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Systemic Pathology > Liver > Flashcards

Liver Flashcards

1
Q

Major source of billirubin

A

Catabolism of haemoglobin

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2
Q

Minor and other sources of bilirubin

A

Cytochrome p-450
Destruction of premature RBC

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3
Q

Enzyme which converts heme to biliverdin

A

Heme oxygenase

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4
Q

Which enzyme converts biliverdin to bilirubin

A

Biliverdin reductase

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5
Q

Is unconjugated billirubin water soluble or not

A

Not

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6
Q

Within hepatocyte, bilinebin binds to several proteins in the cytosof known as

A

Glutathione - s-transferase also known as ligandin

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7
Q

Which enzyme helps in conjugation of bilirubin with glucoronic acid

A

UDP - glucoronyl transferase

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8
Q

Is the conjugated bilirubin excreted in urine or into the intestine

A

Intestine

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9
Q

What happens to the conjugated, Bilirubin in the small intestine and colon

A

By bacterial betaglucoronidases they are degraded to colour less urobilinogens

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10
Q

What is responsible for normal colour of the stool?

A

Stercobilinogen

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11
Q

How urobilinogen is excreted in urine

A

As some urobilinogen are reabsorbed in terminal ileum and colon

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12
Q

Why unconjugated bilirubin is not excreted in urine

A

As the tightly bound to albumin

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13
Q
  • Irreversible brain injury in infants due to high conc of free unconjugated bilirubin which cross BBB
A

Kernicterus

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14
Q

What are the cells found in space of disse

A

Ito cells

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15
Q

Function of stellate cells or Ito cells

A

High lipid content
Rich in VIT a
Synthesize extracellular collagen

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16
Q

What happens to urine and stool in obstructive jaundice

A

Urine with no urobilinogen
Pale and clay coloured stools with sternobilinggen absent

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17
Q

Impaired bile flow and systemic retention of bilirubin is known as:-

A

Cholestasis

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18
Q

Yellowish pigmentation of skin, mucus membrane, and sclera due to deposition of bilirubin is known as

A

Jaundice

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19
Q

Why sclera is involved in jaundice

A

As sclera has lot of elastic tissue which has affinity for bilirubin.

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20
Q

Normal serum bilirubin level

A

0.3 to 1.2 mg/dl

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21
Q

Serum bilirubin in jaundice

A

2.0 - 2.5mg /dl

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22
Q

Cause of unconjugated hyperbilirubinemia

A

↑ extrahepatic production of bilirubin
↓ reduced hepatocyte uptake
Impaired conjugation

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23
Q

Causes of conjugated hyperbilirubinemia

A

Decreased hepatocellular excretion
Impaired bile flow

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24
Q

Why prehepatic jaundice also known as acholuric jaundice

A

No bilirubin in urine

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25
Q

Which abnormal liver function test seen in hemolytic jaundice

A

↑ LDH

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26
Q

Raised AST and alt is seen in which type of jaundice

A

Hepatic jaundice

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27
Q

Why chole static jaundice usually a surgical jaundice

A

As it requires surgical intervention

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28
Q

↑ in alp, GG T is seen in which type of jaundice

A

Obstructive / post hepatic

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29
Q

Bilirubin present but urobilinogen absent in urine in

A

Obstructive jaundice e

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30
Q

Billirubin absent but urobilinogen absent in which jaundice

A

Hemolytic jaundice

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31
Q

AST > alt in which hepatitis

A

Alcoholi and other toxic hepatitis

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32
Q

Alt > AST in which hepatitis

A

Viral hepatitis

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33
Q

Complete absence of hepatic UGTIA1 leads to

A

Crigler - najjar syndrome type1

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34
Q

Partial absence of UGTIA1 leads to

A

Crigler - najjar syndrome type -2

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35
Q

Treatment of crigler - najjar syndrome type - 2

A

Phenobarbital

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36
Q

Crigler- najjar type - 2 is autosomal dominant /recessive

A

Dominant

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37
Q

Gilbert syndrome is due to deficiency of which enzyme

A

UGT1A1

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38
Q

All hereditary hyperbilirubinemia are autosomal recessive except

A

Crigler najjer type2

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39
Q

Conjugated hyperbilirubinemia seen in which 2 hereditary condition

A

Dubin Johnson syndrome
Rotor syndrome

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40
Q

Dubin Johnson syndrome caused by which protein absence

A

MRP2 protein

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41
Q

What ions are transported through MRR2 protein channel

A

Conjugated bilirubin and other related organic anions

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42
Q

What happens to lysosomes in dubin Johnson syndrome

A

Enlarged with black melanin like pigment deposition of epinephrine metabolites

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43
Q

Carcinoma of bile duct

A

Cholangio carcinoma

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44
Q

Cholangiocarcinoma present in extra hepatic or perihilar regions are known as

A

Klatskin tumors

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45
Q

Location of klatskin tumors

A

Junction of right and left hepatic ducts forming common bile ducts

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46
Q

Extrahepatic forms of cholangiocarcinoma

A

Perihilar
Distal bile duct tumors

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47
Q

Distal bile duct fumors arise at

A

‘Ampulla of vater

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48
Q

Name a liverfluke which cause cholangio carcinoma

A

Opisthorchis sinensis
Clonorchis sinensis

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49
Q

Metastatic / primary tumors of liver more common

A

Metastasis

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50
Q

Most common sites of primary tutors causing metastases at liver

A

Git
Breast
Lung
Pancreas
Leukemia lymphoma

Melanoma

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51
Q

Reason of umblication in metastatic tumnors

A

Necrosis and haemorrhage

52
Q

Marker of choice in differentiating HCC and its fibrolomellar variant

A

AFP = alpha feto protein

53
Q

Workers exposed to polyvinyl chloride can get which hepatic cancer

A

Angiosarcoma

54
Q

Non neoplastic false positive alphafetoprotein are

A

Cirrhosis
massive liver necrosis
Chronic hepatitis HCV
Pregnancy
Neural tube defects anencephaly ) spina bifida

55
Q

Neoplasms with alpha feet protein

A

Hepatocellular carcinoma
Non seminomatous germ cell tumors
Endoderm sinus tumor
Yolksac tumour

56
Q

Most common symptom of hepatocellular carcinoma

A

Abdominal pain) > weight loss

57
Q

Major risk factors of HCC

A

ABCC
Aflatoxin
HBV
HCV
Cirrhosis

58
Q

Minor HCC causes

A

HCC
Hemochromatosis
Cigarette
Contraceptive

59
Q

Hall mark of HCC

A

Bile production by neoplastic cells

60
Q

Tumor marker of fibrolamellar HCC

A

Neurotensin

61
Q

Characteristic feature of fibro lamellar HCC

A

Scirrhous = single large hard well circumscribed tumor with central stellate fibrous scar

62
Q

Primary turner’s of liver

A

HCC
Hepatoblastomas
angiosarcomas

63
Q

Three morphologically gross patterns of HCC

A

Unifocal
Multinodular
Diffuse infiltrative

64
Q

Microscopical gradation of HCC

A

Well differentiated
Moderately differentiated
Poorly differentiated

65
Q

Name a marker of mitochondria used for diagnosing HCC

A

Hep -par1

66
Q

Serum markers of HCC

A

Alpha fetoprotein
Alpha-l - fucosidase

Des - alpha - carboxy - prothrombin

67
Q

Cause of amoebic liver abscess

A

Entamoeba hystolytica

68
Q

Fungal abscess of liver caused by

A

Candida

69
Q

Major route of infection of liver in liver abscess

A

Portal vein

70
Q

Most common extra intestinal complication of amoebic dysentry

A

Amoebic liver abscess

71
Q

Location of amoebic abscess

A

Subdiaphrogmatic region

72
Q

Content of abscess cavity

A

Thick dark material likened to anchovy sauce or chocolate

73
Q

Microscopy of arnoebic liver abscess

A

Trophozoite’s in necrotic region

74
Q

Primary biliary cholangitis involves which bile ducts

A

Small and medium sized intrahepatic bile ducts
No involvement of large intra hepatic ducts and extrahepatic biliary tree

75
Q

Primary scherosing cholangities affects which bile ducts

A

Intrahepatic and extrahepatic bile ducts

76
Q

Autosomal recessive disorder of copper metabolism

A

Wilson’s disease

77
Q

Copper toxicity principally cause end organ damage in

A

Liver
Brain
Eye

78
Q

Mutation of ATP 7b gene leads to

A

Wilson’s disease

79
Q

How copper toxicity leads to liver damage.

A

Through ROS produced by Fenton reaction

80
Q

Does fatty change and Mallory bodies seen in Wilson’s disease

A

Yes both

81
Q

How Wilsons disease affects brain

A

Basal ganglia (putamen) atrophy

82
Q

Kaiser - Fletcher - rings in patients of Wilson’s disease (location)

A

Descemet’s membrane of cornea

83
Q

What happens to ceruloplasmin levels in Wilson disease

A

Decreased

84
Q

Why scrum copper levels not useful for diagnosis of Wilson’s disease

A

As they may be Lowe, normal or elevated depending on the stage of disease.

85
Q

Post necrotic cirrhosis also known

A

Macronodular cirrhosis

86
Q

Jig saw puzzle piece nodules in liver are present in

A

Secondary biliary cirrhosis

87
Q

Liver cells shows feathery degeneration and formation of bile lakes in which disorder

A

Secondary biliary cirrhosis

88
Q

Excessive accumulation of body iron leads to

A

Herochromatosis

89
Q

Mutation in HJV, tfr2, Hfe leads to

A

Absence in hepcidin →↑ iron in liver storage

90
Q

Secondary or acquired hemochromatosis also known as

A

Hemosiderosis

91
Q

Hemosiderin deposition occurs in

A

Liver, pancreas, myocardium, pituitary, adrenal, thyroid gland

92
Q

Chocolate brown liver seen in

A

Hemochromatosis

93
Q

Hemosiderin can be recognized by which stain

A

Prussian blue stain

94
Q

Classic triad in hemochromatosis

A

Micronodular cirrhosis
Bronze diabetes
Skin pigmentation

95
Q

3 major distinctive overlapping lesions in alcoholic liver disease

A

Hepatic steatosis
Alcoholic hepatitis
Alcoholic cirrhosis

96
Q

Main organ for ethanol metabolism

A

Liver

97
Q

3 enzymes which convert ethanol to acetaldehyde

A

Alcohol dehydrogenase
Cytochrome p-450 2e1
Catalase

98
Q

Acetaldehyde gets converted to acetic acid by use of which enzyme in which organelle

A

Acetalehyde dehydrogenase
mitochondria

99
Q

Use of acetic acid in mitochondria

A

Respiratory chain

100
Q

Which gender is more susceptible to alcoholic liver disease

A

Females

101
Q

Why females are at higher risk than males in alcoholic liver disease

A

Oestrogen increase get permeability to endotoxins, cytokines,chemokines

102
Q

Reversible hepatic steatosis

A

’ 80 g of alcohol over one to several days

103
Q

At what dose, severe hepatic injury occurs

A

Daily intake of 80 g alcohol
Or daily consumption of 16og of alcohol for 10-20 years

104
Q

How oxidation of ethanol reduces oxidation of fatty acids

A

Decrease in NAD
Increase in NADH
Inhibits oxidation of fatty acids

105
Q

Hour mitochondrial dysfunction occurs in alcoholic liver disease

A

Decrease in nad/nadh ratio
Antioxidant glutathione is not transported from cytoplasm to mitochondria
Increase in reactive oxygen species

106
Q

How Mallory bodies are formed in alcoholic liver disease

A

Ubiquitin-proteosome pathway is impaired
Inefficient degradation of ubiquitin
Accumulates in hepatocytes

107
Q

More TNF - alpha and TGF - alpha are released ed in circulation in alcoholic liver disease

A

Alcohol → LPs release from grannegative bacteria → enter portal circulation → stimulate production of cytokines

108
Q

Hypoxia damage to liver. Occurs in which region

A

Centric lobular region

109
Q

Abnormal metabolism of methionine leads to

A

Decreased levels of glutathione
Oxidative injury

110
Q

Which cells help in fibrosis inalcholic liver injury

A

Peri sinusoids cells / Ito cells / stellate cells

111
Q

Reversible manifestation of chronic alcoholism

A

Steatosi’s

112
Q

Microvesicular steatosis occurs in which zone

A

Acinar zone 3 or centrilobular zone

113
Q

Why at Centris lobular zone in microvesícular steatosis is affected

A

Alcohol dehydrogenase is located here

114
Q

Is macrovascular steatosis reversible?.

A

Yes

115
Q

Alcoholic hepatitis 4 characteristic features

A

Ballooning degeneration of hepatocyte
Mallory bodies
Neutrophilic infiltration
Alcoholic steatofibrosis

116
Q

In alcoholic fibrosis the microscopic pattern

A

Chicken wire fence pattern

117
Q

Mallory body

A

Tangled cytokeratin intermediate filaments that appear as dense eosinophilia ropy cytoplasmic clumps

118
Q

Chronic irreversible end stage of alcoholic liver disease

A

Cirrhosis

119
Q

Other names of alcoholic cirrhosis

A

Laennac cirrhosis
Portal cirrhosis
Nutritional cirrhosis

120
Q

Size of liver in steatosis, hepatitis, cirrhosis

A

Enlarged, enlarged, shrunken

121
Q

Specific macroscopic features in alcoholic cirrhosis

A

Pig skin and hobnail appearance of nodules

122
Q

Microscopic features of alcoholic cirrhosis

A

Loss of architecture
Regenerating nodules
Vascular reorganization
Fibrosis

123
Q

Are Mallory bodies seen in liver cirrhoens

A

No

124
Q

Lab findings in alcoholic steatosis

A

AST: alt >1
Increased gama glatamyl transpeptidase

125
Q

Lab findings in alcoholic hepatitis

A

AST: alt >2
Serum bill Rubin raised
prothrombin time increased
Serum albumin decreased
Neutrophilic leukocytosis (12000 to 14000) per microlitre

Systemic Pathology (8 decks)

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