Gastrointestinal Tract Pathology

GASTROINTESTINAL TRACT PATHOLOGY Mary Yvonnette C. Nerves, RMT, MD, FPSP

Congenital abnormalities

Esophagus

Atresia/Fistulae/Duplications

Esophageal Obstruction Achalasia Diverticulum Esophageal Mucosal Web Esophageal rings Esophagitis/ Reflux Esophagitis Hiatal Hernia Barrett’s Esophagus Dysplacia

Imperforate Anus Diaphragmatic Hernia/ /Omphalocele/Gastroschisis Meckel’s Diverticulum Pyloric Stenosis

Hirschsprung Disease

Esophageal Varices

GIT PATHOLOGY: Stomach

Small intestine and colon

Peritoneal cavity

Acute gastritis

Intestinal obstruction

Congenital abnormalities

Chronic gastritis Acute Gastric Ulceration

Ischemic bowel disease Angiodysplasia

Esophagus Stomach

Peptic ulcer Gastric polyps

Infectious enterocolitis Inflammatory bowel disease

Small intestine and colon Peritoneal cavity

Hypertrophic gastropathies Tumors Dysplacia

Sigmoid diverticulitis Hemorrhoids/anal cancer Acute appendicitis/appendiceal tumors Tumors Familial syndromes

Carcinoma

Esophageal Tumors

CONGENITAL ABNORMALITIES: ABNORMALITIES: I. ATRESIA / FISTULAE:  Atresia is a condition in which a body orifice or passage in the body is



Gastric heterotopia: patches of ectopic gastric mucosa in the small

bowel colon rd  –  upper 3   of the  Most common site of ectopic gastric tissue  –  esophagus  release acid in eso  dysphagia, esophagitis, Barretts or adenoCA

abnormally closed or absent  Fistula is an abnormal connection or passageway between two epithelium-lined organs or vessels that normally do not connect.

VII. MECKEL DIVERTICULUM: Type A: pure esophageal atresia (7.6%) Type B: esophageal atresia with proximal tracheoesophageal fistula (0.8%) Type C: esophageal atresia with distal tracheoesophageal fistula (86.5%) Type D: esophageal atresia with proximal and distal tracheoesophageal

 Most common type of true diverticulum

fistula (0.7%)



Type E: "H-type"  tracheoesophageal fistula without esophageal atresia

- 2% of the pop’n - present within 2 feet of the ICV - approx. 2 inches long - 2x as common in males - symptomatic by age 2  TRUE DIVERTICULUM: blind outpouching lined by mucosa that communicates with the lumen and includes all 3 layers of the bowel wall

 Occurs in the

omphalomesenteric

(vitelline) duct

(4.4%)

II. IMPERFORATE ANUS: Most common form of congenital intestinal atresia; due to failure of the cloacal diaphragm

ileum

 Occurs as a result of f ailed involution of the

to involute;

III. DIAPHRAGMATIC HERNIA: Intestine protruding through hole in diaphragm

IV. OMPALOCELE (EXOMPHALOS):

RULE of 2s:

 Defect of the anterior abdominal wall at the insertion of the

VIII. PYLORIC STENOSIS:

umbilical cord  Occurs in 1 in 5000 to 1 in 20,000 live births

 Due to progressive thickening of the circular muscle of the pylorus

 Associated with chromosomal defects,(trisomies 13, 18, and 21),

 gastric outlet narrowing

and with other disorders such as Beckwith-Wiedemann Syndrome  Closure of abdominal musculature is incomplete   abdominal viscera herniate into a ventral membranous sac

 3-4x more common in MALES

Five common features used to define BWS are: macroglossia, macrosomia ma crosomia (birth weight and length greater than the 90th percentile), midline abdominal wall defects (omphalocele/exomphalos, umbilical hernia, diastasis recti), ear creases or ear pits, and neonatal hypoglycemia (low

 Generally presents in the

2nd or 3rd  week of life

  new-onset regurgitation and persistent, projectile, nonbilious vomiting  P.E.: hyperperistalsis; ovoid abdominal abdominal mass ’

IX. HIRCHSPRUNG DISEASE DISE ASE A.k.a. Congenital Aganglionic Megacolon

blood sugar after birth).

V. GASTROCHISIS (LAPAROSCHISIS):  A small (generally < 5 cm) defect of the abdominal wall just to the

right of the umbilical cord insertion, allowing evisceration of bowel loops, stomach, and sometimes the gonads  Prevalence: 1 in 10,000 livebirths  ventral wall defect involving all layers of the abdominal wall

Normal migration of neural crest cells from the cecum to rectum is arrested prematurely or when the ganglion cells undergo premature death Distal intestinal segment lacks both Meissner submucosal and the

Auerbach myenteric plexus Clinical Features: earliest and most common presentation is delayed (> 48 hrs) passage of meconium in the newborn newborn Infants and older children: chronic constipation, abdominal distention and vomiting

Pathologic Feature: distal narrow aperistaltic hypertonic segment (aganglionic) and a dilated proximal segment caused by obstruction Aganglionic region may have a grossly normal or contracted appearance while the normally innervated proximal colon May undergo progressive dilation

VI. ECTOPIA (DEVELOPMENTAL RESTS):  Ectopic gastric mucosa (inlet patch):  esophagus  Ectopic pancreatic tissue: stomach/esophagus

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ESOPHAGUS:  A muscular tube connecting the throat (pharynx) with the stomach.

V. ESOPHAGITIS:  LACERATIONS: Mallory-Weiss tears  longitudinal tears in the

 8 inches long, and is lined by moist pink tissue called mucosa.

esophagus near the GEJ assoc with severe retching or vomiting sec to acute alcohol intoxication  Boerhaave syndrome:  char by distal esophageal rupture and mediastinitis

 Runs behind the windpipe (trachea) and heart, and in front of the

spine. Just before entering the stomach, the esophagus passes through the diaphragm.  The upper esophageal sphincter (UES)  is a bundle of muscles at the top of the esophagus. The muscles of the UES are under conscious control, used when breathing, eating, belching, and vomiting. They keep food and secretions from going down the windpipe.  The lower esophageal sphincter (LES) is a bundle of muscles at the low end of the esophagus, where it meets the stomach. When the LES is closed, it prevents acid and stomach contents from traveling backwards from the stomach. The LES muscles are not under voluntary control.

VI. REFLUX ESOPHAGITIS: A.k.a. Gastroesophageal Reflux Disease (GERD) Reflux of gastric contents into the lower esophagus (most frequent

cause of esophagitis) Most

common clinical symptoms : dysphagia, heartburn, regurgitation of sour-tasting gastric contents Pathogenesis: reflux of gastric juices is central to the devt of mucosal injury Conditions that decrease LES tone or increase abdominal pressure:

I. DIVERTICULUM: An outpouching of the alimentary tract

a) alcohol and tobacco use b) obesity c) central nervous system depressants d) pregnancy e) hiatal hernia f) delayed gastric emptying g) increased gastric volume Gross: marked hyperemia with focal hemorrhage Morphology: intraepithelial eosinophils and basal zone hyperplasia

that contains one or more

layers of the wall ZENKER’S DIVERTICULUM (Cricopharyngeal / Pharyngoesophageal): located above the UES; results from increased intrapharyngeal pressure in areas of weakness along the esophageal wall; An outpouching of the esophageal mucosa at points of weaknesses in the wall of the esophagus at the junction with the pharynx (inferior constrictor muscle and obliquely passing fibers of the cricopharyngeal muscles as they descend on the posterior wall of the esophagus to become longitudinal) Traction diverticulum: located immediately above the UES; located in rd the lower 3  of the esophagus and in the region of the hilum of the lung; attributed to fibrosing mediastinal processes or abnormal motility. Epiphrenic diverticulum: immediately above the LES; located just above the diaphragm; Cause: unclear

VII. HIATAL HERNIA:  Characterized by separation of the diaphragmatic crura and

protrusion of the stomach into the thorax through the resulting gap  Of the three major tubes that traverse the diaphragm, the esophagus has the weakest surroundings, much more muscular and less fibrous than the aorta and IVC.  HH can be thought of as a sequela of chronic gastric overdistention.

II. ESOPHAGEAL MUCOSAL WEBS  Ledge-like protrusions of mucosa  

Pathogenesis: unknown Paterson-brown-kelly or Plummer-vinson syndrome: webs + IDA

VIII. BARRETTS ESOPHAGUS: Can be defined as intestinal metaplasia of a normally SQUAMOUS

+ glossitis + cheilosis; found in women and associated with IDA  Most common in upper esophagus

esophageal mucosa. The presence of GOBLET CELLS in the esophageal mucosa is DIAGNOSTIC. SINGLE most common RISK FACTOR for esophageal adenocarcinoma 10% of GERD patients get it Most common in white males; between 40-60 years of age You can think of Barrett’s as REVERSE squamous me taplasia. GROSS: patches of red, velvety mucosa extending upward from the GEJ (You should have, by now, a good feel for squamous (shiny) vs. columnar (mucoid) surface mucosas anywhere in the body.) Intestinalized (gastricized)  mucosa is AT RISK for glandular dysplasia. Searching for dysplasia when BARRETT’s is present is of utmost importance

III. ESOPHAGEAL RINGS A.k.a. Schatzki’s / Lower esophageal  Esophagogastric rings Similar to webs but are circumferential and thicker Rings include mucosa, submucosa and,

in

some

cases,

hypertrophic muscularis propria A rings: present in distal esophagus, above the GEJ B rings: located at the squamocolumnar junction of the lower esophagus Treatment: endoscopic dilatation and surgical myomectomy

IV. ACHALASIA:  A.k.a. Cardiospasm or megaesophagus

MOST/ALL

adenocarcinomas arising in the esophagus arise from

previously existing BARRETT’s

 An esophageal motility disorder characterized by an inability of the

LES to relax after swallowing, resulting  In periodic esophageal obstruction  Nearly complete loss of myenteric ganglion cells is present in the rd lower 3  of the esophagus  Generally synonymous with the word “esophagospasm”

IX. DYSPLASIA:  Glandular “dysplasia”: Find the atypical cells. Increased epithelial

proliferation, often with atypical mitoses, nuclear hyperchromasia and stratification, irregularly clumped chromatin, increased nuclear-tocytoplasmic ratio, and a failure of epithelial cells to mature as they migrate to the esophageal surface are present in both grades of dysplasia

TRIAD: Aperistalsis, Incomplete relaxation of the LES, Increased LES tone  Barium swallow: dilated, aperistaltic esophagus with a beak-like 

tapering at distal end  Progressive dysphagia starting in teens  Pathogenesis: unknown

X. VARICES: 

Dilated, tortuous veins within the lamina propria and submucosa that bulge into the esophageal lumen because of portal hypertension and portosystemic; shunting  Three common areas of portal/caval anastomoses: Esophageal, Umbilical, Hemorrhoidal 

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100% related to portal hypertension

 Found in 90% of cirrhotics

Massive, sudden, fatal hemorrhage is the most feared consequence 

XI. TUMORS:  BENIGN: Leiomyomas, Fibrovascular polyps, Condylomas (hpv)

Lipomas, “granulation” tissue (pseudotumor) The very BEST way to classify ALL tumors of a major organ is to remember its basic HISTOLOGY. You do NOT need to memorize a stupid list from a pathology lecture,  just remember an organ’s native cells!

 Any chronically increased venous pressure phenomenon which

dilates a vein, will also make it more tortuous---legs or esophagus! Varices appear as tortuous dilated veins lying primarily within the submucosa of the distal esophagus and proximal stomach. 

 ,

FACTORS that lead to RUPTURE:



MALIGNANT: Squamous cell carcinoma and Adenocarcinoma

- inflammatory erosion of thinned overlying mucosa - increased tension in progressively dilated veins - increased vascular hydrostatic pressure associated w/ vomiting

ADENOCARCINOMA Commonest type in US Risk factor: Barrett esophagus Distal 1/3 of esophagus Symptoms: insidious onset; late obstruction

SQUAMOUS CELL CARCINOMA Commonest type worldwide Risk factors: esophagitis, smoking, alcohol, genetics Middle 1/3 of esophagus Symptoms: insidious onset; late obstruction

Arises in a background of Barrett esophagus & long-standing GERD

Adults over age 45, affects MALES 4x more than females

RISK FACTORS:

RISK FACTORS: Alcohol and tobacco use, caustic esophageal injury, achalasia, Plummer-Vinson syndrome or Paterson-Kelly syndrome

documented dysplasia, tobacco use, obesity, prior

radiation therapy

FACTORS that DECREASE RISK: Diet rich in fresh fruits and vegetables, H.

presents as a classical triad of dysphagia, iron-deficiency anemia and esophageal webs; and frequent consumption of very hot beverages rd Half of SCCs occur in the middle 3  of the esophagus; Begins as an in-situ lesion (SQUAMOUS DYSPLASIA) Sixfold more common in African-American

pylori serotypes Most frequent in CAUCASIANS; M > F rd Usually occur in the distal 3  of the esophagus DYSPLASIA IN-SITU NFILTRATION Pathogenesis:  Chromosomal abnormalities & mutation or Pathogenesis:  incompletely defined; loss of tumor suppressor genes, overexpression of p53 are present at early stages; Other genetic changes: including p53 and p16/INK4a amplification of c-ERB-B2, cyclin D1 and cyclin E genes; mutation of retinoblastoma tumor suppressor gene; allelic loss of the cyclindependent kinase inhibitor p16/INK4a Would you call this squamous “dysplasia”? A nswer: YES Would your fear it would develop into squamous cell carcinoma? Answer: YES Does it always? Answer: NO Does it usually? Answer: With time, YES, but that time may be years and years.

STOMACH: I. ACUTE GASTRIC ULCEERATION:



 prevents synthesis of prostaglandins, which enhance HC03

 Focal, acutely developing gastric mucosal defect

secretion, inhibit acid secretion, promote mucin synthesis, and increase vascular perfusion  Intracranial injury:   caused by direct stimulation of vagal nuclei   hypersecretion of gastric acid   systemic acidosis  contribute to mucosal injury by lowering the intracellular pH of mucosal cells.

 Occur after severe physiologic stress

Stress ulcers: shock, sepsis, or severe trauma o Curling ulcers: occur in proximal duodenum; severe burns & o

trauma o

NSAID-induced ulcers  are related to cyclooxygenase inhibition

Cushing ulcers:  gastric, duodenal, esophageal; intracranial

disease

ACUTE GASTRITIS A transient inflammatory process

mucosal

 

CHRONIC GASTRITIS H. pylori gastritis: most common cause of chronic gastritis Autoimmune gastritis:  most common cause of atrophic gastritis and most common cause of chronic gastritis in patients w/o H. pylori infection

Pathogenesis: disruption of the protective mechanisms:



Mucin secreted by surface foveolar cells prevents large food particles from directly touching the epithelium

Rich vascular supply to the

H. pylori gastritis: H. pylori:  spiral shaped or curved bacilli; present in almost ALL duodenal ulcers & majority of individuals with gastric ulcers or chronic gastritis; present in 90% of individuals w/ chronic gastritis affecting the ANTRUM  Increased acid secretion may result in PUD  H. pylori infection confers increased risk of gastric Ca  H. pylori transmission: oral-oral; fecal-oral; and environmental spread  H. heilmannii: has reservoir in cats, dogs, pigs

4 Features linked to H. pylori virulence:

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Autoimmune gastritis: Spares the antrum and includes hypergastrinemia

Characterized by: a) Abs to parietal cells & IF b) Reduced serum pepsinogen I concentration c)Antral endocrine cell hyperplasia d) Vit. B12 def. e) defective gastric acid secretion (achlorhydria)

Pathogenesis:

gastric mucosa delivers O2, HCO3, & nutrients and wash away acid

a)Flagella: allow motility in viscous mucus b)Urease: generates NH3 from endogenous urea & elevates local gastric pH

c)Adhesins: enhance bacterial adherence to surface foveolar cells d) Toxins: cytotoxin-assoc gene A (cagA): involved in ulcer & cancer development

 Loss

of parietal cells (responsible for secretion of gastric acid and IF)  Loss of gastric acid  stimulates gastrin release  hypergastrinemia & hyperplasia of antral gastrinproducing G cells  Lack of IF  disables ileal vit. B12 abs.   B12 def.  megaloblastic anemia

Helicobacter pylori, gastric biopsy, silver stain on left, Giemsa stain on right. As a rule, these bugs ADHERE closely to the gastric mucin rather

Morphology:

than invade the epithelial cells.

Intestinal metaplasia

Diffuse atrophy Antral endocrine hyperplasia

Located in the antrum PMNs, subepith plasma cells Acid production: Increased to sl. decreased Gastrin: Normal to decreased Other lesion: Hyperplastic/inflam polyps

Located in the body Lymphocytes, macrophages Decreased acid prodution Gastrin: Increased Other lesion: Neuroendocrine hyperplasia Serology: Abs to H. pylori Serology: Abs to H. Parietal cells Sequela: Peptic ulcer, adenoCA Sequela: Atrophy, PA, AdenoCA, carcinoid tumor Associations: Low socioeconomic status, poverty, residence in rural Associations: Autoimmune areas disease; thyroiditis, DM, Graves dse The acute/chronic patterns of gastritis generally conform to the poly/mono principles we so often have referred to. The “oth er” categories o f gastritis are also histologically based.

II.PEPTIC ULCER DISEASE:

Penetration, perforation:  Pain in BACK, CHEST, LUQ

Most often associated with H. pylori- hyperchlorhydric chronic gastritis Present in 85-100% persons with duodenal ulcers and 65% with gastric ulcers Pathogenesis:  imbalances of mucosal defenses and damaging forces that cause chronic gastritis  H. pylori & NSAID use: primary underlying cause of PUD  Gastric hyperacidity:H. pylori infection, parietal cell hyperplasia, excessive secretory responses or impaired inhibition of stimulatory mechanisms such as gastrin release

MALIGNANT TRANSFORMATION: very rare

III. MUCOSAL ATROPHY and INTESTINAL METAPLASIA:  Strongly associated with increased risk of gastric adenoCA  The risk of adenoCA is greatest in autoimmune gastritis

IV. DYSPLACIA:  Chronic gastritis

exposes epith to inflam-related free radical damage & proliferative stimuli  genetic alterations

Common co-factors in peptic ulcerogenesis:

- Chronic NSAID use: direct chemical irritation & suppress PG release necessary for mucosal protection - Cigarette smoking: impairs mucosal blood flow & healing - high-dose corticosteroids: suppress PG synthesis & impair healing Solitary in > 80% of patients < 0.3 cm: shallow ulcers > 0.6 cm: deeper ulcers Round or oval, sharply; punched-out defect  –  mucosal surface; overhang the base (heaped up margins   cancer) Gnawing, burning, aching pain, epigastric Fe deficiency anemia Acute hemorrhage



o o o

Variations in epithelial size, shape and orientation coarse chromatin texture hyperchromasia and nuclear enlargement

V. HYPERTROPHIC GASTROPATHY:  Rugal prominence (cerebriform)  No inflammation  Hyperplasia of mucosa *Probably better termed “hyperplastic” by the traditional classical definition, but, conventionally, called “hypertrophic”.

MÉNÉTRIER DISEASE Caused by excessive secretion of TGF-α Diffuse hyperplasia of the foveolar epith of the body & fundus & hypoproteinemia due to protein-losing enteropathy Micro: hyperplasia of foveolar mucous cells

Morphologic HALLMARKS:

ZOLLINGER-ELLISON SYNDROME Caused by gastrin-secreting tumors, gastrinomas Most commonly found in the SI and pancreas Micro: Doubling of oxyntic mucosal thickness due to a fivefold increase in the number of aprietal cells; Medium-power view of gastric mucosa in a patient with Zollinger  –Ellison syndrome. Note the large increase in the number of parietal cells 60-90% of gastrinomas are malignant Note prominence or “cerebrated” appearance of rugae Hyperplastic gastric mucosa necessitates an increase in surface area

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VI. GASTRIC POLYPS:  Polyps: nodules or masses that project above the level of the

true benign neoplasms and MAY turn into carcinomas, particularly if the exhibit DYSPLASIA on biopsy.  This SAME general principle, is even MORE true of the colon!  But in general, you know the drill: 1) Benign, 2) Malignant on one axis, and 1) epithelial, 2) stromal, and 3) lymphoid on the other axis.’  Micro: irregular, cysticaly dilated and elongated foveolar glands A Gross appearance of gastric polyps of hyperplastic type. Many of the lesions show central umbilication. B  Low-power microscopic view of gastric polyps of hyperplastic type. The cystic dilatation of the glands

surrounding mucosa  Inflammatory and Hyperplastic Polyps:

approx. 75% of all gastric polyps usually develop in assoc with chronic gastritis o Gross:  majority are smaller than 1 cm. & frequently multiple; ovoid w/ smooth surface  In general, a “ polyp ” can be thought of as ANYTHING which projects as a bump or nodule from a mucosal surface.  Hyperplastic polyps  are considered to be NON-neoplastic, and therefore NEVER turn into cancers. ADENOMATOUS polyps are o o

FUNDIC GLAND POLYPS

GASTRIC ADENOMA

Occur sporadically and in individuals w/ familial adenomatous polyposis 5x more common in females (ave. 50 y/o) Occur in the gastric fundus

Gross: well-circumscribed & smooth Micro: cystically dilated, irregular glands lined by flattened parietal or chief cells

Almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia 3x more common in males (50-60 y/o) Most commonly located in antrum

Gross: solitary, < 2 cm. Micro: ALL GI adenomas have epithelial dysplasia Increased incidense in pts w/ FAP Risk of adenoCA is related to the size of the lesion (> 2 cm.) CA may be present in up to 30% of gastric adenomas

VII. CARCINOMA:

VIII. ADENOCARCINOMA:

 Arise from the generative or basal cells of the foveolae, on a

 







background of chronic atrophic gastritis w/ intestinal metaplasia and preceded by various stages of dysplasia, CIS, and superficial CA Accompanied by hypochlorhydria in 85-90% of cases High intragastric ph promotes the growth of bacteria that reduce dietary nitrate to nitrite and then convert dietary amines, in the presence of nitrite into carcinogenic N-nitroso-compounds Pathogenesis:  germline mutations in CDH1 which encodes Ecadherin (a protein that contributes to epithelial intercellular adhesion)   loss of E-cadherin function a key step in the devt of diffuse gastric CA; Mutations in Beta-catenin (a protein that binds to both E-cadherin & APC), microsatellite instability and hypermethylation of some genes  sporadic intestinal-type gastric CA (2) Major categories of gastric adenocarcinoma: a. INTESTINAL-TYPE: arise from metaplastic epithelium b. DIFFUSE-TYPE:  best represented by linnitis plastica or signet ring (adeno)carcinoma Adenocarcinoma growth patterns: These are logical anatomic or “geometric” descriptions, and NOT exact classifications. o LINITIS PLASTICA: Most spectacular, and most feared , of all gastric adenocarcinomas. It grows diffusely through all layers of the stomach, greatly thickening its wall, and giving the stomach a classic LEATHER BOTTLE appearance. It has a horrible prognosis. DIFFUSE WALL THICKENING of ALL FOUR STOMACH LAYERS IS THE RULE . Not only does it behave like wildfire but is also poorly differentiated “signet” cells, diffusely infiltrative. o Signet ring cells are POORLY differentiated adenocarcinoma cells, and are OFTEN seen with linitis plastica. Could those large “holes” in the cytoplasm possibly be mucicarmine positive” Answer: YES

 Depth of invasion & extent of nodal and distant metastasis at time

of diagnosis: MOST powerful prognostic indicators for gastric cancers  Advanced CA:  first detected as mets to the supraclavicular sentinel LN (Virchow’s node)  Sister Mary Joseph nodule : marker of metastatic CA; subcutaneous nodule in periumbilical region

IX. LYMPHOMA:   

 

5% of gastric malignancies Most common are extra-nodal marginal zone B-cell lymphomas (lymphoma of mucosa-associated lymphoid tissue or MALToma) Pathogenesis: Usually arise at sites of chronic inflammation pro-lymphomatous inflam: H. Pylori infection o translocations: t(11;18)(q21;q21) most common  o activation of NF-kB, a transcription factor that promotes B cell growth & survival Micro:  dense lymphocytic infiltrate in the lamina propria  lymphoepithelial lesions; express B cel markers CD19 and CD20 Clinical Features : most common presenting symptoms  dyspepsia & epigastric pain

X. CARCINOID TUMOR:

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  



Arise from the diffuse components of the endocrine system Gross:  intramural or submucosal masses that create small polypoid lesions Micro: islands, trabeculae, strands, glands, or sheets of uniform cells with scant, pink granular cytoplasm and a round to oval, stipples nucleus Immuno: (+) for endocrine granule markers (synaptophysin and chromogranin A)



The most important prognostic factor for GI carcinoid tumors is LOCATION



Foregut carcinoid tumors rarely metastasize

FEATURES OF GASTROINTESTINAL CARCINOID TUMOR: Feature Esophagus Stomach Fraction of GI carcinoids Mean patient age (yr) Location

Proximal Duodenum

Jejunum and Ileum

Appendix

Colorectum