GASTROINTESTINAL

TRACT PATHOLOGY

by

Mary Yvonnette C. Nerves, RMT, MD, FPSP

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

CONGENITAL ABNORMALITIES

Atresia/Fistulae

Diaphragmatic Hernia/

Omphalocele/Gastroschisis

Meckel’s Diverticulum

Pyloric Stenosis

Hirschsprung Disease

ATRESIA / FISTULAEAtresia is a condition in which a body orifice or

passage in the body is abnormally closed or absent

Fistula is an abnormal connection or passageway

between two epithelium-lined organs or vessels that

normally do not connect.

OMPHALOCELE (Exomphalos)

defect of the anterior abdominal wall at the

insertion of the umbilical cord

occurs in 1 in 5000 to 1 in 20,000 live births

associated with chromosomal defects,

(trisomies 13, 18, and 21), and with other

disorders such as Beckwith-Wiedemann

syndrome

OMPHALOCELE (Exomphalos)

• Closure of abdominal musculature is incomplete abdominal viscera herniate into a ventral

membranous sac

GASTROSCHISIS (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

GASTROSCHISIS (Laparoschisis)

ventral wall defect involving all layers of theabdominal wall

MECKEL DIVERTICULUM

most common type of true diverticulumoccurs in the ileumoccurs as a result of failed involution ofthe omphalomesenteric (vitelline) duct

RULE of 2s: - 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

MECKEL DIVERTICULUM

TRUE DIVERTICULUM: blind outpouching lined by mucosa that communicates with the lumen and includesall 3 layers of the bowel wall

MECKEL DIVERTICULUM

PYLORIC STENOSIS

due to progressive thickening of the circular muscle of the pylorus gastric

outlet narrowing3-4x more common in MALESgenerally presents in the 2nd or 3rd week of

life new-onset regurgitation and persistent, projectile, nonbilious vomiting

P.E. – hyperperistalsis; ovoidabdominal mass

Tx: Fredet-Ramstedt pyloromyotomy

http://www.google.com.ph/url?sa=i&rct=j&q=pyloromyotomy&source=images&cd=&cad=rja&docid=BANqV3riUxxGqM&tbnid=1OkhbjsjNyP4hM:&ved=0CAUQjRw&url=http%3A%2F%2Fwww.pediatricsurgerymd.org%2FAM%2FTemplate.cfm%3FSection%3DList_Of_Conditions%26TEMPLATE%3D%2FCM%2FContentDisplay.cfm%26ContentID%3D1619&ei=_8o0Ua6nEaidiAeayYCICQ&bvm=bv.43148975,d.aGc&psig=AFQjCNGlZV9Zs-OX0FDFW_XDz5NLCELNyA&ust=1362500345463348

HIRCHSPRUNG DISEASE

A.k.a. Congenital aganglionic megacolonwhen normal migration of neural crestcells from the cecum to rectum is arrested prematurely or when the ganglion cellsundergo premature deathdistal intestinal segment lacks both Meissner submucosal and the Auerbach myenteric plexus

HIRCHSPRUNG DISEASE

Clinical Features: earliest and mostcommon presentation is delayed (> 48 hrs) passage of meconium inthe 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

http://www.google.com.ph/url?sa=i&rct=j&q=treatment+of+Hirschprung%27s&source=images&cd=&cad=rja&docid=Vg0o1GBt2ZPGJM&tbnid=eIwQ_E6Lkh-15M:&ved=0CAUQjRw&url=http%3A%2F%2Fwww.chw.org%2Fdisplay%2FPPF%2FDocID%2F22806%2Frouter.asp&ei=gsw0UbuaIKyviQeAx4B4&psig=AFQjCNEFZWUqYhW5Y8VUNthjxXJ5j5dcvA&ust=1362500846917885

IMPERFORATE ANUS

most common formof congenital intestinal atresia

due to failure of the

cloacal diaphragm

to involute

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

ESOPHAGUS

Esophageal Obstruction

- Achalasia

Esophagitis

Barrett’s Esophagus

Esophageal Varices

Esophageal Tumors

DIVERTICULUM

an outpouching of the alimentary tract that contains one or more layers of the wallZENKER’S DIVERTICULUM (Cricopharyngeal / Pharyngoesophageal): locatedabove the UES

- results from increased intrapharyngeal

pressure in areas of weakness along the

esophageal wall

DIVERTICULUM

ZENKER’S DIVERTICULUM

Diverticulectomy with myotomy

DIVERTICULUM

TRACTION DIVERTICULUM: locatedimmediately above the UES

- located in the lower 3rd of the esophagusand in the region of the hilum of the lung

- attributed to fibrosing mediastinalprocesses or abnormal motility.

EPIPHRENIC DIVERTICULUM: immediately above the LES

- located just above the diaphragm- Cause: unclear

ESOPHAGEAL MUCOSAL WEBS

ledge-like protrusions of mucosaPathogenesis: unknownPATERSON-BROWN-KELLY or PLUMMER-VINSON SYNDROME: webs+ IDA + glossitis + cheilosis

most common in upper esophagus

ESOPHAGEAL RINGS

A.k.a. Schatzki’s / Lower esophagealEsophagogastric rings

similar to webs but are circumferentialand 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 squamocolumnarjunction of the lower esophagus

ESOPHAGEAL RINGS

ACHALASIA

A.k.a. Cardiospasm or megaesophagus

failure of the cardiac mechanism to open

when peristaltic waves conveying food

through the esophagus reach it

nearly complete loss of myenteric

ganglion cells is present in the lower 3rd

of the esophagus

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

ACHALASIA

Technique for pneumatic dilation of

achalasia.

Technique for intrasphincteric injection of

botulinum toxin for achalasia.

REFLUX ESOPHAGITISA.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

REFLUX ESOPHAGITIS

Pathogenesis:

- Conditions that decrease LES tone or

increase abdominal pressure:

a) alcohol and tobacco use, obesity

b) central nervous system depressants

c) pregnancy

d) hiatal hernia

e) delayed gastric emptying

f) increased gastric volume

REFLUX ESOPHAGITIS

Gross: marked

hyperemia with

focal hemorrhage

REFLUX ESOPHAGITIS

REFLUX ESOPHAGITISMorphology: intraepithelial eosinophils

and basal zone hyperplasia

HIATAL HERNIACharacterized by separation of the

diaphragmatic crura and protrusion of

the stomach into the thorax through the

resulting gap

VARICESTHREE common areas of portal/caval

anastomoses

Esophageal

Umbilical

Hemorrhoidal100% related to portal hypertension

Found in 90% of cirrhotics

MASSIVE, SUDDEN, FATAL hemorrhage

is the most feared consequence

VARICES

VARICES

VARICESFACTORS that lead to RUPTURE:

- inflammatory erosion of thinned

overlying mucosa

- increased tension in progressively

dilated veins

- increased vascular hydrostatic

pressure associated w/ vomiting

VARICES

VARICES

BARRETT’S ESOPHAGUSCan be defined as intestinal metaplasia of a

normally SQUAMOUS 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

BARRETT’S ESOPHAGUS

GROSS: patches of red, velvety mucosaextending upward from the GEJ

http://apps.pathology.jhu.edu/blogs/barretts/wp-content/uploads/2008/10/barnfdlo.jpg

INTESTINALIZED (GASTRICIZED)

mucosa is AT RISK for glandular

dysplasia.

Searching for dysplasia when

BARRETT’s is present is of utmost

importance

MOST/ALL adenocarcinomas arising in

the esophagus arise from previously

existing BARRETT’s

BARRETT’S ESOPHAGUS

BARRETT’S ESOPHAGUS

BARRETT’S ESOPHAGUS

TUMORS

BENIGN

MALIGNANT

–Squamous cell carcinoma

–Adenocarcinoma

BENIGN TUMORSLEIOMYOMAS

FIBROVASCULAR POLYPS

CONDYLOMAS (HPV)‏

LIPOMAS

“GRANULATION” TISSUE (PSEUDOTUMOR)‏

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

RISK FACTORS: documented dysplasia

tobacco use

obesity

prior radiation therapy

FACTORS that DECREASE RISK:

- diet rich in fresh fruits and vegetables

- H. pylori serotypes

Most frequent in CAUCASIANS; M > F

Usually occur in the distal 3rd of the esophagus

ADENOCARCINOMA

ADENOCARCINOMA

ADENOCARCINOMA

ADENOCARCINOMA

ADENOCARCINOMA

SQUAMOUS CELL CARCINOMA

Adults over age 45, affects MALES 4x

more than females

RISK FACTORS:

a) alcohol and tobacco use

b) caustic esophageal injury

c) achalasia

RISK FACTORS: d) Plummer-Vinson syndromee) frequent consumption of very hot

beveragessixfold more common in African-American

SQUAMOUS CELL CARCINOMA

Half of SCCs occur in the middle 3rd

of the esophagus

Begins as an in-situ lesion

(SQUAMOUS DYSPLASIA)

SQUAMOUS CELL CARCINOMA

SQUAMOUS CELL CARCINOMA

• DYSPLASIAIN-SITUINFILTRATION

SQUAMOUS CELL CARCINOMA

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

FACTORS that influence survival:1. Sex – F > M2. Stage – In situ, mucosal CA, superficial CA > deeper tumors3. LN mets – 2 or more involved nodes:

worse prognosis4. Other microscopic findings: vascular/lymphatic

invasion & marked tumor necrosis5. Involvement of circumferential surgical margins high probability of recurrence6. Overexpression of EGFR/p53 – worse prognosis

ESOPHAGEAL CARCINOMA

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

STOMACH

CHRONIC GASTRITIS

PEPTIC ULCER

GASTRIC POLYPS

HYPERTROPHIC GASTROPATHY

TUMORS

CHRONIC GASTRITISH. 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

CHRONIC GASTRITISH. 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

CHRONIC GASTRITISH. pylori gastritis:

- 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

CHRONIC GASTRITISH. pylori gastritis:

- 4 Features linked to H. pylori virulence:

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 devt

CHRONIC GASTRITISAutoimmune gastritis: spares the

antrum and includes hypergastrinemia

- char by:

a) Abs to parietal cells & IF

b) Reduced serum pepsinogen I conc

c) Antral endocrine cell hyperplasia

d) Vit. B12 def.

e) defective gastric acid secretion

(achlorhydria)

CHRONIC GASTRITISAutoimmune gastritis:

- Pathogenesis: loss of parietal cells

(responsible for secretion of gastric

acid and IF)

loss of gastric acid stimulates

gastrin release hypergastrinemia &

hyperplasia of antral gastrin-

producing G cells

Lack of IF disables ileal vit. B12

abs. B12 def. megaloblastic

anemia

CHRONIC GASTRITISAutoimmune gastritis:

- Morphology:

Diffuse atrophy

Intestinal metaplasia

Antral endocrine hyperplasia

GASTRITISH. PYLORI-ASSOCIATED AUTOIMMUNE

LOCATION antrum body

INFLAM INFILTRATE PMNs, subepith plasma cells Lymphocytes, macrophages

ACID PRODUCTION Increased to sl. decreased Decreased

GASTRIN Normal to decreased Increased

OTHER LESIONS Hyperplastic/inflam polyps Neuroendocrinehyperplasia

SEROLOGY Abs to H. pylori Abs to parietal cells

SEQUELAE Peptic ulcer, adenoCA Atrophy, PA, AdenoCA, carcinoid tumor

ASSOCIATIONS Low socioeconomic status, poverty, residence in rural areas

Autoimmune disease; thyroiditis, DM, Graves dse

COMPLICATIONS of CHRONIC GASTRITIS

Peptic Ulcer Disease

Mucosal atrophy and intestinal

metaplasia

Dysplasia

PEPTIC ULCER DISEASE• Most often associated with H. pylori-

hyperchlorhydric chronic gastritis

• Present in 85-100% persons with duodenal ulcers and 65% with gastric ulcers

PEPTIC ULCER DISEASEPathogenesis: 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

PEPTIC ULCER DISEASECommon 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)

PEPTIC ULCER DISEASE

Gnawing, burning, aching pain, epigastric

Fe deficiency anemia

Acute hemorrhage

Penetration, perforation:

Pain in BACK

Pain in CHEST

Pain in LUQ

MALIGNANT TRANSFORMATION – very

rare

PEPTIC ULCER DISEASE

PEPTIC ULCER DISEASE

COMPLICATIONS of Gastric Ulcers

Bleeding–Occurs in 15% to 20% of patients

–Most frequent complication

–May be life-threatening

–Accounts for 25% of ulcer deaths

–May be the first indication of an ulcer

Perforation–Occurs in about 5% of patients

–Accounts for two thirds of ulcer deaths

–Rarely, is the first indication of an ulcer

COMPLICATIONS of Gastric Ulcers

Obstruction from edema or scarring–Occurs in about 2% of patients

–Most often due to pyloric channel ulcers

–May also occur with duodenal ulcers

–Causes incapacitating, crampy abdominal pain

–Rarely, may lead to total obstruction with intractable vomiting

COMPLICATIONS of Gastric Ulcers

MUCOSAL ATROPHY and INTESTINAL METAPLASIA

• Strongly associated with increased risk of gastric adenoCA

• The risk of adenoCA is greatest in autoimmune gastritis

Chronic gastritis exposes epith to

inflam-related free radical damage &

proliferative stimuli genetic

alterations

Morphologic HALLMARKS:

a) Variations in epithelial size, shape and

orientation

b) coarse chromatin texture

c) hyperchromasia and nuclear enlargement

DYSPLASIA

HYPERTROPHIC GASTROPATHY

Rugal prominence (cerebriform)

No inflammation

Hyperplasia of mucosa

HYPERTROPHIC GASTROPATHY

Ménétrier disease: resulting from profound hyperplasia of the surface mucous cells with accompanying glandular atrophy, ass. w/ CMV, H. Pylori, ↑TGF-α

Hypertrophic-hypersecretory gastropathy: associated with hyperplasia of the parietal and chief cells within gastric glands

(normal gastrin)

MENETRIER DISEASE

HYPERTROPHIC GASTROPATHY

Gastric gland hyperplasia secondary to

excessive gastrin secretion, in the setting

of a gastrinoma (Zollinger-Ellison syndrome)

ZOLLINGER-ELLISON SYNDROME

GASTRIC POLYPSPolyps: nodules or masses that project

above the level of the surrounding

mucosa

Inflammatory and Hyperplastic Polyps:

approx. 75% of all gastric polyps

usually develop in assoc with chronic

gastritis

Gross: majority are smaller than 1 cm. &

frequently multiple; ovoid w/ smooth

surface

HYPERPLASTIC

POLYP

Micro: irregular,

cysticaly dilated

and elongated

foveolar glands

GASTRIC POLYPSFundic Gland Polyps:

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

GASTRIC POLYPSGastric adenoma:

almost always occur on a background of

chronic gastritis with atrophy and

intestinal metaplasia

3x more common in males (50-60 y/o)

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

GASTRIC POLYPSGastric adenoma:

most commonly located in antrum

Gross: solitary, < 2 cm.

Micro: ALL GI adenomas have epithelial

dysplasia

GASTRIC ADENOMA

CARCINOMAPathogenesis: closely related to environmental factors

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

CARCINOMA(2) Major categories of gastric adenocarcinoma:

a. INTESTINAL-TYPE

- arise from metaplasticepithelium

B. DIFFUSE-TYPE

- best represented by linnitisplastica or signet ring(adeno)carcinoma

ADENOCARCINOMAGROWTH PATTERNS

LINITIS PLASTICA

LINITIS PLASTICA

ADENOCARCINOMADepth 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 periumbilicalregion

GASTRIC CARCINOMAFACTORS related to prognosis:

1. Patient’s age – CA in the young: worse

2. Tumor stage – the deeper the penetration, the greater the chance of mets; polypoid, large intraluminal tumors have lower mets < tumorsgrowing within the wall

3. Location within the stomach: 80% of 5-yr survivors, the lesion is in the distal half of the stomach

4. Tumor margins: pushing/expanding border vs. Diffuse infiltration

GASTRIC CARCINOMAFACTORS related to prognosis:

5. Microscopic type and grading – intestinal

type > diffuse type

6. Inflammatory reaction: cellular infiltrate at

the interface bet tumor & normal tissue: GOOD

px sign

7. Perineural invasion: poor px

8. Regional LN involvement: if NEG, >50% may

survive for 5 years

GASTRIC CARCINOMAFACTORS related to prognosis:

9. Type of surgery – radical subtotal

gastrectomy: best survival

10. Overexpression of c-erbB2 protein, p53 –

poor prognosis

11. Detection of cathepsins and cyclin-

dependent kinase inhibitor (p27Kip1)

expression by IHC: reduced survival

LYMPHOMA5% 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

- translocations: t(11;18)(q21;q21) most

common activation of NF-kB, a transcription

factor that promotes B cell growth & survival

LYMPHOMAMicro: dense lymphocytic infiltrate in the

lamina propria lymphoepithelial lesions

- express B cell markers CD19 and CD20

Clinical Features: most common presenting

symptoms dyspepsia & epigastric pain

CARCINOID TUMORArise from the diffuse components of the

endocrine system

Gross: intramural or submucosal masses that

create small polypoid lesions

CARCINOID TUMORMicro: islands, trabeculae, strands, glands, or

sheets of uniform cells with scant, pink

granular cytoplasm and a round to oval,

stipples nucleus

CARCINOID TUMORImmuno: (+) for endocrine granule markers

(synaptophysin and chromogranin A)

The MOST important prognostic factor for GI

carcinoid tumors is LOCATION

Foregut carcinoid tumors RARELY

METASTASIZE

G.I.S.T. Can behave and/or look benign or

malignant

Usually look like smooth muscle, i.e.,

“stroma”, “spindly”

tumor cells are derived from the

interstitial cells of Cajal, a “neural”

type of cell, similar to the neural plexi

found in the intestines (pacemaker

cells for gut peristalsis)

G.I.S.T. Pathogenesis: 75-80% of all GISTS

have oncogenic, gain-of-function

mutations of the gene encoding the

tyrosine kinase c-KIT (receptor for

stem cell factor)

Gross: solitary, well-circumscribed,

fleshy mass

G.I.S.T.

G.I.S.T.

Spindle cell type

Epithelioid type

G.I.S.T.

CD 117

G.I.S.T. Can behave and/or look benign or

malignant

Usually look like smooth muscle, i.e.,

“stroma”, “spindly”

Are usually POSITIVE for c-KIT

(CD117)

tumor cells are derived from the

interstitial cells of Cajal, a “neural”

type of cell, similar to the neural plexi

found in the intestines.

G.I.S.T.

G.I.S.T.

G.I.S.T.

CD 117

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

SMALL/LARGE INTESTINE

INFLAMMATORY BOWEL DISEASE

Crohn’s Disease

Ulcerative Colitis

OBSTRUCTION

TUMORS

IBD

CROHN’S DISEASE (granulomatous

colitis)

ULCERATIVE COLITIS

IBD DIFFERENCES

Crohn’s disease Ulcerative colitis

CHROHN’S DISEASE

CHROHN’S DISEASE

CHROHN’S DISEASE

ULCERATIVE COLITIS

ULCERATIVE COLITIS

ULCERATIVE COLITIS

OBSTRUCTION

Small Intestine – most often involved

Clinical manifestations:

- abdominal pain & distention, vomiting and constipation

OBSTRUCTIONANATOMY– ADHESIONS (post-surgical)

– IMPACTION

– HERNIAS

– VOLVULUS

– INTUSSUSCEPTION

– TUMORS

– INFLAMMATION, such as IBD (Crohn) or diverticulitis

– STRICTURES/ATRESIAS

– STONES, FECALITHS, FOREIGN BODIES

– CONGENITAL BANDS, MECOMIUM, INPERF. ANUS

OBSTRUCTION

HERNIAS

Any weakness in the wall of the peritoneal cavity that permits protrusion of a serosa-lined pouch of peritoneum (hernial sac)

Acquired hernias: most commonly occur anteriorly via the femoral and inguinal canal or umbilicus or sites of surgical scars visceral protrusion

(external herniation)

HERNIAS

ADHESIONS

Surgical procedures, infection or other causes of peritoneal inflam (eg. Endometriosis) adhesions between bowel segments, abdominal wall & operative sites fibrous bridges create closed loops internal herniation

INTUSSUSCEPTIONA length of intestine (intussuscipiens)

literally swallows part of the bowel just

proximal to it (intussusceptum)

most cases are seen during the first 5

yrs of life

Infants & children: rotavirus infection

Older children and adults: intraluminal

mass or tumor serves as point of traction

PHYSIOLOGY– ILEUS, esp. postsurgical

– INFARCTION

– MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE

OBSTRUCTION

TUMORS

NON-NEOPLASTIC (POLYPS)

BENIGN

MALIGNANT

POLYPS

Inflammatory Polyps

- forms as a result of chronic cycles of

injury and healing

POLYPS

Hamartomatous Polyps

- occur sporadically

- hamartoma: tumor-like growths of

mature tissues that are normally

present at the site in which they

develop

- assoc w/ genetically determined or

acquired syndromes

POLYPSHamartomatous Polyps

POLYPS

Juvenile Polyp

- focal malformations of the mucosal

epith & lamina propria

- majority occur in children <5 y/o

- majority are located in rectum

rectal bleeding

Juvenile (retention) polyp.

Note the ulcerated, highly

hyperemic surface.

POLYPS

Hyperplastic Polyp

- epithelial proliferations discovered in

the 6th and 7th decades of life

- Pathogenesis: decreased epith

turnover & delayed shedding of surface

epith cells piling up of goblet &

absorptive cells

- NO malignant potential

Gross appearance of multiple

hyperplastic polyps. The lesions are

characteristically small, sessile, and

pale.

Microscopic appearance of hyperplastic

polyp. The individual glands show a

typical serration of their mid portion.

POLYPS

Neoplastic Polyp (Adenomas)

- precursors to the majority of

colorectal adenocarcinomas

- char by the presence of epithelial

dysplasias

POLYPS

Sessile polyp Pedunculated polyp

POLYPSNeoplastic Polyp (Adenomas)

- Micro: HALLMARK of epithelial

dysplasia nuclear hyperchromasia,

elongation and stratification

- classified as TUBULAR,

TUBULOVILLOUS OR VILLOUS

Adenomatous polyp showing marked contrast between the dysplastic glands

of the polyp and adjacent normal glands.

Microscopic appearance of

villoglandular polyp. There is an

admixture of villous and

glandular structures.

ADENOCARCINOMA

Most common malignancy of the GIT

Dietary factors assoc w/ increased risk:

low intake of unabsorbable vegetable

fiber & high intake of refined CHOs &

fat

Pathogenesis: APC/Beta-catenin

pathway and microsatellite instability

pathway

GROWTH PATTERNSPOLYPOID: proximal colon

ANNULAR, CONSTRICTING: distal colon

DIFFUSE

Polypoid pattern of growth in a rectal lesion.Cake-like configuration with

central ulceration.

Deeply penetrating and ulcerated

tumor.

Moderately differentiated colonic

adenocarcinoma.

Polypoid pattern of growth in a rectal lesion.Cake-like configuration with

central ulceration.

Gross appearance of signet ring carcinoma. This tumor type is highly malignant,

narrows the lumen, and has a pebbly mucosal surface and thickened muscular

wall.

Stage A tumors invade through the muscularis

mucosae into the submucosa but do not reach the muscularis propria

Stage B1 tumors invade into the muscularis propria

Stage B2tumors completely penetrate the smooth

muscle layer into the serosa

Stage Ctumors encompass any degree of

invasion but are defined by regional lymph node involvement

Stage C1 tumors invade the muscularis propria with fewer than four positive nodes

Stage C2tumors completely penetrate the smooth muscle layer into the serosa with four or

more involved nodes

Stage D lesions with distant metastases

Carcinoma in situ

(may be referred to as high grade dysplasia) – intramucosal carcinoma that does not penetrate the muscularis

mucosae

Dukes’ Classification (Astler-Coller modification)

Tumor Stage Histologic Features of the Neoplasm

Tis Carcinoma in situ (high-grade dysplasia) or intramucosal carcinoma (lamina propria invasion)

T1 Tumor breaches the musc. Muc. invades into submucosa

T2 Extending into the muscularis propria but not penetrating through it

T3 Penetrating through the muscularis propria into subserosa

T4 Tumor directly invades other organs or structures

Nx Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Metastasis in 1 to 3 lymph nodes

N2 Metastasis in 4 or more lymph nodes

Mx Distant metastasis cannot be assessed

M0 No distant metastasis

M1 Distant metastasis

TNM Staging

COLORECTAL CARCINOMAClinical:

- Right-sided: fatigue & weakness due to

IDA

- Left-sided: occult bleeding, changes in

bowel habits or cramping LLQ

discomfort

- Most important prognostic factors:

depth of invasion & +/- LN mets

COLORECTAL CARCINOMAFACTORS related to prognosis:

1. Patient’s age – very young and very old: poor px

2. Sex – better px: F > M

3. CEA serum levels > 5.0 ng/ml

4. Tumor location: favorable px - lesions located in the left colon > lesions in sigmoid colon and rectum

5. Local extent – focal microscopic CA in a polyp/tumor restricted to mucosa & submucosa: good px

COLORECTAL CARCINOMAFACTORS related to prognosis:

6. Obstruction – poor px

7. Perforation – poor px

8. Tumor margins & inflammatory reaction –better px

9. Vascular/perineural invasion: poor px

10. Microscopic tumor type – Mucinous CA, signet ring CA and anaplastic CA: worse px

11. LN involvement - > 6 LNs: <10% survive >5 yrs.

HEMORRHOIDS

Develop secondary to persistently elevated

venous pressure w/in the hemorrhoidal

plexus

Most common predisposing influences:

straining at stool fr constipation & venous

stasis of pregnancy

Pathogenesis: variceal dilatations of anal &

perianal venous plexus that forms collaterals

that connect portal & caval venous systems

to relieve venous HPN

HEMORRHOIDS

External hemorrhoids: collateral vessels w/in

the inferior hemorrhoidal plexus located

below the anorectal line

Internal hemorrhoids: dilatation of the

superior hemorrhoidal plexus within the

distal rectum

HEMORRHOIDS

Micro: thin-walled, dilated, submucosal vessels that

protrude beneath the anal or rectal mucosa

HEMORRHOIDS

ANAL CARCINOMAS

MORE LIKELY TO BE SQUAMOUS, or “basaloid”

F > M (3:1)

Worse in prognosis

HPV – related (HPV16)

ANAL CARCINOMAS

NORMAL

ANAL CARCINOMAFACTORS related to prognosis:

1. Tumor stage– depth of invasion & regional

LN involvement; inguinal LN involvement

(grave px sign)

2. Tumor size – inversely related to px

3. Tumor recurrence - tumor recurrence in the

pelvic or perineal regions following APR:

ominous px

GIT PathologyCONGENITAL ABNORMALITIES

ESOPHAGUS

STOMACH

SMALL/LARGE BOWEL

APPENDIX

ACUTE APPENDICITISA normal TRUE DIVERTICULUM of the cecum

GENERALLY, a disease of YOUNGER people

Pathogenesis: OBSTRUCTION by FECALITH

the classic cause but fecaliths present only

about half the time

- Other causes: gallstones, tumor, mass of

worms eg. O. vermicularis

- Ischemic injury & stasis of luminal contents

bacterial proliferation trigger inflam

response eg. tissue edema, PMN infiltration

ACUTE APPENDICITISDDx:

- mesenteric lymphadenitis (sec. to

unrecognized Yersinia infection or viral

enterocolitis)

- acute salpingitis

- ectopic pregnancy

- mittelschmerz (pain fr minor pelvic bleeding

during ovulation)

- Meckel diverticulitis

ACUTE APPENDICITIS

ACUTE APPENDICITISEARLY APPENDICITIS:

NEUTROPHILSMucosa, submucosa

NEED NEUTROPHILS in the MUSCULARIS to

confirm the DIAGNOSIS

Classic clinical finding: MCBURNEY’S SIGN

Perforationperitonitis the rule, if no surgery

Perforationperitonitis the rule, if no surgery

Complications: perforation, pyelophlebitis,

portal venous thrombosis, liver abscess and

bacteremia

ACUTE APPENDICITIS

TUMOR

Carcinoid: most common

- incidental finding

- most frequent location: DISTAL TIP

- distant spread: rare

Mucocele (common): obstructed

appendix w/ inspissated mucin

Mucinous Cystadenoma (rather rare)

Mucinous Cystadenocarcinoma (rare)

- invasion of wall peritoneal implants

MUCOCELECOMMON CYST on APPENDIX filled with MUCIN

Can RUPTURE to become:

PSEUDOMYXOMA PERITONEI

(mucinous ascites and mucinous tumordisseminated on peritoneal surfaces)

MUCOCELE

MUCOCELE

MUCINOUS CYSTADENO(CARCINO)MA

MUCINOUS CYSTADENO(CARCINO)MA

Have a nice day!