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Pathology MBBS > Stomach, IBD, Malabsorption syndromes, polyps and colon cancer > Flashcards

Stomach, IBD, Malabsorption syndromes, polyps and colon cancer Flashcards

1
Q

Zones of ulcer

A
  1. Necrosis
  2. Inflammatory cells
  3. Granulation tissue
  4. Fibrosis
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2
Q

Stomach ulcer (compared to duodenal ulcer)

A
  • the less common peptic ulcer
  • lesser curvature near incisura angularis
  • poorer prognosis
  • perforations more common
  • no night pain
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3
Q

Duodenal ulcer (compared to stomach ulcer)

A
  • the more common peptic ulcer
  • D1 zone
  • better prognosis
  • bleeding is more common
  • night pain (relieved by food) is present
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4
Q

Causes of acute gastritis

A
  1. Smoking🚬
  2. Aspirin and other NSAID
  3. Alcohol🍺
  4. Uremia
  5. Stress
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5
Q

Type B chronic gastritis

A 
M/C
H. pylori associated
Usually affects antrum
H&E:
 Intraepithelial neutrophils and sub-epithelial plasma cells
H. pylori strained by different stains
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6
Q

H. pylori virulence factor

A 
Gram negative bacteria with tuft of flagella at one end
Only host is humans 
Virulence factors:
1. Flagella
2. Urease against acid
3. cag A and Vac A toxins - carcinogenic
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7
Q

Diseases caused by H. pylori

A
  1. Chronic gastritis
  2. Gastric adenocarcinoma
  3. MALToma
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8
Q

Stains used for H. pylori

A
  1. Warthin Starry silver stain
  2. Non silver stain:
    • Giemsa stain
    • Acridine orange
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9
Q

Type A chronic gastritis

A

Autoimmune gastritis
Affects fundus, body; spares antrum
Clinically:
1. Pernicious anaemia
2. Increased risk of other autoimmune diseases
Gross: loss of rugal folds
H&E: infiltrate of lymphocytes and plasma cells

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10
Q

Pathogenesis of type A chronic gastritis

A
  1. Antibodies against parietal cells and IF
  2. Reduced production of HCl, IF
  3. Hypergastrinemia
    Also:
    • Vit B12 absorption decreases ➡️ megaloblastic anaemia
    • Chief cell destruction ➡️ reduced serum pepsinogen
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11
Q

Risk factors for gastric adenocarcinoma

A
  1. Smoking 🚬
  2. H. pylori - antral
  3. Japanese people
  4. High intake of smoked fish
  5. Food rich in preservatives
  6. Blood group A
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12
Q

Site of occurrence of gastric adenocarcinoma

A

Most common to least common

  1. Antrum
  2. Lesser curvature
  3. Greater curvature
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13
Q

Lauren’s classification

A 
Of gastric adenocarcinoma
1. Intestinal:
 Bulky polypoidal lesions
2. Diffuse:
 Infiltrative lesions
Both presents as dyspepsia and gastritis
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14
Q

Intestinal gastric adenocarcinoma

A 
Bulky polypoidal lesions
H&E: glands lined by malignant cells
Better prognosis
Pathogenesis:
1. Mutation in WNT pathway
2. p53 mutation
3. Loss of function in APC
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15
Q

Diffuse type of gastric adenocarcinoma

A

Infiltrative lesion
H&E: mucin secretion and signet ring cell
Poorer prognosis
Pathogenesis:
CDH-1 gene mutation ➡️ loss of E-cadherin

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16
Q

Linitis plastica

A

Leather bottle
Diffusely infiltrate the entire gastric wall without an intraluminal mass
Wall of stomach is thickened UTI 2-3 cm
Leathery and elastic consistency
Develops into desmoplasia (extreme fibrosis)

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17
Q

Virchow’s node

Irish node

A

Virchow’s node is when left supraclavicular lymph node is affected and swollen
Irish node is when left axillary lymph node is affected

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18
Q

Sister Mary Joseph’s nodule

A

Periumbilical nodule affected by gastric adenocarcinoma

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19
Q

Blumer shelf

A

Gastric adenocarcinoma or similar carcinoma metastasised to pouch of Douglas

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20
Q

Most important prognostic factor of gastric carcinoma

A

Depth of invasion

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21
Q

GIST Gastrointestinal stromal tumour

A 
M/C mesenchymal tumour of stomach
From interstitial cells of cajal
Part of Carney’s triad
Pathogenesis:
1. C-kit mutation
2. PDGF R-A mutation
Gross - well circumscribed fleshy mass 
H&E:
1. Spindly cells M/C
2. Epitheloid cells
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22
Q

Carney’s triad

A

In young females

  1. Gastric GIST
  2. Pulmonary chondroma
  3. Paraganglioma
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23
Q

Immunohistochemical markers for GIST (Gastrointestinal stromal tumour)

A
  1. DOG I - most specific
  2. CD-117 (C-KIT) - most sensitive
  3. CD-34
24
Q

Prognostic criteria of GIST (Gastrointestinal stromal tumour)

A 
1. Tumour size:
• <5 cm good
• >10 cm bad
2. Location: 
• Gastric good
• intestinal bad
3. Mitosis:
>10/HPF bad prognosis
25
Q

MALToma

A

Usually H. pylori associated
M/C stomach
Associated with t(11:18), t(14:18)
Usually DLBCL (diffuse large B cell lymphoma)
H&E: lymphoepithelial lesions (lymphocytes entering into a gland)

26
Q

Carcinoid tumour

A 
From enterochromaffin cells
Gross: pan brown/yellow colour
H&E: salt and pepper collation
e- microscopy: dense core neurosecretory granules
IHC markers:
1. MSE neuron specific enolase
2. Chomogranin 
3. Synaptophysin
27
Q

Inflammatory bowel disease

A 
1. Crohn’s disease:
Any area of GIT, transmural 
2. Ulcerative colitis:
 Colon and rectum (Backwash ileitis)
 Submucosal
3. Indeterminate colitis:
 8-10 % of cases
28
Q

Pathogenesis of IBD

A
  1. Hygiene hypothesis:
    Because of use of lot of preservatives and packed food, lack of development of mucosal immune response
  2. Genetics
29
Q

Genetic factors for IBD

A
  1. NOD2 gene polymorphism ➡️ NFK-β pathway ➡️ increased cellular population ➡️ Crohn’s disease
  2. ATG 16L1 - autophagy related
  3. IRGM immune related GTPase M

• IL-23 receptor polymorphism is protective for both Crohn’s disease and ulcerative colitis
• HLA association:
Crohn’s disease HLA DR1
Ulcerative colitis HLA DR2

30
Q

Crohn’s disease

A

Any area of GIT, but commonly in ileum, caecum, ileocaecal valve
• Transmural
• Bimodal (15-20 years and elderly) like Hodgkin lymphoma
• More common in females
• More common in Caucasians
• smoking 🚬 is a risk factor
Higher risk of CAN (colitis associated neoplasia)
Barium enema: string sign of Kantor
Anti saccharomyces cereviseae antibody is present

31
Q

Crohn’s disease

clinical manifestations

A
  1. Intermittent diarrhoea attacks
  2. Abdominal pain
  3. Fever
  4. Uveitis
  5. Primary sclerosing cholangitis
  6. Ankylosing spondylitis
  7. Migratory polyarthritis
32
Q

Crohn’s disease

Gross features

A
  1. Skip lesions
  2. Deep knife like and serpentine ulcer
  3. Rubbery thick intestinal wall
  4. Cobblestone appearance
  5. Creeping fat
  6. Higher risk of structure, fissure, fossils and sinus
33
Q

Microscopy of Crohn’s disease

A
  1. Transmural involvement
  2. CD4-TH1 cells increased: non caseating granuloma
  3. Cryptitis
  4. Crypt abscess
    Last two are more prominent in ulcerative colitis
34
Q

Ulcerative colitis

A 
Site: colon, rectum submucosa
Smoking is protective 
CD4 TH2 cells increased 
Extra intestinal: primary sclerosis cholangitis
P-ANCA is present
Less risk of CAN
On barium enema - lead pipe appearance
35
Q

Ulcerative colitis

gross features

A
  1. Continuous involvement
  2. Superficial broad based ulcer
  3. Pseudopolyps - islands of regenerating mucosa
  4. Mucosal bridges from pseudopolyps
  5. Toxic megacolon
36
Q

Ulcerative colitis

microscopy

A
  1. Submucosal involvement
  2. Cryptitis
  3. Crypt abscess
37
Q

Malabsorption syndromes

A 
Clinically steatorrhea 
 Frothy, bulky and greasy stools
1. Celiac disease
2. Whipple’s disease
3. Tropical sprue
38
Q

Celiac disease

A 
Gluten sensitive enteropathy
Cannot have:
B. Barley
R. Rye 
O. Oats 
W. Wheat 
Can have rice, maize
Usually affects 2nd part of duodenum
Marsh score for grading
39
Q

Pathogenesis of celiac sprue

A

Ab mediated:
1. Anti-gliadin
2. Anti tissue transglutaminase IgA (most sensitive)
3. Anti endomysial antibody IgA (most specific)
Gluten contains α-gliadin, can’t be broken by digestive enzyme
Increased CD8+ T lymphocytes
Associated with HLA-DQ2, DQ8

40
Q

Clinical features of celiac sprue

A
  1. Steatorrhea
  2. Diarrhoea
  3. Abdominal pain
  4. Increased risk of dermatitis herpetiformis
  5. Increased risk of enteropathy associated T cell lymphoma
41
Q

Celiac sprue microscopy

A
  1. Villous atrophy
  2. Crypt hyperplasia
  3. Increased intraepithelial lymphocytes
42
Q

Whipple’s disease

A 
Caused by Actinomycete whipplei
Gram positive organism
Rare
Multisystem:
1. GIT
2. Lymph node
3. Joints
4. CNS
43
Q

Whipple’s disease

microscopy

A

Lamina propria is stuffed with foamy macrophages, PAS diastase resistant organisms
Differential diagnosis for giant macrophages on intestinal biopsy:
• TB - AFB positive
• Whipple’s disease - AFB negative

44
Q

Tropical sprue

A 
Caused by E. coli
Can effect:
• duodenum-iron deficiency
• jejunum-FA deficiency
• ileum-Vit B12 deficiency
Microscopy:
• Villous atrophy
• Regional arthritis
45
Q

Ulcers of intestine

A 
1. Typhoid:
• ileocaecal junction
• longitudinal ulcer ➡️ low chance of stricture
• microscopy: erythrophagocytosis
2. TB:
• transverse ulcer
• stricture
3. Amoebiasis:
• caecum M/C, liver
• flask shaped ulcer limited to submucosa 
• microscopy: erythrophagocytosis
46
Q

Polyps and their classification

A 
Polyps are protrusion of mucosa
Classification of polyps
1. Sessile: more malignant
2. Pedunculated: less malignant
Classification:
1. Neoplasia- adenoma
2. Non-neoplastic:
• inflammatory
• hyperplastic
• hamartomatous
47
Q

Microscopic classification of adenoma

A 
1. Tubular polyp:
 Has tubules
 Also known as adenomatous polyp
2. Villous polyp:
 Has villous projections 
3. Tubulovillous polyp:
 Has both tubules and villous architecture
 Has highest malignant potential
48
Q

Peutz-Jeghers syndrome

A

Jejunum M/C
Loss of function of LKB1/ STK11 gene
Features:
1. Multiple hamartomatous polyp
2. Perioral/ mucocutaneous hyperpigmentation
3. Increased risk of carcinoma colon, breast, thyroid, lung,…

49
Q

Familial Adenomatous Polyp (FAP)

pathogenesis

A

APC is a negative regulator of β-catenin ➡️ degrades β-catenin

  1. APC mutation
  2. β-catenin not degraded
  3. β-catenin enters nucleus
  4. Proliferation
  5. FAP
50
Q

Familial Adenomatous Polyp (FAP)

A
  • Autosomal dominant
  • APC (Adenomatous polyposis coli) gene mutation on chromosome 5q21
  • Diagnosis: >100 polyps
  • If left untreated, colon cancer is 100%
  • Congenital hypertrophy of retinal pigment epithelium
51
Q

Gardner syndrome

Turcot syndrome

A 
Gardner syndrome:
FAP + osteoma, epidermal cyst, abnormal dentition
Turcot syndrome:
FAP + brain 🧠 tumours
 (Medulloblastoma > glioblastoma)
52
Q

Colon cancer risk factors

A
  1. FAP - APC gene mutation on chromosome 5q21
  2. HNPCC - mismatch gene defect of HMPH1, MSH-1,2,6
  3. Smoking, alcohol
  4. High fat diet and highly processed food
  5. Less fibre diet
  6. IBD (ulcerative colitis > Crohn’s disease)
    Fish 🎣 intake is protective
53
Q

Adenocarcinoma sequence

A 
1. APC gene
Normal epithelium ➡️ epithelium at risk
2. K-RAS
Epithelium at risk ➡️ Adenoma
3. p53
Adenoma ➡️ carcinoma
AK-53 🔫
54
Q

Mismatch repair (microsatellite instability) pathway

A

Hereditary non-polyposis colon cancer
1. Mismatch repair gene mutation
Normal colon ➡️ sessile serrated adenoma
2. TGF-β, BAX, TCF-4, IGF2R gene mutations:
Sessile serrated adenoma ➡️ carcinoma

55
Q

Mismatch repair genes

A

MLH-1
MSH-2
(MSH-6, PMS-1, 2)

Pathology MBBS (17 decks)

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