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๐Ÿ“š GIT Pathology 2 โ€” Easy Point Notes

1. ๐ŸŸ  BARRETT'S ESOPHAGUS

What is it? The normal squamous (flat) lining of the lower esophagus gets replaced by intestinal-type columnar cells โ€” this is called intestinal metaplasia. It happens because of long-term acid reflux (GERD).
Who gets it? Males, usually 40โ€“60 years old.
Key Points:
  • Appears as red, velvety patches/tongues extending upward from the gastroesophageal junction
  • Goblet cells (with mucous vacuoles) are the diagnostic hallmark โ€” MUST be present
  • It is a major risk factor for adenocarcinoma of the esophagus

2. ๐ŸŸก STOMACH โ€” KEY DEFINITIONS

TermMeaning
ErosionOnly the superficial lining is lost; doesn't go through the muscularis mucosae
UlcerDeeper defect >5mm; penetrates through muscularis mucosae into submucosa
GastritisInflammation of the stomach lining (diagnosed by microscopy)
GastropathyWhen there is stomach damage but NO inflammatory cells (e.g., hypertrophic gastropathy)

3. ๐Ÿ”ด ACUTE GASTRITIS

What is it? Short-term (transient) inflammation of the stomach lining.
Causes:
  • NSAIDs and Aspirin
  • H. pylori infection
  • Alcohol
  • Chemicals
  • Severe stress (burns, trauma, major surgery)
  • Bile reflux (after stomach surgery)
  • Viral infections (CMV)
Types by severity:
MildSevere
No major changesErosions + hemorrhage = Acute Erosive Hemorrhagic Gastritis
Microscopy: Dense neutrophil infiltration; pit abscesses (neutrophils collecting in gland pits)
Stress Ulcers โ€” Remember:
  • Curling ulcers โ†’ Burns/trauma โ†’ proximal duodenum
  • Cushing ulcers โ†’ Brain/intracranial disease โ†’ stomach/duodenum/esophagus โ†’ highly prone to perforation

4. ๐ŸŸค CHRONIC GASTRITIS (H. pylori)

How H. pylori causes damage:
  1. Urease โ†’ breaks down urea โ†’ releases ammonia โ†’ raises gastric pH โ†’ stimulates G cells โ†’ hypergastrinemia โ†’ excess acid
  2. Adhesins โ†’ helps bacteria stick to stomach lining
  3. Cytotoxins (cagA + vacA genes) โ†’ cause gastritis, ulcers, and cancer
Immune response:
  • Increases pro-inflammatory cytokines (IL-1ฮฒ, TNF)
  • Decreases anti-inflammatory cytokines (IL-10)
Microscopy hallmarks:
  • Intraepithelial neutrophils
  • Plasma cells in lamina propria
  • Lymphoid follicles
  • Plasma cells are characteristic of H. pylori gastritis

5. ๐Ÿ”ต PEPTIC ULCER DISEASE (PUD)

Stomach protects itself by:
  • Mucus secretion (by foveolar cells) โ†’ forms protective layer
  • Bicarbonate secretion
  • Tight junctions between cells
  • Prostaglandins โ†’ increase mucus + bicarbonate, increase blood flow, reduce acid
Risk factors (things that break down protection):
  1. H. pylori โ€” most common cause; nearly all duodenal ulcers have H. pylori
  2. NSAIDs/Aspirin โ€” irritate mucosa + block prostaglandins + reduce bicarbonate
  3. Smoking โ€” reduces blood flow + impairs healing
  4. Hypercalcemia/Zollinger-Ellison syndrome โ€” excess acid
Ulcer Layers (Microscopy):
  1. Necrotic zone (surface)
  2. Neutrophilic exudate
  3. Granulation tissue (mononuclear cells)
  4. Fibrous/collagenous scar (base)
Symptoms:
  • Burning/aching epigastric pain
  • Worse 1โ€“3 hours after meals and at night (11 PMโ€“2 AM)
  • Nausea, vomiting, bloating, weight loss
  • Antacids provide relief
Complications:
  • Bleeding (most common) โ†’ coffee-ground vomit, melena, iron-deficiency anemia
  • Perforation (~5% patients)
  • Pyloric obstruction (~10%) due to scarring or edema
  • Duodenal ulcers โ†’ NEVER become malignant
  • Gastric ulcers โ†’ small % may undergo malignant change

Gastric vs Duodenal Ulcer โ€” Comparison Table

FeatureGastric UlcerDuodenal Ulcer
SiteLesser curvature1st part of duodenum
IncidenceLess commonMore common
Age>60 years, M>F25โ€“50 years, M>F
H. pyloriLess commonStrong association
Acid levelUsually normalHigh
Food & painFood aggravatesFood relieves
AntacidsInconsistent reliefPrompt relief
Night painNot observedCommon
HeartburnNot commonCommon
BleedingHematemesis > melenaMelena > hematemesis
Weight lossPresentAbsent
MalignancySmall riskNever
Key facts:
  • Gastroduodenal artery โ†’ bleeds in duodenal ulcer
  • Left gastric artery โ†’ bleeds in gastric ulcer
  • Urea breath test โ†’ used to confirm H. pylori treatment success

6. ๐ŸŸฃ GASTRIC ADENOCARCINOMA

Most common malignancy of the stomach
Protective factors (DECREASE risk):
  • Aspirin
  • Fresh fruits and vegetables
  • Vitamins A and C
  • Calcium, Selenium, Zinc, Iron
  • Alcohol is NOT a risk factor
Risk factors:
EnvironmentalHost/GeneticPredisposing Conditions
H. pylori (5โ€“6ร— risk)Blood group AChronic gastritis
Nitrites, smoked/salted foodsFamily historyIntestinal metaplasia
Low socioeconomic statusCDH1 mutationsPartial gastrectomy
Rubber/coal workersBRCA2, TP53 mutations
H. pylori โ†’ cancer pathway: Chronic H. pylori โ†’ mucosal inflammation โ†’ hypochlorhydria โ†’ bacterial overgrowth โ†’ mucosal atrophy โ†’ intestinal metaplasia โ†’ dysplasia โ†’ carcinoma
Genetics:
  • CDH1 gene encodes E-cadherin (cell adhesion protein)
  • Germline CDH1 mutations โ†’ familial gastric cancer
  • CDH1 loss in ~50% of sporadic diffuse gastric cancers
  • TP53 mutation in majority of both diffuse and intestinal type sporadic cancers
Sites (most to least common):
  • Pylorus & antrum: 50โ€“60%
  • Cardia: 25%
  • Body & fundus: 15โ€“25%
  • Lesser curvature most affected (~40%)
Macroscopic types:
  1. Polypoid
  2. Fungating
  3. Ulcerated
  4. Infiltrative (Linitis plastica = "leather bottle stomach")
Signet ring cell carcinoma: Signet ring cells >50% of tumor (part of diffuse type)
Spread of Stomach Cancer:
RouteHow
Local/DirectInto muscularis โ†’ serosa โ†’ duodenum, pancreas, liver, colon
LymphaticTo Virchow's node (supraclavicular) = Troisier's sign (first sign of cancer)
Periumbilical nodesSister Mary Joseph nodule (subcutaneous nodule at umbilicus)
BloodVia portal vein โ†’ liver; also lungs, bones
OvariesKrukenberg tumor
Clinical features:
  • Early satiety, bloating, distension, vomiting
  • Iron-deficiency anemia (tumor bleeds)
  • Gastric outlet obstruction (pyloric tumors)
  • Elevated CEA (carcinoembryonic antigen) tumor marker

7. ๐ŸŸข CROHN'S DISEASE (IBD)

What is it? Chronic inflammatory bowel disease that can affect any part of the GI tract (mouth to anus), with transmural (full-thickness wall) inflammation.
Key microscopic features:
  1. Chronic inflammation โ€” lymphocytes, plasma cells, macrophages throughout
  2. Crypt abscesses โ€” clusters of neutrophils inside crypts โ†’ destroy crypts
  3. Non-caseating granulomas โ€” the HALLMARK of Crohn's
    • Found in ~35% of cases
    • Located mainly in submucosa
    • Made of epithelioid cells + lymphocyte rim ยฑ giant cells
  4. Transmural inflammation โ€” all layers of bowel wall involved; lymphoid aggregates in submucosa/subserosa
  5. Skip lesions โ€” areas of normal bowel between diseased areas

8. ๐ŸŸค ULCERATIVE COLITIS (UC)

What is it? Chronic inflammatory bowel disease limited to the colon and rectum; inflammation involves only mucosa and submucosa (not full thickness).
Key features:
  • Always starts in rectum, extends proximally (continuous โ€” no skip lesions)
  • No skip lesions (unlike Crohn's)
  • Mucosa looks red, granular like sandpaper; bleeds easily; covered with yellowish exudate
  • Pseudopolyps โ€” islands of surviving mucosa surrounded by ulcers (seen in chronic UC)

Crohn's vs UC โ€” Quick Comparison

FeatureCrohn's DiseaseUlcerative Colitis
LocationEntire GI tract (any part)Colon + rectum only
Inflammation depthTransmural (all layers)Mucosa + submucosa only
Skip lesionsYesNo (continuous)
GranulomasYes (non-caseating)No
Ulcer shapeDeep fissures, "cobblestone"Superficial, broad
Rectal involvementNot alwaysAlmost always

9. ๐Ÿ”ด COLORECTAL CANCER (Adenocarcinoma)

Most common malignant tumor of the entire GI tract
Diet-related risk factors:
  • Low fiber โ†’ slow stool transit โ†’ more time for carcinogens to act
  • High animal fat/red meat โ†’ increases bile acids โ†’ bacteria convert to carcinogens
  • Deficiency of vitamins A, C, E (antioxidants) โ†’ more oxidative damage
  • Protective: Cruciferous vegetables (cauliflower, broccoli, cabbage), vitamins A, C, E
Molecular pathogenesis (how it develops):
  1. APC gene inactivation (tumor suppressor)
    • APC normally destroys beta-catenin (stops cell growth)
    • When APC is lost โ†’ beta-catenin accumulates โ†’ binds TCF โ†’ activates c-MYC, cyclin D1 โ†’ uncontrolled cell proliferation
    • Both copies of APC must be lost (mutation or methylation)
  2. Other mutations: KRAS, TP53, SMAD2/4 (TGF-ฮฒ pathway) accumulate over time
Investigation of Colon Cancer:
  1. Guaiac test โ€” detects occult (hidden) blood in stool
  2. CEA (carcinoembryonic antigen) โ€” elevated tumor marker
  3. Flexible sigmoidoscopy
  4. Colonoscopy
  5. Biopsy โ†’ Investigation of choice
Symptoms:
  • Right-sided: anemia, weight loss (silent bleeding)
  • Left-sided: change in bowel habits, obstruction
  • Discomfort in left lower quadrant

๐Ÿ—‚๏ธ Quick Memory Tricks

FactRemember
Goblet cells = Barrett's diagnosis"Goblet = Gatekeeper"
Cushing ulcer = brain โ†’ perforation"Cushing = Cranium = Catastrophic perforation"
Virchow's node = Troisier's signLeft supraclavicular node enlargement
Krukenberg = ovariesStomach cancer โ†’ ovary metastasis
Sister Mary Joseph nodule = umbilicusPeriumbilical spread
APC loss โ†’ colorectal cancer"APC = Anti-Proliferation Controller"
Non-caseating granuloma = Crohn'sGranuloma = Crohn's signature
No skip lesions = UCUC = Uniform and Continuous
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