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Histopathology > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

Describe the histology of liver cirrhosis

A

Fibrosis, hepatocyte necrosis, nodules of regenerating hepatocytes, disturbance of vascular architecture

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2
Q

What is liver cirrhosis?

A

Diffuse abnormality of liver architecture interfering with blood flow and function. Fibrotic bridges form between the portal triad and central vein, with extra-hepatic shunting leading to anastomoses

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3
Q

State the seven major causes of cirrhosis

A

Alcoholic liver disease, non-alcoholic fatty liver disease, chronic viral hepatitis, autoimmune hepatitis, biliary pathology, genetic conditions, drugs

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4
Q

Name a drug that causes cirrhosis

A

Methotrexate

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5
Q

State at least three genetic causes of cirrhosis

A

Haemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency, galactosaemia, glycogen storage disease

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6
Q

State two causes of micronodular cirrhosis

A

Alcoholic hepatitis, biliary tract disease

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7
Q

State three causes of macronodular cirrhosis

A

Viral hepatitis, Wilson’s disease, alpha-1 antitrypsin deficiency

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8
Q

Name the prognostic scoring system for liver cirrhosis

A

Modified Child’s Pugh Score

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9
Q

Which gene causes haemochromatosis?

A

Mutation of the HFE gene on chromosome 6

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10
Q

Which gene causes Wilson’s disease?

A

Mutation of the ATP7B gene on chromosome 13

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11
Q

State the 5 components of prognostic scoring in liver cirrhosis

A

ABCDE: Albumin, bilirubin, clotting (prothrombin time), distension (ascites), encephalopathy

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12
Q

State the score required for Child’s Pugh A, B, and C, and the prognosis they represent

A

A: total score <7, 45% 5 year survival
B: total score 7-9, 20% 5 year survival
C: total score >9, <20% 5 year survival

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13
Q

Describe the macroscopic appearance of hepatic steatosis

A

Large, pale, yellow, greasy liver

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14
Q

Describe the microscopic appearance of hepatic steatosis

A

Accumulation of fat droplets in hepatocytes. If later stage, fibrosis

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15
Q

Describe the macroscopic appearance of alcoholic hepatitis

A

Large, fibrotic liver

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16
Q

Describe the microscopic appearance of alcoholic hepatitis

A

Hepatocyte ballooning and necrosis, Mallory Denk bodies, fibrosis

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17
Q

What is the mortality of an episode of acute alcoholic hepatitis?

A

10-20%

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18
Q

Describe the macroscopic appearance of alcoholic cirrhosis

A

Yellow-tan, fatty, enlarged liver progresses to shrunken, non-fatty, brown liver

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19
Q

What % of those with autoimmune hepatitis are female?

A

78%

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20
Q

Which HLA is associated with autoimmune hepatitis?

A

HLA-DR3

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21
Q

State at least two antibodies associated with autoimmune hepatitis type 1

A

Antinuclear (ANA), anti-smooth muscle (anti-SMA), anti-actin, anti-soluble liver antigen

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22
Q

State the autoantibody associated with autoimmune hepatitis type 2

A

Anti-liver-kidney microsomal (anti-LKM)

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23
Q

Name the two biliary causes of cirrhosis

A

Primary biliary cirrhosis, primary sclerosing cholangitis

24
Q

What is the female to male ratio of primary biliary cirrhosis?

25
What is primary biliary cirrhosis?
Autoimmune inflammatory destruction of medium sized intrahepatic bile ducts leading to cholestasis and the slow development of cirrhosis over many years
26
When is the peak incidence of primary biliary cirrhosis?
40-50
27
Describe the blood test results in primary biliary cirrhosis
Raised serum ALP, raised cholesterol, raised IgM, anti-mitochondrial antibodies in >90% Late in disease, hyperbilirubinaemia
28
Describe the histology of primary biliary cirrhosis
Bile duct loss with granulomas
29
Describe the clinical features of primary biliary cirrhosis
Fatigue, pruritis, abdominal discomfort. Secondary symptoms include skin pigmentation, xanthelasma, steatorrhoea, vitamin D malabsorption, and inflammatory arthropathy
30
How is primary biliary cirrhosis managed?
Ursodeoxycholic acid leads to remission in 25%
31
What is primary sclerosing cholangitis?
Inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts, leading to multifocal structure formation with dilation of preserved segments
32
Is primary sclerosing cholangitis more common in males or females?
Males
33
When is the peak incidence of primary sclerosing cholangitis?
40-50
34
Which condition is primary sclerosing cholangitis associated with?
IBD (especially ulcerative colitis)
35
Describe the blood test results in primary sclerosing cholangitis
Raised serum ALP, p-ANCA autoantibodies
36
Describe the difference between primary biliary cirrhosis and primary sclerosing cholangitis on ultrasound
PBC: No bile duct dilatation PSC: Bile duct dilatation
37
Describe the appearance of primary sclerosing cholangitis on ERCP
Beading of bile ducts from multifocal strictures
38
Describe the appearance of primary sclerosing cholangitis on histology
Onion skin fibrosis (concentric fibrosis)
39
What is the main complication of primary sclerosing cholangitis?
Cholangiocarcinoma
40
State the incidence of haemochromatosis
1 in 400 Caucasians (1 in 10 are carriers)
41
State the incidence of Wilson's disease
1 in 30,000
42
Describe the pathophysiology of haemochromatosis
Mutated HFE gene at chromosome 6p21.3 leads to increased iron absorption in the gut, which deposits in the liver, heart, pancreas, adrenals, pituitary, joints, and skin, leading to fibrosis
43
Describe the pathophysiology of Wilson's disease
Mutated ATP7B gene on chromosome 13 - which encodes a copper transporting ATPase expressed on the canalicular membrane - leads to decreased biliary copper excretion and consequently copper deposition in the liver, CNS, and iris
44
At what age does Wilson's disease typically present?
11-14
45
Describe the pathophysiology of alpha-1 antitrypsin deficiency
Mutations in the SERPINA1 gene located in the long arm of chromosome 14 prevent alpha-1 antitrypsin from leaving hepatocytes .Alpha-1 antitrypsin accumulates in hepatocytes, leading to intracytoplasmic inclusions and hepatitis. The lack of alpha-1 antitrypsin in the lungs disrupts the protease-antiprotease balance in the lungs, allowing proteases, specifically neutrophil elastase, to act uninhibited and destroy lung matrix and alveolar structures, causing emphysema.
46
Describe the histological appearance of the liver in haemochromatosis
Iron deposits in the liver, stain with Prussian blue
47
Describe the histological appearance of the liver in Wilson's disease
Mallory bodies and fibrosis. Copper deposits stain with Rhodanine
48
Describe the histological appearance of the liver in alpha-1 antitrypsin deficiency
Intracytoplasmic inclusions of alpha-1 antitrypsin which stain with Periodic acid Schiff
49
Describe the clinical features of haemochromatosis
Skin bronzing, diabetes, hepatomegaly with micronodular cirrhosis, cardiomyopathy, hypogonadism, pseudogout
50
Describe the clinical features of Wilson's disease
Acute hepatitis, fulminant liver failure/ cirrhosis, parkinsonism, psychosis, dementia, Kayser-Fleischer rings
51
What causes Kayser-Fleischer rings?
Copper deposits in Descemet's membrane in the cornea
52
Describe the investigation results in haemochromatosis
Increased serum iron and ferritin, transferrin saturation >45%, decreased total iron binding capacity (TIBC)
53
Describe the investigation results in Wilson's disease
Decreased serum caeruloplasmin and copper, increased urinary copper
54
Describe the investigation results in alpha-1 antitrypsin deficiency
Decreased serum alpha-1 antitrypsin, absent alpha-globulin band on electrophoresis
55
State the management of haemochromatosis
Venesection, desferrioxamine
56
State the management of Wilson's disease
Lifelong penicillamine
57
What % of patients with haemochromatosis-induced cirrhosis will develop hepatocellular carcinoma?
30%

Histopathology (30 decks)

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