GI Overview

 

I.         Esophagus

a.        Normal

b.        Congenital Abnormalities of Esophagus

                                                               i.      Agenesis

                                                             ii.      Atresia

                                                           iii.      Fistulas

c.        Acquired Abnormalities of Esophagus

                                                               i.      Mucosal webs

                                                             ii.      Schatzki’s ring

                                                           iii.      Stenosis

                                                            iv.      Varices

d.        Lesions ó Motor Dysfunction

                                                               i.      Achalasia

                                                             ii.      Hiatal hernia

                                                           iii.      Diverticula

                                                            iv.      Lacerations

e.        Inflammatory conditions (Esophagitis)

                                                               i.      Acid reflux

                                                             ii.      Infections

                                                           iii.      Chemical Injury

                                                            iv.      Thermal Injury

                                                              v.      Metabolic

f.         Tumors

                                                               i.      Benign

                                                             ii.      Neoplasms

1.        SCC

2.        Adenocarcinoma

3.        Miscellaneous

II.       Stomach

a.        Normal

b.        Gastritis

                                                               i.      Acute Gastritis

                                                             ii.      Chronic Gastritis

1.        Autoimmune Gastritis

c.        Chronic Peptic Ulcer Disease

                                                               i.      Duodenal Ulcers

                                                             ii.      Gastric Ulcers

d.        Acute (Stress) Ulcers

e.        Hypertrophic gastropathy

                                                               i.      Menetrier’s disease

                                                             ii.      Zollinger-Ellison syndrome

f.         Tumors

                                                               i.      Benign

                                                             ii.      Malignant

1.        Gastric Carcinoma

2.        Lymphoma

3.        Mesenchymal Tumors

III.     Small Intestine

a.        Normal

b.        Congenital Abnormalities

                                                               i.      Atresia

                                                             ii.      Meckel’s Diverticulum

c.        Malabsorption

                                                               i.      Defective Intraluminal Solubility

                                                             ii.      Mucosal Cell Abnormalities

                                                           iii.      Reduction in Intestine Surface

                                                            iv.      Lymphatic Obstruction

                                                              v.      Iatrogenic Causes

                                                            vi.      Drugs

                                                          vii.      Infection

1.        Giardiasis

2.        Viral gastroenteritis

                                                        viii.      Unexplained Causes

IV.     Pancreas

a.        Normal

b.        Acute Pancreatitis

c.        Chronic Pancreatitis

                                                               i.      Chronic calcifying pancreatitis

                                                             ii.      Chronic obstructive pancreatitis

d.        Tumors

                                                               i.      Carcinoma of the Pancreas

                                                             ii.      Islet Cell Tumors

1.        Insulinoma

V.       Small Bowel and Colon

a.        Congenital

                                                               i.      Duplications

                                                             ii.      Malrotations

                                                           iii.      Omphalocele

                                                            iv.      Gastroschisis

                                                              v.      Heterotopia

                                                            vi.      Atresia, Stenoses, Fistulas

                                                          vii.      Hirschsprung’s Disease

b.        Traveler’s diarrhea

c.        Infective enterocolitis

                                                               i.      Bacterial

                                                             ii.      Viral

                                                           iii.      Parasitic

                                                            iv.      GI + HIV

                                                              v.      Pseudomembranous colitis

1.        Clostridium difficile

d.        Inflammatory (idiopathic)

                                                               i.      Crohn’s Disease (= Regional enteritis)

                                                             ii.      Ulcerative Colitis

e.        Ischemic Bowel Disease

f.         Bowel Obstruction

g.        Diverticular Disease

h.       Tumors

                                                               i.      Benign

1.        Hyperplastic polyps

2.        Hamartomatous polyps

a.        Juvenile (Retention) polyps

b.        Peutz-Jeghers polyps

3.        Inflammatory polyps

                                                             ii.      Neoplastic

1.        Adenomatous polyps

a.        Tubular adenomas

b.        Villous adenomas

c.        Serrated adenomas

d.        Heredofamilial Polyposis

                                                                                                                                       i.      Familial polpyposis

                                                                                                                                     ii.      Gardner’s syndrome

                                                                                                                                   iii.      Turcot’s syndrome

2.        Carcinoma of the colon

3.        Lymphomas

4.        Mesenchymal tumors

5.        Carcinoid Tumors

6.        Metastatic tumors

VI.     Appendix

a.        Appendicitis

b.        Tumors


I.         Esophagus

a.        Normal

Esophagus = inferior extension of the pharynx

Conducts food and prevents regurgitation

Upper esophageal sphincter: level of cricopharyngeus muscle

Lower esophageal sphincter: level of diaphragm (proximal to epithelial junction)

Layers

1.  mucosa

                a. non-keratinizing stratified squamous epithelium

                b. lamina propria: loose connective tissue

                c. muscularis mucosa (often quite thick in esophagus)

2. submucosa

                3. muscularis propria: skeletal muscle proximally, smooth muscle lower 2/3

                                a. inner circular layer

                                b. outer longitudinal layer

b.        Congenital Abnormalities of Esophagus

                                                               i.      Agenesis

    failure to form

                                                             ii.      Atresia

    segment fails to form (usually adjacent to tracheal bifurcation)

                                                           iii.      Fistulas

    communication between lumen to bronchus or trachea

c.        Acquired Abnormalities of Esophagus

                                                               i.      Mucosal webs

proximal, semicircular, middle aged-women

                                                             ii.      Schatzki’s ring

distal, circumferential

                                                           iii.      Stenosis

chemical injury related

                                                            iv.      Varices

etiology: portal hypertension (cirrhosis)

morphology: dilated veins (mucosal and submucosal)

    40% mortality on first bleed if ruptured

d.        Lesions ó Motor Dysfunction

                                                               i.      Achalasia

    failure to relax, increased LES tone, bag-like esophagus

    etiology: destruction of myenteric ganglia, scleroderma

    symptoms: dysphagia, regurgitation

    can be primary or secondary to infection, neoplasm, etc.

                                                             ii.      Hiatal hernia

    up to 20% of adults (stomach enters thoracic cavity)

                                                           iii.      Diverticula

proximal (Zenker’s), traction (mid), epiphrenic (distal)

                                                            iv.      Lacerations

    Mallory-Weiss tear

    linear, retching-induced bleeding

    if transmural rupture à Boerhaave syndrome [mediastinitis (high mortality rate)]

e.        Inflammatory conditions (Esophagitis)

                                                               i.      Acid reflux

    most common cause of esophagitis

    decreased LES tone

    symptoms: dysphagia, pain, dyspepsia

    hallmark: rich eosinophilic infiltrate

                        complications: bleeding, stricture, Barrett’s metaplasia (10%)

Barrett’s metaplasia

                - squamous à metaplastic columnar (glandular) epithelium

                                        the longer the segment, the greater the chance of complications (ulceration, bleeding, stricture, malignancy)

                                        à dysplasia of metaplastic glandular mucosa (à screen every 6 months)

                                        à adenocarcinoma (30-40X risk)

                                        if Barrett’s is high-grade, 40% à invasive adenocarcinoma (therefore, resection)

                                                             ii.      Infections

- fungal (candida albicans: immunocompromise, gray-white pseudomembranes)

- viral (HSV: punched out ulcers, CMV: immunocompromise)

- bacterial (usually a consequence of disease elsewhere)

                                                           iii.      Chemical Injury

    acid, alkali, alcohol, drugs

                                                            iv.      Thermal Injury

    hot liquid, radiation

                                                              v.      Metabolic

    uremia

f.         Tumors

                                                               i.      Benign

usually of mesenchymal origin (leiomyoma)

                                                             ii.      Neoplasms

1.        SCC

poor prognosis

keratin pearls

4% of all cancer deaths

males, black, (higher in China, Iran)

etiology: alcohol, smoking, nitrosamines (no hereditary role)

predisposing factors: achalasia, stricture, esophageal webs

subforms:

- fungating exophytic tumor

- flat diffuse neoplasm (infiltrates wall)

- ulcerated, excavated mass (grows deeply)

2.        Adenocarcinoma

poor prognosis

middle-aged white males

predisposing factors: chronic reflux à Barrett’s metaplasia

3.        Miscellaneous

leiomyosarcoma, melanoma, Kaposi sarcoma, metastatic SCC

II.       Stomach

a.        Normal

 

Parietal cells

HCl

digestive acid

fundus

Chief cells

pepsinogen

à pepsin; digests protein

fundus

Mucous neck cells

mucous

lubricant

fundus, cardia, antrum

G cells

gastrin

stimulates HCl production

antrum

 

                                3 phases of digestion

                                                1. cephalic phase (mediated by vagal activity; initiated by food stimuli)

                                                2. gastric phase (stimulation of gastric juice; direct: parietal; indirect: G cells

                                                3. intestinal phase (ends gastric secretion)

                                Gastric defenses against autodigestion (pH 1.0-3.0)

                                                1. Mucous secretion (physical barrier to acid and pepsin)

                                                2. Bicarbonate secretion (creates alkaline environment immediately adjacent to epithelium)

                                                3. Cellular barriers (tight junctions, rapid repair)

                                                4. Mucosal blood flow (removes excess H+ and supplies nutrients)

b.        Gastritis

inflammation of the gastric mucosa

                                                               i.      Acute Gastritis

neutrophilic infiltrate

very common

etiology: drugs (aspirin), alcohol, smoking, staphyolococcal enterotoxin, helicobacter pylori, etc.

pathogenesis: gastric mucosal barrier breakdown, blood shunting (injury)

complications: ulceration, bleeding

                                                             ii.      Chronic Gastritis

lymphocytic, plasmocytic infiltrate (neutrophils may be present)

association: gastric carcinoma, helicobacter pylori, pernicious anemia, bile reflux, etc.

pathology: swollen and boggy à flat and thin

complications: gastric carcinoma, hypochlorhydria/achlorhydria (à pernicious anemia), ulceration (gastric or duodenal)

- chronic active gastritis = neutrophil component is significant and H. pylori in superficial mucous layer

- chronic superficial gastritis = chronic inflammatory cells predominate

                - chronic atrophic gastritis = atrophy of gastric glands is present

1.        Helicobacter pylori gastritis

gram negative spiral rod (produces urease à direct damage)

clinical/histological picture resembles acute gastritis

antrum is more severely affected

does not invade (lives in mucous)

2.        Autoimmune gastritis

<10% of cases of chronic gastritis

autoantibodies against parietal cells and intrinsic factor

fundus is more severely affected

c.        Chronic Peptic Ulcer Disease

chronic, solitary ulcers occurring at any level of the GI tract exposed to acid-pepsin juices

etiology: increase in damaging forces or breakdown of protective mechanisms, stress, aspirin, alcohol, coffee, smoking, increase in serum calcium levels, H. pylori, altered gastric secretion

ulcers are deep and punched out

complications: bleeding, perforation, obstruction, pain (probably do not lead to malignancy)

deep, single, large, scarred, sharp margins

                                                               i.      Duodenal Ulcers

associated with increased gastric acidity

                                                             ii.      Gastric Ulcers

not associated with increased gastric acidity

d.        Acute (Stress) Ulcers

multiple, small, shallow, ragged margins, not associated with chronic gastritis

etiology: stress, severe illness (ICU setting: brain damage, burns, shock, trauma, aspirin, NSAIDS)

granulation tissue, fibrinoid necrosis, no scarring

symptoms: bleeding, pain

e.        Hypertrophic gastropathy

                                                               i.      Menetrier’s disease

expansion of stomach surface epithelium

30-50 y.o. men

very rare

hypochlorhydria

                                                             ii.      Zollinger-Ellison syndrome

expansion of parietal cell compartment

caused by a pancreatic or duodenal gastrinoma

causes enlarged gastric folds and peptic ulcers

f.         Tumors

                                                               i.      Benign

polyps and adenomas of the stomach are rare and usually benign

                                                             ii.      Malignant

1.        Gastric Carcinoma

Japan>>USA; associated with blood type A or Lewis subtype

Hypochlorhydria à increased risk for gastric carcinoma

exophytic, fungating tumor from mucosa (may be flat or excavated = linitis plastica)

most common: pylorus or antrum

staging based on depth: early (mucosa and submucosal); advanced (muscular wall)

5-year prognosis: early (95%) late (10%)

2.        Lymphoma

3.        Mesenchymal Tumors

spindle cell neoplasms (interstitial cells of Cajal = GI pacemaker cells)

have smooth muscle and neural features

III.     Small Intestine

a.        Normal

lined by villi separated by pit-like crypts extending into muscularis mucosa (normal villous:crypt height = 5:1)

villi (terminal digestion and absorption of food)

crypts (secrete ions, water, deliver IgA and antimicrobials)

mucus cells (mucus protects and facilitates uptake of nutrients)

surface epithelial cells (uptake intrinsic factor-vitamin B12 complex)

Digestion, Absorption, Transport

1.        Intraluminal breakdown of food (digestion)

a.        pancreatic phase: proteins, fats, carbohydrates

b.        biliary phase: solubilize fats

2.        Intestinal absorption

a.        luminal surface of brush border cells

b.        additional digestion of carbohydrates and peptides

c.        intracellular modification/mobilization of amino acids, fats

3.        Removal of nutrients (transport)

a.        lymphatics, capillaries

b.        Congenital Abnormalities

                                                               i.      Atresia

rare; most commonly: duodenum

                                                             ii.      Meckel’s Diverticulum

persistence of vitelline duct on antimesenteric side of bowel à diverticulum (within 30cm of ileocecal valve)

contains all three layers of normal bowel wall (true diverticulum)

heterotopic (gastric or pancreatic) rests are possible (50%) à peptic ulceration of mucosa

complications: bleeding, intussusception, incarceration, perforation

c.        Malabsorption

abnormal secretion of fat (steatorrhea)

decreased absorption of fat, fat-soluble vitamins, proteins, carbohydrates, minerals, water

                                                               i.      Defective Intraluminal Solubility

pancreatic insufficiency

bacterial overgrowth (reduces bile salt levels)

                                                             ii.      Mucosal Cell Abnormalities

disaccharidase deficiency (rare) = difficult to digest milk/dairy (congenital or acquired)

                                                           iii.      Reduction in Intestinal Surface

Gluten sensitive enteropathy = Celiac Disease (Celiac Sprue)

- Toxic effect of gluten (wheat, rye) on mucosal epithelial cells

- hypersensitivity to gliadin (component of gluten)

- flattened mucosa

- treatment: remove gluten from diet

- complications: T-cell lymphoma, adenocarcinoma

                                                            iv.      Lymphatic Obstruction

interfering with transport of nutrients:

1.        tuberculosis

2.        lymphoma

3.        lymphangiectasia (dilated lacteals and lymphatics)

                                                              v.      Iatrogenic Causes

gastrectomy, radiation enteritis

                                                            vi.      Drugs

cholestyramine, colchicines, para-aminosalicylic acid, cathartics, neomycin

                                                          vii.      Infection

1.        Giardiasis

Giardia Lamblia: parasitic (usually coats, no invasion)

drinking contaminated water

2.        Viral gastroenteritis

rotavirus, Norwalk virus, adenovirus

3.        Other Parasitic

        strongyloidiasis

4.        Whipple’s Disease

multi-system, treatable (antibiotics)

morphology: foamy macrophages in lamina propria (PAS positive)

Actinomyces (gram+, PAS+, rod-shaped bacilli)

defective T-cell function (?)

villous architecture maintained

                                                        viii.      Unexplained Causes

mechanism unknown: DM, carcinoid syndrome, endocrine abnormalities

IV.     Pancreas

a.        Normal

                main function: secretion (endocrine, exocrine)

duodenal enzymes

secretin: controls electrolyte, water production by pancreas

choecystokinin: controls enzyme production by pancreas

pancreatic enzymes: exocrine

trypsin, chymotrypsin, amylase, lipases, phospholipases, elastases, ribonucleases

released in proenzymes form à pancreatic duct (activated in duodenum) à protects pancreas

pancreatic enzymes: endocrine (Islet of Langerhans)

A cells: glucagons

B cells: insulin (70% of Islet cells)

D cells: somatostatin

PP cells: pancreatic peptide

D1 cells: vasoactive intestinal polypeptide (VIP)

b.        Acute Pancreatitis

sudden destruction of pancreas (escape of activated pancreatic enzymes into parenchyma)

common, life-threatening

etiology: Biliary tract disease (women), alcoholism (men), trauma, iatrogenic, infections, hyperlipidemia, AIDS

gross: necrosis, hemorrhage, chalky white fat necrosis

histology: acute inflammation, necrosis, mild to severe hemorrhage

pathogenesis: premature activation.  Possible mechanisms:

1.        duct obstruction (pressure build-up)

2.        acinar cell injury (viruses, chemicals, trauma)

3.        proenzymes are packaged (lysosomes) instead of secreted

complications:

1.        abscess, pseudocyst (necrotic debris, enzymes)

2.        rupture of abscess, pseudocyst

3.        hemorrhage (blood vessel erosion)

4.        fat necrosis (lipase release, pancreas and/or distal sites)

5.        duodenal obstruction (secondary to pancreatic inflammation)

6.        systemic organ failure (ARDS, renal failure, shock, etc.)

c.        Chronic Pancreatitis

etiology: alcoholism, biliary tract disease, pancreas divisum (two parts of pancreas), CF, hyperlipidemia, hypercalcemia

pathogenesis: repeated flare ups of pancreatitis (not classic acute pancreatitis)

repeated bouts of classic acute does not à chronic pancreatitis

40%: no identifiable cause

necrosisàfibrosis theory

relentless, progressive

steatorrhea

                                                               i.      Chronic calcifying pancreatitis

predominantly in alcoholics

atrophy of parenchymal cells, calcification of insterstitium

gross: hard, calcification and/or stones (diagnosed on x-ray)

                                                             ii.      Chronic obstructive pancreatitis

stenosis of sphincter of Oddi

fibrosis, atrophy, no calcification

head of pancreas

d.        Tumors

                                                               i.      Carcinoma of the Pancreas

very poor prognosis (3%, 5 years)

painless jaundice

most are ductal adenocarcinomas

etiology: unclear (smoking, diet, benzidine, chronic pancreatitis, DM)

morphology: 60% (head: may present earlier)

elevated CA 19-9

Trousseau’s sign

                                                             ii.      Islet Cell Tumors

glucagonoma, insulinoma, somatostatinoma, Werner-Morrison (VIP), Zollinger-Ellison (gastrinoma: ectopic)

1.        Insulinoma

rare; most common islet cell tumor

most occur singly, encapsulated

good prognosis

Whipple’s triad

1.        insulin shock with fasting (periodic hypoglycemia)

2.        low fasting blood glucose

3.        relief of symptoms with IV or oral glucose

V.       Small Bowel and Colon

a.        Congenital

                                                               i.      Duplications

                                                             ii.      Malrotations

                                                           iii.      Omphalocele

                                                            iv.      Gastroschisis

                                                              v.      Heterotopia

                                                            vi.      Atresia, Stenoses, Fistulas

                                                          vii.      Hirschsprung’s Disease

congenital aganglionic megacolon

b.        Traveler’s diarrhea

symptoms: diarrhea, abdominal pain

may be enteroinvasive, or enterotoxin-related

c.        Infective enterocolitis

                                                               i.      Bacterial

E-coli, salmonella, staphylococcal, vibrio cholera, shigella

                                                             ii.      Viral

Norwalk virus, rotavirus

                                                           iii.      Parasitic

strongyloides, entameba histolytica, taenia, trichinella spiralis

                                                            iv.      GI + HIV

                same as above, but with the addition of: mycobacterium avium-intracellulare (MAI), CMV, HSV, Adenovirus, etc.

                                                              v.      Pseudomembranous colitis

                caused by bacterial toxins

                etiology: iatrogenic - long-term antibiotics (ampicillin, etc.), nosocomial

                morphology

                gross: friable freckles, superficial ulceration, sparing of adjacent mucosa

                histology: pseudomembrane (fibrin, acute inflammatory cells), “volcanic eruption

1.        Clostridium difficile

                associated with pseudomembranous colitis

                gram+, non-invasive, enterotoxin

d.        Inflammatory Bowel Disease (idiopathic) = IBD

overlap exists in symptoms and diagnosis

                                                               i.      Crohn’s Disease (= Regional enteritis)

hallmarks: granulomas, transmural, skip lesions

may involve entire GI tract

epidemiology: females, whites, family history of IBD

etiology: unknown (autoimmune? infectious?)

morphology: linear, skip ulcers (abscesses are rare), cobblestone mucosa, “creeping fat”, non-caseating granulomas

complications

                localized: fistulas, strictures, hemorrhage

                systemic: hepatic inflammation, arthritis, ocular inflammation, erythema nodosum, nutritional deficiencies

                                                             ii.      Ulcerative Colitis

large bowel always and only (begins in rectum)
hallmark: intermittent cramping bloody diarrhea

may involve terminal ileum = backwash ileitis

diffuse, superficial mucosal ulceration (crypt abscesses); mucus secretion impairment

etiology: unknown

prone to remissions

complications

                localized: toxic megacolon, hemorrhage, stricture, adenocarcinoma

                systemic: hepatitis, hemolytic anemia, arthritis, thromboembolism, erythema nodosum

e.        Ischemic Bowel Disease

resembles UC

lack of inflammatory response (blood supply is cut-off)

etiology: hypoperfusion (heart failure, shock, etc.)

f.         Diverticular Disease

mucosa herniations (through muscularis)

most common site: mesenteric side of sigmoid colon

associated: high fat, low fiber diet

complications: diverticulitis, fistula, obstruction (secondary to inflammation), bleeding, bladder irritation, mimics carcinoma

tend to be next to tenia coli

g.        Bowel Obstruction

hernias, adhesions, intussusception, volvulus

h.       Tumors

polyp = protrusion of mucosa into gut lumen

- pedunculated polyp: stalk (can be excised endoscopically)

- sessile polyp: no stalk

                                                               i.      Benign

1.        Hyperplastic polyps

increased proliferation of cells in colonic crypt (lower 1/3)

normal location, normal cell differentiation (but expanded)

rectosigmoid in shape (“saw-tooth”)

not associated with malignancy

2.        Hamartomatous polyps

a.        Juvenile (Retention) polyps

most common polyp in children

Juvenile Polyposis syndrome (autosomal dominant): multiple adenomatous polyps (à carcinoma)

acute inflammation seen

b.        Peutz-Jeghers polyps

part of a clinical syndrome (autosomal dominant)

- melanin pigmentation of lips

- buccal mucosa

- webs of fingers/toes

- harmartomatous polyps GI tract (small bowel and stomach)

3.        Inflammatory polyps

occur in long-standing inflammatory bowel disease (not true polyps)

                                                             ii.      Neoplastic

1.        Adenomatous polyps

                                                                increased risk of cancer (villous > mixed > tubular)

        increased size à increased cancer risk

        10-15 years for polyp à cancer

a.        Tubular adenomas

most common adenomatous polyp

mutation in adenomatous polyposis coli (APC) gene

abnormal tissue involvement (whole crypt and surface of cells à proliferation)

dysplasia (may be pedunculated or sessile)

morphology: “test-tube”-like

b.        Villous adenomas

usually sessile

morphology: arranged in papillary fronds (finger-like)

complications: bleeding, water and electrolyte loss

c.        Tubulo-villous adenomas

20-50% villous features

d.        Serrated adenomas

colon (right-side)

sessile or pedunculated

distribution similar to hyperplastic poly (but stratified and dysplastic)

morphology: goblet cell immaturity, mitoses, prominent nucleoli

pre-malignant

e.        Heredofamilial Polyposis

                                                                                                                                       i.      Familial polpyposis

autosomal dominant

polyps are adenomatous, but very numerous (fuzzy appearance)

cancer is inevitable

                                                                                                                                     ii.      Gardner’s syndrome

adenomatous polyps + soft tissue tumors elsewhere in body

autosomal dominant

cancer is inevitable

                                                                                                                                   iii.      Turcot’s syndrome

adenomatous polyps + brain tumors (gliomas)

autosomal recessive

cancer is inevitable

2.        Carcinoma of the colon

second most common cause of death from cancer

etiology: diet (high fat, low-fiber diet with cholesterol); bile salts à bacterial products

colon (left-side) most common

left-side: napkin-ring (present earlier with obstruction)

right-side: fungating (clinically silent for a longer duration)

3.        Lymphomas

rare; MALT (B-cell origin); Burkitt’s

4.        Mesenchymal tumors

rare; smooth muscle, neural, vascular, fibrohistiocytic, lipomatous

5.        Carcinoid Tumors

malignant neoplasms in slow motion

most carcinoid tumors (90%) occur in GI

neoplastic (serotonin, histamine, bradykinin, prostaglandins)

increased tryptophan metabolism àHIAA increase (diagnostic)

few mitoses

silver-stain

carcinoid syndrome

1. vasoactive disturbances (flushing, sweating, hypotension)

2. intestinal hypermotility (diarrhea)

3. bronchoconstrictive attacks (asthma)

4. cardiac involvement (right-side plaques)

6.        Metastatic tumors

from lung, breast, melanoma

VI.     Appendix

a.        Appendicitis

fecal stone obstruction à decreased blood flow à ischemia, bacteria overgrowth

acute (neutrophilic) inflammation of muscularis propria

complications: perforationàperitonitis, abscesses, pylephlebitis, septicemia

b.        Tumors

1. carcinoid (most common)

2. benign hyperplastic polyps

3. mucocele (neoplastic mucin-filled appendix)

                - cystadenoma or cystadenocarcinoma

                - pseudomyxoma peritonei (neoplastic cells throughout peritoneal cavity)

4. invasive adenocarcinoma: very unusual