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GI2 #02 Mon. 02/23/04 9am Dr. Cunningham J.

Uxer for Jenny Wiggins Page 1 of 6

I.

Introduction to GI Pathophysiology Esophagus A. Gastroesophageal Reflux Disease Pathophysiology (not discussed. Ppt included for completeness)

Erosive esophagitis ranges from slight redness to erosions. Complications are stricture, Barretts epithelium, perforation, ulcer, and hemorrhage.

Therapy includes pharmacologic suppression of gastric acid & anti-relux surgery (Nissen fundoplication to hiatal hernia & create new GE junction competence). B. Barrett Esophagus (not discussed. Ppt included for completeness)

Adaptation to chronic persistent gastric reflux Replacement of squamous epithelium of esophagus by columnar epithelium. Cardia type mucous glands; fundal-type glands with parietal and chief cells; intestinal type epithelium.

Metaplastic epithelium, dysplasia, adenocarcinoma C. Achalasia Pathophysiology


Lower esophageal sphincter (LES) does not completely relax, basal tone

Controlled by hormones and neural (vagus) to or the muscle tone


Lacks propulsive peristaltic ability

Food accumulates at the LES


Decreased myenteric ganglion cells Disorder doesnt allow complete relaxation of basal tone in the LES and the food accumulates at the LES leading to esophageal dilitation. Cant find anything blocking esophageal outflow, so this is a functional obstruction and is usually mediated by hormones or nerves. (As opposed to a mechanical obstructionfibrous tissue, tumor, something physically blocking the outflow.) D. Esophageal Carcinomas The esophagus lacks a serosa which facilitates spread of esophageal carcinoma (squamous cell or adenocarcinoma) by direct extension and rapid involvement of regional lymph nodes. Can extend into the tracheaclinical implications of work-up and prognosis. E. Regional Lymph Node Mets: Clinical Significance of Lymphatic Drainage Follow blood vessels: Upper 1/3: cervical, internal jugular, supraclavicular

GI2 #02 Mon. 02/23/04 9am Dr. Cunningham J. Uxer for Jenny Wiggins Page 2 of 6

Middle 1/3: paratracheal and hilar, aortic, cardiac, and paraesophageal Lower 1/3: retroperitoneal, celiac, left gastric Visceral metastases: Liver and lung Pictureslide 28: cross section thru the lungs, esophagus, and trachea rigid looking structure. See both direct invasion and lymph spread. o Cancer started in the mucosa extends thru the wall (no serosa) extends into adjacent structures. o See isolated islands of firm white tissue surrounded by loose, fibrous tissue = metastatic focus of cancer in esophagusHilar lymph nodes o In epithelium, carcinomas spread via lymphatics to regional lymph nodes, direct invasion thru wall, & hematogenous spread to lungs. F. Esophageal Varices Clinical Significance of Venous Drainage

From the speakers notes for the picture in slide29: Venous layers of the esophagus. 3 parts of venous system related to esophagus: intrinsic veins, associated veins, & extrinsic veins. 2 layers of veins in the wall of esophagus are superficial venous plexus (located in the lamina propria & muscularis mucosa) & submucosal plexus (within the circular muscle). In distal esophagus, venous blood drains 1st from a superficial mucosal network of small intraepithelial blood vessels into submucosal, longitudinally oriented deep intrinsic veins. Once in intrinsic veins, blood drains through a system of transverse perforating veins with unidirectional valves into extrinsic serosal & periesophageal veins & ultimately into the left gastric vein inferiorly and the azygos vein superiorly. Veins of upper drain into the SVC Veins of middle drain into the azygous Veins of lower drain into the portal vein by way of the LEFT gastric coronary veins. This is an anatomy ?can be asked for portal HTN. Veins are present in tissue in adventitia, submucosa ,lamina propria mucosa, circular & longitudinal muscle. Submucosal veins dilate in portal HTN and esophageal varices.

Review clinical significance of this. o Cirrhosisslide 31 Fibrous tissue disrupts livers vasculature. This obstructs tributaries of portal vein. pressure flow into short gastric veins of the left coronary artery dilatation in submucosa. High P area of portal veins and esophageal varices. Q: How can you tell the difference between direct extension & lymphatic spread?

GI2 #02 Mon. 02/23/04 9am Dr. Cunningham J. Uxer for Jenny Wiggins Page 3 of 6

A: Common in GI. Important because used to stage cancer. Direct extension: see a direct extension thru the wall into adjacent structures, and even lymph nodes. Metastatic spread: see cancer in an isolated lymph node due to lymphatic spread III. Small Intestinenot much was said here. Look at the following:

Serosa Muscularis Propia Submucosa o Enteric Plexus o Peyers Patches (ileum)very prominent in the ileum Mucosal Epithelial Cells

IV. Stomach: Five Anatomically Defined Zones Review the histo of these Cardia Fundusdome shaped area Body or Corpushas majority of gastric glands, including the parietal cells o Parietal cells secrete acid (HCl) & intrinsic factor Antrum o Favorite site for ulcersLesser curvature, near body o Peptic ulcers tend to occur at the junction of acid secreting epithelial tissue (body) and non-acid secreting epithelial tissue (antrum) Pylorus o Carcinomas Lesser curvature, near antrum Proximal duodenum


V.

Small intestine, again to follow w/ppts A. Pictures: Slide 6 7

Shows surface area of small intestine for absorption, which is its major function. Will talk about this in malabsorptive disorders. Has circular folds, vili, microvili to absorptive ability Slide 8: small intestine. Vili, goblet cells, muscularis mucosa, background inflammatory cells.

GI2 #02 Mon. 02/23/04 9am Dr. Cunningham J. Uxer for Jenny Wiggins Page 4 of 6

Slide 9: Normal is on left. Right shows disorders that disrupt mucosa surface area: no vili = celiac sprue, no microvili = cant absorb food components B. Meckels diverticulum

Disorder due to embryology of small intestine. Remnant of the vetilline duct (omphalomesenteric) True diverticulum: Has all 3 layers of the GI tract. Meckels diverticulum. Vermiform appendix is an example. False diverticulum: Does not have all layers of the GI tract. Contains all layers of the bowel wall. Can have small intestine epithelium. May have acid secreting gastric mucosa. Will have parietal cells that secrete acid. Ulceration/diverticulitis/bleedingulcer will develop in the non-acid secreting epithelium outside the diverticulum. AGAIN: peptic ulcers develop at the junction of acid secreting and nonacid secreting epithelium. 2% / 2 feet from ICV (ileocecal valve) / 2inches long. o Think of 2s. 2% of the population has this. Of this 2%, 2% are symptomatic & present like acute appendicits. o Slides 11 & 12 show Meckels diverticulum. o Slide 13 is the vermiform appendix.

VI. Colon A. Anatomy of the Colon

Six (6) regions, the caliber of lumen progressively diminishes from cecum to sigmoid colon o 1st part reabsorbs remainder of water Right colon vs. left colon carcinomas o Right carcinomas: polypoid infiltrative lesion: larger lumen, presents later. Present with occult blood loss. o Left carcinomas: change in bowel habits and obstruction because lumen is smaller Taeniae coli = longitudinal muscle bundles separated into short segments, haustra = evaginations of the colonic wall between taeniaeimportant in development of false diverticulum False diverticulumdiverticular disease of colon

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Picture: small intestine, colon, arrows to teniae, haustra, can see mucosal evaginations (can include mucosa or mucosa & submucosa)look like balloons. Pouchevagination into surrounding structure; can get appendicitis of colon = diverticulitis. More common on the left. Disease of aging, low fiber diet. Due to pressures at that point of the colon. Sphincter action of the ileocecal valve o Differentiate inflammatory bowel disease based on affected sections of colon. o Incompetence due to inflammatory process that is limited to the colon and backwash ileitisbackwash into terminal ileum o Ulcerative colitis only affects the colon. If seen affecting the small bowel, its due to incompetent ileocecal valve. Limited to terminal ileum Meissner and Auerbach enteric plexus o Lack of leads to megacolon (dilated colon), acquired and congenital o Acquired: Chagras diseaseinfection that destroys enteric plexus. Ulcerative colitistoxic changes & severe inflammatory process that destroys the enteric plexus o Congenital: Hirschsprung disease.

Lymphatic plexus in submucosa o Lymphatic invasion and metastatic spread o Determines opportunity for metastatic spread. o In colon, higher concentration of lymphatics beyond muscularis mucosa o survival rate as tumor spreads through wall because risk of lymph node invasion. o Stomach has the same factor. B. Hirschsprung Disease

Congenitalfailure of ganglion cell migration. A segment of colon, usually the distal segment that lacks the enteric plexus. Creates a functional obstruction because theres no neural stimulation. In collapsed segment of colon and beyond it, pt is missing enteric plexus. So dilated segment looks diseased but its actually good because the enteric plexus allows it to dilate. Resect collapsed part. Junction of two separate blood vessel systems Arterial blood supply of the inferior mysenteric and superior circulation o At overlap theres a watershed area @ the splenic flexure and rectosigmoid junction. Have 2 separate blood vessel systems. o Risk of ischemic injury Arterial blood supply of the inferior mysenteric and the internal iliac artery

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o Watershed area @ rectosigmoid junction and mid-rectum o Risk of ischemic injury C. Colon Adenocarcinoma and Anatomy

Anatomy of Colon and Spread of Carcinoma into the Wall- Dukes Stages o Mucosa and submucosa

Mucosa: columnar adenocarcinoma wall regional paracolonic lymph nodes In mucosa the tendency is not to metastasize.

Lymphatics are in submucosa. If carcinoma penetrates here, get lymph node invasion. o Muscularis mucosa o Circular and longitudinal muscular o Serosathink about cancer. Have epicolonic lymph nodes here. o Regional Lymph nodes o Distant Mets

Colon Adenocarcinoma o Spread-Invasion o Into the wall, o Spread-Lymphatics o Regional pericolonic lymph nodesworst prognosis o Distant-Vascular o Livercheck for liver invasion as part of work up. Slide 30colon resection for cancer. See the mucosal surface. Slide 31Diagram to show regional lymph nodes in serosal tissue.

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