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Pathology > Pathology of the Liver > Flashcards

Pathology of the Liver Flashcards

1
Q

4 causes of acute liver failure and acute onset of jaundice?

A

Alcohol
Viruses
Drugs
Bile duct obstruction

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2
Q

Outcomes of acute liver failure?

A

Complete regeneration
Chronic liver disease
Death from liver failure

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3
Q

Classifications of jaundice by site and causes?

A

Pre-hepatic (increased requirement of haem breakdown increases bilirubin) - causes include haemolysis, of any type, and haemolytic anaemias; there is unconjugated bilirubin

Hepatic (injury/necrosis of hepatocytes) - causes include acute liver failure, alcoholic hepatitis, decompensated cirrhosis, bile duct loss (atresia, PBC, PSC), pregnancy

Post-hepatic (obstructive) - causes include congenital biliary atresia (no bile duct), gallstones in CBD, strictures and tumours of the head of the pancreas

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4
Q

Classifications of jaundice by type?

A

Conjugated - has been conjugated in the liver; causes are post-hepatic and hepatic

Unconjugated - has not been conjugated in the liver; causes are pre-hepatic and hepatic (problem with the conjugating capacity of the liver)

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5
Q

What is liver cirrhosis?

A

Bands of fibrosis separate regenerating nodules of hepatocytes; this is irreversible and a common end-point for liver disease

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6
Q

Complications of cirrhosis?

A

Portal hypertension (oeosphageal varices at the porto-caval anastamoses, caput medusae)

Ascites (accumulation of fluid in the peritoneal cavity due to raised hydrostatic pressure and hypoalbuminaemia)

Liver failure

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7
Q

What are other causes of portal hypertension?

A

Budd-chiari syndrome - narrowing and occlusion of the hepatic veins

Portal vein thrombosis

Portal fibrosis in sarcoidosis

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8
Q

Explain the causes of CLD clinical features?

A

Oedema - hypoalbuminaemia; ascites arises with portal hypertension as well

Haematemesis - ruptured oesophageal varices, due to portal hypertension

Spider naevi and gynecomastia - hyperoestrogenemia

Purpure and haemorrhaging - reduced clotting factor synthesis

Coma (hepatic encephalopathy) - failure to eliminate toxic gut bacterial metabolites

Infection - reduced Kupffer cell number and function

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9
Q

Pathogenesis of alcoholic liver disease?

A

Increased peripheral release of fatty acids and increased synthesis of fatty acids and triglycerides within the hepatocyte; acetaldehyde causes hepatocyte injury

Increased collagen synthesis by fibroblasts

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10
Q

How does the duration of alcohol consumption affect the prognosis?

A

2-3 days causes a fatty liver - steatosis is infiltration of hepatocytes with fat (reversible)

4-6 weeks causes hepatitis (reversible)

Months-years causes fibrosis (irreversible)

Years causes cirrhosis (irreversible)

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11
Q

Histopathological features of alcoholic fatty liver?

A

Fat vacuoles appear clear in the hepatocytes

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12
Q

Histopathological features of alcoholic hepatitis?

A

Hepatocyte necrosis and a neutrophil infiltrate

Mallory bodies (inclusions within cells) and pericellular fibrosis

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13
Q

Histopathological features of alcoholic fibrosis?

A

Collagen laid down around cells

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14
Q

Histopathological features of alcoholic cirrhosis?

A

Bands of fibrosis separate regenerating nodules of hepatocytes

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15
Q

What is non-alcoholic steatohepatitis (NASH)?

A

Caused by fat deposition in hepatocytes, due to a reason other than alcohol consumption; it is pathologically identical to alcoholic steatohepatitis

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16
Q

Risk factors for NASH?

A

Diabetes, obesity, hyperlipidaemia

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17
Q

What is viral hepatitis?

A

Inflammation of hepatocytes due to viral infection with Hep A-E, EBV, herpes simplex virus and CMV

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18
Q

Describe hepatitis A

A

Spread by faecal-oral route and it has a short incubation period

The virus kills hepatocytes DIRECTLY

There is no carrier state and it usually causes a mild illness

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19
Q

Describe hepatitis B

A

Spread via blood, blood products, intercourse and in utero; it has a long incubation period

There is a carrier state

Bystander hepatocyte damage due to anti-viral immune response

20
Q

Describe hepatitis C

A

Spread by blood, blood products and (possibly) via intercourse; it has a short incubation period and is often asymptomatic

The disease is dynamic (comes and goes) and tends result in carriers or chronic disease

21
Q

Histopathological findings in chronic viral hepatitis?

A

Dense portal chronic inflammation

Interface hepatitis (dense portal and peri-portal lymphocyte and plasma cell infiltrate that disrupts the parenchymal limiting plate)

Lobular inflammation

Fibrosis and cirrhosis

22
Q

Outcomes of Hep B infection?

A

Asymptomatic (carrier - unaffected but able to transmit the infection)

Chronic hepatitis

Cirrhosis

Hepatocellular carcinoma

Fulminant hepatic failure

23
Q

Outcomes of Hep C infection?

A

Chronic hepatitis

Cirrhosis

24
Q

What are the autoimmune diseases of the liver?

A

Primary biliary cirrhosis (PBC)

Autoimmune hepatitis

Primary sclerosing cholangitis

25
Q

What is primary biliary cirrhosis (PBC)?

A

A rare autoimmune disease; it is assoc. with auto-antibodies to mitochondria (AMA - anti-mitochondrial)

26
Q

Aetiology of PBC?

A

Unknown aetiology but majority of cases are in females (90%)

27
Q

Histopathology of PBC?

A

Progressive damage and loss of interlobular bile ducts

Progressive chronic granulomatous inflammation on biopsy

28
Q

What is autoimmune hepatitis (AIH)?

A

Attack to hepatocytes that mimics chronic hepatitis; there may be a trigger, e.g: a drug

29
Q

Antibodies in autoimmune hepatitis?

A

Assoc. with production of auto-antibodies to smooth muscle, anti-nuclear antibodies and anti-LKM (liver, kidney, microsomal) antibodies

30
Q

What is chronic drug-induced hepatitis?

A

Features similar to that of chronic hepatitis and may trigger autoimmune hepatitis; this can be caused by numerous drugs

31
Q

What is primary sclerosing cholangitis (PSC)?

A

Chronic inflammation and onion-skin PERI-DUCTAL FIBROSIS; appearance of “beads on a string”

32
Q

Aetiology of

A

More commonly affects males and is assoc. with UC; there is an increased risk of malignancy of the bile duct and of the colon

33
Q

What are 3 liver storage diseases?

A

Haemochromatosis
Wilson’s disease
α1-antitrypsin deficiency

34
Q

What is haemochromatosis?

A

Excess iron within the liver

35
Q

Causes of haemochromatosis?

A

Primary - genetic condition increasing Fe absorption

Secondary - Fe overload from diet, transfusions and iron therapy

36
Q

What is primary haemochromatosis?

A

Autosomal recessive condition that leads to excess Fe absorption from the intestine and abnormal Fe metabolism; it is worse in homozygotes and in males (do not have menstrual excretion of Fe)

After menopause, women will be just as susceptible as males

37
Q

Pathogenesis of primary haemochromatosis?

A

Deposited in portal connective tissue and leads to fibrosis and cirrhosis

It predisposes to carcinoma and can cause diabetes, cardiac failure, impotence and haemosiderin deposition in the skin

38
Q

What is Wilson’s disease?

A

Inherited autosomal recessive disorder of Cu metabolism; Cu accumulates in the liver and brain (basal ganglia)

It can cause chronic hepatitis and neurological deterioration

39
Q

Signs of Wilson’s disease?

A

Kayser-Fleischer rings (dark rings around iris)

Low serum caeruloplasmin

40
Q

What is α1-antitrypsin deficiency?

A

Inherited autosomal recessive disorder of production of anti-trypsin (anti-protease); causes emphysema, in non-smokers, and cirrhosis

41
Q

Histopathology of α1-antitrypsin deficiency?

A

Cytoplasmic globules of unsecreted protein globules remain in liver cells

42
Q

Tumours of the liver?

A

Primary (rare):
Hepatocellular adenoma
Hepatocellular carcinoma

Secondary (common):
Multiple metastases from colon, pancreas, stomach, breast, lung, etc

43
Q

Describe hepatocellular adenoma

A

Benign and most common in females; they can rupture and bleed but most remain assymptomatic

44
Q

Describe hepatocellular carinoma

A

Assoc. with HBV, HCV and cirrhosis

45
Q

Presentation of hepatocellular carcinoma

A

Usually presents as a mass, pain and obstruction; often advanced on finding

Pathology (25 decks)

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