ESOPHAGEAL PATHOLOGY
Esophogus: Normal Anatomy
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Extends from C6 to T11/12
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10-11 cm long in infants, 25 cm long in adults
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Endoscopy measures from incisors
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3 points of contriction:
u Cricoid Cartiladge
u Under left mainstem bronchus
u Diaphragm
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No serosa; lesions easily spread
Esophagus: Benign Pathology
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Fistulas
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Heterotopic Tissue
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Rings & Webs
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Diverticula
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Hiatal Hernia
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Lacerations
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Varicies
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Dysmotility
CONGENITAL ANOMALIES:
TRACHEOESOPHAGEAL FISTULA
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Segmental absence of esophageal canalization
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May end in blind pouches, or may communicate with the trachea forming a fistula.
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Complications: aspiration  pneumonia, asphyxia †
Esophagus: Heterotopic Tissue
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Gastric Mucosa
u Most common just distal to the cricoid cartiladge
u May ulcerate
u May give rise to adenocarcinoma
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Salivary Gland
u RARE
u Usually middle to distal 3rd
ESOPHAGUS: WEBS AND RINGS
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Exaggerated mucosal folds
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Sx: dysphagia
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Upper (above aorta): “webs”
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Lower (distal 5 cm): “rings”
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Plummer-Vinson syndrome:
u web, glossitis, iron-deficiency anemia
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Webs
u Usually women
u Usually > 40 yrs old
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Rings
u Most commonly at the EG juction
u Usually 2-4 mm thick and protrude 5mm
ESOPHAGUS: DIVERTICULA
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Location: upper at junction with pharynx (“Zenkers”), middle & lower thirds (“Traction”)
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Mechanism: acquired lumen pressure 
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Sx: positional regurgitation – food looks like what you ate = no digestion
HIATAL HERNIA
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Sliding: 90%
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Rolling (paraesophageal): 10%
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Symptoms: heartburn
u Gastric juice reflux
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Complications: bleed, infarct
Esophagus: Lacerations and Varicies
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Lacerations (Mallory Weiss Syndrome
u Occur following fits of vomiting, most common in alcoholics
u May be full thickness
u Account for 5-10 % of massive hematemesis
u Linear, oriented longitudinally from GE junction
u Cause: relaxation failure during prolonged vomiting.
u Complication: rupture  left thorax (Boerhaave’s syndrome)
ESOPHAGEAL VARICES (1)
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Dilated valcular channels from portal hypertension (cirrhosis)
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Causes massive hematemesis with a 40% fatality rate
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Conditions:
thrombosis of portal veins
u thrombosis of hepatic veins
u cirrhosis
u Cancer
ESOPHAGEAL VARICES (2)
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Rx:
u Primary prophylaxis: PharmacoRx:
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▬ reduce portal vein pressure with beta blockers and also vasodilators. May add endoscopic ligation/thombosis.
Acute bleeding: PharmacoRx: octreotide (“synthetic somatostatin”)
▬ Endoscopy: ligation or scleroRx; balloon tamponade: rescue only — “last resort”
Rx (cont.):
u Prevent recurrent bleeding:
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beta blockers plus vasodilator isosorbide mononitrate plus endoscopic procedure (ligation; scleroRx).
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Surgical shunts (portocaval or splenic vein anastomosis to renal veins) rapidly being replaced by pharmacoRx &
endoscopy.
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TIPS (transjugular portosystemic shunt) now used only to “buy time” for liver transplantation (survival 85% 1 yr, 60%
5 yr).
Dysmotolity: ACHALASIA
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Motor dysfunction causing decreased peristalsis, incomplete relaxation of LES, and increased basal LES tone.
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Other causes: Myenteric plexus absent for unknown reasons orChagas’ disease
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Complications: aspiration, cancer (2-7%)
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Rx:
u Dilatation (but unsatisfactory)
u Botulinum toxin (paralytic agent) injection into lower esophageal sphincter (experimental)
u Surgical myotomy
GASTRO-ESOPHAGEAL REFLUX (GERD)
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Reflux of gastric content ® esophagus
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Older age group
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Sx: "Heartburn"
u Mechanism: Esophageal sphincter tension ¯ ;
delayed gastric emptying; drugs, cough
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Dx: Sx, esophageal pH monitor, biopsy
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Complications: Barrett's esophagus
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Rx: Medical: Positional; drugs to ¯ gastric secretion.
Endoscopic surgical “pleating”
BARRETT ESOPHAGUS
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Columnar/Gastric epithelium in esophagus
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Reflux ® esophagitis ® healing ® metaplasia ® glandular epithelium
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Complications: esophageal epithelium ® ulceration
® stricture
® dysplasia ® adenocarcinoma 8-10%
® no adequate, noninvasive screening test
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Pulmonary complications: Acid laryngitis; asthma & pulmonary fibrosis?
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“Short segment” Barrett’s = metaplasia < 3 cm from G-E junction
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Complications: esophageal epithelium ® ulceration
ESOPHAGUS: STENOSIS
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Congenital
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Acquired:
u Post-inflammatory
▬
u
u
lye
▬ ulcer (reflux)
Scleroderma (systemic sclerosis)
Neoplasm
ESOPHAGUS: CANCER
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Cause:
u mucosal erosion  repair  dysplasia  carcinoma
u Exposure:
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Acid reflux
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Alcohol (especially concentrated alcoholic drinks)
▬ Smoking = squamous cell carcinoma
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Geographic frequency differences
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Location: 50% middle third, 30% lower, 20% upper
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Types: SCC 80-85%, adenocarcinoma 10%
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Past 3 decades:  incidence of adenocarcinoma (Barrett?)
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Polypoid, ulcerative, diffuse
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Sx: obstruction
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Complications: aspiration, bleed, invasion
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Invasion: tracheo-esophageal fistula; artery
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Mets: nodes, late-distant
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Rx:
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Resectable less than 50%
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ChemoRx
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Radiation Rx
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Prognosis: 30% 1 yr; 5-10% 5 yr
Adenocarcinoma
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Predominantly white and male (5:1)
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Occurs most commonly in the middle to lower 3rd, and often at the GEJ.
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Vast majority arise from Barrett’s.
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Often appers as a nodular mass with intact epithelium.
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As with SCC, usually quite advance at diagnosis.
Gastric Pathology
STOMACH: CONGENITAL LESIONS
 Diaphragmatic hernia: viscera in chest often fatal at birth (lung compression  pulmonary hypoplasia)
 Pyloric stenosis — pyloric muscle hypertrophy
 Cause: ¯ nitric oxide (smooth muscle relaxant) synthase
 Clinical features:
○ Projectile vomiting second week
○ Visible abdominal peristalsis
○ Mass (palpation (olive), ultrasound; radiology)
 Male/female = 4:1; familial
 Rx: antral muscle incision — pyloromyotomy (Ramstedt)
STOMACH: INFLAMMATORY LESIONS
 Acute Gastritis
 Causes:
 NSAIDS block prostaglandin synthesis  microvascular injury  focal mucosal necrosis
 ETOH
 smoking
 uremia
 Stress ulcers:
 sepsis, brain (Cushing’s)
 burns (Curling’s), shock, trauma
Chronic Gastritis
 Autoimmune Gastritis
 Involves Fundus, Antrum usually spared
 Antibodies to Parietal Cells/Intrinsic Factor present
 ê HCL, Gastrin, and Parietal cells
 Significant atrophy
 10% will develop pernicious anemia
 Associated with other autoimmune disorders
 Helicobacter Pylori Gastritis
 No associated antibodies or PA (pernicious anemia)
 FOUR TIMES MORE COMMON
 inimal fundic involvement
 Involves the antrum predominantly
 Hyperacidity, duodenal ulcers may be present.
 Normal Gastrin levels
 H. pylori has four virulence factors:
 Flagella (can swim in mucin)
 Urease (elevate local pH)
 Adhesins
 Toxins
 Environmental (non-specific)
 MOST COMMON
 Involves antrum and fundus
 Strong association with atrophy, metaplasia, and carcinoma
 Related to ETOH use
 The Histologic View:
 Chronic Superficial:
 Superficial inflammation and mild flattening
 Chronic Atrophic:
 Full thickness inflammation with atrophy of glands
 Gastric Atrophy
 No further inflammation
 End stage of CG
PEPTIC ULCER DISEASE: CAUSES
 Helicobacter pylori ,NSAIDS, HCl 
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Peptic Ulcers
Usually a solitary lesion
Most commonly in 1st part of duodenum (80%), lesser curvature of stomach (20%)
Appear oval with over-hanging mucosal margins
Nearly all have antral gastritis (HP), those who don’t are usually NSAID users
5% fatality rate (70% perf, 10% bleed)
M>F
Duodenal Ulcers:
 Genetic influences appear at work
 increased HCL, and gastric emptying
 Anterior wall of duodenum most common
Gastric Ulcers:
 No apparent genetic influences
 Low to normal HCL
 1-3 % delelope CA
PEPTIC ULCER: DIAGNOSIS
 Gastric acidity (duodenal ulcer , gastric ulcer )
 X-ray (5% falsely benign gastric ulcer)
 [Problem: benign vs. carcinoma in gastric]
 Endoscopy (biopsy and cytology)  $ but provides definitive diagnosis
PEPTIC ULCER: THERAPY
 Eradicate H. pylori
 Maintenance Rx necessary only if eradication fails or recolonization occurs
 If NSAIDS responsible, discontinue or substitute
 Antisecretory Rx
 Zollinger-Ellison syndrome: excise gastrinoma
PEPTIC ULCER: COMPLICATIONS
 Bleeding (chronic anemia; massive:may die) 20%.
 Perforation (peritoneum; pancreas) 3-4%.
 Obstruction <2%.
 ? Cancer ? — only if in stomach and if initially ulcerating carcinoma (benign gastric ulcers do NOT become malignant over time).
PEPTIC ULCER: UPPER GI HEMORRHAGE
 Unrelated to degree of acid production.
 NSAIDS = risk factor. NSAIDS and steroids = risk  10 times.
 Immediate Tx: Drugs don’t help.
 Stabilize hemodynamics
 Endoscopy (thermal contact, injection)
 Surgery (vagotomy; antrectomy)
 Dieulafoy’s lesion: congenital abnormally large artery in center of gastric mucosal erosion within 5 cm of gastroesophageal junction 
bleed
 Rx: Endoscopic cautery
 Recurrence prevention:
 Control H. pylori
 No NSAIDS
HYPERTROPHIC GASTROPATHY
 Pathology: mucosal hyperplasia ® giant rugae
 Menetrier's: M/F = 4/1 mucous glands (foveolar cells)increased ; rugal folds Inc; HCl ¯ decr
 Hypersecretory: mucous, parietal and chief cells Incr, HCl Incr , rugal folds Incr
 Zollinger-Ellison syndrome: rugal folds incre, HCl and gastrin incre, increa (gastrinoma)
HYPERTROPHIC GASTROPATHY
ZOLLINGER-ELLISON SYNDROME
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Definition: gastric HCl hypersecretion and peptic ulceration due to increased serum gastrin secreted by pancreatic (sometimes in
duodenal wall) islet cell tumor (gastrinoma).
 50% > multiple gastrinomas
 10% = multiple ulcers
 60% of gastrinomas malignant (mets  nodes)
 Age: peak 30-50
 10% = MEN I (multiple endocrine neoplasia): adenomas of pancreas, pituitary, parathyroid, and adrenal cortex along with peptic ulcers
 Regulator gene (tumor suppressor) mutation (MEN I). Chromsome 11.
 Dx: serum gastrin , gastric HCL 
 Rx:
 Medical: HCl control
 Surgery: tumor
STOMACH: BENIGN TUMORS
 Gastrointestinal Stromal Cells Tumor (Leiomyoma)
 Ulcerate and bleed.
 Ectopic asymptomatic pancreas (mass)
 Polyps:
 Hyperplastic: benign, inflammatory, non-neoplastic
 Adenomatous: premalignant (carcinoma  > 2 cm)
 Multiple polyps syndromes:
○ FAP: Familial adenomatous polyposis (neoplastic)
○ Peutz-Jeghers (hamartomas)
 Leiomyoma (ulcerate and bleed)
 Ectopic asymptomatic pancreas (mass)
 Polyps:
 Hyperplastic: benign, inflammatory, non-neoplastic
 Adenomatous: premalignant (carcinoma  > 2 cm)
 Multiple polyps syndromes:
○ FAP: Familial adenomatous polyposis (neoplastic)
○ Peutz-Jeghers (hamartomas)
Gastric Adenocarcinoma
 85-90% of gastic ca
 Incidence high in asia, lower in US
 US incidence dropping over several decades.
 Risk factors: salts and nitrates with low fats
 Often presents at advanced stages, only 50% resectable.
 “Virchow’s Node,” mets to left supraclavicular node.
Histologic Types
 Intestinal type: cells cohesive–localized, ulcerate, distal (body & pylorus), related to polyps, H. pylori, atrophic gastritis, intestinal
metaplasia
 Diffuse type (linitis plastica): cells not cohesive; widely & deeply infiltrative, proximal (esophageal-cardial junction).
 10% familial, but only 2% of all gastric Ca = E-cahedrin (CDHI) gene mutations autosomal dominant, signet-ring histology of
early diffuse gastric Ca
 Cause: Role of H. pylori. Hereditary. Diet?
 Sx: 0; weight loss, pain anorexia, anemia, obstruction, Virchow’s node
 Dx: melena, x-ray, endoscopy with biopsy, carcinoembryonic antigen (CEA) (25%), HCl = achlorhydria in 2/3
 Path: superficial (limited to mucosa an submucosa), ulcerative, polypoid, leather-bottle (linitis plastica)
 Tx: surgery
 Mets: nodes, peritoneum, liver, ovaries (Krukenberg)
 Prognosis: five-year survival 5-25% (but “early gastric cancer (EGC)” = 90%)
 Frequency: In USA, distal Ca , proximal  (barrettes?)
STOMACH: LYMPHOMA
 Frequency: 3-5% of all stomach cancer.
 Most common site for G.I. lymphoma
 H. pylori role uncertain, but probably plays a major role
 May be treated with antibiotics (very early if HP related) or radiation alone.