Alcoholic Liver Disease

Question 1

Definition

Answer 1

chonic liver disease from alcoholic fatty liver to alcoholic hepatitis and cirrhosis, due to excessive long term alcohol consumption.

Question 2

Pathophysiology

Answer 2

Direct hepatocyte effects-
- altered redox state
- oxidative stress and lipid peroxidation due to CYP and ETC induction
- Transcription factor effects
- Protein adduct formation
- Altered methionine and folate metabolism
Increased gut permeability causing kupffer cell activation-
- proinflammatory cytokine release
- hepatocyte apoptosis
- stellate cell activation
- collagen production and fibrosis
Basically fatty change, alcoholic hepatitis then cirrhosis.
- FA production as NAD used in alcohol metabolism.
- steatosis= hepatocyte injury/inflammation= stellate activation= myofibroblast proliferation, contraction, chemotaxis, fibrogenesis.
Also activated kuppfer cells= cytokines= hepatocyte apoptosis.
- perivenular and peisinusoidal fibrosis= cirrhosis.
- alcoholic hep= cirrhosis.
The cirrhosis =
- clotting dysfunction, oncotic pressure, N elimination, bilirubin conjugated problems.
- complications of HTN eg varicies, ascites, encephalopathy, spider naevi, malnutrition, splenomegaly, testicular atrophy.
- HCC
- liver failure.

Question 3

Signs

Answer 3

Palmar erythema
Spider naevi
Bilateral gynaecomastia
Testicular atrophy
Bilateral parotid enlargement
Dupuytrens contracture
If decompensated liver disease- jaundice, coagulopathy, ascites, encephalopathy, splenomegaly. 
(NOT jaundice, ascites, or splenomegaly usually)

Question 4

Symptoms

Answer 4

Generally asymptomatic
Anorexia
Fatigue
RUQ discomfort
Tender hepatomegaly
Fever
Easy bruising
Poor concentration

Question 5

Diagnosis

Answer 5

Leukocytosis, macrocytic anaemia, thrombocytopenia, increase prothrombin time.
Elevated AST to ALT ratio over 2.
Gamma glutamyl transpeptidase high.
ALP high. 
Total bilirubin high.
Low serum albumin. 
HypoK, Mg, Ca, P. 
US
Biopsy.
AUDIT or CAGE questionnaire
Cirrhosis biopsy mallory bodies

Question 6

Management

Answer 6

Abstinence support, maybe disulfiram.
No further treatment for fatty liver, and is generally reversible.
Steroids for alcoholic hepatitis, and infection screen. High mortality.
Nutrition, vits B,K.
Manage complications.
Transplant.

Question 7

Complications

Answer 7

HCC
Liver failure (transplant only option)
Wernicke korsakoff syndrome
Encephalopathy
Dementia
Epilepsy
Oesophageal varices (L gastric to azygos)
Prone to drug toxicity eg paracetamol.

Question 8

Differentials

Answer 8

Hepatitis
Galactosaemia
Haemorrhagic virus
Cholecystitis (positive Murphys)
Wernickes encephalopathy

Question 9

Basic pathophysiology

Answer 9

Direct hepatocyte affects.
Alcohol metabolism uses NAD= more FA production.
Seatosis= hepatocyte injury and inflammation= stellate and kupffer activation= collagen production and cytokines= hepatocyte apoptosis.
Repeated nodular regneration= cirrhosis.
Decreased liver function and portal HTN.

Question 10

Withdrawal

Answer 10

Symptoms- tachyc, hypotension, tremor, confusion, fit, hallucination.
Treatment- chlordiazepoxide, vitamins K and B.

Question 11

Explanation

Answer 11

-liver deals with toxins like alcohol. Long term this causes damage- initally fatty change, the inflammation, and eventually scarring.
-it can lead on to cancer and problems in the brain.
-lifestyle stop drinking, avoid paracetamol, good nutrition.
-pharmacological steatosis reversible w/o meds but hepatitis may requires steroids. Also alcohol abstinence support eg disulfiram.
Nutrition. Monitoring. Transplant.