2.TRAKTUS DIGESTIVUS

8/10/2019 2.TRAKTUS DIGESTIVUS

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TRAKTUSDIGESTIVUS

Pieri Kumaladewi, Dr, SpPA (UGM)

Wien Wiratmoko, Dr, SpPA(UNAIR)


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Upper digestive tract

I. Diseases of the Mouth & Jaw

A. Congenital DisordersB. Inflammatory disorders

C. Tumors and tumor-like conditions

II. Diseases of the Salivary GlandsA. Sialadenitis

B. Acute parotitis

C. Sjogren syndromeD. Mucocele

E. Ranula

F. Tumors of the salivary gland

III. Diseases of the EsophagusA.Tracheoesophageal fistula

B. Esophageal diverticulaC. Achalasia

D. Esophageal varices

E. Hiatus hernia

F. Inflammatory and related disorders

of the esophagus

G. Carcinoma of the esophagus


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I.A. CONGENITAL DISORDERS

SCHISIS / CLEFT MICROGNATHIA

* Failure of mesodermal penetrance betweenthe 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


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TONGUE

CONGENITAL DISORDER OF THE TONGUEMICROGLOSSI MACROGLOSSI MEDIAN RHOMBOID GLOSSITIS

TIE TONGUE BIFID TONGUE


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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)


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Glositistuberculosa Glositisluetica

Geographic tongue Hairry tongue

GLOSSITIS


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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


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LEUKOPLAKIA

- white patches of keratosis- premalignant lesion

- hyperkeratosis, hyperplasia of the squamous epithelium

- dysplastic changes

SQUAMOUS CELL CARCINOMA


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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 complicationrheumatic fever, acute

proliferative glomerulonephritis, Henoch Schonlein purpura

-Ulcerative pharyngitis & tonsillitisdiphtheria

Tonsilitis:-Follicular tonsilitis, streptococcus/ Borrelia / virus

-Parenkhimal tonsilitis: quincy, Peritonsiler abses

-Angina agranulositic netropenic

-Tonsilitis morbili: Warthin Finkeldey giant cells

Pharynx & Tonsil


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A. Sialadenitis

B. Mucocele

C. Ranula

D. TumorsPleomorphic adenoma (Mixed tumor)

Warthin tumor / adenolymphoma / Papillary cystadenomalymphomatosum

OncocytomaAdenoid cystic carcinoma

Mucoepidermoid tumor

II. Diseases of the SALIVARY GLAND


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II. A. Sialadenitis

Acute

- Suppurative parotitis- Non-suppurative parotitis

- Parotitis epidemica / Mumps: paramyxovirus

Orchitis/ Oophoritis

- Cytomegalic inclusion disease

Chronic1. SJOGRENS SYNDROME :

- Autoimmune disease

- Keratoconjungtivitis sicca

- Xerostomia

- Parotitis hyperplasia

2. MIKULICZ SYNDROME :- Idiophatic

- Keratoconjungtivitis sicca

- Xerostomia

- Unilateral parotitis hyperplasia


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Mucocele A cyst-like pool of mucus, lined by granulation tissue,

near a minor salivary gland

Results from mucus leakage caused by rupture ofobstructed or traumatized ducts

Ranula

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


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Tumors of the Salivary Glands

1. Pleomorphic adenoma (Mixed tumor)

2. Warthin tumor / adenolymphoma / Papillary

cystadenoma lymphomatosum3. Oncocytoma

4. Adenoid cystic carcinoma

5. Mucoepidermoid tumor


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Anatomy of parotid gland


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Anatomy of parotid gland


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Pleomorphic adenoma (parotid)


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Pleomorphic adenoma (gross)


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Pleomorphic adenoma


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Warthin tumor

Benign tumor mostly occur in parotid gland


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Warthin tumor

Cystic spaces lined by double-layered eosinophilic epithelium,

and all embedded in lymphoid stroma


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Oncocytoma

Mostly in parotid gland


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Oncocytoma

Large granular appearing, eosinophilic-staining epithelial cells


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Adenoid cystic carcinoma

Minor salivary gland


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Most characteristic appearance consists of cribriform pattern

with masses of small, dark-staining cells arrayed arround

cystic spaces


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Mucoepidermoid tumor(Palatal gland)

Mostly in parotid gland


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III. Diseases of the Esophagus

A.1. Tracheoesophageal fistula

Congenital 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 communicates

With the trachea near the tracheal bifurcation, the upper esophagus ends in a blindpouch

Associated 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


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A.2. Heterotopic tissue

patches of fundic-type gastric mucosa are

occasionally found above the distal sphincter

separated from the columnar lining of the distalesophagus

congenitally misplaced gastric tissue (heterotopic)

can lead to ulceration and stricturing due to

local acid/pepsin secretion


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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


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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

dilatationdysphagia


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D. Esophageal varices

-Localized dilatation of veins

-Portal hypertension

-cirrhosis hepatis

- Haematemesis


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III. Diseases of the esophagus

E. HIATUS HERNIA

The presence of part of the stomach above the diaphragmatic orifice, mostly acquired

Increased intra-abdominal pressure and loss of diaphragmatic muscular tone with aging

herniation of the stomach and subsequent retraction of the esophagus.


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F. Inflammatory and related disorders

of the esophagus

1. Gastroesophageal reflux

2. Barrets esophagus3. Candida esophagitis

4. Viral esophagitis

5. Esophageal stricture


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F. 1. Gastroesophageal reflux

Reflux of gastric acid contents into the esophagusesophagitis,stricture, ulceation, or columnar metaplasia (Barrets esophagus)

Usually characterized by burning pain (often manifests by substernalpain 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


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F.2. BARRETS 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


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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


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F. 4.a. Viral esophagitis

Herpetic esophagitis Characterized by painful and difficult swallowing

Tends to occur in immunosuppressed patient, causedby HSV-1 infection

Cytomegalovirus (CMV) infection Less common


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F. 4.b. Other esophagitis

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

(GVH) disease


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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)


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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


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G.1. Squamous Cell Carcinoma

Arises most frequently in the upper and middle thirdsof the esophagus


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G2. Adenocarcinoma

Arises most frequently in the lower third, and mostly from

aberrant gastric mucosa or Barrets esophagus


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Part 2


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Pathology ofthe

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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STOMACH


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A. Congenital Pyloric Stenosis

B. Gastritis

C. Peptic Ulcer of the StomachD. Malignant Tumor of the Stomach


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A. Congenital Pyloric Stenosis

Is caused by hypertrophy of circular muscular layer of the pylorusoften results as papable mass

obstruction of gastric outletepisodes 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

I Diseases of the Stomach


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a. Causes

- Nonsteroidal anti-inflammatory drugs (NSAIDs)

- Cigarette smoking

- heavy alcohol intake- Burn injury (severe)Curling ulcer

- Brain injuryCushing ulcer

b. Characteristic

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

- may be manifest as gastric ulceroften multiple


B. Gastritis:1. Acute (erosive) gastritis


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Acute gastritis


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- Helicobacter pyloriassociated gastritis- gramneg. 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


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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 mucous andsubmucous layerswith germinal center

1. Inflammatory cells: activenetrophil (+)2. Metaplasia: intestinal metaplasiapre-malignant

condition

3. Glandular atrophy: glandular tissue is reduced in

amount and undergoes to intestinal metaplasia

4. 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 ?

Granulomatus gastritis: tuberculosis,

syphilis, sarcoidosis, fungi, Crohn disease

Reflux gastritis: duodenal and bile reflux

Menetrier disease (giant hypertrophic

gastritis)

M t i di


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Menetrier disease(HYPERTROPHIC GASTROPATHY)

Severe hyperplasia of mucosal layer

cells + glandular atrophyextremeenlargement of gastric rugae

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

Gastrinomaexcessive gastrinexcretiongastric 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 secretionbut rarely

occur in association with absolute achlorhydria

Middle-later age group

Male > female, 1.5 to 2:1

Often solitary

>50% 4cm 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 ioninjury 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 and

destroy the muscle coat.


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ACUTE GASTRIC ULCER

Multiple

Gastric > duodenum

Erosionulceration

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/traumaCurling ulcer NSAID


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TRIGER F CTORS OF PEPTIC ULCER

Cylindric epithelia


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PEPTIC ULCER

Necrotic debris

Granulation tissue with lymphocytic infiltratio

Glands hyperplasia

Edema

I Diseases of the stomach


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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

neoplasm5-10% of gastric polyp

Sessile / pedunculated

distalantrum 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)


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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


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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 infiltrategastric wall leather bottle appearance

Histology intestinal gland type

Diffuse: signet-ring cell


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The Growth of Gastric Cancer

Other gastric tumors


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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 TUMORCarcinoid syndrome

Low grade malignancy

Metastasis to the liver Multiple lesions

LEIOMYOMA

SECONDARY TUMORS (METASTASIS)

rare

Mostly from leukemia or general lymphoma From breast / lung cancerdiffuselinitis

plastica


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GASTRIC CARCINOMA

Prognosis:

Depend on the depth of tumor invasion

and metastasis process

Adenocarcinoma, NOS


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Adenocarcinoma, NOS

ULCUS CARCINOMATOSA


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ULCUS CARCINOMATOSA

Diseases of the Intestine


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REDUPLICATION STENOSIS DIVERTICULUM ATRESIA

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


B. INTESTINAL OBSTRUCTION

Invagination/ intususeption Volvulus


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Invagination/ intususeption Volvulus

Vascular obstruction HaemorrhoidIntern/ extern


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A. Peptic Ulcer

B. Crohn Disease

C. 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 syndromegastric acid hypersecretiondue 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, orhyperplasias associated with hypergastrinemia and peptic ulcer


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B. Crohns Disease

Chronic inflammatory condition of unknown etiology

Tends to affect young people in 2ndand 3rddecades 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 intestinebladder, vagina, skin


B Crohns Disease


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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 productcom-

plication (peptic ulceration bleedingperforation)

Occasionally associated with: intussusception and

volvulus


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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

Diagnosisbiopsyblunting of small intestinal villi

10-15%small intestinal malignancy: most often enteropathy-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 changeabnormalities

similar to those of celiac disease

Probable infectious origin;

often respond to antibiotics

Whipple disease PAS+ macrophages in mucosal

Tropheryma whippeliiEM

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 intoleranceAbetalipoproteinemia 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 losshypoproteinemia


MALABSORPTION


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Coeliac disease

Tropical sprue

Whipples 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 T f th ll i t ti


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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)


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III Di f th C l


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A. Hirschprung disease

B. Diverticula

C. Vascular diseases of the colon

D. 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


B Di ti l


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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


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Diverticulosis of the Sygmoid



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C. Vascular diseases of the colon


D I fl t di d f th l


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D. Inflammatory disorders of the colon

ENTERITIS TUBERCULOSA


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ENTERITIS TUBERCULOSA

Primer: milk + mycobacterium tuberculosa

Secunder: sputum + mycobacterium tuberculosa


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Ulcerative Colitis


E T


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E. Tumors

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


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Type Comments

Non-neoplastic polypsHyperplastic 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 polyposissyndrome)increased risk of malignancy

Greater malignant potential

High potential for malignant change

Intestinal Polyps


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Familial Adenomatous Polyposis

Adenomatous polyp


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Adenomatous polyp

Dukes Stage


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ASTLER - COLLER


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Five-year survival rate

Atumor terbatas di mukosa - 100%

B1 sampai dengan muskularis propria,

belum sampai ke limfonodi 67%

B2menembus muskularis propria,belum sampai ke limfonodi 54%

C1sampai dengan muskularis propria,

sudah sampai limfonodi 43%

C2menembus muskularis propria,

sudah sampai limfonodi 22%

Dmetastasis jauh sangat rendah

IV Di f th A di


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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 : carcinoid tumor


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2.TRAKTUS DIGESTIVUS

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