to injury.
Subsequent inflammation, necrosis and fibrosis.

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9
Q

Differential diagnosis

A

Jaundice and abdominal pain/distension:

Alcoholic liver disease (what stage?)
GI malignancy with liver metastasis
Infective hepatitis

CNS symptoms:

Hepatic encephalopathy
Wernicke-Korsakoff’s

GI bleed:

Bleeding varices
Perforated ulcer
Malignancy

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