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Pathology > GIT Disorders Part 3 > Flashcards

GIT Disorders Part 3 Flashcards

1
Q

Most common Malignant tumor of stomach

A

Gastric adenocarcinoma

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2
Q

Gastric Adenocarcinoma is most prevalent in which country

A

Japan

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3
Q

Risk factors of Gastric Adenocarcinoma

A

Smoked/salted foods
Low socio-economic status
Previous gastric surgery
Partial anterectomy
Pernicious anemia
Atrophic gastritis
H pylori
EBV
Tobacco use
Gastric adenomatous Polyps
Menetrier’s disease
Blood group A
Nutrient deficiencies (Zn,Mo,Se, Vit A)
Genetic factors

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4
Q

Genetic risk factors of gastric Adenocarcinoma

A

P53 gene - Liframeni Syndrome
APC gene down regulation
Beta Catenin upregulation - increases epithelial cell proliferation
CDH1 gene - loss of E-cadherin
BRCA2 gene
HNPCC Syndrome

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5
Q

Commonest site of Gastric Adenocarcinoma

A

Antrum (lesser curvature)

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6
Q

Common site of gastric adenocarcinoma in Pernicious anemia

A

Fundus/Body

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7
Q

Clinical features of Gastric Adenocarcinoma

A

Right upper quadrant discomfort
Early/recent onset dyspepsia
Post -prandial heaviness
Abdominal pain
Weight loss

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8
Q

Paraneoplastic syndromes seen in Gastric Adenocarcinoma

A

Acanthosis nigricans - Hyperpigmentation of skin (axillary region)
Lesser Trelat sign - multiple seabouric keratosis on back and trunk
MAHA
Migratory thrombophlebitis

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9
Q

Metastasis of Gastric Adenocarcinoma

A

Hematogenous spread - Liver, lungs, ovary
Lymphogenous spread - Lymph nodes, Ovaries

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10
Q

Supraclavicular lymph node on left side is termed as

A

Virchow’s LN

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11
Q

Axillary lymph node on left side is termed as

A

Irish LN

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12
Q

Periumbilical skin nodules termed as

A

Sister Mary Joseph Nodule

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13
Q

Metastasis of gastric tumor to Pouch of Douglas termed as

A

Blumer’s Shelf

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14
Q

Investigation of choice in Gastric Adenocarcinoma

A

Endoscopy + Biopsy

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15
Q

Gastric Adenocarcinoma can be classified on the basis of

A

On basis of Morphology
Depth of invasion
Lauren’s classification

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16
Q

Classification of gastric Adenocarcinoma on the basis of Morphology

A

3 types - Exophytic growth
Flat growth
Lesion or ulcer

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17
Q

Classification of gastric Adenocarcinoma on the basis of depth of invasion

A

Early
Late

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18
Q

Which layer is involved in early gastric Adenocarcinoma

A

Mucosa/submucosa involvement

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19
Q

Prognosis of early gastric Adenocarcinoma

A

Better prognosis

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20
Q

Layers involved in late Gastric Adenocarcinoma

A

Muscle/serosa involvement

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21
Q

Prognosis in late Gastric Adenocarcinoma

A

Bad Prognosis

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22
Q

Best prognosis in which gastric Adenocarcinoma

A

Superficial spreading of stomach cancer

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23
Q

Lauren’s classification includes

A

Intestinal type
Diffuse type

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24
Q

In intestinal type, there is overactivity of

A

APC gene
Beta -Caterin

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25
Q

In intestinal type, tumor cell makes

A

Intestinal gland like pattern

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25
Q

Intestinal type is seen in which age group

A

Elderly patients

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26
Q

Prognosis of intestinal type Gastric Adenocarcinoma

A

Better prognosis

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27
Q

In Diffuse type gastric Adenocarcinoma, tumor cells are

A

Scattered

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28
Q

According to Lauren’s classification which type have localized tumors

A

Intestinal type

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29
Q

According to Lauren’s classification,Non-localized tumor is seen in

A

Diffuse type

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30
Q

Diffuse type gastric Adenocarcinoma affects which age group

A

Younger patients

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31
Q

Mutation seen in Diffuse type gastric Adenocarcinoma

A

CDH1 gene mutation - loss of E cadherin

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32
Q

Prognosis in diffuse type gastric Adenocarcinoma

A

Bad prognosis

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33
Q

Condition seen in diffuse type gastric Adenocarcinoma due to increased connective tissue

A

LINITIS PLASTICA

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34
Q

Treatment of gastric Adenocarcinoma

A

Surgical
Anticancer drugs

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35
Q

ECF Regime for gastric Adenocarcinoma

A

Epirubicine
Cisplatin
Flifluorouracil

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36
Q

Most common mesenchymal tumor in abdomen

A

Gastro-intestinal Stromal tumor (GIST)

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37
Q

Locations involved in GIST

A

Stomach > SI > LI > Esophagus

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38
Q

Most common site in GIST

A

Stomach

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39
Q

Rarest site in GIST

A

Esophagus

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40
Q

Cell of origin in GIST

A

Cell of CAJAL - Pacemaker of GI tract - controls Peristaltic activity

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41
Q

Mutations seen in GIST

A

C-Kit Mutation
PDgFR-A(Platelet derived growth factor receptor alpha) mutation
Succinate dehydrogenase mutation

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42
Q

Commonly affected age group in GIST

A

Elderly patients (around 60 years) , sometimes younger too

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43
Q

Carney Stratakis Syndrome

A

GIST + Paraganglioma

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44
Q

Mode of inheritance in Carney Stratakis Syndrome

A

Autosomal dominant

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45
Q

Mutation seen in Carney Stratakis Syndrome

A

SDH Mutation

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46
Q

Mutation in Familial GIST

A

NF-1 gene mutation

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47
Q

Carney’s triad

A

GIST
Paraganglioma
Pulmonary chondroma

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48
Q

Due to C-Kit or PDgFR alpha mutation there is

A

Increased activity of different growth factors - increased Tyrosine kinase activity - cell proliferation increases - Cancer

49
Q

Clinical features of GIST

A

Bleeding
Abdominal pain
Weight loss

50
Q

GIST spread via

A

Blood vessels, No lymphatic spread

51
Q

Common site of metastasis in GIST

52
Q

Investigation of choice in GIST

A

CT Scan/PET

53
Q

Findings of Biopsy in GIST

A

Epitheloid cells
Presence of spindle cells
Mixed cells

54
Q

Endoscopic finding in GIST

A

Solitary, fleshy mass
“Whorled appearance”

55
Q

Immunohistochemistry markers in GIST

A

DOG-1(Best markers) > C-Kit(CD117) > CD34

56
Q

Treatment of GIST

A

Surgical
TKIs - Imatinib

57
Q

Prognosis of GIST Depends upon

A

Location
Mitotic index
Size of tumor

58
Q

Higher the mitotic index, the prognosis is

59
Q

Depending on the location GIST affecting stomach have prognosis

A

Good prognosis - less aggressive

60
Q

If size of tumor is more than 10cm in GIST, The prognosis is

61
Q

When the size of tumor is less than 5cm , then prognosis is

62
Q

Most common extranodal site in Non Hodgkin’s Lymphoma

A

GIT - Stomach (MC)

63
Q

Most common extranodal site in Non Hodgkin’s lymphoma + HIV Patient

64
Q

Preferred site of GI lymphoma in Follicular Lymphoma

65
Q

Preferred site in Enteropathy associated T cell Lymphoma

66
Q

In case of allogenic BM transplantation or organ Transplantation, effect of Immunosuppressive therapy

A

Decreased T cell activity - leads to increased B cell proliferation

67
Q

Gastric Maltoma also termed as

A

Indolent Marginal zone Lymphoma

68
Q

Role of H pylori in Gastric Maltoma

A

Lymphocytes proliferation in gastric mucosa

69
Q

H pylori induced inflammation leads to

A

Formation of H pylori Specific B cells and T cells - Cytokines secretion - leads to increased BCL-10 and MALT-1 Activity

70
Q

Increased BCL-10 And MALT-1 Activity stimulates

A

Nuclear factor kappa Beta - B cell proliferation - Leads to Low grade MALTOMA

71
Q

Which mutation leads to conversion of Low grade MALTOMA to High grade MALTOMA

A

p16 and p53 mutations

72
Q

Translocation associated Maltoma are resistant to

A

Antibiotics

73
Q

Clinical features of Gastric Maltoma

A

Epigastric pain
Dyspepsia

74
Q

Microscopical finding from Biopsy in Gastric Maltoma

A

Lymphoepithilial lesion - lymphocyte infiltrates into epithelial cells - destroys glands

75
Q

Immunohistochemistry markers in Gastric Maltoma

A

CD20 +ve
CD5/CD23 -ve
CD43 +ve (25%)

76
Q

Treatment of H pylori associated Gastric Maltoma

A

Antibiotics

77
Q

Treatment of High grade MALTOMA

A

Anticancer drugs

78
Q

Malabsorption means

A

Not proper digestion of nutrients and minerals from intestine

79
Q

Classical symptoms of Malabsorption disorders

A

Chronic diarrhea - Steatorrhea
Abdominal pain
Feeling of heaviness
Weight loss

80
Q

Celiac sprue is also known as

A

Gluten sensitive Enteropathy

81
Q

Celiac sprue is genetically associated with

A

HLA DQ2, HLA DQ8 +ve

82
Q

Celiac sprue is associated with which Autoimmune disorders

A

Type 1 DM
Sjogren Syndrome
Thyroiditis
IgA Nephropathy

83
Q

Celiac sprue associated with which Syndromes

A

Down Syndrome
Turner Syndrome
Ataxia
Autism
Depression/Epilepsy

84
Q

Commonly affected part of GIT in Celiac sprue

A

Small intestine
Duodenum > Jejunum

85
Q

Gluten is found naturally in which products

A

Wheat
Barley
Rye
Oat

86
Q

Gluten is converted to

87
Q

Formation of Gliadin from Gluten can leads to activation of

A

CD8 and CD4 T cell

88
Q

Activation of CD4 and CD8 cells due to gliadin leads to

A

Auto- antibody formation
Cytokines secretion
Epithelial cell damage

89
Q

Autoantibodies formed in Celiac sprue

A

Anti-transglutminase antibody
Anti-Endomysial antibody
Anti-gliadin antibody

90
Q

IgA antibodies in Celiac sprue leads to involvement of which organ

A

Skin - dermatitis herpetiformis

91
Q

Clinical features of Celiac sprue

A

Diarrhea
Abdominal pain
Stunted growth
Flatulence
Nutrient deficiencies (Iron/Folic acid) - Anemia

92
Q

Diagnosis of Celiac sprue is done through

A

Clinical history
Intestinal biopsy
Serology

93
Q

Site of intestinal biopsy in Celiac sprue

94
Q

Findings of Duodenal biopsy in case of Celiac sprue

A

Villous atrophy
Crypts hyperplasia
Lymphocytic infiltration

95
Q

In Celiac sprue, there is increased risk of which cancers

A

Enteropathy associated T cell Lymphoma
Small intestine Adenocarcinoma
Esophageal cancer ( Squamous cell)

96
Q

Serological findings in Celiac sprue

A

Anti transglutaminase antibody - most sensitive Ab
Anti Endomysial antibody - overall best Ab

97
Q

Treatment of Celiac sprue

A

Stop gluten containing diet
Nutritional supplementation
In case of Dermatitis herpetiformis - DAPSONE

98
Q

Stages of Celiac sprue

A

Latent disease
Silent disease
Clinic disease

99
Q

Findings in Latent disease

A

Serology +ve

100
Q

Findings in silent disease

A

Serology +ve, Villous atrophy
Asymptomatic

101
Q

Findings in clinical disease

A

Serology +ve, Villous atrophy
Symptomatic

102
Q

Environmental enteropathy also termed as

A

Tropical sprue

103
Q

Most common cause of Environmental enteropathy

104
Q

Which parts of GIT involved in Environmental enteropathy

A

Total involvement of Small intestine - decreases iron/folic acid/B12

105
Q

Treatment of Environmental enteropathy

A

Antibiotics

106
Q

Risk of cancer in environmental enteropathy

107
Q

Causative agent of Whipple’s disease

A

Tropheryma whipplei

108
Q

Pathogenesis of Whipple’s disease

A

Phagocytosis of Tropheryma whipplei by Macrophages - leads to involvement of lamina propria - Fat malabsorption

109
Q

Organs affected in Whipple’s disease

A

Intestine
Joints
LN
Cardiovascular system
CNS

110
Q

Triad seen in Whipple’s disease

A

Diarrhea
Weight loss
Arthralgia

111
Q

Diagnostic method used in Whipple’s disease

A

Intestinal biopsy

112
Q

Finding of intestinal biopsy on routine staining in Whipple’s disease

A

Macrophages infiltration in lamina propria (Foamy macrophages)

113
Q

Finding of intestinal biopsy on Electromicroscopy in Whipple’s disease

A

Bacteria - Rod shaped bacilli present inside Macrophages

114
Q

Finding of intestinal biopsy on PAS stain in Whipple’s disease

A

Diastase resistance granules

115
Q

Treatment of Whipple’s disease

A

Antibiotics - Cotrimoxazole

116
Q

Anal cancer is type of which carcinoma

A

Squamous cell carcinoma

117
Q

Main cause of anal cancer

A

Human Papilloma virus - HPV 16,18

118
Q

Why surgery is not preferred in case of Anal cancer

A

Risk of damage to anal sphincter - can lead to fecal incontinence

119
Q

Chemoradiation Regime used in anal cancer is termed as

A

Nigro’s regime

Pathology (14 decks)

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