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II.

1 – Gastrointestinal Tract
Robbins

A. ANATOMIC ANOMALIES DISEASE ETIOLOGY Atresia  CHD  Other GIT malformations Fistula  GERD, Caustric burns, Radiotherapy  Congenital, Scleroderma  Congenital  Long-standing reflux esophagitis  Chronic graft-vs.-host disease  congenital heart disease, neurologic problems, GU or other GI malformations  Aspiration, suffocation from food, pneumonia, fluid & electrolyte imbalance

I.

THE ESOPHAGUS MORPHOLOGY  Portion of esophagus is replaced by thin, noncanalized cord, with blind pouches above and below the atretic segment  Connection between the esophagus and the trachea or a mainstem bronchus

CLINICAL MANIFESTATIONS

 Incompatible with life

Stenosis

 Episodic dysphagia

 Esophageal wall fibrous thickening

Mucosal webs

 Plummer-Vinson Syndrome: Cheilosis, glossitis, iron deficiency anemia  Episodic dysphagia

 UPPER esophageal muscosal overgrowths

Esophageal rings

 Episodic dysphagia

 LOWER esophageal muscosal overgrowths  “A” ring: if above the gastroesophageal junction  “B” or Schatzki ring: if at the gastroesophageal juction  Muscularis propria hypertrophy

B. LESIONS ASSOCIATED WITH MOTOR DYSFUNCTION DISEASE ETIOLOGY CLINICAL MANIFESTATIONS  inhibitory neuron dysfunction  degeneration of CNS or peripheral nerves (DM, amyloidosis, cancer)  protozoal (Toxoplasma) infection of esophageal myenteric plexus of nerves.  Progressive dysphagia  Aperistalsis  Nocturnal regurgitation and aspiration of undigested food. COMPLICATIONS  Inc risk of SCC (~5%).  Candida esophagitis.  Aspiration pneumonia.  Airway obstruction.

MORPHOLOGY

Achalasia

 Proximal esophageal dilation  Thickened or thinned muscular walls  Regurgitation with mucosal dage

•Secondary Achalasia

   

Chagas disease Disorders of the vagal dorsal motor nuclei (polio, surgical ablation) Diabetic autonomic neuropathy Infiltrative disorders (malignancy, amyloidosis, sarcoidosis)  Crura (muscles) of diaphragm and the esophagus are not close enough. COMPLICATIONS  ulceration with bleeding & perforation.  Rolling hernias can have strangulation & obstruction.

Hiatal Hernia

 unknown.  Rolling hernias can be secondary to surgery.

Sliding (axial):  Shortened esophagus  Traction of upper stomach into thorax  Bell-like dilation of stomach w/in the thoracic cavity Paraesophageal (rolling):  Cardia of stomach dissects into the thorax adjacent to the esophagus  Outpouchings of the alimentary tract containing one or more wall layers

Diverticula •Zenker Diverticulum  disordered cricopharyngeal motor function  Dysphagia, food regurgitation, mass in the neck  Aspiration with pneumonia

 UPPER esophagus

From 2015 2B edited by Anj. Anne. How. Jerro. Mark. Joseph. Tin

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boggy.or radiotherapy. Chemo. radiation.5 – The Thyroid Gland (Robbins) Page 2 of 8 . Autoimmune diseases. EtOH. with linear streaks or patches of similar mucosa in the distal esophagus  Microscopic: Normal squamous mucosa of distal esophagus replaced by metaplastic intestinal-like columnar epithelium Infectious and Chemical Esophagitis Causes:  Prolonged gastric intubation  Ingestion of irritants: alcohol corrosive acids or alkalis. ESOPHAGITIS DISEASE  Reflux Esophagitis ETIOLOGY CLINICAL MANIFESTATIONS In adults Dysphagia Heartburn Regurgitation of gastric contents in the mouth  Hematemesis  Melena  Stricture or Barrett esophagus     MORPHOLOGY antireflux mechanisms  Sliding hiatal hernias  Delayed gastric emptying and gastric volume  the esophageal mucosa  Hyperemia and edema  Thickened basal zone & thinning of superficial epithelial layers  Neutrophil or eosinophil infiltration  Superficial necrosis and ulceration with adherent inflammatory exudate Barrett Esophagus  long-standing gastroesophageal reflux disease (GERD). aspergillosis) infection  Uremia. acute hemorrhagic erosive gastritis  Microscopic: neutrophil invasion. viral (Herpesvirus. erosion Pyloric Stenosis B. velvety mucosa at the gastroesophageal junction. Acute Gastritis Chronic Gastritis  H. adherent blood clots C. Graft-vs-host disease. tobacco.  In adults  may lead to adenocarcinoma  Gross: irregular circumferential band of red. inflammation. Gastritis I. obstruction. chemotherapy.  Pressure rupture of the esophagus just above the diaphragm  Tortuous. tobacco. THE STOMACH MORPHOLOGY  In the gastric muscle wall CLINICAL MANIFESTATIONS  Fatal if with respiratory impairment with pulmonary hypoplasia  Male to female ratio 4:1  In utero displacement of the stomach cephalad  Hypertrophy or hyperplasia of pyloric muscularis propria  Visible peristalsis  Palpable firm ovoid mass  Gross: edema and hyperaemia. coarse-textured mucosa Histologically: Lymphocyte and plasma cell infiltrate in lamina propria Intraepithelial neutrophilic infil8s Mucosal gland atrophy Metaplasia of surface columnar epithelium to intestinal-type Dysplasia in long standing C.  Irregular luminal protrusion of overlying mucosa  Superficial ulceration.•Traction Diverticulum •Epiphrenic Diverticulum Lacerations (Mallory-Weiss Syndrome) Boerhaave Syndrome Esophageal Varices  congenital or result of motor dysfunction  discoordination of peristalsis & lower sphincter relaxation  Episodes of excessive vomiting  Failure of LES relaxation  Alcohol  Large amounts of alcohol  Portal hypertension  90% of patients with alcoholic cirrhosis have esophageal varices. Crohn disease        Gross: reddened.  Schistosomiasis  asymptomatic  Nocturnal regurgitation of massive amounts of fluid        no symptoms until rupture with hematemesis  90% chance of recurrence Massive hematemesis Inflammation Residual ulcer Mediastinitis Peritonitis  Mid-esophageal  Just above lower esophageal sphincter  longitudinal tears across the esophagogastric junction or in the upper stomach are mucosal or sometimes entirely through the wall with perforation. mucormycosis. excessive hot fluids. stress. CONGENITAL ANOMALIES DISEASE ETIOLOGY Pancreatic heterotopia Diaphragmatic Hernia  Weakness of the diaphragm II. ischemia. pylori colonization of mucosa EtOH. epidermolysis bullosa) A. post-surgical. smoking  Bacteria. uremia. systemic infections. dilated veins in distal esophageal submucosa/mucosa. GASTRITIS  NSAIDs. CMV) or fungal (candidiasis. Chron disease  Systemic desquamative disorders (pemphigoid.

belching. clean ulcer bases  Microscopic: necrotic debris.  Nausea. Rectum)  Arrested (proximal to distal) migration of neural crest cells into the gut  Assoc with Down syndrome  Male female ratio 4:1  Neonatal failure to pass meconium or abdominal distention  Risk: perforation. extensive burns. vomiting. ENTEROCOLITIS  >250 gm daily stool production with 70%-90% water  Dysentery  low volume painful diarrhea  Secretory  Net intestinal fluid secretion >500 mL/day. enterocolitis  Occur in Chagas disease.  Astroviruses I. anorexia. A. inflammatory bowel disease. fever. gastric rupture Bezoars Eosinophilic gastritis Hypertrophic Gastropathy •Menetrier disease •Hypertrophichypersecretory gastropathy •Gastric Gland hyperplasia Gastric Varices  Luminal concretions  Hyperplasia of mucosal epithelial of gastric rugal folds  Hyperplasia of surface mucous (foveolar) cells  Fundic gland atrophy  Hyperplasia of parietal and chief cells (fundic glands)  Parietal cell hyperplasia  Occurs near the gastroesophageal junction  Hyperchlorydia III. lined by mucosa and communicating with the gut lumen  Absence of ganglion cells and ganglia in muscle wall and submucosa of affected segment (usu. and psychosomatic disorders B. peritonitis. virus). diarrhea  Osmotic  >500 mL stool/day. MISCELLANEOUS CONDITIONS  Gastric outlet obstruction (pyloric stenosis. or aching pain.  Calicivirus (Norwalk/Norwalk-like  Acute illness: 1-7 days  Viral Entercolitis virus. weight loss  COMPLICATIONS: Hemorrhage. bowel obstruction. tumors)  Gastric and intestinal atony (ileus)  Phytobezoar  trichobezoar (hairball)  Heavy eosinophilic infiltration of the mucosa or submucosa  Idiopathic. sepsis. bloating. osmotic gap diarrhea  Malabsorption  Voluminous. isotonic with plasma.5 – The Thyroid Gland (Robbins) persists during fasting  Shortened villi  lamina propria inflammation  enterocyte amage (brush border loss & cytoplasmic vascuolization  crypt hyperplasia Page 3 of 8 . scarring Peptic Ulcer  exposure to acid and peptic juices  Gross: sharply punched-out defect with overhanging mucosal borders. headache  Enteric adenoviruses. sever trauma (Curling ulcers)  ICP (Cushing ulcers)  NSAIDs  Acute gastric erosions or ulcers  Ulcers less than 1cm in diameter  Ulcer base is brown (blood) D. Allergy  Hypoalbuminemia  risk for PUD  Protein-losing enteropathy  TGF-α overexpression (?)  Hypochlorydia  Hypoproteinemia  Hyperchlorydia  Excessive gastrin secrxn  Gastrinoma (ZollingerEllison)  In portal hypertension Gastric Dilation  Rarely. perforation. granulation tissue. deep scarring Acute Gastric Ulceration  Severe stress – shock. PEPTIC ULCER DISEASE  Epigastric gnawing. Sapporo-like  Diarrhea. bulky stools w/ excess fat and ↑ osmolality  Exudative  Purulent bloody stools diseases Infectious Enterocolitis  Rotavirus. CONGENITAL ANOMALIES DISEASE ETIOLOGY Meckel Diverticulum Congenital Aganglionic Megacolon\ (Hirschsprung Disease) Acquired Megacolon Diarrhea SMALL AND LARGE INTESTINES CLINICAL MANIFESTATIONS MORPHOLOGY  Blind pouch leading off the alimentary tract. worse at night and 1-3 hrs after meals. smooth. burning.C.

frothy. migratory lamina propria arthritis. distention. dermatitis Peripheral neuropathy  Diarrhea. impotence. dehydration. rye Tropical  Travel or habitation (Postinfectious) Sprue exposure Whipple Disease  Tropheryma whippelii Lactase Deficiency Abetalipoproteinemia  Cannot synthesize apolipoprotein B  Diarrhea. sepsis. Enterocolitis Protozoa  Immature gut immunity  Onset of oral feeding  Necrotizing  Bacterial colonization Entercolitis  Mucosal injury  Impaired intestinal blood flow  Collagenous Colitis  Autoimmune disease. anorexia. malabsorption  No abnormalities of mucosa  Failure to thrive. heart disease  (+) PAS  In whites and males  Diarrhea. flatus. bulky. MALABSORPTION SYNDROME Defects in:  Intraluminal digestion  Terminal digestion  Transepithelial transport  NSAID  Explosive diarrhea & abd pain  Hrs-days incubation. distended macrophages in the weight loss. abdominal  mucosa becomes laden w/ cramps. retinitis  Burr cells pigmentosa D. flatulence. cholangitis.5 – The Thyroid Gland (Robbins) MORPHOLOGY  Non-caseating sarcoid-like granulomas  Transmural inflammation  Goblet cell population  Maintenance of gladular architecture  Skip lesions Page 4 of 8 . dysentery  Yersinial & mycobacterial infections  Right colon – plaquelike adhesion of fibrinopurulent necrotic. Ingestion of preformed  Bacterial Enterocolitis  Infection w/ enteric   Antibiotic Clostridium difficile toxin Associated Colitis overgrowth after (Pseudomem-branous antibiotic therapy Colitis)  Parasitic  Nematodes.  Genetic fever. fatgue  marked atrophy of villi  Antibodies to tissue  elongated regenerative crypts transglutaminase and  surface epithelial damage with gliadin intraepithelial lymphocytes  Dermatitis herpetiformis  exuberant lamina propria chronic  COMPLICATIONS: iron inflammation and vitamin deficiencies. sacroiliitis. steatorrea. erythema immunoreactivity nodosum. Cestodes. hemorrhage. hyperparathyroidism  Purpura and petechiae. I. neurologic and  Lipid vacuolation liver disorders. pain. malabsorption. IDIOPATHIC INFLAMMATORY BOWEL DISEASE DISEASE ETIOLOGY CLINICAL MANIFESTATIONS  Intermittent attacks of diarrhea. weight loss. cystically dilated glands surrounded by proliferating smooth muscle cells  Rectal bleeding  Mucosal discharge MALABSORPTION SYDROME Celiac Disease  Gluten in wheat. risk for GI lymphoma  Villous blunting  Abundant lymphocytes and eosinophils in lamina propria  Diarrhea. shock  Chronic watery diarrhea with abdominal pain  Mucosal edema.  Abnormal host ankylosing spondylitis. fever.greasy stools  Anemia. necrosis in terminal ileum and proximal colon or entire gut  Patches of bandlike collagen under the surface epithelium  Intraepithelial infiltrates of lymphocytes  In mucosal epithelium     Mild lymphocytic infiltrate Crypt epithelial cell apoptosis Focal ulceration Mucosal inflammation  Inflammatory diarrhea  Bone marrow transplant  Enterostomy  Inadequate nutrition  Acute inflammatory destruction of the cecal region  Chronic lymphoplasmacytic inflammation  Lymphoid follicular hyperplasia  Acute angulation of anterior rectal shelf  Mechanical abrasion  Distorted. oat. grayyellow debris and mucus to the damaged colonic mucosa  In low-birth-weight or premature neonates  Mild diarrhea to fulminant illness with gangrene. barley. diarrhea. sprue Miscellaneous Intestinal Inflammatory Disorders  AIDS-associated  HIV diarrheal illness  Lymphocytic Colitis  Transplantation  Drug-induced interstinal injury  Radiation enterocolitis  Neutropenic colitis (Typhlitis)  Diversion colitis  Colitis cystic profunda “solitary rectal ulcer syndrome” C. weight loss. abdominal pain. bleeding  Ostopenia. tetany  Amenorrhea. steatorrhea. perforation. infertility.  Infectious weight loss Chron Disease  Mucosal integrity  Migratory polyarthritis. edema. uveitis. diarrhea.

erythema nodosum. . fibrosis. strangulation  Fibrous bridging between viscera  Telescoping of one intestinal segment into immediately distal segment Intussusception Volvolus  Obstruction and infarction  Twisting of a bowel loop about its mesenteric vascular base IV.5 – The Thyroid Gland (Robbins) . calculus. radiation  Children – rotaviral vaccination or infection  Adults – tumor  Complications: internal herniation. dysplasia  Non-granulomatous  No skip lesions  Mucosa reddened. gangrene. sinus tracts.000 cells/mm3 Acute Appendicitis  Early:  scant appendicial wall neutrophil exudates  congestion of subserosal vessels  perivascular neutrophil emigration  Advanced/Acute suppurative:  Severe neutrophilic infiltration  Fibrinopurulent serosal exudates  Luminal abscess formation  Ulceration  Suppurative necrosis  Dilation of appendiceal lumen by mucinous secretions  Peritoneum distended  Tenaceious semisolid. fibrosis. abd discomfort. uveitis. stricture  Tortuous abnormal dilations of submucosal veins to lamina propria of cecum or ascending colon Angiodysplasia Hemorrhoids  Constipation  Venous stasis during pregnancy  Cirrhosis (portal HPN)  Usu asymptomatic  Cramping. intraluminal pressure ischemia bacterial invasion  Periumbilical pain migrating to RLQ  Nausea or vomiting  Abdominal tenderness  Mild fever  Leukocytosis >15. cholangitis  Risk: carcinoma  cobblestone appearance  aphthous ulcers  Chrronic mucosal damage. sacroiliitis. peforation  Venous thrombosis: acute mesenteric venous occlusion  Chronic ischemia: mucosal inflammation. malabsorption. APPENDIX  Obstruction of appendicial lumen by fecalith. mucinproducing anaplastic Page 5 of 8 Mucocele Pseudomyxoma peritonei  Innocuous obstruction with inspissated mucus  Mucin secreting adenomas  Adenocarcinoma I. ankylosing spondylitis. ulceration. granular or friable iwth inflammatory pseudopolyps and easy bleeding E.Ulcerative Colitis amyloidosis  COMPLICATIONS: fistulas. INTESTINAL OBSTRUCTION DISEASE ETIOLOGY  Peritoneal wall weakness or defect MORPHOLOGY  Hernia sac  Incarceration  Hernias Adhesions  Peritonitis following surgery. peritonitis CLINICAL MANIFESTATIONS  Variceal dilations of anal and perianal submucosal venous plexi Diverticular Disease  Focal bowel wall weakness  Multi flask-like outpouchings F.abd pain  Toxic megacolon  Migratory polyarthritis. VASCULAR DISORDERS DISEASE ETIOLOGY CLINICAL MANIFESTATIONS Ischemic Bowel Disease     Arterial thrombosis Arterial embolism Venous thrombosis Nonocclusive ischemia        Severe abdominal pain Bloody diarrhea Gross melena Nausea Vomiting Bloating Abdominal wall rigidity MORPHOLOGY  Mucosal infarction: patchy mucosal hemorrhage  Mural infarction: complete mucosal necrosis  Transmural infarction: sudden and total occlusion of major vasculature. obstruction. protein-losing enteropathy  Risk: bowel cancer  Intermittent attacks of bloody mucoid diarrhea. infection. malnutrition. endometriosis. constipation  COMPLICATION: pericolic abscesses.

cholecystitis. pancreatic pseudocyts. hemangioma. or  Dysphagia Lifestyle. nephritic syndrome. acute salpingitis. neurofibroma. or walled-off infections B. with or w/o keratinisation (SCC)  Hemorrhage Genetic  Begin as in situ gray-white. abd trauma. exudates and frank suppuration  Localized abscesses  Tuberculous peritonitis – exudates studded with minute pale granulomas 1. Mesenteric Cysts  Arise from sequestered lymphatic channels. plasma cell. plaquelike  Sepsis Predisposition  Respiratory tree fistulas with longitudinally/circumferential aspiration  Gross: exophytic nodules to excavated and  Patients older than 40. Fibrovascular polyp. fibroma. lipoma.  More often in men and blacks  Dietary. lymphangioma b. TUMORS Primary tumors Mesothelioma Desmoplastic small round cell tumor Secondary tumors TUMORS OF THE GASTROINTESTINAL TRACT ESOPHAGUS 1. Intramural or submucosal: Leiomyoma. cirrhosis CLINICAL MANIFESTATIONS MORPHOLOGY  Peritoneal membranes – dull and gray. peritoneal dialysis. Peritoneal Infection  Can resolve spontaneously or with therapy 2. Mucosal (larger than 3cm): Squamous papilloma.5 – The Thyroid Gland (Robbins) Page 6 of 8 . PERITONEUM A. bowel strangulation. pinched-off enteric diverticula of developing foregut or hindgut. Malignant Tumors DISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY  Adults older than 50 years  Gross: lesions may be polypoid (60%). Benign Tumors: a. diverticulitis. neutrophil infiltrate 3. Sclerosing Retroperitoni tis  Methydergide use  Fibrosing disorders (carcinoid tumors. diffusely infiltrative (15%) Squamous Cell  Obstruction Esophageal  Microscopic: tumors well differentiated. Benign Tumors a. Inflammatory polyp 2. sclerosing cholangitis. more deeply infiltrative masses  Barrett Adenocarcinoma often in men  Microscopic: mucin-producing glandular esophagus  Symptoms of GERD and SCC tumors with intestinal futures. INFLAMMATION DISEASE ETIOLOGY  Appendicitis. peptic ulcer. Carcinoma  Weight loss disorders. developmental cysts of urogenital orgin. sessile or pedunculated  Epithelial tubules and cysts interspersed  Inflamed stroma  Fundic gland dilation  Fibroblast proliferation in submucosa with eosinophil infiltrate  Occur with FAP I. Non-Neoplastic Polyps DISEASE ETIOLOGY  Hyper-plastic or inflammatory polyps  Fundic gland polyps  Inflammatory fibroid polyps  Hamartomatous polyps  Occur with Peutz-Jeghers syndrome or.adenocarcinoma cells V. Diffusely infiltrative signet ring cells STOMACH 1. Riedel fibrosing thyroiditis)  Hydronephrosis  Dense infiltrative fibrosing overgrowth of retroperitoneal tissues  Lymphocyte. exhibit necrotizing excavation (25%).  Juvenile polyposis syndrome  Assoc with chronic gastritis CLINICAL MANIFESTATIONS  90% of gastric polyps MORPHOLOGY  Smooth.

autoimmune gastritis. vomiting. Malignant  Assoc with MSI  ↑ risk for carcinomas  Asyptomatic or may cause occult bleeding with anemia  SI adenomas – cause obstruction and intusseption  Tubular glands. pylori infection  c-KIT gene mutation  Usu. anorexia. weakness. regional lymph nodes. weight loss. DNA methylation  K-RAS. smooth surface  Villous frondlike projections of epithelial surface  Mixture of first two  Features of both hyperplastic polyp and adenoma Colorectal Carcinoma (FAP)  APC gene mutation. abdominal painm. Neoplastic Polyps – Gastric Adenoma 2. flat. progressive bowel obstruction. Asymptomatic  Weight loss. rounded. Diet. iron deficiency anemia. bleeding MORPHOLOGY  Metastatic spread to mesentery. can be sessile or pedunculated Gastric Carcinoma  Environment. SMADs. chronic gastritis. columnar cells with invasion II. abd discomfort. liver enlargement  Gross: polypoid exophytic mass or annular mass with “napkin-ring” obstruction  Histological: tall. partial gastrectomy  H. altered bowel habits. dysphagia. liver TUMORS OF THE COLON AND RECTUM 1. Non-neoplastic polyps DISEASE  Hyperplastic polyp ETIOLOGY CLINICAL MANIFESTATIONS  6th decade MORPHOLOGY  Nipple like hemispheric protrusions  Well-formed mature glands with crowding  Focal sporadic hamartomatous malformations of SI and colon mucosa  Large polyps.b. Smoking. telomerase mutation  Asymptomatic at first  Fatigue. lobulated with arborizing smooth muscle surrounding normal glands  Juvenile polyp  Children <5yrs  Peutz-Jeghers polyp b. nausea. or depressed or excavated  (See Lauren classification)  Lymphoma (MALT)  Gastrointestinal stromal tumor (GIST)  Carcinoid Tumors  Schwannomas  Lipomas  Solid tumor of the gastric mucosa or wall  Tumor cells are either epithelioid or spindle cell shaped  Enterochromaffin-like cell tumor TUMORS OF THE SMALL INTESTINE DISEASE ETIOLOGY Adenomas Adenocarcinoma  In Px with familial polyposis syndromes CLINICAL MANIFESTATIONS  Clinically silent unless they obstruct the intestinal lumen or CBD  Obstruction (cramping pain. hemorrhage  Gastric mucosa dysplasia  Tumors are exophytic. Benign a. vomiting). p53. and pedunculated w/ cystically dialted glands and abundant laminar polyp  Sporadic hamartomatous mucosal polyps of SI and colon  Large polyps. anemia. Adenoma (Neoplastic polyps)  Tubular adenoma  Villous adenoma  Tubulovillous adenoma  Serrated adenoma 2. pedunculated.1 – The Gastrointestinal Tract (Robbins) .Trans Page 7 of 8 . Malignant  Chronic gastritis  Genetic polyposis syndrome  40% harbour carcinoma  Proliferative dysplastic epithelium  Single.

stippled nuclei  (+) for chromogranin and synaptophysin  Early lesions: plaquelike mucosal or submucosal expansions  Advanced: full mural thickness or polypoid exophytic masses protruding to lumen  Microscopic: atypical lymphocytes infiltrate b. Gastrointestinal Lymphoma c. firm. yellow-tan intramural or submucosal masses  Fibrosis of muscularis – kinking and obstruction  Microscopic: islands to sheets of uniform chohesive cells with scant. granular cytoplasm and oval.Trans Page 8 of 8 . or intusseption  In SI or colon submucosa  Spindle shaped ore epitheloid. chemoresponsive  Asymptomatic  Larger lesions: mucosal ulcerations with bleeding. c-KIT positive  Spindle shaped lesions with smooth muscle phenotype  Visceral involvement II. obstruction. Mesenchymal Tumors  Lipomas  GIST  Smooth muscle tumors  Kaposi Sarcoma  (Most common GI mesenchymal tumor)  Amenable to surgical resection. Carcinoid Tumors  Asymptomatic but Sx caused by tumor secretory products  Tumors are small.1 – The Gastrointestinal Tract (Robbins) .a.