Month: February 2019

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



Some Notes on Cardiac Pathology

Please note that I made these for my own use but thought they may be useful to others!

Cardiac Pathology


Divided into diseases of the:

  1. Coronary arteries
  2. Endocardium (including valves)
  3. Myocardium (including congenital heart disease)
  4. Pericardium


  1. Coronary arteries


Any vascular disease can involve these (e.g. vasculitis) but atheroma is the important one.

Clinically: angina, unstable angina and myocardial infarction (due to superimposed thrombosis secondary to ulceration or fissuring).


Left coronary artery >

  • anterior descending > anterior septum and wall of left ventricle
  • circumflex branch > lateral wall of left ventricle


Right coronary artery > posterior septum and wall of left ventricle


Distribution of infarction:

  1. Subendocardial infarction due to severe, generalized disease.
  2. Focal due to blockage of a major artery.


 Complications of myocardial infraction:



Arrhythmias: ventricular fibrillation / heart block

Acute cardiac failure / cardiogenic shock




  • Mural (over the infract) which may be followed by systemic embolisation
  • Atrial thrombus (due to atrial fibrillation)
  • (DVT which may be followed by pulmonary embolization)



Rupture (due to softening of muscle):

  • Myocardium (leading to cardiac tamponade and death)
  • Papillary muscle (mitral incompetence)
  • Septum (left to right shunt)





  • Chronic cardiac failure.
  • Immune pericarditis (Desslers’s syndrome)



Cardiac aneurysm (due to fibrosis)


At any time:

Another infarct


  1. B) Myocardium





  • Viral e.g. Coxsackie
  • Bacterial e.g. Borrelia (Lyme Disease)


Toxic: e.g. Diphtheria


Immunological e.g. Rheumatic fever



Definition: Heart muscle disease not due to ischaemia, hypertension, valvular disease or inflammation


  1. Dilated cardiomyopathy: end stage of the above (which has burnt out), alcohol or pregnancy
  2. Hypertrophic cardiomyopathy: autosomal dominant
  3. Restrictive cardiomyopathy: endomyocardial, fibro-elastosis, amyloid, haemochromtosis


Rheumatic fever

Preceded by streptococcal sore throat.

Type 2 hypersensitivity reaction (antibodies to streptococci cross react with antibodies to myocardium.


Clinical features

  • General: fever etc.
  • Skin: nodules
  • CNS: chorea
  • Heart:
  • Pericarditis
  • Myocarditis (Aschoff bodies- collections of macrophages)
  • Endocarditis including valves – may lead to chronic valve disease (see below)


Congenital Heart Disease


Risk factors: e.g. Down’s syndrome, rubella, thalidomide


  1. Left to right shunts e.g. atrial or ventricular septal defects ( if untreated may reverse
  2. Right to left shunt “ Cyanotic”

e.g. Tetralogy of Fallot:

  • large ventricular septal defect
  • pulmonary stenosis

3)  overriding of the aorta

4)  right ventricular hypertrophy



  1. C) Endocardium


Valve disease


Mitral valve:


Leads to dilation and hypertrophy of the left atrium

In incompetence there is, also, dilatation of the left ventricle



  • Post -inflammation: rheumatic fever
  • Infective endocarditis
  • Left ventricular failure
  • Myocardial infarction
  • “Floppy mitral valve syndrome”



  • Post-inflammation: rheumatic fever



  • Atrial fibrillation
  • Infective endocarditis



Aortic valve:



  • Age related calcification
  • Calcification of abnormal valve:

Congenital bicuspid

Post -inflammation: rheumatic fever


Leads to marked cardiac hypertrophy and the risk of sudden death



  • Post -inflammation: rheumatic fever
  • Infective endocarditis
  • Dilatation of valve ring e.g. Marfan’s syndrome


Leads to dilatation and hypertrophy



Infective endocarditis


Vegetations form on the valves


  1. Acute:

Pathogenic organism (e.g. staphylococcus aureus) and normal valve


  1. Subacute:

Less pathogenic organism (e.g. streptococcus viridans, from the mouth, or enterococci, from the gut) and an abnormal valve




  • Systemic features: Fever etc.
  • Embolisation of vegetations

Infected infarcts in the brain or kidneys

Splinter haemorrhages



Other causes of valve vegetations

e.g. marantic in patients with cancer



  1. D) Pericardium


Classified according to appearance

  1. Fibrinous e.g. myocardial infarction
  2. Serous e.g. rheumatic fever
  3. Purulent e.g. bacterial infection
  4. Haemorrhagic e.g. traumatic, tumour
  5. Fibrotic +/- calcification (chronic) = constrictive pericarditis g. TB



Pericardial haemorrhage:

  1. Myocardial infarction
  2. Dissecting aortic aneurysm