Gastro02-IntroGIPath

7/31/2019 Gastro02-IntroGIPath

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GI2 #02

Mon. 02/23/04 9am

Dr. Cunningham

J. Uxer for Jenny Wiggins

Page 1 of 6

Introduction to GI Pathophysiology

I. EsophagusA. Gastroesophageal Reflux Disease Pathophysiology (not discussed. Ppt included

for completeness)

• Erosive esophagitis ranges from slight redness to erosions.

• Complications are stricture, Barrett’s 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 doesn’t allow complete relaxation of basal tone in the LES and the

food accumulates at the LES leading to esophageal dilitation. Can’t find

anything blocking esophageal outflow, so this is a functional obstruction

and is usually mediated by hormones or nerves. (As opposed to a

mechanical obstruction—fibrous 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 trachea—clinical

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


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

•

Picture—slide 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 esophagus—Hilar 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 speaker’s 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 distalesophagus, 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 ⅓ drain into the SVC

• Veins of middle ⅓ drain into the azygous

• Veins of lower ⅓ 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 Cirrhosis—slide 31

Fibrous tissue disrupts liver’s 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


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 Intestine— not much was said here. Look at the following:

• Serosa

• Muscularis Propia

• Submucosa

oEnteric Plexus

oPeyer’s Patches (ileum)— very prominent in the ileum

• Mucosal Epithelial Cells

IV. Stomach: Five Anatomically Defined Zones

• Review the histo of these

• Cardia

• Fundus— dome shaped area

• Body or Corpus— has majority of gastric glands, including the parietal cells

o Parietal cells secrete acid (HCl) & intrinsic factor

• Antrum

o Favorite site for ulcers—Lesser curvature, near bodyo Peptic ulcers tend to occur at the junction of acid secreting epithelial

tissue (body) and non-acid secreting epithelial tissue (antrum)

• Pylorus

oCarcinomas – Lesser curvature, near antrum

• Proximal duodenum

V. Small intestine, again to follow w/pptsA. 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


Page 4 of 6

• Slide 9: Normal is on left. Right shows disorders that disrupt mucosa

surface area: no vili = celiac sprue, no microvili = can’t absorb food components

B. Meckel’s diverticulum• Disorder due to embryology of small intestine. Remnant of the vetilline duct

(omphalomesenteric)

• True diverticulum: Has all 3 layers of the GI tract. Meckel’s

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/bleeding— ulcer will develop in the non-acid

secreting epithelium outside the diverticulum.

• AGAIN: peptic ulcers develop at the junction of acid secreting and non-

acid 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 Meckel’s diverticulum.

o

Slide 13 is the vermiform appendix.

VI. ColonA. Anatomy of the Colon

• Six (6) regions, the caliber of lumen progressively diminishes from cecum to

sigmoid colon

o 1 st 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 becauselumen is smaller

• Taeniae coli = longitudinal muscle bundles separated into short segments,

haustra = evaginations of the colonic wall between taeniae— important in

development of false diverticulum

• False diverticulum— diverticular disease of colon



GI2 #02

Mon. 02/23/04 9am

Dr. Cunningham


Page 5 of 6

• Picture: small intestine, colon, arrows to teniae, haustra, can see mucosal

evaginations (can include mucosa or mucosa & submucosa)—look likeballoons. Pouch—evagination 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 ileitis”—backwash into terminal ileum

o Ulcerative colitis only affects the colon. If seen affecting the small

bowel, it’s due to incompetent ileocecal valve. Limited to terminal ileum

• Meissner and Auerbach enteric plexus

o Lack of leads to megacolon (dilated colon), acquired and congenitalo Acquired: Chagra’s disease—infection that destroys enteric plexus.

Ulcerative colitis—toxic 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

• Congenital—failure of ganglion cell migration. A segment of colon, usually

the distal segment that lacks the enteric plexus. Creates a functional

obstruction because there’s no neural stimulation.

• In collapsed segment of colon and beyond it, pt is missing enteric plexus. So

dilated segment looks diseased but it’s 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 there’s 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



GI2 #02

Mon. 02/23/04 9am

Dr. Cunningham


Page 6 of 6

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 Serosa— think about cancer. Have epicolonic lymphnodes here.

o Regional Lymph nodes

o Distant Mets

• Colon Adenocarcinoma

o Spread-Invasion

o Into the wall,

o Spread-Lymphatics

o Regional pericolonic lymph nodes— worst prognosis

o Distant-Vascular

o Liver— check for liver invasion as part of work up.

• Slide 30—colon resection for cancer. See the mucosal surface.

• Slide 31—Diagram to show regional lymph nodes in serosal tissue.

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Gastro02-IntroGIPath