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:

 

Minutes:

Arrhythmias: ventricular fibrillation / heart block

Acute cardiac failure / cardiogenic shock

 

Days:

Thromboses:

  • 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)

 

Week:

Rupture (due to softening of muscle):

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

 

Pericarditis

 

Weeks:

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

 

Months:

Cardiac aneurysm (due to fibrosis)

 

At any time:

Another infarct

 

  1. B) Myocardium

 

Myocarditis

Causes:

Infectious:

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

 

Toxic: e.g. Diphtheria

 

Immunological e.g. Rheumatic fever

 

Cardiomyopathy:

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

 

Incompetence:

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

 

Stenosis:

  • Post-inflammation: rheumatic fever

 

Complications:

  • Atrial fibrillation
  • Infective endocarditis

 

 

Aortic valve:

 

Stenosis:

  • Age related calcification
  • Calcification of abnormal valve:

Congenital bicuspid

Post -inflammation: rheumatic fever

 

Leads to marked cardiac hypertrophy and the risk of sudden death

 

Incompetence

  • 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

 

 

Complications:

  • 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