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Pathology MBBS > Liver pathology > Flashcards

Liver pathology Flashcards

1
Q

Zones of liver and diseases affecting each zone

A
  1. Periportal: viral hepatitis
  2. Midzonal: yellow fever
  3. Centrilobular:
    • alcohol
    • acetaminophen toxicity
    • CVC
    • ischemia
    • Budd Chiari syndrome
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2
Q

Zones of liver most susceptible to toxin induced & ischemic damage respectively

A 
To toxin induced damage: zone 1 
 Periportal area (like viral hepatitis)

To ischemic damage: zone 3
(Centrilobular area)

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3
Q

Space of Disse

A

Space between hepatocytes and lining of sinusoids

  1. Vitamin A storage
  2. Ito cells/ Stellate cells- fibrosis in cirrhosis
  3. Amyloid is first seen here
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4
Q

Canals of Herring

Kupffer cells

A

Present between hepatocytes
Contain oval cells/stem cells of liver
Kupffer cells (macrophages) are located in the sinusoids

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5
Q

Cirrhosis

A 
End stage liver disease
Characterised by:
1. Disruption of liver architecture
2. Regenerating parenchymal nodules
3. Bridging fibrous septae 
Types: 3mm
1. Micronodular
2. Macronodular
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6
Q

Micronodular cirrhosis

A

<3 mm

  1. Early ALD
  2. Hemochromatosis
  3. 1° biliary cirrhosis
  4. Indian childhood cirrhosis
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7
Q

Macronodular cirrhosis

A

> 3 mm

  1. Late ALD
  2. Wilson’s disease
  3. α-1 antitrypsin deficiency
  4. Viral hepatitis
  5. Drugs and toxins
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8
Q

Causes of cirrhosis

A
  1. Alcoholic liver disease
  2. Non-alcoholic steatohepatitis NASH
  3. Metabolic disorders:
    • α-1 antitrypsin deficiency
    • Wilson’s disease
    • Hemochromatosis
  4. Viral hepatitis
  5. Autoimmune hepatitis
  6. Drugs and chemicals
  7. Biliary diseases
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9
Q

Pathogenesis of cirrhosis

A

Hallmark: capillarisation of sinusoids
Normal liver:
Type 1 and 3 collagen - periportal and centrilobular area
Type 4 collagen - space of Disse
In cirrhosis: type 1 and 3 collagen occupies space of Disse ➡️
loss of fenestrations of sinusoids ➡️
capillarisation of sinusoids

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10
Q

Minimum amount of alcohol that can cause alcoholic liver disease

A

60-80 ml/day for 10 years

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11
Q

Alcoholic liver disease gross features

A

Soft, yellow, greasy

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12
Q

Manifestations of alcoholic liver disease

A 
1. Steatosis
• Fatty liver
• Reversible
• starts in centrilobular area (zone-3)
• micro or macrovesicular
2. Hepatitis
3. Cirrhosis:
• Irreversible
• Fibrosis seen
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13
Q

Features of hepatitis of alcoholic liver disease

A
  1. Hepatocyte swelling ➡️
  2. Ballooning degeneration
  3. Neutrophilic infiltrate
  4. Mallory hyaline bodies
  5. Some fibrosis
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14
Q

Laennac cirrhosis

A

End stage of alcoholic liver disease

Liver is reduced to a fibrotic scar

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15
Q

Mallory hyaline bodies
Mallory deny bodies
composed of

A

Composed of intermediate filaments like CK8, CK18

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16
Q

Mallory denk bodies or
Mallory hyaline bodies
are seen in

A 
New. NASH
Indian. childhood cirrhosis
W. Wilson’s disease
A. Alcoholic liver disease
T. Tumours like HCC
C. Cirrhosis, 1° biliary
H. Hyperplasia, focal nodular 
Not present in: hemochromatosis and 1° sclerosing cholangitis
17
Q

Microvesicular steatosis is seen in

A

D. Drugs and toxins
A. Acute fatty liver of pregnancy 🤰
R. Reye’s syndrome
E. Early alcoholic liver disease

18
Q

Macrovesicular steatosis is seen in

A 
C. Chronic hepatitis C
L. Late alcoholic liver disease
O. Obesity 
N. NASH
E. PEM
19
Q

NASH

Non Alcoholic Steatohepatitis

A 
Features similar to ASH, except no history of alcohol
Seen in:
1. Obesity
2. Metabolic syndrome
3. Insulin resistance
20
Q

Differences between alcoholic steatohepatitis and NASH

A

ASH has prominent Mallory hyaline bodies and inflammation (with neutrophils) compared to NASH
Macrophages are predominant in NASH
Perisinusoidal damage is predominant in ASH, unlike periportal damage in NASH

21
Q

Reye’s syndrome

A 
Rare disorder
When children suffering from viral illness is treated with aspirin ➡️ severe mitochondrial dysfunction
On H&E, extensive microvesicular steatosis
Clinically, 
1. Rash
2. Vomiting 🤮 
3. Hypoglycaemia
4. Hepatic encephalopathy
22
Q

Haemochromatosis

A 
Excessive iron overload
M/C metabolic cause of liver cirrhosis 
Autosomal recessive
Common pathogenesis:
1. Mutation of HPE gene on chr 6p
2. Decreased hepcidin
3. Increased iron
Treatment: phlebotomy
DoC: Desferoxamine (chelator)
23
Q

Causes of hemochromatosis

A 
Hereditary:
1. HFE gene mutation on chr 6p
2. HAMP gene
3. HJV juvenile hemochromatosis
Secondary:
1. Repeated blood transfusions
2. Bantu siderosis (iron 🍽)
24
Q

Hemochromatosis

clinical features

A 
Clinical triad: 
1. Liver: micronodular cirrhosis (M/C and earliest organ affected)
2. Pancreas: DM
3. Skin: brown due to melanin (> hemosiderin)
Bronze diabetes, 2. and 3. together
4. Restrictive or dilated cardiomyopathy
5. Testicular abnormalities
6. Joint involvement
7. Risk of HCC
25
Q

Lab diagnosis of hemochromatosis

A
  1. Serum iron increases
  2. Serum ferritin increases
  3. Serum transferrin saturation increases
  4. Serum TIBC decreases
    Liver biopsy:
  5. Brownish pigmentation-hemosiderin
  6. Micronodular cirrhosis
  7. On Prussian blue, bluish iron deposits can be seen
26
Q

Wilson’s disease

pathogenesis

A

Excessive copper accumulation
Autosomal recessive
Pathogenesis:
1. Mutation of ATP7B gene on chr 13q
2. Defect in incorporation of copper into ceruloplasmin
3. Increased accumulation of copper in tissues
4. Wilson’s disease

27
Q

Wilson’s disease

clinical manifestations

A
  1. Liver - cirrhosis
  2. Eye 👁: Kayser Fleisher ring
    Brownish discolouration of Descemet’s membrane of cornea
  3. Brain 🧠:
    putamen and basal ganglia are affected ➡️ neuropsychiatric manifestations
28
Q

Wilson’s disease

diagnosis and treatment

A
  1. Increased copper levels
  2. Decreased ceruloplasmin
    Liver biopsy:
    • Stain for Cu: Rhodamine, Rubeanic acid
    • Stain for ceruloplasmin: orcein
    Most sensitive: increased urinary Cu excretion
    Treatment: copper chelators
29
Q

α1-Antitrypsin deficiency

basics and clinical manifestations

A

Autosomal recessive
Pathogenesis: deficiency of α1-Antitrypsin ➡️ elastase activity increases ➡️:
1. Lung: panacinar emphysema
2. Liver: cirrhosis

30
Q

α1-Antitrypsin deficiency

genetics and microscopy

A 
Genetics:
1. PiMM - normal
2. PiMZ - heterozygous
3. PiZZ - α1-Antitrypsin deficiency
Microscopy:
1. Steatosis 
2. Cytoplasmic globules in periportal area:
 PAS +ve
 Diastase resistant
31
Q

Hepatitis viruses

types

A 
A. Picorna 
 Faeco-oral
 2-6 weeks
B. Hepadna, the only DNA virus
C. Flavi 
D. Delta
E. Hep E virus
 Faeco-oral 
 4-5 weeks
 Maximum mortality in pregnancy 🤰
32
Q

Common features among hepatitis B, C and D viruses

A

Parenteral, vertical and sexual transmission
2-26 weeks gestation
B and C viruses are carcinogenic
Hep C is M/C cause of chronic hepatitis among viruses

33
Q

Microscopy of acute hepatitis

A
  1. Ballooning degeneration: swelling of hepatocytes
  2. Disruption of lobular architecture
  3. Inflammation
  4. Spotty necrosis
  5. Councilman bodies- apoptotic bodies
  6. Absence of portal inflammation
  7. Central-portal bridging necrosis
  8. Drop out of hepatocytes
34
Q

Chronic hepatitis

microscopy

A
  1. Ground glass hepatocytes:
    Seen in hep B infection due to deposition of surface antigens
  2. Bridging fibrosis: bridged between the central vein and portal tract
  3. Mononuclear portal inflammation
  4. Interface hepatitis
  5. Cirrhosis
35
Q

Microscopy of hep C infection

A
  1. Steatosis
  2. Lymphoid aggregates
  3. Bile duct damage and proliferation
36
Q

Autoimmune hepatitis

A 
Females > males
Three types
Microscopy:
1. Increased plasma cells infiltration
2. Hepatic rosettes 
3. Emperipolesis
4. Interface hepatitis
37
Q

Types of autoimmune hepatitis

A 
1. Type 1:
• HLA DR3
• Positive for ANCA, SMA and anti-mitochondrial Ag
2. Type 2:
• Ab against LKM +ve
• Three types
3. Type 3:
• No ANCA, LKM
• LSA +ve, liver soluble antigen
38
Q

Types of type 2 autoimmune hepatitis

A

Ab against LKM +ve

  1. LKM 1: Hep C
  2. LKM 2: drugs
  3. LKM 3: Hep D

Pathology MBBS (17 decks)

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