block 9-lower-alimentary-tract-xx.pdf

8/9/2019 BLOCK 9-LOWER-ALIMENTARY-TRACT-XX.pdf

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Pathology of the

LOWER ALIMENTARY TRACT

I. Diseases of the Stomach

II. Diseases of the Small Intestine

III. Diseases of the Colon

IV. Diseases of the Appendix


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1/5/2012 tums-pafkugm-alimentary-tract 2

STOMACH


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A. Congenital Pyloric Stenosis

B. Gastritis

C. Peptic Ulcer of the Stomach

D. Malignant Tumor of the Stomach


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A. Congenital Pyloric Stenosis

Is caused by hypertrophy of circular muscular layer of the pylorus

often results as papable mass

obstruction of gastric outlet episodes of projectile vomiting

(beginning in the first 2 weeks of life)

Much more common in boys Is corrected by surgical incision of the hypertrophied muscle


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a. Causes

- Nonsteroidal anti-inflammatory drugs (NSAIDs)

- Cigarette smoking

- heavy alcohol intake

- Burn injury (severe) Curling ulcer- Brain injury Cushing ulcer

- ingestion of strong acid or alkaline

b. Characteristic

- focal damage of mucosa with acute inflammation, necrosis,and hemorrhage

- may be manifest as gastric ulcer often multiple


B. Gastritis: 1. Acute (erosive) gastritis


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Acute gastritis


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- Helicobacter pylori – associated gastritis

- gram – neg. organism, in the surface

epithelium beneath the mucous barrier

- cells desquamation and lead to polymorph

and chronic inflammatory cells- predominantly affects the anthrum

- most common form of gastritis

- often has increased gastric acid

- young adulthood and early middle age- associated with gastric cancer


B. Gastritis: 2. Chronic gastritis


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HISTOLOGIC PICTURE OF CHRONIC

GASTRITIS

• Early stage: inflammation affects the superficial parts ofthe mucosal layers superficial chronic gastritis

• Next stage: the inflammation affects all mucosal andsubmucosal layers – with germinal center

1. Inflammatory cells: mononuclear cells; active

netrophil (+)2. Metaplasia: intestinal metaplasia pre-malignant

condition

3. Glandular atrophy: glandular tissue is reduced in

amount and undergoes to intestinal metaplasia4. H. pylori

5. Dysplasia: carcinoma


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ATROPHIC

GASTRITIS


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H.pylori


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H. PYLORY AND CHRONIC GASTRITIS


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OTHER GASTRITIS

• Eosinophyillic gastritis: food allergy ?

• Granulomatous gastritis: tuberculosis,

syphilis, sarcoidosis, fungi, Crohn disease

• Reflux gastritis: duodenal and bile reflux

• Menetrier disease (giant hypertrophic

gastritis)


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Menetrier disease (HYPERTROPHIC GASTROPATHY)

• Severe hyperplasia of mucosal layer

cells + glandular atrophy extremeenlargement of gastric rugae

• Hypertrophic gastropathy + hyper-secretion: mucosal cells, parietal andchief cells hyperplasia.

• Gastrinoma excessive gastrinexcretion gastric glandularhyperplasia (Zollinger-Ellisonsyndrome)

• Sometimes with severe loss of plasmaproteins from the altered mucosa

• Risk of peptic ulcer


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C. Peptic Ulcer of the Stomach• Most often at or near lesser curvature, in the anthral & pre-pyloric

region

• Is not a precursor lesion of Ca of the stomach

• Is not dependent on increased gastric acid secretion – but rarelyoccur in association with absolute achlorhydria

• Middle-later age group

• Male > female, 1.5 to 2:1

• Often solitary

• >50% Ø 4cm

• Ø 0,6 cm ulcer


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PEPTIC ULCER

Etiopathogenic mechanism:

- H. pylori : 90-100% duodenal ulcer, 70% gastric ulcer; bacterial

urease & protease break down glycoprotein in gastric mucus interfering with epithelial protection

- NSAID

- alcohol, smoke, blood-group, HLA-B5

- Increased permeability of the gastric mucosa to hydrogen ion

back diffusion of H2 ion injury to gastric mucosa- Bile-induced gastritis leading to gastric ulceration


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PEPTIC ULCER

Complications:

1.Bleeding2.Perforation

3.Obstruction: due to Edema or cicatrix


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G STRIC ULCER

• Destruction of mucosa and sub-mucous

• Almost always single, 2-3 cm,

• Type:

– Acute peptic ulcer: both mucous andsub-mucous layer are involved, 1 cm,

single/ multiple

– Chronic peptic ulcer: penetrated anddestroy the muscle coat.


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ACUTE GASTRIC ULCER

• Multiple• Gastric > duodenum

• Erosion – ulceration

• Ø 1 cm, circular, rarely invade to mucosal layer

• Etiology – Shock, burning ulcer, sepsis, severe trauma

– High intracranial pressure Cushing ulcer

– Proximal the duodenum + severe burning

ulcer/trauma Curling ulcer

– NSAID


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TRIGER F CTORS OF PEPTIC ULCER


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PEPTIC ULCER

Cylindric epithelia

Necrotic debris

Granulation tissue with lymphocytic infiltratio

Glands hyperplasia

Edema


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POLYP – Polypoid mass

– >90% non neoplasm (inflammatory/ hyperplasia)

– Sessile / pedunculated

– 20-25% multiple

– Mostly occur in chronic gastritis – No malignant potential

ADENOMA

– neoplasm 5-10% of gastric polyp

– Sessile / pedunculated

– distal – anthrum predominant

– Six decade, Male: female = 2:1

– Some cases origin from chronic gastritis with intestinalmetaplasia

I. Diseases of the stomach

D. Tumors of the stomach (benign)


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I. Diseases of the stomach

D. Tumors of the stomach (malignant)

• Adenocarcinoma is about 90-95% of gastric malignancy

• High incidence: japan, Chili, Costa Rica, China

• Location: - 40-50% pylorus/anthrum; 25% cardia

- 40% minor curvature; 12% c. major

- Etiology:

- Diet

- Chronic atrophic gastritis

- H. pylori infection

- partial gastrectomy- Gastric Adenoma

- Genetic : A blood group, family factor


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GASTRIC CANCER

– Invasion

• Early ( mucosa and submucosa)

• Advanced (invade the submucosa)

– Macroscopic growth

• Exophytic• flat/ depressed

• Excavation

Linitis plastica – tumor cells diffusely infiltrate gastric wall

leather bottle appearance

– Histology

• intestinal gland type

• Diffuse: signet-ring cell


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The Growth of Gastric Cancer


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Other gastric tumors

• MALIGNANT LYMPHOMA

– 40% malignant lymphoma of GIT – 5% of gastric malignancy

– B cell type predominant, MALT origin

• CARCINOID TUMOR Carcinoid syndrome

– Low grade malignancy

– Metastasis to the liver – Multiple lesions

• LEIOMYOMA

• SECONDARY TUMORS (METASTASIS)

– rare

– Mostly from leukemia or general lymphoma

– From breast / lung cancer diffuse linitisplastica


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GASTRIC CARCINOMA

• Prognosis:

– Depend on the depth of tumor invasion

and metastasis process


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Adenocarcinoma, NOS


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ULCUS CARCINOMATOSA


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REDUPLICATION STENOSIS DIVERTICULUM ATRESIA

Diseases of the Intestine

A. CONGENITAL ABNORMALITIES


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HERNIA

Mechanic obstruction-atresia

-stenosis

-stricture

-hernia

-volvulus

-invagination / intususeption

Neurogenic obstruction-paralytic - adinamic-spastic - dinamic

Vascular obstruction-trombosis-embolism

Diseases of the Intestine

B. INTESTINAL OBSTRUCTION


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Invagination/ intususeption Volvulus

Vascular obstruction


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A. Peptic Ulcer

B. Crohn DiseaseC. Meckel Diverticulum

D. Malabsorption syndrome

E. Tumors of the Small Intestine


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A. Peptic Ulcer of the Intestine

• Most frequently in the first portion of duodenum

• Is not a precursor of malignancy

• Is always associated with hypersecretion of gastric acid

and pepsin

• increased frequency in persons of blood group O

genetic factors?

• Often complicated by hemorrhage with melena,

perforation, obstruction


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A. Peptic Ulcer of the Intestine

Sometimes associated with:

• Aspirin or other NSAID

• Smoker: the incidence is two-fold greater

• Zollinger-Ellison syndrome gastric acid hypersecretiondue togastrin secreting islet cell tumor of the pancreas

• Primary hyperparathyroidisme

• Multiple Endocrine Neoplasia (MEN Wermer syndrome), an

autosomal dominant syndrome characterized by pituitary, thyroid,

parathyroid, adrenal cortical, and pancreatic islet cell adenoma, orhyperplasias associated with hypergastrinemia and peptic ulcer


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B. Crohn’s Disease

• Chronic inflammatory condition of unknown etiology

• Tends to affect young people in 2nd and 3rd decades of life

• Occurs most frequently in Jewish descent

• Cinical manifestations:

– Abdominal pain and diarrhea

– Malabsorption

– Fever

– Intestinal obstruction resulting from fibrous tissue

– Fistulas: inter-intestine, between intestine – bladder, vagina, skin

II Diseases of the Small Intestine


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B. Crohn’s Disease


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Crohn Disease Ulcerative Colitis

May involve any portion of the gastrointestinal

tract, usually the ileocecal region, small intestine,or colon.

Chronic inflammatory reaction extends through

the entire thickness of the intestinal wall.

Fistulous tracts between loops of intestines, or

between the intestine and other site; skip lesionswith mucosal cobblestone appearance.

Non-caseating granulomatous inflammation with

lymphocytic infiltration, fibrosis, and thickening of

intestinal wall.

Incidence of secondary malignancy is much lowerthan in ulcerative colitis

Affects only colon.

Inflammation and ulceration

limited to mucosa and submucosa

Crypt abscess, pseudopolyp

Greatly increased incidence ofcolon cancer in longstanding

cases


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Comparison of the lesions


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C. Meckel Diverticulum

• Most common congenital anomaly of the small intestine

• Remnant of embryonic vitelline duct distal small bowel

• May contain ectopic gastric, duodenal, colon, pancreatic

tissue• Usually asymptomatic, ectopic tissue product com-

plication (peptic ulceration bleeding perforation)

• Occasionally associated with: intussusception and

volvulus


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Celiac Disease• Sensitivity to gluten in cereal product

• Clinically: weight loss, weakness, diarrhea with pale,

bulky, frothy, foul smelling stools• Growth retardation and general failure to thrive

• Most often become symptomatic in infancy when cerealsare first added to the diet

• Diagnosis biopsy blunting of small intestinal villi

• 10-15% small intestinal malignancy: most oftenenteropathy-type T cell lymphoma


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Disorders Morphologic Features CommentsCeliac disease Flat mucosal surface with marked

villous atrophy

Gluten sensitivity

Tropical sprue Micros: no change abnormalities

similar to those of celiac disease

Probable infectious origin;

often respond to antibiotics

Whipple disease PAS+ macrophages in mucosal

Tropheryma whippelii EM

Most common: small intestine;

arthralgia, cardiac & neuro. S

Disaccharidase

deficiency

No characteristic histologic change Sited in brush border of

mucosal cell of small intestine;

Lactase def.milk intolerance

Abetalipoproteinemia No characteristic features in the in-

testine; circulating acanthocytes

Hereditary deficiency of apo-

protein-B

Intestinal

lymphangiectasiaGeneralized dilatation of the small

intestinal lymphatics

Marked gastrointestinal pro-tein loss hypoproteinemia




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E. Tumors of the small intestine

• Make up a small percentage of the gastrointestinal tumor

• Carcinoid tumor:

- most frequently in appendix (in small intestine: 30%)

- slow growing, low-grade malignancy (of appendix almost never

metastasizes

- carcinoid syndrome: caused by elaboration of vasoactive peptidesand amines, especially serotonin, manifest clinically by:

(1) cutaneous flushing

(2) watery diarrhea and abdominal cramp

(3) bronchospasm

(4) valvular lesions of the right side of the heart

• Other tumors: lymphoma, adenocarcinoma (rare)


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The Spread of Tumor


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A. Hirschprung disease

B. Diverticula

C. Vascular diseases of the colonD. Inflammatory disorders of the colon

E. Tumors


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A. Hirschprung disease

• Dilatation of colon due to the absence of ganglion cellsof the submucosal and myenteric neural plexuses

• Dilatation is proximal to aganglionic segment

III Di f th C l


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B. Diverticula

• Most common in old person, and almost always multiple• Most frequently involve the sigmoid colon

• It’s a pulsion/false diverticula (pockets of mucosa and submucosa

herniated through the muscular layer)

• Diverticulosis: multiple diverticula without inflammation

• Diverticulitis:

- inflammation of diverticula, mostly in older person

- may be complicated by perforation peritonitis, abscess, bowel

stenosis (can be with lower abdominal bleeding & tenderness,

fever, leukocytosis, others)- bright red rectal bleeding


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Diverticulosis of the Sygmoid

III Diseases of the Colon


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C. Vascular diseases of the colon

-results in mucosal, mural, and trans mural infarction involving the wall of the intestine

-is almost always caused by arteriosclerotic occlusion (at least 2 of the major mesen-teric vessels)

-most often affects the splenic flexures and rectosigmoid junction (watershed areas)


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Ischemic bowel disease

Almost always caused by atheroscle-

rotic occlusion

Most often affects the splenic flexure

and rectosigmoid junction (watershed

Area = relatively poor vascularized

region, between areas supplied by the

superior and inferior mesenteric artery

and internal iliac arteries

III Diseases of the Colon


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-Are dilated internal and external

venous plexusses in the anal

canal-Predisposed by low-fiber diet

III Di f th C l


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D. Inflammatory disorders of the colon

Ulcerative Colitis

• Often grouped with Crohn disease as inflammatory bowel disease; unknown

etiology; similar geographic & racial distribution family history; similar

extraintestinal manifestation: polyarthritis, uveitis & episcleritis, sclerosing

cholangitis, sacroiliitis, skin: erythema nodosum and pyoderma gangrenosum

•

Characteristics- mucosal inflammation & ulceration limited to the large intestine

- confined to the mucosa & submucosa crypt abscess

- red, granular appearance of the mucosa

- pseudopolyp

- chronic diarrhea with passage of blood & mucus (bleeding is the most frequent

clinical manifestation)


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Ulcerative Colitis


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ENTERITIS TUBERCULOSA

Primer: milk + mycobacterium tuberculosa

Secunder: sputum + mycobacterium tuberculosa


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Others:

Bacillary dysentery

Cholera

Salmonella

Viral

Parasitic (Amebic, giardia, balantidia, schistosoma, etc.)




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Type Comments

Non-neoplastic polyps•Hyperplastic polyp

•Inflammatory polyp

- Lymphoid polyp

- Inflammatory pseudopolyp

•Hamartomatous polyp

- Juvenile polyp

- Peutz-Jeghers polyp

No clinical significance

Rectal mucosa; may be reactive

@ ulcerative colitis and others, granulation tissue

Most frequently in children

@ Peutz-Jeghers syndrome

Neoplastic polyps

•Tubular adenoma

•Tubulovillous adenoma

•Villous adenoma

Often multiple (hereditary multiple polyposis

syndrome) increased risk of malignancy

Greater malignant potential

High potential for malignant change

III. Diseases of the Colon: E. Tumors: Polyps


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Familial Adenomatous Polyposis


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Adenomatous polyp

d i


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• One of the most common neoplasm of the intestine

• Peak age incidence: 6th

– 7th

decades• Associated with increased CEA (carcinoembryonic antigen) to

follow the course of the disease

• Develops through model of: adenoma – carcinoma sequence

• Predisposing factors:

1. Adenomatous polyp

2. Inherited multiple polyposis syndrome

3. Long-standing ulcerative colitis

4. Genetic factors: 4X increase of incidence among relatives of the cancer patients

5. A low fiber, high animal fat diet• Characteristics:

- left colon napkin-ring (annular) often producing early obstruction

- right colon polypoid chronic blood loss anemia

III. Diseases of the Colon: E. Tumors: adenocarcinoma

’ S


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Dukes’ Stage

ASTLER COLLER


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ASTLER - COLLER

Five-year survival rate• A – tumor is limited in the mucosa - 100%

•B1 – reach the muscularis propria,

no lymphonode involvement 67%

•B2 – passing the muscularis propria,no lymphonode involvement 54%

•C1 – reach the muscularis propria,

with lymphonode involvement 43%

•

C2 –

passing the muscularis propria,with lymphonode involvement 22%

•D – metastasis very low FSR


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IV. Diseases of the Appendix

A.Inflammatory diseases

1. Acute appendicitis

2. Chronic appendicitis

B.Tumors of the appendix

The most common : carcinoidtumor

APPENDICITIS


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APPENDICITIS

SIMPLE ACUTE SUPPURATIVE GANGREN

CHRONIC APENDICITIS

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