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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?

A

10:1

25
Q

What is primary biliary cirrhosis?

A

Autoimmune inflammatory destruction of medium sized intrahepatic bile ducts leading to cholestasis and the slow development of cirrhosis over many years

26
Q

When is the peak incidence of primary biliary cirrhosis?

A

40-50

27
Q

Describe the blood test results in primary biliary cirrhosis

A

Raised serum ALP, raised cholesterol, raised IgM, anti-mitochondrial antibodies in >90%
Late in disease, hyperbilirubinaemia

28
Q

Describe the histology of primary biliary cirrhosis

A

Bile duct loss with granulomas

29
Q

Describe the clinical features of primary biliary cirrhosis

A

Fatigue, pruritis, abdominal discomfort. Secondary symptoms include skin pigmentation, xanthelasma, steatorrhoea, vitamin D malabsorption, and inflammatory arthropathy

30
Q

How is primary biliary cirrhosis managed?

A

Ursodeoxycholic acid leads to remission in 25%

31
Q

What is primary sclerosing cholangitis?

A

Inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts, leading to multifocal structure formation with dilation of preserved segments

32
Q

Is primary sclerosing cholangitis more common in males or females?

A

Males

33
Q

When is the peak incidence of primary sclerosing cholangitis?

A

40-50

34
Q

Which condition is primary sclerosing cholangitis associated with?

A

IBD (especially ulcerative colitis)

35
Q

Describe the blood test results in primary sclerosing cholangitis

A

Raised serum ALP, p-ANCA autoantibodies

36
Q

Describe the difference between primary biliary cirrhosis and primary sclerosing cholangitis on ultrasound

A

PBC: No bile duct dilatation
PSC: Bile duct dilatation

37
Q

Describe the appearance of primary sclerosing cholangitis on ERCP

A

Beading of bile ducts from multifocal strictures

38
Q

Describe the appearance of primary sclerosing cholangitis on histology

A

Onion skin fibrosis (concentric fibrosis)

39
Q

What is the main complication of primary sclerosing cholangitis?

A

Cholangiocarcinoma

40
Q

State the incidence of haemochromatosis

A

1 in 400 Caucasians (1 in 10 are carriers)

41
Q

State the incidence of Wilson’s disease

A

1 in 30,000

42
Q

Describe the pathophysiology of haemochromatosis

A

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
Q

Describe the pathophysiology of Wilson’s disease

A

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
Q

At what age does Wilson’s disease typically present?

A

11-14

45
Q

Describe the pathophysiology of alpha-1 antitrypsin deficiency

A

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
Q

Describe the histological appearance of the liver in haemochromatosis

A

Iron deposits in the liver, stain with Prussian blue

47
Q

Describe the histological appearance of the liver in Wilson’s disease

A

Mallory bodies and fibrosis. Copper deposits stain with Rhodanine

48
Q

Describe the histological appearance of the liver in alpha-1 antitrypsin deficiency

A

Intracytoplasmic inclusions of alpha-1 antitrypsin which stain with Periodic acid Schiff

49
Q

Describe the clinical features of haemochromatosis

A

Skin bronzing, diabetes, hepatomegaly with micronodular cirrhosis, cardiomyopathy, hypogonadism, pseudogout

50
Q

Describe the clinical features of Wilson’s disease

A

Acute hepatitis, fulminant liver failure/ cirrhosis, parkinsonism, psychosis, dementia, Kayser-Fleischer rings

51
Q

What causes Kayser-Fleischer rings?

A

Copper deposits in Descemet’s membrane in the cornea

52
Q

Describe the investigation results in haemochromatosis

A

Increased serum iron and ferritin, transferrin saturation >45%, decreased total iron binding capacity (TIBC)

53
Q

Describe the investigation results in Wilson’s disease

A

Decreased serum caeruloplasmin and copper, increased urinary copper

54
Q

Describe the investigation results in alpha-1 antitrypsin deficiency

A

Decreased serum alpha-1 antitrypsin, absent alpha-globulin band on electrophoresis

55
Q

State the management of haemochromatosis

A

Venesection, desferrioxamine

56
Q

State the management of Wilson’s disease

A

Lifelong penicillamine

57
Q

What % of patients with haemochromatosis-induced cirrhosis will develop hepatocellular carcinoma?

A

30%

Histopathology (30 decks)

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