Condition	Pathology	Clinical features	Morphology	
Esophagus	
Anatomic Anomalies	
Atresia & Fistulas	•	Uncommon & incompatible with life.
•	Associated with congenital heart disease & other gastrointestinal tract malformations.	•	Artesia: a segment of the esophagus is only a thin, noncanalized cord, with blind pouches on either side.
•	Fistula: connects one of the pouches with the trachea or bronchus.	•		
Stenosis, Webs & Rings	•	Stenosis: congenital or acquired in adult life after severe esophageal injury.
•	Mucosal rings: smooth ledges of mucosa & a vascularized fibrous core.	•	Progressive dypshagia	•		
Motor Dysfunction	
Achalasia	•	Present in young adulthood.

Secondary achalasia occurs in:
•	Chagas disease
•	Polio
•	Diabetic autonomic neuropathy
•	Malignancy, amyloidosis, sarcoidosis.	•	Aperistalsis of the esophagus.
•	Partial or incomplete relaxation of the lower esophageal sphincter (LES) with swallowing.
•	Increased resting tone of (LES).
•	Esophageal dilation.
•	Dysphagia & regurgitation.

Complications:
•	Candidal esophagitis
•	Diverticula
•	Aspiration pneumonia.	•	Dilated esophagus above LES.
•	Thickened or thinned muscular wall.
•	Diminished myenteric ganglia.
•	Secondary mucosal damage.	
Hiatal Hernia	•	A saclike dilation of stomach with protrusion above the diaphragm.

Sliding hiatal hernia:
•	90% of cases.
•	Shortened esophagus.
•	Traction of upper stomach into thorax.
•	Bell-like dilation of stomach within thoracic cavity.

Paraesophageal hiatal hernia:
•	<10% of cases.
•	Cardia of stomach dissects alongside esophagus into thorax.
•	Vulnerable to strangulation & infarction.	•	Reported in 1-20% of normal adults.
•	Retrosternal chest pain.
•	Regurgitation of gastric juices.
•	A hiatal hernia may ulcerate or strangulate, causing bleeding or perforation.	•		
Diverticula	•	An outpouching of the alimentary tract that contains one or more layers of the wall, result of motor dysfunction.
•	Pharyngeal: upper esophagus.
•	Traction: more distal location, attributed to fibrosing mediastinal processes or abnormal motility.
•	Epiphrenic: immediately above esophageal sphincter, unknown cause.	•		•		
Lacerations (Mallory-Weiss Syndrome)	•	Longitudinal tears in the esophagus at the esophagogastric junction.
•	Caused by episodes of excessive vomiting in toxic gastritis.
•	Seen most frequently in alcoholics.	•	Potentially massive hematemesis.
•	Inflammation
•	Residual ulcer
•	Mediastinitis
•	Peritonitis
•	Not usually fatal &healing tends to be prompt.	•		
Esophagitis	
Reflux Esophagitis	•	Foremost cause of esophagitis.
•	Decreased efficacy of esophageal antireflux mechanisms
•	Presence of a sliding hiatal hernia.	•	Occurs usually in adults.
•	Dysphagia
•	Heartburn
•	Regurgitation of sour brash
•	Hematemesis
•	Melena
•	Can lead to stricture or Barrett esophagus.	•	Hyperemia & edema
•	Thickening of basal zone & thinning of superficial layers of stratified squamous epithelium
•	Polymorphonuclear or eosinophilic leukocyte infiltrate.
•	Superficial necrosis & ulceration.	
Barrett Esophagus	•	Replacement of distal esophageal squamous epithelium by a metaplastic columnar epithelium, in response to prolonged injury.
•	Inflammation & ulceration of squamous mucosa.
•	Healing is by re-epithelization by pluripotent stem cells.	•	Risk of ulceration & stricture.
•	Risk of adenocarcinoma is 30 times normal.	•	Gross: red, velvety mucosa as irregular circumferential band at gastroesophageal junction, linear streaks or patches in distal esophagus.
•	Histology: mixture of gastric-type & intestinal-type columnar epithelial cells.	
Infectious & Chemical Esophagitis	•	Prolonged gastric intubation
•	Ingestion of irritants: alcohol, excessive hot fluids, smoking.
•	Uremia
•	Bacteremia or viremia: herpesvirus, CMV
•	Fungal infection: candidiasis, mucormycosis, aspergillosis
•	Radiation
•	Cytotoxic anticancer therapy	•		•		
Varices	•	Occur in 90% of cirrhotic patients.
•	Hepatic schistosomiasis is a common cause worldwide.
•	Portal hypertension induce formation of collateral bypass channels through the coronary veins of stomach into eosphageal subepithelial & submucosal veins.	•	Clinically silent until rupture, with hematemesis –fatality rate is 40%.
•	90% chance of recurrence within a year in survivors.	•	Tortuous dilated veins lying within submucosa of distal esophagus & proximal stomach.
•	Irregular protrusion of overlying mucosa into lumen.
•	Superficial ulceration, inflammation, or adherent blood clot.	
Squamous cell carcinoma	•	Occurs in adults older than age 50, more often in men.
•	Pathogenesis is multifactorial.

Dietary:
•	Vitamin deficiency
•	Deficiency of trace metals
•	Fungal contamination of foodstuffs
•	High content of nitrites/nitrosamines
•	Betel chewing

Lifestyle:
•	Alcohol consumption
•	Tobacco use

Esophageal disorders:
•	Long-standing esophagitis
•	Achalasia
•	Long-standing celiac disease.	•	Insidious in onset, symptoms develop late in the course.
•	Dysphagia
•	Obstruction
•	Weight loss
•	Hemorrhage
•	Sepsis, secondary to ulceration
•	Fistula formation into respiratory tree with aspiration.
•	5-year survival: 75% (superficial), 25% (advanced)	•	Being as in-situ lesions: gray-white, plaquelike thickenings or elevations of mucosa.
•	With progression, the lesions extend longitudinally along axis, circumferentially, & deep with invasion.	
Adenocarcinoma	•	One half of esophageal cancers.
•	Evolve through dysplastic change in Barrett mucosa.

Genetic alterations:
•	Overexpression of p53 protein.
•	Allelic losses at 17p.
	•	Arise in patients older than age 40, more commonly in men than in women.
•	Overall 5-year survival is less than 30%; screening programs detect disease earlier.	Gross:
•	Exophytic nodule
•	Excavated & deeply infiltrative.

Histology:
•	Mucin-producing glandular tumors.
•	Diffusely infiltrative signet ring cells.	
Stomach	
Pyloric Stenosis	Congenital pyloric stenosis:
•	Hypertrophy & hyperplasia of circular muscle of muscularis propria of pyloris.
•	Occurs in 1:300-1:900 live births.
•	Male-female ratio is 4:1.

Acquired pyloric stenosis:
•	Long term complication of chronic antral gastritis.
•	Peptic ulcers close to pylorus & malignancy.	•	Visible peristalsis
•	Firm ovoid palpable mass by physical examination.
•	Mucosal edema & inflammation.
•	Regurgitation & vomiting by third week of life.		
Acute Gastritis	•	Chronic use of NSAIDs.
•	Excessive alcohol consumption.
•	Heavy smoking
•	Cancer chemotherapy
•	Ischemic & shock

Mechanism of action:
•	Increased acid production
•	Decreased production of surface bicarbonate buffer
•	Reduced mucosal blood flow, disruption of mucus layer.
•	Direct damage to mucosal epithelium.	•	Asymptomatic or minor abdominal pain.
•	Acute abdominal pain with hematemesis.	•	Moderate edema & hyperemia
•	Entry of neutrophils into epithelial layer
•	Sloughing of superficial epithelium
•	Hemorrhage	
Chronic Gastritis	•	Presence of chronic mucosal inflammatory changes leading to mucosal atrophy & epithelial metaplasia.
•	Chronic infection with Helicobacter pylori.
•	Antibodies to parietal cells.
•	Toxic: alcohol & tobacco
•	Postsurgical: reflux of bile.
•	Granulomatous conditions: Crohn disease	•		•		
Autoimmune Gastritis	•	Antibodies to gastric parietal cells.
•	Associated with Hashimoto thyroiditis & Addison disease.	•	Few symptoms
•	Nausea & vomiting
•	Upper abdominal discomfort
•	Overt pernicious anemia is rare
•	Long-term risk of cancer: 2-4%	•	Reddened, coarse-textured mucosa.
•	Inflammatory infiltrate of lymphocyte & plasma cells in lamina propria.
•	Variable atrophy.
•	Metaplasia to intestinal-type epithelium.
•	Dysplasia	
Peptic Ulcer disease	•	A breach in the mucosa of the alimentary tract that extends through the muscularis mucosa into the submucosa or deeper.
•	Produced by an imbalance between gastroduodenal mucosal defenses & damaging forces of gastric acid & pepsin.
•	No genetic tendencies.

Duodenal ulcer is more frequent in patients with:
•	Alcoholic cirrhosis
•	Chronic obstructive pulmonary disease
•	Chronic renal failure

Promotors:
•	Gastric hyperacidity
•	Chronic use of NSAIDs
•	Cigarette smoking
•	Alcoholic cirrhosis
•	Corticosteroids
•	Hypercalcemia	•	Epigastric burning, gnawing or aching pain which is worse at night & 1-3 hours after meals.
•	Nausea & vomiting.
•	Bloating & belching
•	Weight loss

Complications:
•	Anemia
•	Hemorrhage
•	Perforation
•	Obstruction	•	98% of ulcers found in duodenum & stomach in a ratio of 4:1.
•	Gross: a sharply punched-out defect with overhanging mucosal borders & smooth clean ulcer base.

Histology:
•	Thin superficial layer of necrotic debris.
•	Zone of inflammation
•	Granulation tissue
•	Scar
•	Chronic gastritis in surrounding mucosa.	
Acute gastric ulceration	•	Focal, acutely developing gastric mucosal defects.
•	Encountered in shock, extensive burns or severe trauma.
	•	Acute gastric erosions or ulcers	•	Ulcers are <1cm in diameter, multiple & shallow.
•	Ulcer base is brown.	
Hypertrophic Gastropathy	•	Giant cerebriform enlargement of gastric rugal folds, caused by hyperplasia of mucosal epithelial cells.
•	Menetrier disease: surface mucosal cells.
•	Hypertrophic-hypersecretory gastropathy: parietal & chief cells.
•	Gastric gland: secondary to excessive gastrin secretion in Zollinger-Ellison syndrome.	•	Patients are at risk for peptic ulceration.
•	Excess secreted proteins may cause hypoalbuminemia & protein-losing gastroenteropathy.
•	Hyperplastic mucosa may become dysplastic, with risk of adenocarcinoma.		
Benign Tumors	Gastric polyps (90%):
•	Nodule or mass that projects above level of surrounding mucosa.
•	Majority are hyperplastic or inflammatory.
•	Smooth surfaced, sessile or pedunculated with epithelial tubules & cysts.
•	Multiple & are seen in chronic gastritis.

Gastric adenomas (5-10%):
•	Single & maybe sessile or pedunculated.
•	True neoplasm with proliferative dysplastic epithelium.
•	Incidence increases with age.	•			
Gastric Carcinoma	Contributing factors:
•	Diet: lack of refrigeration, use of preservatives, lack of fresh fruit & vegetable.
•	Cigarette smoking
•	Infection by H.pylori leading to chronic gastritis.
•	Autoimmune gastritis
•	Partial gastrectomy

Genetic alterations:
•	Lead to dysplasia of gastric mucosa.
•	Genetic instability in DNA repair genes
•	Expression of telomerase	•	Insidious disease, initially asymptomatic.
•	Weight loss
•	Abdominal pain
•	Anorexia
•	Vomiting
•	Altered bowel habits
•	Dysphagia
•	Anemia
•	Hemorrhage
•	Dissemination to ovaries generate Krukenberg tumors.

Prognosis:
•	Resected early: 90-95% 5-year survival.
•	Advanced: 15% 5-year survival.	Gross locations:
•	Pylorus & antrum: 50-60%
•	Cardia: 25%
•	Body & fundus: 15-25%
•	Lesser curvature: 40%
•	Greater curvature: 12%

Features:
•	Early gastric carcinoma is confined to mucosa & submucosa.
•	Advanced gastric carcinoma extends beyond submucosa.
•	Tumors are exophytic, flat, depressed, or excavated.

Intestinal subtype:
•	Gland-forming columnar epithelium.
•	Mucin-producing.
•	Polypoid expansile growth pattern.
•	Mean age: 55
•	Male-female ratio: 2:1

Diffuse subtype:
•	Poorly differentiated
•	Single signet-ring cells
•	Mucin-producing
•	Infiltrative growth patterh
•	Mean age: 48
•	Male-female ratio: 1:1	
Small and Large Intestines	
Congenital Anomalies	
Meckel Diverticulum	•	A blind pouch leading off the alimentary tract, lined by mucosa.
•	Persistence of the vitelline duct leaves a solitary diverticulum 30cm from the ileocecal valve.	•	Usually asymptomatic
•	May intussuscept, incarcerate or perforate.		
Hirschsprung Disease	•	Arrested migration of neural crest cells into gut.
•	Functional obstruction & dilation proximal to affected segment.
•	Male-female ratio: 4:1
•	Associated with Down syndrome

Acquired megacolon:
•	Chagas disease
•	Bowel obstruction
•	Inflammatory bowel disease
•	Psychosomatic disorders
	•	Failure to pass meconium in neonate.
•	Abdominal distention.
•	Risk of perforation, sepsis & enterocolitis with fluid derangement.	•	Absence of ganglion cells & ganglia in muscle wall & submucosa of affected segment.
•	Rectum is always affected.
•	Progressive dilation & hypertrophy of unaffected proximal colon.	
Enterocolitis	
Diarrhea & Dysentery	•	Diarrhea: daily stool production in excess of 250gm, containing 70-95% water.
•	Dysentery: low-volume, painful diarrhea.

Secretory:
•	Infectious
•	Neoplastic

Osmotic:
•	Disaccharidase deficiencies
•	Prescribed gut lavage
•	Latulose therapy
•	Antacids

Exudative:
•	Infectious: bacterial damage to mucosal epithelium
•	Idiopathic inflammatory bowel disease

Malabsorption:
•	Defective intraluminal digestion
•	Infectious: Giardia lamblia
•	Lymphatic obstruction

Deranged motility:
•	Decreased intestinal transit time
•	Decreased motility	•			
Viral Gastroenterocolitis	•	Rotavirus
•	Enteric adenoviruses
•	Astroviruses
•	Norwalk virus	•	Incubation period ranges from hours to several days.
•	Acute illness occurs from 1-7 days.
•	Anorexia, headache & fever.		
Bacterial enterocolitis	•	Ingestion of preformed toxin in contaminated food: S.aureus, Vibrios, Clostridium perfringens.
•	Infection by toxigenic organisms
•	Infection by enteroinvasive organisms.

Mechanism:
•	Bacterial adhesion & replication
•	Enterotoxins: secretagogues & cytotoxins
•	Invasion: E.coli, Shigella, Salmonella & Yersinia enterocolitis	•	Ingestion of toxins: explosive diarrhea & abdominal pain within hours.
•	Infection with enteric pathogens: incubation period of hours to days, followed by diarrhea, dehydration or dysentery.
•	Insidious infection: Yersinial & mycobacterial infection.	•	Salmonella: ileum & colon with Peyer patch involvement.
•	Shigella: colonic inflammation, erosion & exudate.
•	Campylobacter jejuni: small intestine, appendix, colon, ulcers, inflammation & exudate.
•	Y.enterocolitica: ileum Peyer patches, appendix, colon, & mesenteric lymph nodes with necrotizing granulomas & systemic spread.	
Necrotizing enterocolitis	•	Acute, necrotizing inflammation of small intestine & colon in low-birth-weight or premature neonates.
•	Result of immaturity of immune system, initiation of oral feeding, mucosal injury & impaired intestinal blood flow.
	•	Mild gastrointestinal illness
•	Fulminant illness with gangrene, perforation, sepsis & shock.
	•	Mucosal edema
•	Hemorrhage
•	Necrosis	
Pseudomembranous Colitis	•	Acute colitis caused by toxins of C.difficile in setting of antibiotic therapy.
•	Formation of an adherent inflammatory membrane.	•		•	Plaquelike adhesion of fibrinopurulent necrotic debris & mucus to damaged colonic mucosa.	
Parasite-caused Inflammatory disorders	Nematodes: 
•	Strongyloides
•	Ascaris
•	Hookworms

Flatworms:
•	Tapeworms
•	Flukes

Protozoa:
•	Entamoeba histolytica
•	Giardia lamblia

AIDS patients:
•	Microsporidia
•	Crytosporidia	•		•		
Malabsorption	•	Characterized by suboptimal absorption of fats, fat-soluble & other vitamins, proteins, carbohydrates & electrolytes.
•	Result of disturbed intraluminal & terminal digestion, transepithelial transport through enterocyte.	•	Diarrhea
•	Flatus
•	Pain
•	Weight loss
•	Passage of bulky, frothy, greasy stools
•	Anemia & bleeding
•	Osteopenia & tetany
•	Ameorrhea, impotence & infertility
•	Purpura & petechia, edema, dermatitis
•	Peripheral neuropathy
•	Hyperparathyroidism	•		
Celiac Spruce	•	A chronic disease with small intestinal mucosal lesion & impaired nutrient absorption.

Pathogenesis:
•	Sensitivity to gluten, which contains the gliadin protein component shared by wheat, oat, barley & rye.
•	Genetic susceptibility: 90-95% of patients express DQw1 & HLA-B8.
•	Immune-mediated: cross reactivity with type 12 adenovirus.	•	Diarrhea
•	Flatulence
•	Weight loss
•	Fatigue

Complications:
•	Iron & vitamin deficiencies
•	10-15% of gastrointestinal lymphoma, usually T-cell.	•		
Tropical Spruce	•	Occurs almost exclusively in people living in tropics.
•	Responds to long-term board-spectrum antibiotic therapy.	•		•	Lamina propria has abundant lymphocytes & more eosinophils than celiac disease.
•	Brunt of injury is distal in contrast to celiac disease	
Whiple disease	•	Rare, systemic condition involving intestine, CNS & joints.
•	Due to infection by Tropheryma whippelii, a gram-positive actinomycete.	•	Diarrhea
•	Steatorrhea
•	Abdominal cramps
•	Fever
•	Weight loss
•	Migratory arthritis	•	Small intestine mucosa is laden with distended macrophages in lamina propria & in lymphatics, joints & brain.
•	Rod-shaped bacilli.
•	Inflammation is absent.	
Disaccharidase deficiency	•	An apical membrane enzyme of surface absorptive cells.
•	Deficiency: lactose remains in lumen & exerts osmotic effect.	•	Diarrhea
•	Malabsorption	•	No abnormalities of mucosa.	
Abetalipoproteinemia	•	Familial autosomal recessive inheritance.
•	Inability to synthesize apoproteins required for lipoprotein export from mucosal cells – lipid vacuolation
•	Depressed levels of chylomicrons VLDL & LDL.	•	Failure to thrive
•	Diarrhea
•	Steatorrhea	•		
Idiopathic Inflammatory Bowel Disease:
•	Crohn disease: granulomatous disease affecting any portion of gut.
•	Ulcerative colitis: colonic disease, no granulomas	
Crohn Disease	•	Sharply delimited & transmural involvement of the bowel by inflammatory processes with mucosal damage.
•	Presence of noncaseating granulomas.
•	Fissuring & fistula formation.	Intermittent attacks of:
•	Diarrhea
•	Fever
•	Abdominal pain
•	Anorexia & weight loss

Complications:
•	Fibrotic strictures
•	Fistulas to adjacent viscera
•	Abdominal & perianal skin
•	Loss of abdumin
•	Vitamin B12 deficiency with pernicious anemia
•	Malabsorption of bile salts with steatorrhea.

Systemic manifestations:
•	Migratory polyarthritis
•	Sacroilitis
•	Ankylosing spondylitis
•	Erythema nodosum
•	Uveitis
•	Cholangitis
•	Amyloidosis
•	Risk of bowel cancer	Gross:
•	Granular serosa with adherent creeping mesenteric fat.
•	Rubbery thick intestinal wall with edema, inflammation, fibrosis, muscular hypertrophy & stricture.
•	Mucosal punched-out ulcers.
•	Tendency to fistula & sinus tract formation.
•	Skip lesions: affected areas with intervening normal areas.

Histology:
•	Mucosal inflammation with intraepithelial neutrophils & crypt abscesses, laminar propria mononuclear inflammation.
•	Ulceration.
•	Chronic mucosal damage: villus blunting, atrophy, metaplasia.
•	Transmural inflammation with lymphoid aggregates.
•	Noncaseating granulomas
•	Fibrosis, muscle & neural hypertrophy, vasculitis.	
Ulcerative Colitis	•	Affects only mucosa & submucosa of colon.
•	Extends in a continuous fashion.
•	Granulomas are absent.	•	Intermittent attacks of bloody mucoid diarrhea.
•	Migratory polyarthritis
•	Sacroilitis
•	Ankylosing spondylitis
•	Uveitis
•	Cholangitis
•	Primary sclerosing cholangitis
•	Skin lesions
•	Risk of carcinoma higher in patients with colitis > 10 years.	Gross:
•	Extends retrograde from rectum to involve entire colon in a continuous fashion.
•	Mucosa may be reddened, granular or friable with inflammatory pseudopolyps.
•	No mural thickening or stricture.

Histology:
•	Crypt abscesses
•	Ulceration
•	Chronic mucosal damage & atrophy
•	Epithelial dysplasia may progress to carcinoma.	
Vascular Disorders	
Ischemic Bowel Disease	Predisposing conditions:
•	Arterial thrombosis: atherosclerosis, vasculitis, dissecting aneurysm.
•	Arterial embolism: cardiac vegetations.
•	Venous thrombosis: hypercoagulable states, cirrhosis, sepsis
•	Nonocclusive ischemia: cardiac failure, shock, dehydration.	•	Total infarction: 50-75% death rate.
•	Occurs in severely ill patients.
•	Severe abdominal pain & tenderness.
•	Bloody diarrhea
•	Nausea & vomiting
•	Bloating & abdominal wall rigidity	Transmural infarction:
•	Infarction of all bowel layers.
•	Bowel segment in hemorrhagic.
•	Bowel appears rubbery & dusky.
•	Bacteria produce gangrene.
•	Perforation develops within days.

Mural & mucosal infarction:
•	Incomplete necrosis or necrosis of mucosa only.
•	Mucosa appears hemorrhagic.
•	Distribution is patchy.

Chronic ischemia:
•	Cause mucosal inflammation, ulceration, fibrosis & stricture.
•	Segmental patchy distribution.	
Angiodysplasia	•	Tortuous, abnormal dilations of submucosal veins that dilate into lamina propria, cecum & ascending colon.
•	Tend to bleed.
•	Due to partial, intermittent occlusion of submucosal veins in the cecum & ascending colon.	•		Range from small, focal ectasias to large, dilated, tortuous venous formation.	
Hemorrhoids	•	Variceal dilation of anal & perianal submucosal venous plexuses.
•	Associated with constipation, venous stasis of pregnancy & cirrhosis.	•		•	Ectasia of inferior hemorrhoidal plexus below anorectal line.
•	Secondary thrombosis, strangulation or ulceration with fissure.	
Diverticular Disease	•	Acquired diverticula may occur anywhere in gut.
•	Focal weakness in bowel wall at sites of penetrating blood vessels.
•	Increased intralaminal pressure from exaggerated peristaltic contractions.
•	Diverticulitis: inflammation of diverticulum after obstruction or perforation.	•	Usually asymptomatic.
•	Cramping, abdominal discomfort & constipation.
•	Diverticulitis: pericolic abscesses, sinus tracts & peritonitis.	•	Multiple flasklike outpouchings 0.5-1cm in diameter in distal colon.
•	Occur alongside taeniae coli & dissect into appendices epiploicae.
•	Muscularis of intervening bowel wall is hypertrophic.	
Intestinal Obstruction	
Hernias	•	Weakness or a defect in wall of peritoneal cavity permits protrusion of a peritoneal sac.
•	Segments of viscera become trapped in them.
•	Sites: inguinal & femoral canals, umbilicus, surgical scars, retroperitoneal	•	Stasis & edema leads to incarceration.
•	Vascular compromise leads to strangulation.	•		
Adhesions	•	Localized peritoneal inflammation after surgery, infection, endometriosis or radiation.
•	Healing leads to fibrous bridges between viscera.	Complications:
•	Internal herniation
•	Obstruction & strangulation of viscera.	•		
Intussusception	•	Telescoping of one segment of intestine into immediately distal segment.
•	Children: spontaneous & reversible.		•		
Volvulus	•	Complete twisting of a bowel loop about its mesenteric base.
•	Obstruction & infarction.
•	Occurs in small bowel or redundant loops of sigmoid colon.		•		
Tumors of the Small and Large Intestine	
Small intestinal neoplasms	•	3-6% of tumors
•	Benign lesions: leiomyomas, adenomas, lipomas, neuromas & hamartomas.
•	Adenomas frequently occur in the region of ampulla of Vater, especially in patients with polyposis syndromes.	•	Adenomas are silent, unless they obstruct the intestinal lumen or common bile duct.
•	Cramping pain
•	Nausea & vomiting
•	Bleeding
•	Spread of mesentery, regional lymph nodes & liver.
•	5-year survival is 70% with wide en bloc excision.	•		
Non-neoplastic polyps	•	90% of epithelial polyps in colon.

Hyperplastic polyp:
•	Found in more than one half of persons older than 60 years.
•	Nipple-like protrusions less than 5mm in diameter.
•	Composed of well-formed mature glands & scant lamina propria.

Juvenile polyp:
•	Focal hamartomatous malformations of small intestine & colon mucosa, usually sporadic.
•	Occur in children less than 5 years old.
•	Rare juvenile polyposis syndrome: large (1-3cm) & numerous, autosomal dominance, pedunculated with cystically dialated glands & increased risk of adenocarcinomas.

Peutz-Jeghers polyp:
•	Hamartomatous mucosal polyps of small intestine & colon, often sporadic.
•	Rare Peutz-Jeghers syndrome exhibits autosomal dominance, melanotic pigmentation of mucosal & skin surfaces, & increased risk of carcinoma.
•	Large, pedunculated, lobulated polyps with arborizing smooth muscle surrounding normal abundant glands.	•		•		
Adenomas	•	Prevalence: 50% after age 60.
•	Frequently multiple.
•	Arise as the result of epithelial dysplasia.
•	Histologic subtype: tubular, villous & tubulovillous
•	Large villous adenomas are more likely to harbor severe dysplasia or carcinoma.
•	Adenomas are slow growing.

Risk of malignancy is correlated with:
•	Polyp size
•	Histologic architecture
•	Severity of dysplasia	•	May be asymptomatic or cause anemia & occult bleeding.
•	Small intestine: adenomas may cause obstruction & intussusception.
•	Severe dysplasia
•	Intramucosal carcinoma is still confined to mucosa; has little or no metastatic potential.
•	Invasive adenocarcinoma is a malignant lesion with metastatic potential as it has crossed into submucosa.
•	Only adequate treatment for any adenoma is resection.	•	90% of adenomas are in the colon.

All adenomas exhibit:
•	Dysplastic epithelium
•	Tall hyperchromatic disorderly cells with increased nuclear-cytoplasmic ratio, cigar-shaped nuclei.

•	All adenomas may harbor intramural or intramucosal carcinoma.

Tubular adenomas:
•	Involve only a few adjacent crypts.
•	Become bulky neoplasms with growth & protrude into lumen.
•	Branching dysplastic glands are embedded in lamina propria.

Villous adenomas:
•	Larger than tubular adenomas.
•	May carpet up to 10cm of colonic mucosa.
•	Finger-like projections are lined by dysplastic epithelium with a lamina propria core.	
Familial syndromes	Familial adenomatous polyposis:
•	Innumerable adenomatous polyps in colon.
•	Risk of progression to adenocarcinoma is 100%.
•	Minimum of 100 colon adenomas required for diagnosis.
•	Prophylactic colectomy is curative.
•	Average age of onset: teens to 20s.
•	Progression to cancer occurs in 10-15 more years without surgery.

Gardner syndrome:
•	A familial adenomatous polyposis variant.
•	Exhibits multiple osteomas, epidermal cysts, fibromatosis, abnormal dentition & higher frequency of duodenal & thyroid cancer.

Genetic alterations:
•	Somatic mutation in tumor-suppressor APC gene.
•	Inherited mutations in DNA mismatch repair genes in hereditary nonpolyposis colorectal cancer syndrome.
•	DNA methylation: loss of DNA methyl groups occurs early in colonic cancer.
•	Mutations of K-ras gene & other oncogenes.
•	Losses on 18q & 17p.
•	Expression of telomerase.	•		•		
Colorectal Carcinoma	•	Arise in polypoid adenomas
•	Hereditary nonpolyposis colorectal syndrome.

Risk of cancer is associated with:
•	Excess energy intake.
•	Low vegetable fiber intake.
•	High content of refined carbohydrates.
•	High intake of red meat.
•	Decreased intake of vitamins A, C, E.	•	Asymptomatic for years.
•	Fatigue
•	Weakness
•	Iron deficiency anemia
•	Abdominal discomfort
•	Progressive bowel obstruction
•	Liver enlargement
•	Prognosis is based on extent of invasion at diagnosis
•	5-ear survival depends on depth of penetration & lymph node involvement; 100% for lesions limited to mucosa & 25% of extensively invasive tumors.
•	Surgery is only hope for cure.	Sites of occurrence:
•	Cecum/ascending colon: 38%
•	Transverse colon: 18%
•	Descending colon: 8%
•	Rectosigmoid: 35%
•	Multiple sites: 1%

Presentation:
•	Polypoid, fungating masses
•	Annular, encircling masses.
•	Poorly differentiated neoplastic cells.
•	Tumors incite inflammation & fibrosis of mesenchyme.
•	Minority produces copious mucin.
•	Foci of neuroendocrine differentiation, signet-ring features or squamous differentiation.	
Carcinoid Tumors	•	Tumors of gut endocrine cells.
•	Peak incidence: 50s
•	Appendiceal, rectal carcinoids seldom metastasize.
•	Ileal, gastric, & colonic carcioids are often aggressive.	•	Usually asymptomatic
•	Symptoms occur from obstruction & bleeding.
•	Inconstant secretory products: gastrin, ACTH & insulin.
•	Carcinoid syndrome arises from tumor secretion of serotonin & seen only with metastases or with carcinoids outside of gut.

Features of Carcinoid syndrome:
•	Vasomotor: flushing, cyanosis
•	Intestinal hypermotility: diarrhea, cramps, nausea & vomiting
•	Asthmatic bronchoconstriction: cough, wheezing, dyspnea
•	Hepatomegaly: hepatic metastases.
•	Systemic fibrosis: pulmonic & tricuspid valve thickening & stenosis, endocardial fibrosis.
•	Diagnosed by excess 5-hydroxyindoleacetic acid.	•	Intramural or submucosal masses: small, firm & yellow-tan.
•	Appendix & rectum: solitary masses; elsewhere, there tend to be multiple nodules.
•	Nodules may cause kinking & obstruction of intestine.
•	Metastases tend to be small & dispersed.

Histology:
•	Discrete islands, trabeculae, glands.
•	Sheets of monotonou uniform cells with scant, pink, granular cytoplasm.
•	Oval, stippled nuclei, separated by a fibrous stroma.	
Gastrointestinal Lymphoma	•	Gut is most common location: 40% of lymphomas other than lymph nodes.

Predisposing factors:
•	Chronic spruelike malabsorption syndromes
•	Natives of Mediterranean region
•	Immunodeficiency states.

Sporadic lymphomas:
•	Stomach: 55-60%
•	Small intestine: 25-30%
•	Colon: 20-25%

Spruce-associated lymphomas:
•	Affects younger individuals (30-40 years).
•	Long duration of malabsorption disorders.
•	Usually T-cell lymphoma.
•	Poor prognosis

Mediterranean lymphoma:
•	B-cell lymphoma in children & young adults of Mediterranean ancestry.
•	Background of chronic diffuse mucosal plasmacytosis.
•	Prognosis is poor.	•	Sporadic lymphomas are amenable to surgical resection & are chemoresponsive.
•	Lymphomas associated with H.pylori infection may be treatable by eradication of H.pylori.	•	Early lesions are plaquelike expansions of mucosa & submucosa.
•	Advanced lesions are full-thickness mural lesions or polypoid, fungating masses protruding into lumen.
•	Atypical lymphocytes infiltrate mucosa & wall.	
Appendix	
Acute Appendicitis	•	Most common cause of abdominal condition requiring surgery.

Obstruction of lumen:
•	Due to fecalith, calculus, tumor, worms
•	Predisposes to buildup of intraluminal pressure, ischemic injury & bacterial invasion.	•	Mainly a disease of adolescents & young adults.
•	Periumbilical pain, then localizing to right lower quadrant.
•	Nausea or vomiting
•	Abdominal tenderness
•	Mild fever
•	Leukocytosis
•	False-positive clinical diagnosis rate of 20-25%.

Complications:
•	Perforation
•	Pyelophlebitis
•	Thrombosis of portal venous drainage
•	Liver abscess
•	Bacteremia

Mimics:
•	Enterocolitis
•	Mesenteric lymphadenitis
•	Acute salpingitis
•	Ectopic pregnancy
•	Cystic fibrosis
•	Meckel diverticulitis	Early acute appendicitis:
•	Scant neutrophil exudations throughout mucosa, submucosa & muscularis.
•	Congestion of subserosal vessels
•	Perivascular neutrophil emigration.
•	Serosa is dull, granular & red.

Advanced acute appendicitis:
•	More severe neutrophilic infiltration.
•	Fibrinopurulent serosal exudate
•	Luminal abscess formation with ulceration & suppurative necrosis
•	Further worsening leads to gangrenous necrosis followed by rupture.	
Tumors of Appendix	Mucocele:
•	Dilation of appendiceal lumen by mucinous secretions.
•	Caused by mucosal hyperplasia.
•	Nonneoplastic elongated columnar mucous cells produce copious mucin.

Mucinous cystadenoma:
•	Neoplastic mucin-producing columnar epithelium.
•	Mechanical distention leads to appendiceal rupture & spillage of mucin & neoplastic cells into abdomen.

Mucinous cystadenocarcinoma:
•	Invasion of appendiceal wall by non-malignant neoplastic cells.
•	Spread beyond appendix as peritoneal implants.
•	Peritoneal cavity becomes distended with semisolid, mucin-containing anaplastic adenocarcinoma cells.	•			
Peritoneum	
Inflammation	•	Sterile peritonitis: result from spillage of bile or pancreatic enzymes.
•	Surgical procedures: incite foreign body reaction followed by development of adhesions.
•	Endometriosis: introduce irritant blood into peritoneal cavity.	•			
Peritoneal Infection	Causes:
•	Appendicitis
•	Ruptured peptic ulcer
•	Cholecystitis
•	Diverticulitis
•	Bowel strangulation
•	Acute salpingitis
•	Abdominal trauma
•	Peritoneal dialysis
•	Perforated inflammatory conditions of intestines
•	Ascites
•	Nephrotic syndrome in children
•	Cirrhosis in adults	•	Infection may heal spontaneously or with therapy.
•	Residual, walled off abscess may persist, serving as foci for new infection.
•	Exudate may organize, leaving fibrous adhesions.	•	Dull, gray transformation of normally glistening peritoneal membranes.
•	Development of exudate & outright suppuration.
•	Localized abscesses
•	Inflammation remains superficial
•	Tuberculous peritonitis: plastic exudate with myriad minute granulomas.	
Sclerosing Retroperitonitis	•	Dense fibromatous overgrowth of retroperitoneal tissues.	•	Overgrowth may encroach on ureters (leading to hydronephrosis) or bowel segments.	•	Fibrous overgrowth is infiltrative accompanied by inflammatory cells.