Category: Hepato-biliary Pathology

Some Notes on Liver Disease

This was tricky for me to write as the subject is  the closest to my heart! I  really found it hard to leave so much out.


Acute hepatitis:

  1. Viruses
  2. Drugs


Chronic hepatitis (liver disease lasting more than 6 months)

  1. Viruses
  2. Autoimmune
  3. Drugs


Pathological features of chronic hepatitis

Grade = inflammation (can be in 3 places: portal tracts, interface and lobular)

Stage = fibrosis (portal tract expansion > bridging > cirrhosis)


The commonest causes of cirrhosis are:

  1. viral hepatitis
  2. alcoholic liver disease
  3. non-alcoholic fatty liver disease


Viral hepatitis

There are 5 hepatitis viruses (all RNA except for HBV): A-E

A and E: spread by faecal oral route, cause only an acute hepatitis

B, C and D (which can only infect people who have HBV, as well): spread by blood etc., cause the full range of liver disease:

  1. acute hepatitis
  2. chronic hepatitis – scarring begins
  3. cirrhosis – nodules of hepatocytes surrounded by scar tissue


Alcoholic liver disease and non-alcoholic fatty disease (risk factors: obesity, diabetes) produce the same pathological changes:

  1. fatty change
  2. fatty liver hepatitis (alcoholic hepatitis / non-alcoholic steatohepatitis (NASH) respectively): ballooning, neutrophils and scarring
  3. cirrhosis

NB These 3 stages often con-exist


There are (many) other liver diseases which may  cause of cirrhosis:

  1. Autoimmune hepatitis: anti smooth muscle actin autoantibodies, plasma cells, associated with other AI diseases, response to steroids
  2. Drug induced liver injury (DILI): “any kind of liver disease can be caused by a drug’
  3. Haemochromatosis = genetic (AR) increased iron absorption from the gut

deposited in the liver and many other organs (including the pancreas).

  1. Wilson’s disease = genetic (AR) decreased copper excretion (by hepatocytes into the bile duct).
  2. Primary sclerosing cholangitis (PSC): sclerosis (= fibrosis) of the bile ducts leading to their loss. Associated with Ulcerative Colitis
  3. Primary biliary cholangitis (PBC): inflammation (with granulomas) of the bile ducts leading to their loss


Complications of cirrhosis:

  1. Portal hypertension with varices
  2. Liver failure with hepatic encephalopathy,
  3. Liver cell cancer (the same as hepatocellular carcinoma)


Tumours of the liver:

The commonest are secondary tumours (many via the portal vein)


Primary tumours

  1. Benign
  2. Bile duct adenomas
  3. Hepatic adenomas (associated with the contraceptive pill)


  1. Malignant
  2. Liver cell carcinoma

Most commonly associated with cirrhosis.

Spread via the portal vein.

Carry a poor prognosis.


  1. Cholangiocarcinoma (an adenocarcinoma)

Divided into intrahepatic and extra hepatic (including gall bladder)

May be associated with ulcerative colitis and worm infections

Spread to lymph nodes

Carry a poor prognosis



Not “Everyone Must Get Stoned” *

My first blog is going to be about gallstones. There is no special reason for this other than they are common (and, therefore, I hope this will be of interest to lots of people) and I happen to find gallbladder pathology interesting!

Below is a picture of a case I cut up yesterday:

As a medical student, I remember that the risk factors for gallstones were described as being “fat, fair, female and forty/ fertile ”  (depending on the specific version of the mnemonic).

How does this shape up now?  In this blog my core reference is Robin’s Pathology (in its range of formats) but will use a range of others. I will return to the topic of textbooks another time.

According to Robbins Basic Pathology (page 673):

Age: The prevalence of gallstones increases with age; over a 1/4 of people aged over 80 years have stones.

Sex: At every age, they are twice as common in women.

Ethnicity: They are very common in certain Native American groups.

Hereditary:  Family history and genetic disorders of bile salt metabolism. Although not mentioned in Robbins,  patients with haemolytic anaemias, including genetic ones such as Sickle Cell Anaemia, are at increased risk of pigment stones.

Environment:  Any factor that increases cholesterol excretion will increase the risk of stones. Oestrogens do this  (obviously contributing to the increased risk in women) as does obesity, rapid weight loss and drugs which increase cholesterol excretion, such as clofibrate.

Disorders affecting gallbladder motility: These includes pregnancy which contributes to the female and fertile risk.

So how does the mnemonic stand up? I came  across a paper (Postgrad Med J. 2013 Nov;89(1057):638-41. ) which directly addresses this question and concluded: “Our study found that the validated ‘students’ 5Fs’ mnemonic retains a role in clinical diagnosis of patients suspected of cholelithiasis but the factor ‘familial’ should be substituted for ‘forty’ in recognition of the role of inheritance and the changing demographics of gallstone incidence.”.

* Bob Dylan: