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Flashcards in Liver and biliary pathology Deck (84)
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1
Q

Deescribe the basic structure of the liver

A

Basic structural unit is the hepatic lobule – thought of as a hexagon.

At the centre are the terminal branches of the hepatic vein (= centrilobular vein). The points of the hexagon are formed by the portal tracts, which contain 3 structures (portal triad): branches of the bile ducts, hepatic artery and portal vein. The liver cells can be split into three zones.
Zone 1 (closest to the portal triad) – periportal hepatocytes receive more oxygen and
• Zone 2 – mid zone
Zone 3 (close to terminal hepatic vein) – perivenular hepatocytes are the most mature
and metabolically active. Zone 3 has most liver enzymes

2
Q

Which zone receives the most oxygen?

A

Zone 1- closest to the portal triad

3
Q

Which zone is the most metabolically active?

A

Zone 3- closest to the central vein

4
Q

Which protein is NOT synthesised by the liver?

A

Gamma globulin

5
Q

Where is the space of Disse?

A

Between the hepatocytes and endothelieal cells

6
Q

Where are the stellate cells?

A

In the space of disse

7
Q

What is the function of stellate cells?

A

store vitamin A

Usually lie quiescent in the space of disse

when activated due to injurt to the hepatocytes, they produce collagen

They become myofibroblasts–>deposit collagen in the space of disse

Myofibroblasts contract constricting sinusoids and increasing vascular resistance

8
Q

What causes acute hepatitis? + define acue hepatitis

A

Viruses or drugs

Hepatitis last <6 months

9
Q

Histology of acute hepatitis

A

Spotty necrosis

small foci of inflammation + infiltration

lymphocytes and macrophages with damaged hepatocytes

10
Q

Grade vs stage of chronic inflammation

A

Grade- severity of inflammation

Stage - severity of fibrosis - this is more important in chronic hepatitis

11
Q

Histopathology of chronic hepatitis

A
  1. Portal Inflammation: inflammation has not crossed the limiting plate
  2. Interface hepatitis (PEICEMEAL NECROSIS) – cannot see the border between the portal tract and parenchyma
  3. Lobular inflammation- looks similar to spotty necrosis in acute hepatitis
  4. Fibrosis: Bridging from the portal vein to central vein due to fibrosis- intraheptic shunting- (critical stage in the evolution of hepatitis to cirrhosis)
12
Q

What is the key stage in evolution of hepatitis to cirrhosis?

A

Bridging between the portal vein and central vein

13
Q

Histopathology of cirrhotic liver

A

whole liver is affected

Hepatocyte necrosis

Fibrosis

Nodules of regenerating hepatocytes with surrouding fibrosis

Disturbance of vascular architecture (formation of intrahepatic and extrahepatic shunts)

14
Q

Explain intrahepatic and extrahepatic shunting

A
15
Q

Major causes of cirrhosis

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease
  3. Chronic viral hepatitis (hep B+/-D and C)
  4. Autoimmune hepatitis
  5. Biliary causes: Primary biliary cirrhosis & Primary sclerosing cholangitis
  6. Genetic causes:
    a) Haemochromatosis- HFE gene Chr 6 b) Wilson’s disease- ATP7B gene Chr 13 c) Alpha 1 antitrypsin deficiency (A1AT) d) Galactosaemia e) Glycogen storage disease
  7. Drugs e.g. methotrexate
16
Q

Haemochromatosis gene mutation

A

HFE gene Ghr 6

17
Q

Wilson’s disease mutation

A

ATP7B gene Chr 13

18
Q

Alpha 1 antitrypsin: gene mutation

A

A1At gene

19
Q

Micronodular vs macronodular cirrhosis

A

Micro: <3mm and uniform nodules throughout the liver

Maco: >3mm, variable nodule size throughout the liver

20
Q

What causes micronodular cirrhosis?

A

alcoholic hepatitis, biliary tract disease

(a, b)

non alcoholic Fatty liver disease

Haemchromatosis

**think haemachromatosis is bronzed diabetes; diabetes, NAFLD all similar pathology…**

21
Q

Causes of macronodular cirrhosis

A

viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency

VWA

22
Q

Outline the child’s pugh score

A
23
Q

Outline the spectrum of alcoholic liver disease

A
24
Q

What type of cirrhosis is alcoholic cirrhosis?

A

Micronodular

25
Q

Most common cause of chronic liver disease in the West

A

NAFLD

26
Q

Spectrum of NAFLD

A

a) simple steatosis - fatty change
b) non-alcoholic steatohepatitis (NASH) - progressed to inflammation

27
Q

HLA association of Autoimmune hepatitis

A

HLA-DR3

28
Q

Antibodies seen in autoimmune hepatitis

A

Type 1: ANA (antinuclear Ig), anti-SMA (anti-smooth muscle Ig), anti-actin Ig, anti- soluble liver antigen Ig

Type 2: Anti-LKM Ig (anti liver-kidney-microsomal Ig)

29
Q

PBC biochemical features

A

↑serum ALP, ↑cholesterol, ↑IgM, hyperbilirubinaemia (late)

30
Q

Anti-mitochondrial antibodies

A

PBC

31
Q

Bile duct loss with granulomas secondary to chronic inflammation

A

PBC

  • Hallmark: granulomatous inflammatory destruction of bile ducts.
32
Q

signs & symptoms of PBC

A

Fatigue, pruritis, abdominal discomfort

skin pigmentation, xanthelasma (part. eyelid),
steatorrhoea, vitamin D malabsorption, inflammatory arthropathy.

33
Q

Which bile ducts are affected in PBC vs PSC?

A

PBC- intrahepatic

PSC- intrahepatic and extrahepatic

34
Q

Treatment of PBC

A

ursodeoxycholic acid

35
Q

Male vs female incidence of PBC vs PSC

A

PBC: F>M

PSC: M>F

36
Q

Association of PSC

A

UC

37
Q

Biochemical features of PSC

A

↑ serum ALP, several associated auto-Ig, particularly p-ANCA

38
Q

USS of PSC vs PBC

A

PBC- no dilatation of bile ducts

PSC - dilatation of bile ducts: beading of the bile ducts (multi-focal strictures with dilation of preserved segments)

39
Q

ERCP findings of PSC

A

beading of bile ducts (due to multifocal strictures)

40
Q

What type of fibrosis do you get in PSC?

A

Onion skinning - concentric fibrosis

41
Q

Which cancer is associated with PSC?

A

Cholangiocarcinoma

42
Q

What is the most common benign liver lesion?

A

Haemangioma

43
Q

3 benign liver tumours

A

Liver cell adenoma

Bile duct Adenoma

Haemangioma

44
Q

What is the main risk factor of hepatic adenoma?

A

OCP use, associated with to oestrogen levels

Treated with stopping OCP; if doesn’t resolve –> resection

45
Q

Malignant liver lesions

A

HCC

Chlangiocarcinoma

Haemangiosarcoma

Hepatoblastoma

Secondary tumours

46
Q

Causes of HCC

A

Most commonly occurs in patients with chronic liver
disease – closely linked with viral hepatitis, alcoholic cirrhosis,
haemochromatosis, NAFLD, Aflatoxin, androgenic steroids

47
Q

IVx of HCC

A

AFP and USS

48
Q

RF for cholangiocarcinoma

A

primary sclerosing cholangitis

(worm)parasitic liver disease

chronic liver disease-Cirrhosis

congenital liver abnormalities

Lynch syndrome type II

49
Q

when are hepatic adenomas resected

A

when symptomatic

>5mm

non shrinkage despite stopping OCP

50
Q

Most common malignant liver lesion

A

Secondary tumours - GI tract, breast or bronchus

51
Q

Genetic causes of cirrhosis

A

haemochromatosis

Wilson’s

Alpha 1 antitrypsin deficiency

52
Q

Haemochromatosis mode of inheritance

A

Autosomal recessive mutation of HFE gene on chrmosome 6

53
Q

Wilson’s disease mode of inheritance

A

Autosomal recessive mutation of ATP7B gene on chr 13

54
Q

Alpha 1 antitrypsin deficiency mode of inheritance

A

Autosomal dominant

mutation of A1AT

55
Q

Histology of haemochromatosis

A

Fe deposits in liver – stains with Prussian blue stai

micronodular cirrhosis

Liver turns chocolatey brown colour

56
Q

Wilson’s disease histology

A

Cu stains with Rhodanine stain
Mallory bodies and fibrosis on microscopy

57
Q

A1AT deficiency histology

A

Intracytoplasmic inclusions of A1AT which stain with Periodic acid Schiff

58
Q

Ivx of haemochromatosis

A

↑ Fe, ↑ Ferritin
● Transferrin saturation > 45% ● ↓ TIBC

59
Q

Treatment of haemochromatosis + prognosis

A

Venesection

iron chelation

Desferrioxamine

30% with cirrhosis → HCC

60
Q

Biochemical findings of wilson’s disease

A

↓ serum caeruloplasmin ●

↓ serum copper (as it’s depositing everywhere else)

↑ urinary copper

61
Q

Treatment of wilson’s disease

A

Lifelong pencillamine

62
Q

Absent α-globulin band on electrophoresis

A

Alpha 1 antitrypsin deficiency

63
Q

in drug injury which zone of the liver is most affected/damaged

A
  • The damaged hepatocytes are in zone 2 and 3- mostly zone 3

Zone 3 is most affected because that is where the most drug metabolising hepatocytes are so where most of the toxic metabolites of drug metabolism is formed

64
Q

Difference between PBC and PSC

A

PBC: intrahepatic and bile duct loss secondary to inflammation

PSC: Extrahepatic and intrahepatic: bile duct loss due to peridcutal fibrosis

65
Q

which liver conditions cause granulomas

A

PBC

Drugs

66
Q

sturcture of hepatic adenoma

A

round circumscribed lesion

Sharply demarcated borders

67
Q

HCC- main causes in the west and developing countries

A

west- cirrhosis

developing countries -viruses

68
Q

difference between haemchromatosis and haemsiderosis

A

haemchromatosis: Fe accumulation in hepatocytes, develops into cirrhosis and HCC

HAemosiderosis: Fe accumulation in macrophages, does not develop into cirrhosis, secondary to repeated blood transfusions, not somethign to be worried about

69
Q

whihc malignancy is common in thailand and due to worms

A

cholangiocarcinoma

70
Q

Which of these is NOT associated with fatty change in the liver?

  • Diabetes
  • Hepatitis B
  • Hepatitis C
  • Alcohol
A
  • Answer: Hep B
  • Diabetes and alcohol are classic causes of fatty change
  • There is a genotype of Hepatitis C which can cause fatty change so it is also technically correct
71
Q

3 Cirrhosis defining features

A

WHOLE liver is involved

Characterised by scarring and fibrosis surrounding nodules of regenerating hepatocytes

Distortion of liver vascular architecture: development of intra- and extrahepatic shunts

72
Q

3 Complications of Cirrhosis

A

Portal hypertension:oesophageal varices + splenomegaly: palpable slpeen due to backlog of blood into spleen

Hepatic encephalopathy

Liver cell cancer

73
Q

is cirrhosis reversible

A

cirrhosis may be REVERSIBLE If the underlying cause is aggressively treated

74
Q

which stages of alcoholic liver disease are reversible and irreversible

A

Fatty liver disease- reversible

Alocohlic hepatits- irreversible

75
Q

in alcolhilic liver disease, which zone is alcoholic hepatits mostly affecting

A

changes are MAINLY seen in Zone 3

cells that get damaged are the ones that contain the most alcohol dehydrogenase that convert alcholic in toxic metabolise of acetaladehyde

76
Q

what type of firbosis is very characteristic of alcoholic liver disease

and what else do you see (cell types)

A

Pericellular fibrosis: Fibrosis around individual cells

inflammation: lots of inflammatory cells will be seen but the most characteristic inflammatory cell seen is the neutrophil polymorph but can be lymphocytic too.

77
Q

features of haemchromatosis

A

deposition in:

testes: fertility
pancreas: Bronzed diabetes

Liver: hepatocyte damage >> HCC

cardiovascular: cardiomyopathy
skin: tanned complexion

78
Q

what is Haemosiderosis

A

is a type of iron overload

accumulation of iron in macrophages

usually occurs as a result from repeated blood transfusion

79
Q

presentation of Wilson’s disease

A

depositio of copper in:

lentiform nucleus of the basal ganglia: Parkinsonian features, dementia, psychosis

iris- Kayser-Fleischer rings

liver- liver disease: : acute hepatitis, fulminant liver failure or cirrhosis

80
Q

other associated conditons of autoimmune hepatits:

A

autoimmune conditions: SLE, rheumatoid arthritis, thyroiditis, UC etc.

81
Q

what type of cell accumulaiton do you find in autoimmune hepatitis + why

A

active form of chronic hepatits: lots of inflammatory cells + plasma cells

lots of plasma cells

Lots of plasma cells because lots of autoantibodies are secreted

82
Q

treatment for autoimmune hepatits:

A

Responds to STEROIDS

83
Q

a1-Antitrypsin Deficiency clinical features:

A

hepatocyte can make a1-antitrypsin but cannot secrete it so deficinecy in blood but excess in liver causes:

emphysema in the lung

COPD in NON SMOKERS

A1AT: deficiency can present in neonates as giant cell hepatitis (giant cell hepatocytes are multinuclear)

84
Q

what can the skin look like in haemochromatosis?

A

bronzed or slate grey