Pathology of Peptic Ulcer

Normal Stomach

Esophagus & Stomach Normal

Benign tumors
usually small, polypoid and asymptomatic, but may be confused with malignancies Most common- leiomyomas – GIST Smooth muscle tumors

Most common benign tumor of esophagus Minute tumors 1-2 mm are often near the gastroesophageal junction and are asymptomatic Median age 35 years, 2/3 men


Circumscribed, mural, solitary mass, 2-5 cm, bulges into lumen, may be polypoid; gray-white and whorled cut surface;

similar to classic leiomyomas; circumscribed lesion composed of intersecting fascicles of bland spindle cells with variable fibrosis

Other benign tumors
Fibromas Lipomas Hemangiomas Neurofibromas Lymphangiomas Fibrovascular polyps Squamous papillomas Inflammatory polyps

Esophageal Carcinoma
shift from squamous cell carcinoma arising in upper/middle third of esophagus to adenocarcinomas arising in distal esophagus Since most patients are asymptomatic during early stages, they often present with advanced or metastastic disease Metastases usually to liver, lungs, pleura

Squamous cell carcinoma
Most common type of esophageal cancer Highest incidence in northern Iran, northern China (? due to polycyclic aromatic hydrocarbons,

deficiency of vitamins A, C, thiamine, B6, riboflavin zinc, molybdenum; fungal contamination, nitrates / nitrosamines, Betel nuts, alcohol, tobacco, urban environment

Other causes
achalasia, corrosive strictures, long standing esophagitis, Plummer-Vinson syndrome, HPV in high risk regions

Usually men age 50+ in low risk areas; more common in blacks (4:1) in US dysphagia, anorexia, weight loss (due to advanced stage at presentation) 90% in mid/lower esophagus Often multifocal Most present with invasion into muscularis propria

(a) deep irregular ulcers with nodular margins that may perforate and enter trachea, aorta or mediastinum; (b) gray-white plaque-like thickenings of mucosa that cause thick, rigid esophageal wall and luminal narrowing or (c) polypoid exophytic lesion

Esophageal Carcinoma

most are moderate to well differentiated; tumor clusters may exist several cm from main mass due to lymphatic spread through submucosa ; may have focal glandular or small cell differentiation or lymphoid stroma

Superficial squamous cell carcinoma
Tumor confined to mucosa and submucosa (T1) regardless of lymph node status Intramucosal tumors have no lymph node involvement vs. 30% of submucosal tumors Account for 20% of resections in US/Western Europe Patients may also have bronchial or oropharyngolaryngeal carcinoma 5 year survival is 85% without vs. 40% with nodal involvement

Gross: polypoid masses, thin plaques or eroded mucosal depressions Micro: invasive nests with irregular borders

Primary tumor (T) TX: primary tumor cannot be assessed T0: no evidence of primary tumor Tis: carcinoma in situ T1: tumor invades lamina propria or submucosa T2: tumor invades muscularis propria T3: tumor invades adventitia T4: tumor invades adjacent structure

Staging (clinical and pathologic)

Regional lymph nodes (N)   NX: regional lymph nodes cannot be assessed N0: no regional lymph node metastases N1: regional lymph node metastases

Distant Metastasis (M)   MX: distant metastasis cannot be assessed M0: no distant metastasis M1: distant metastasis   

Stage grouping and 5 year survival
Stage 1 : T1 N0 M0, 80-90% Stage 2A: T2 or T3, N0 M0, 40-50% Stage 2B: T1 or T2, N1 M0, 25-40% Stage 3 : T3 N1 M0 or T4 any N M0, 15-25% Stage 4 : Any T, any N, M1, < 5% Stage 4a: Any T, any N, M1a Stage 4b: Any T, any N, M1b

Features to report
Tumor type Histologic grade Depth of invasion Tumor size
Anatomic site Angiolymphatic invasion

Perineural invasion Margin involvement (proximal, distal, radial) Lymph node involvement (total involved, total examined) Other features (esophagitis, Barrett’s esophagus, dysplasia, specific types of infection)

30-40% of primary esophageal cancers; increasing incidence over past 20 years for unknown reasons Previously confused with gastric carcinomas, particularly in lower 1/3 of esophagus Age 40+, median 50’s, usually white men In Barrett’s esophagus patients, 73% had hiatal hernia, 63% were smokers, 45% alcohol users

Tend to invade via submucosal lymphatics, emphasizing importance of margin evaluation Similar prognosis as squamous cell carcinoma when grouped by stage

usually distal esophagus with invasion of gastric cardia; appear as flat patches to nodular masses Deep ulcerative lesions

Mucin producing glandular tumors Intestinal type features Signet ring cells – gastric types – less common

Clinical features
Over 40 yrs More common in men More in whites Dysphagia Progressive weight loss Bleeding Chest pain vomiting

Prognostic factors
depth of invasion, lymph node metastases, status of resection margins

Mucosal protection
(a) mucus secretion: mucus is relatively impermeable to H+; also fluid with acid or pepsin exits gastric glands as “jets” and penetrates surface mucus layer without contacting surface epithelial cells (b) bicarbonate secretion creates pH neutral microenvironment adjacent to cell surface

(c) intercellular tight junctions prevent backdiffusion of H+; disruptions are quickly repaired (d) rich blood flow supplies bicarbonate and nutrients and removes acid (e) muscularis mucosa limits injury; if intact, repair occurs in hours/days vs. weeks if not intact

Acute gastritis
Acute mucosal inflammatory process, usually transient May be accompanied by local hemorrhage or mucosal sloughing Severe erosive disease may cause acute GI bleeds Associated with heavy use of NSAIDs (non-steroidal anti-inflammatory drugs, including aspirin),

excessive alcohol use, heavy smoking, cancer chemotherapy, bile reflux, uremia, systemic infections (Salmonella), severe stress (trauma, burns, surgery),

ischemia and shock, acid/alkali ingestion as part of suicide attempts, gastric irradiation mechanical trauma (nasogastric tube), distal gastrectomy Major cause of massive hematemesis in alcoholics Occurs in 25% of those who take daily aspirin for rheumatoid arthritis

Acute Gastritis

Acute Esophagitis & Gastritis

mild: modest edema of lamina propria, slight vascular congestion, intact epithelium, scattered neutrophils; severe: erosion and hemorrhage in mucosa

none, or Pain in epigastrium nausea and vomiting Hemorrhage & massive hemetemesis melena

Chronic gastritis
Chronic mucosal inflammatory changes leading to mucosal atrophy and epithelial metaplasia, usually without erosions Most cases are type B or non-autoimmune gastritis Increases with age; in Europe/Japan, affects 50% at age 60+ Histology does not correlate well with symptoms

Chronic Helicobacter pylori infection, toxins (alcohol, tobacco), reflux of bilious duodenal secretions (post-antrectomy or other), obstruction (bezoars, atony), radiation

Helicobacter pylori gastritis
Present in 90% with chronic gastritis affecting the antrum non-spore forming, curvilinear gram negative rod, 3.5 x 0.5 microns Colonizes 50% of asymptomatic American adults by age 50; 80% of Puerto Rican adults Most people with H. pylori infection in North America have gastritis but no symptoms

Has adapted to niche provided by gastric mucus by motility (flagella) to swim through viscous mucous, urease to buffer gastric acid, adhesin to bind to gastric epithelial cells (better binding with cells that express type O antigen)

H. pylori sits on surface or in lumen, needs acid to survive, otherwise urease causes pH to be too high Biopsy - Toludine blue stain, silver stain Urease test, Breath test.

Helecobacter pylori

Present in superficial mucus layer and along microvilli of epithelial cells; are NOT invasive; are usually not seen in areas of intestinal metaplasia; associated with chronic inflammatory infiltrate with germinal centers (follicular gastritis) and plasma cells in lamina propria;

Ulcers: breach in mucosa of GI tract Extends from muscularis mucosae into submucosa or deeper Peptic ulcer: chronic, usually solitary, due to acid-peptic juices Remitting relapsing lesions Middle aged to older adults M : F – 3 : 1 for duodenal ulcers 2 : 1 for gastric ulcers

Peptic ulcer disease

Duodenum – 1st part antrum, GE junction, margins of gastrojejunostomy, adjacent to Meckel diverticulum containing ectopic gastric mucosa, lower esophagus

Imbalance b/w mucosal defense mech & damaging forces mucosal injury due to Helicobacter pylori infection – all duodenal ulcers & 2/3 rd gastric ulcers NSAID use, alcohol, bile/pancreatic juice reflux smoking, corticosteroids use, Zollinger-Ellison syndrome (multiple peptic ulcerations in stomach, duodenum and jejunum due to excess gastrin secretion by a tumor),

Impaired defenses – ischemia,shock Hyperacidity present in a minority of duodenal ulcers and only rarely in gastric ulcers

usually < 4 cm, Round to oval, punched out defect clean base (due to peptic enzymes), surrounded by erythematous mucosa Presence of thrombosed artery or blood vessel at base Scarring – puckering of surrounding mucosa

gastritis; H. pylori; Ulcer may be transmural or limited to mucosa and submucosa 4 zones in active ulceration1) thin layer of necrotic debris 2) nonspecific acute inflammation 3) granulation tissue 4) fibrosis

Clinical features
Epigastric pain – burning or aching worse at night Usually 1 to 3 hrs after meals Relieved by alkalis or food Referred pain- back or lt upper quadrant Anemia Frank hemorrhage Perforation Nausea, vomiting, belching, wt. loss

Gastric Ulcer

Peptic ulcer - Endoscopy

Duodenal Peptic Ulcer

Gastric Ulcer

Gastric Ulcer

Gastric Ulcer

Benign Vs Malignant ulcer
Young adults Duration – wks or years Normal or hyperacidity Locatn- lesser curvature pre or pyloric Size < 4 cm Punched out edges Positive response to antacids

Older age Wks or months Normal or hypoacidity Greater curvature pre or pyloric region Usually >4 cm Rolled out edges No response to antacids

Bleeding- frequent & life threatening Perforation Obstruction from - Edema or scarring Pain – excessive


Causes: NSAIDs, steroid use, severe physiologic stress (shock, extensive burns, sepsis, severe trauma, increased intracranial pressure, postintracranial surgery, intensive care unit), post-chemotherapy, post-radiation therapy

Acute gastric ulcer

Stress ulcers
Cushing ulcers: ulcers in esophagus to duodenum associated with intracranial injury or surgery; have high incidence of perforation Curling ulcer: stress ulcer in proximal duodenum associated with severe burns or trauma Stress ulcers heal in days-weeks

Morphologic types of Carcinoma Stomach
Fungating Ulcerating Diffuse

Fungating Carconoma Stomach

Gastric Adenocarcinoma

Linitis Plastica – Schirrhous Carcinoma diffuse.

Spread of Gastric Ca

“You get ulcer, not from what you eat, but from what’s eating you..!”

Toludine Blue stain – H pylori

Urease production test



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