TRAKTUS DIGESTIVUS

TRAKTUS DIGESTIVUS

Pieri Kumaladewi, Dr, SpPA (UGM)

Wien Wiratmoko, Dr, SpPA(UNAIR)

Upper digestive tract

I. Diseases of the Mouth & JawA. Congenital DisordersB. Inflammatory disordersC. Tumors and tumor-like conditions

II. Diseases of the Salivary GlandsA. SialadenitisB. Acute parotitisC. Sjogren syndromeD. MucoceleE. RanulaF. Tumors of the salivary gland

III. Diseases of the EsophagusA.Tracheoesophageal fistulaB. Esophageal diverticulaC. AchalasiaD. Esophageal varicesE. Hiatus herniaF. Inflammatory and related disorders of the esophagus

G. Carcinoma of the esophagus

I.A. CONGENITAL DISORDERS

SCHISIS / CLEFT MICROGNATHIA* Failure of mesodermal penetrance between the maxillary, median nasal, and lateral nasal.

- Unilateral/ Bilateral - Simplex/ complex: Labioschisis

LabiognatoschisisLabiognatopalatoschisis

Oblique facial clef- Sporadic/ congenital

- May be it is associated with other anomalies

TONGUE

CONGENITAL DISORDER OF THE TONGUEMICROGLOSSI MACROGLOSSI MEDIAN RHOMBOID GLOSSITIS

TIE TONGUE BIFID TONGUE

I.B. INFLAMMATORY DISORDERS

1. Herpes Labialis- most common lesion caused by HSV (HSV-1)- tends to recur, with activation by febrile illness, trauma, sunshine, menstruation

2. Aphthous stomatitis- characterized by painful, recurrent, erosive oral ulceration

3. Oral candidiasis (thrush, moniliasis)- local lesion, white, membranous, caused by Candida albicans- occurs most commonly in debilitated infants and children, immunocompromized patient, and diabetics

4. Acute necrotizing ulcerative gingivitis (trench mouth, Vincent infection, fusospirochetosis)- severe gingival inflammation occuring in patient with decresed resistance to infection- due to concurrent infection with symbiotic bacteria (Fusobacterium species and Borrelia vincentii)

Glositis tuberculosa Glositis luetica

Geographic tongue Hairry tongue

GLOSSITIS

I.C. TUMORS & TUMOR-LIKE CONDITIONS

1. Benign tumors of the oral mucosaa. Papilloma: the most common benign epithelial oral mucosal tumor tongue, lips, gingivae, buccalb. Fibroma: it is often a non-neoplastic hyperplastic lesion due to chronic irritationc. Hemangioma: tongue, lips, buccal mucosad. Epulis: any abnormal swelling of the gingiva, as a reparative growth rather than a true neoplasm

2. Leukoplakia: - clinical term describing irregular white mucosal patches - pre-cancer

3. Odontogenic tumors

a. Odontoma: hamartoma derived from odontoblastic epithelium b. Ameloblastoma:

- epithelial tumor arising from precursor cells of the enamel organ- usually before age 35, and most fequently in mandible- irregular local extension

4. Oral cancer

- mostly squamous cell carcinoma- often associated with abuse of tobacco and alcohol- may be associated with irritants: pipe smoking, chewing tobacco or betel nuts

I.C. TUMORS & TUMOR-LIKE CONDITIONS

LEUKOPLAKIA- white patches of keratosis- premalignant lesion- hyperkeratosis, hyperplasia of the squamous epithelium- dysplastic changes

SQUAMOUS CELL CARCINOMA

Malignant tumors: NPC, squamous cell ca, lymphoma

Pharyngitis-Viral pharyngitis: common feature of the CC, influenza, measles, etc-Streptococcal pharyngitis: less common but more important than viral pharyngitis because the complication rheumatic fever, acute proliferative glomerulonephritis, Henoch Schonlein purpura -Ulcerative pharyngitis & tonsillitis diphtheriaTonsilitis:-Follicular tonsilitis, streptococcus/ Borrelia / virus-Parenkhimal tonsilitis: quincy, Peritonsiler abses-Angina agranulositic netropenic-Tonsilitis morbili: Warthin Finkeldey giant cells

Pharynx & Tonsil

A. SialadenitisB. Mucocele

C. RanulaD. Tumors

Pleomorphic adenoma (Mixed tumor) Warthin tumor / adenolymphoma / Papillary cystadenoma

lymphomatosum Oncocytoma

Adenoid cystic carcinomaMucoepidermoid tumor

II. Diseases of the SALIVARY GLAND

II. A. Sialadenitis

Acute- Suppurative parotitis- Non-suppurative parotitis- Parotitis epidemica / Mumps: paramyxovirus Orchitis/ Oophoritis- Cytomegalic inclusion disease

Chronic1. SJOGREN’S SYNDROME :

- Autoimmune disease- Keratoconjungtivitis sicca- Xerostomia- Parotitis hyperplasia

2. MIKULICZ SYNDROME : - Idiophatic- Keratoconjungtivitis sicca- Xerostomia- Unilateral parotitis hyperplasia

Mucocele

• A cyst-like pool of mucus, lined by granulation tissue, near a minor salivary gland

• Results from mucus leakage caused by rupture of obstructed or traumatized ducts

Ranula• Is a large mucocele, of salivary gland of origin, characteristically localized to the floor of the mouth

Tumors of the Salivary Glands

1. Pleomorphic adenoma (Mixed tumor) 2. Warthin tumor / adenolymphoma / Papillary

cystadenoma lymphomatosum 3. Oncocytoma

4. Adenoid cystic carcinoma5. Mucoepidermoid tumor

Anatomy of parotid gland

Pleomorphic adenoma (parotid)

Pleomorphic adenoma (gross)

Pleomorphic adenoma

Warthin tumor

Benign tumor mostly occur in parotid gland

Warthin tumor

Cystic spaces lined by double-layered eosinophilic epithelium, and all embedded in lymphoid stroma

Oncocytoma

Mostly in parotid gland

Oncocytoma

Large granular appearing, eosinophilic-staining epithelial cells

Adenoid cystic carcinoma

Minor salivary gland


Most characteristic appearance consists of cribriform pattern with masses of small, dark-staining cells arrayed arround

cystic spaces

Mucoepidermoid tumor(Palatal gland)

Mostly in parotid gland

III. Diseases of the Esophagus

A.1. Tracheoesophageal fistulaCongenital disorder, is suggested in a newborn by copious salivation associated with

choking, coughing, and cyanosis on attempts at food intake

The most common variant (90%), the lower portion of the esophagus communicatesWith the trachea near the tracheal bifurcation, the upper esophagus ends in a blind pouchAssociated abnormality: maternal polyhydramnion

The second most common variant, fistulous connection between the upper esophagus and the trachea; the lower esophageal segment is not connected to the upper esophagus

The third variant, fistulous connection between the tachea and a completely patent esophagus

III. Diseases of the Esophagus A.2. Heterotopic tissue

• patches of fundic-type gastric mucosa are occasionally found above the distal sphincter separated from the columnar lining of the distal esophagus

• congenitally misplaced gastric tissue (heterotopic) can lead to ulceration and stricturing due to local acid/pepsin secretion


B. Esophageal diverticula- Outpouchings of the wall of hollow viscus- herniation of the mucosa or full thickness - effects: dysphagia, diverticulitis

- pharyngoesophageal diverticula

-Traction: external forces pulling on the wall (true divericula)-Pulsion: forcible distention (false diverticula): result from periesophageal inflammation and scarring


C. Achalasia

-Contractility of the lower esophagus is lost and there is failure of relaxation at the sphincter (cardiospasm)

-Mechanism: fibrosis and atrophy of smooth muscle (reduced number number of ganglion cells in the myenteric plexus: Chagas’ disease & other unknown etiology).

-Clinically: slowing / retention of the food dilatation dysphagia


D. Esophageal varices

-Localized dilatation of veins

-Portal hypertension

- cirrhosis hepatis

- Haematemesis

III. Diseases of the esophagus

E. HIATUS HERNIA

The presence of part of the stomach above the diaphragmatic orifice, mostly acquiredIncreased intra-abdominal pressure and loss of diaphragmatic muscular tone with aging herniation of the stomach and subsequent retraction of the esophagus.


F. Inflammatory and related disorders of the esophagus

1. Gastroesophageal reflux2. Barret’s esophagus3. Candida esophagitis

4. Viral esophagitis5. Esophageal stricture


F. 1. Gastroesophageal reflux

• Reflux of gastric acid contents into the esophagus esophagitis, stricture, ulceation, or columnar metaplasia (Barret’s esophagus)

• Usually characterized by burning pain (often manifests by substernal pain or heartburn) relieved by antacids

• Often precipitated by assuming recumbent position• Associated:

- most commonly with hiatal hernia and incompetent lower esophageal sphincter - with excessive use of alcohol & tobacco, and with increased gastric volume- with pregnancy and scleroderma


F.2. BARRET’S ESOPHAGUS

Columnar metaplasia (often of intestinal type with prominent goblet cells) ofesophageal squamous epithelium.Complication of long-standing gastroesophageal reflux, to be a well-known precursor of esophageal adenocarcinoma


F. 3. Candida esophagitis• Etiology: Candida (Monilia) albicans• Manifest clinically by white adherent mucosal patches and

painful, difficult swallowing• Often assciated with:

- antibiotic therapy- diabetes mellitus- malignancy- immunodeficiency


F. 4.a. Viral esophagitis

Herpetic esophagitis• Characterized by painful and difficult swallowing • Tends to occur in immunosuppressed patient, caused

by HSV-1 infection

Cytomegalovirus (CMV) infection• Less common


F. 4.b. Other esophagitis

Less common form of esophagitisCaused by: uremia, radiation therapy, graft-versus-host

(GVH) disease


F. 5. Esophageal stricture

Most often results from prolonged esophageal gastric acid reflux

May also be caused by suicidal or accidental ingestion of corrosive agent (acid or alkaline)


G. Carcinoma of the esophagus

Aggressive tumor manifest clinically by dysphagia, weight loss,and anorexia, and occasionally by pain or hematemesis

In the USA the incidence of SC and adenocarcinoma are equal

May be manifest pathologically by protrusion into the esophageal lumen

Spread by local extension to adjacent structure: trachea, bronchi, aorta, or diffuse infiltration into esohageal wall


G.1. Squamous Cell Carcinoma

Arises most frequently in the upper and middle thirds of the esophagus


G2. Adenocarcinoma

Arises most frequently in the lower third, and mostly from aberrant gastric mucosa or Barret’s esophagus

Part 2

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

STOMACH


A. Congenital Pyloric Stenosis

B. Gastritis

C. Peptic Ulcer of the Stomach

D. Malignant Tumor of the Stomach


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

a. Causes- Nonsteroidal anti-inflammatory drugs (NSAIDs)

- Cigarette smoking

- heavy alcohol intake

- Burn injury (severe) Curling ulcer

- Brain injury Cushing ulcer

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

Acute gastritis

- 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

HISTOLOGIC PICTURE OF CHRONIC GASTRITIS

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

• Next stage: the inflammation affects all mucous and submucous layers – with germinal center

1. Inflammatory cells: active netrophil (+) 2. Metaplasia: intestinal metaplasia pre-malignant condition3. Glandular atrophy: glandular tissue is reduced in amount and undergoes to intestinal metaplasia4. H. pylori5. Dysplasia: carcinoma

ATROPHICGASTRITIS

H.pylori

H. PYLORY AND CHRONIC GASTRITIS

OTHER GASTRITIS

• Eosinophyillic gastritis: food allergy ?• Granulomatus gastritis: tuberculosis,

syphilis, sarcoidosis, fungi, Crohn disease• Reflux gastritis: duodenal and bile reflux• Menetrier disease (giant hypertrophic

gastritis)

Menetrier disease (HYPERTROPHIC GASTROPATHY)

• Severe hyperplasia of mucosal layer cells + glandular atrophy extreme enlargement of gastric rugae

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

• Gastrinoma excessive gastrin excretion gastric glandular hyperplasia (Zollinger-Ellison syndrome)

• Sometimes with severe loss of plasma proteins from the altered mucosa

• Risk of peptic ulcer


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 rarely

occur in association with absolute achlorhydria• Middle-later age group• Male > female, 1.5 to 2:1• Often solitary• >50% Ø <2cm; 10% Ø >4cm• Ø <0,3 cm erosion; Ø>0,6 cm ulcer

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

PEPTIC ULCER

Complications:

1.Bleeding2.Perforation

3.Obstruction: due to Edema or cicatrix

GASTRIC ULCER

• Destruction of mucosa and sub-mucous • Almost always single, 2-3 cm, • Type:

– Acute peptic ulcer: both mucous and sub-mucous layer are involved, 1 cm, single/ multiple

– Chronic peptic ulcer: penetrated and destroy the muscle coat.

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

TRIGER FACTORS OF PEPTIC ULCER

PEPTIC ULCER

Cylindric epithelia

Necrotic debris

Granulation tissue with lymphocytic infiltration

Glands hyperplasia

Edema

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 – antrum predominant – Six decade, Male: female = 2:1– Some cases origin from chronic gastritis with intestinal

metaplasia

I. Diseases of the stomach

D. Tumors of the stomach (benign)

I. Diseases of the stomach

D. Tumors of the stomach (malignant)• 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

GASTRIC CANCER– Invasion

• Early ( mucosa and submucosa)• Advanced (invade the submucosa)

– Macroscopic growth• Exophytic• flat/ depressed• ExcavationLinitis plastica – tumor cells diffusely infiltrate

gastric wall leather bottle appearance– Histology

• intestinal gland type• Diffuse: signet-ring cell

The Growth of Gastric Cancer

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

linitis plastica

GASTRIC CARCINOMA

• Prognosis:– Depend on the depth of tumor invasion

and metastasis process

Adenocarcinoma, NOS

ULCUS CARCINOMATOSA

REDUPLICATION STENOSIS DIVERTICULUM ATRESIA

Diseases of the Intestine

A. CONGENITAL ABNORMALITIES

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

Invagination/ intususeption Volvulus

Vascular obstruction HaemorrhoidIntern/ extern


A. Peptic Ulcer

B. Crohn Disease

C. Meckel Diverticulum

D. Malabsorption syndrome

E. Tumors of the Small Intestine


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


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 hypersecretion due to

gastrin 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, or hyperplasias associated with hypergastrinemia and peptic ulcer


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


B. Crohn’s Disease

Crohn Disease Ulcerative ColitisMay 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 lesions with mucosal cobblestone appearance. Non-caseating granulomatous inflammation with lymphocytic infiltration, fibrosis, and thickening of intestinal wall.Incidence of secondary malignancy is much lower than in ulcerative colitis

Affects only colon.

Inflammation and ulceration limited to mucosa and submucosaCrypt abscess, pseudopolyp

Greatly increased incidence of colon cancer in longstanding cases

Comparison of the lesions


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


D. Malabsorption syndrome• 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 cereals are first

added to the diet• Diagnosis biopsy blunting of small intestinal villi• 10-15% small intestinal malignancy: most often enteropathy-type

T cell lymphoma

Disorders Morphologic Features CommentsCeliac disease Flat mucosal surface with marked

villous atrophyGluten 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 mucosalTropheryma 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 lymphangiectasia

Generalized dilatation of the small intestinal lymphatics

Marked gastrointestinal pro-tein loss hypoproteinemia


D. Malabsorption syndrome

MALABSORPTION

Coeliac disease

Tropical sprue

Whipple’s disease

Secondary malabsorptiona. Interference with digestion-Mucosa destruction-Hepatic/ pancreatic disease-Resection of bowel-Congenital disaccharidase defect-Drug influence

Primary syndromes

b. Diminish of absorption-intestinal stasis-chronic obstruction

c. Altered transport-Lymphatic obstruction-Mesenteric blood supply disease-Abetalipoproteinemia


E. Tumors of the small intestine• Make up a small percentage of the gastrointestinal tumor• Carcinoid tumor:

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

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

metastasizes

- carcinoid syndrome: caused by elaboation of vasoactive peptides

and 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)


A. Hirschprung disease

B. Diverticula

C. Vascular diseases of the colon

D. Inflammatory disorders of the colon

E. Tumors


A. Hirschprung disease

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

• Dilatation is proximal to aganglionic segment


B. Diverticula

• Most common in old person, and almost always multiple• Most frequently involve the sigmoid colon• Type: pulsion/false diverticula pockets of mucosa and

submucosa

Diverticulosis of the Sygmoid


C. Vascular diseases of the colon


D. Inflammatory disorders of the colon

ENTERITIS TUBERCULOSA

Primer: milk + mycobacterium tuberculosa

Secunder: sputum + mycobacterium tuberculosa

Ulcerative Colitis


E. Tumors

Type CommentsNon-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 malignancyGreater malignant potentialHigh potential for malignant change

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

Intestinal Polyps

Familial Adenomatous Polyposis

Adenomatous polyp

Dukes’ Stage

ASTLER - COLLER

Five-year survival rate•A – tumor terbatas di mukosa - 100% •B1 – sampai dengan muskularis propria, belum sampai ke limfonodi 67%•B2 – menembus muskularis propria, belum sampai ke limfonodi 54%•C1 – sampai dengan muskularis propria, sudah sampai limfonodi 43%•C2 – menembus muskularis propria, sudah sampai limfonodi 22%•D – metastasis jauh sangat rendah

IV. Diseases of the Appendix

A.Inflammatory diseases

1. Acute appendicitis

2. Chronic appendicitis

B.Tumors of the appendix

The most common : carcinoid tumor

TRAKTUS DIGESTIVUS

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