Liver pathology

Question 1

The normal liver weight

Answer 1

1500-2000g

Question 2

Describe the anatomical and functional areas of the liver

Answer 2

Hexagonal anatomical lobules based around hepatic vein
Acini functional zone that is entered along the line of two portal triads and extends out to points at two central veins on either side.Split into 3 zones, zone 1 closest to portal triads, zone 3 to veins

Question 3

How much liver needs to be ‘lost’ before symptomatic

Answer 3

80-90%!

Question 4

Functions of the liver

Answer 4

Protein productions, albumin
Clotting factors
Detoxification

Question 5

Symptoms of liver failure

Answer 5

Low albumin- peripheral oedema
Bleeding-loss of coagulation factors
Low concentration- ammonia, toxins
Jaundice, direct bilirubin
Portal hypertension- varices, ascites

Question 6

Features of a cirrhotic liver

Answer 6

Liver is smaller, nodules over the surface, increasing fibrosis around lobules.

Question 7

Cellular activity in cirrhosis

Answer 7

The normally quiescent stellate cells become active and moves towards injured hepatocytes (chemotaxis), cells proliferate and cause fibrogenesis.
Inflammatory response from kupffer cells causes release of cytokines that result in cell apoptosis and chemotaxis of stellate cells which proliferate and cause fibrogenesis

Question 8

Different causes of portal hypertension

Answer 8

Intrahepatic (cirrhosis) most common 90%
Prehepatic (thrombus within the portal vein)
Posthepatic (severe right sided heart failure)

Question 9

What do patients with portal hypertension present with?

Answer 9

Ascites- fluid in the abdomen due to increased pressure pushing fluid out of vessels. Also low serum albumin lower blood osmolarity. Legs swelling maybe low albumin levels
Bruising- low clotting factors
Shunts- caput medusae, oesphageal varices, anal varices
Anglomata (spider veins)
Hepatic encephalopathy failure of the liver to detoxify substances (ammonia)

Question 10

Hepatitis eitiologies

Answer 10

Hepatitis A, B, C, D, E most common (90%).
CMV herpes like virus present typically in immunosuppressed.
Epstein Barr (glandular fever).

Question 11

Hepatitis A

Answer 11

DNA virsus
Self-limiting (doesn’t progress typically)
Spread by poor hygiene
Can be asymptomatic
May have malaise, fatigue, jaundice, elevated ALT, AST

Question 12

Hepatitis B and C

Answer 12

DNA/ RNA virus
Spread by body fluids
Associated with chronic infection and the development of cirrhosis.
Can result in acute or chronic hepatitis
Damage caused by bodies immunological response to the antibodies on the hepatocytes

Question 13

Complication of cirrhosis

Answer 13

Cancer

Question 14

Hepatitis B vs C prognosis

Answer 14

Hep B only 25% develop acute hepatitis, and 5% chronic. The majority of infections result in recovery.
Hep C most develop chronic hepatitis, more than 20% develop cirrhosis eventually. Increased risk of carcinoma

Question 15

Autoimmune hepatitis, diagnosis and treatment.

Answer 15

Primary biliary cirrhosis
Primary sclerosing cholangitis
Diagnoses involves exclusion of viral and toxic causes. And also association with other autoimmune disorders (SLE etc.)
Patients may respond to immunosupressant therapy.

Question 16

Drug and toxin induced liver injury

Answer 16

Predictable and non-predictable hepatotoxins.
Toxin maybe directly toxic to hepatocytes or the liver may convert a substance into a toxic form.
Pattern of injury; cholestasis, hepatocellular necrosis, fatty liver, granulomas, vascular lesions, neoplasms.

Question 17

Most common toxins involved in liver injury

Answer 17

Paracetamol, acute

Alcohol. Acute and chronic

Question 18

Alcoholic liver disease

Answer 18

Cell injury caused by reactive oxygen species and cytokines
Changes in lipid metabolism
Decreased export of lipoproteins
All result in
-hepatic steatosis
-alcoholic hepatitis
-cirrhosis

Question 19

Non alcoholic fatty liver disease

Answer 19

Associated with metabolic syndromes, type 2 diabetes, obesity, dislipidaemia, hypertension.
Around 10% of patients with NASH will go on to develop cirrhosis.

Question 20

Haemochromatosis

Answer 20

Autosomal recessive genetic disorder whereby there is a mutation on the HFE (hereditary Fe) gene causing excessive absorption of iron.
Iron builds up in liver and patients can develop cirrhosis.

Question 21

Circulatory diseases (portal hypertension) of the liver and their manifestations

Answer 21

Impaired blood inflow: portal vein obstruction (thrombosis). Cirrhosis. Manifestations- splenomegaly, intestinal congestions, varices.
Impaired intrahepatic blood flow: cirrhosis, sinusoid occulsion. Manifestations- ascites, varices, hepatomegaly, elevated transaminases.
Outflow obstruction: Hepatic vein thrombosis (Budd-chiari syndrome), right sided heart failure. Manifestations- ascites, hepatomegaly, abdo pain, elevated transaminases, jaundice.

Question 22

Most common cause of elevated transaminase elevation

Answer 22

Viral

Question 23

Hepatitis C

Answer 23

RNA virus
Spread through blood
Majority of people infected are unable to eliminate the virus
85% actutely infected end up with chronic infection

Question 24

Liver cirrhosis

Answer 24

Irreversible scarring
Advanced liver disease
Liver initially enlarges then shrinks
Surface becomes irregular and nodular

Question 25

Ulcerative colitis

Answer 25

A form of inflammatory bowel disease causing inflammation and ulcers in the colon.

Question 26

Signs of chronic liver disease

Answer 26

Ascites
Encephalopathy
Spider nevae

Question 27

Budd chiari syndrome

Answer 27

Acute thrombosis of hepatic veins- outflow obstructed
Acutely congested liver, hepatocellular injury
Portal hypertension with ascites developing.
Presents with progressive sever upper ado pain, jaundice, hepatomegaly, ascites, hepatic encephalopathy.

Question 28

Management of budd chiari

Answer 28

Shunt
Anticoagulation
Diuretics