IDIOPHATIC !

NFLAMATORY BOWEL DISEASE

CROHNS Disease
1932 Py idiopatik terminal ileitis

Skip area regional enteritis

any level GIT Crohns Dis

Patol Khas :
1. Sharply delimited

- Trasmural ----- Pr inflam + kerusakkan

mucosa
2.Non Caseating granulomatous
3. Fissure , fistula
4. Mainfest, Sistemik
Epid : Any age - anak 2 s/d usia lanjut. Peak
decade 6 - 7

Morfol
Small

intest 40 %
Small intest + Colon 30 %
Colon 30 %
- Creeping Fat
Tebal , Edem , Fibrotik Rubbery , inflam
Propria muskularis hipertrop lumen sempit
Ro string Sign
: KHAS Sharp Demarcation , Multiple Bowel
Segmen SKIP LESSIONS
-

Early : Focal Mucosal Ulcer ~ Canker Sures

( APHTHOUS ULCERS ), Edem , Texture

mucosa normal hilang
COBBLESTONE APP
fissure
fistula / sinus
perforasi , abses lokal
HISTOL : - inflam mucosa
- ulcerasi
- chronic mucosal damage Distorsi
- atropi, metaplasia : Piloric metaplacia
Paneth cell Metaplasia

- Inflam transmural , agregat limfoid

- granuloma non kaceosa ( sarcoid like gran )
- other mural change : Musc mucosa - Reduplikasi
Tebal, ireg, fibrosis Striktura
Limfangiektasis, saraf hipertrop, vaskulitis fokal
KLINIK : Diare,demam ,abdominal pain
feses + darah
Komplikasi : Fibrosis , fistula
Protein losing enteropathy
General mal absorption B12 , bile salt
Manifestasi extra intes poli artritis
migrans,sacroilietis, ankylos spondilitis,eritem nodosum

Kolitis ulseratifa

Ulsero inflammatory dis

Kolon Mukosa

Submukosa
severe CASE
Berbd dgn CD,K UExtends in a Continuous
fashion prox.from Rectum
Py Imun
Morfol
Rectum retrograde fashion kolon
pancolitis

continuity,mukosa merah , granuler ,

pdrh,ulcerasi ,pseudo polip ,serosa normal
Dapat toxic mega kolon ( gangren )
Displasia Ca ( low + high grade )
Klinik : Diare + Pdrh

Colonic Diverticulosis
Blind

Pouch dilapisi mukosa

Ileum yeyenum divert. Multipel jrg
Kolon --- sering multipel divertikulosis

Morfol : Small flask like , sferikal

0,5 1 cm kolon sigmoid
Histol : dd tipis,mukosa Flattened, atropi menekan
submukosa , musk propria tak ada , M. sirc hipertropi.
Divertikolitis fibrosis abses peritonitis.
Patogenesis : 1. Dd Weakness fokal
2.Tek intra lumen

Mayor causes of intestinal obstruction

Mechanikal

obstruction

Adhesions

Hernia , internal / external

Volvulus
Intussusception
TUMORS
Inflam . Strik
Obstruction gall stone , fecolith, Bd asing
Cong. Stricture , Atresia
Cong. Band
Meconeum in mucoviscidosis ( Cystic fibrosis )
Imperforate anus

 PSEUDO
Paralytic

OBSTRUCTION

ileus ( Post OP )
Vascular infark
Miopathi, neuropati ( HIRSCHSPRUNGS
DIS )

Tumours of the SMALL and large

intestinalis
Non

neoplastic polyps
Hyperplasia polyps
Hamartomatous polyp

juvenile polyp
Peutz jegher polyp

Inflam. Polyp
Lymphoid Polyp

Neoplastik Epithelial Lesions

Benign

Polyp Tub. Adenoma

_ Tub. Villous Adenoma

Villous Adenoma
Malignant Lesions Adenoma Ca 70 % KGNS GIT
- Carcinoid T
- Anal Zone Ca
Mesenchymal Lesions
Benig lesions: Leiomio,lipoma,neuroma,angioma
Malignant
: leiomio sarcoma, Liposarc, Malignant
spindle cell

Limfoma

kaposi sarc

Polip Masa T dalam lumen

- Polip pedunculated
- Sessile
dpt sbg akibat * Maturasi abnormal ( Mukosa )
* Inflamasi

Non Neoplastik spt polip hiperpl

Polip Epitelial Akbt Prol. Displ Polip Adenoma /
Adenoma True Neoplasia ( New Growth )
precusor Ca
Polipoid Lesions Tumor Submucosa / Mural

Polip Non neoplastik

Sporadik
Tu

kolon
~ Usia
Large intest 90 % Polip hiperpl

> 50 % 60 th
Polip inflam ( Pseudo Polip ) disekitar inflam
mukosa Yg regenerasi ulcerasi tu UC / CD
Polip limfoid normal Tdd jar limpoid intra
mukosa

Morfol :
Polip hiperplastik : Polip epit, kecil < 5 mm
Segala gol usia ( dekade 5,7 )

Diatas fold mukosa , nipple like , hemisferik ,

smooth singel / multiple
Histol : Well formed glands / crypt dilapisi sel
non neopl ( mature goblet / absorptive cells )
L. propria < <
Potensial malignant negatif

Histol :
-

inflam mucosa
-ulcerasi
-chronic mucosal damage distrosi
atropi , metaplasia : Piloric Metaplasia

Paneth cell metapl

Inflamasi trans mural , agregat limfoid
Granuloma non kaseosa . ( sarcoid like gran )
Other mural change : musc. mucosa reduplikasi
Tebal, irreg,fibrosis Strictura
Limfangiektasis,saraf hipertropi ,vasculitis focal

Yuvenile Polip
fokal

hamartomatous malformation elemen

mukosa sporadik / ~ rare autosomal dominant
sindr. Yuvenile poliposis

< 5 thn 80 % rectum / tersebar kolon

1 3 cm , bulat , smoot / lesi lobulated,tangkai 2 cm
Histol : L. Propria bulk polip , kel dilatasi kistik
imflam , permukaan kongesti , ulcerasi
Singel / Multiple
Potensial malignant ( - )
Juvenile poliposis - Adenoma
Adeno karcinoma

Polip Peutz Jegher

Lesi hamartomatous
Singel / Multiple
Rare autosomal dominant syndr
KHAS : Polip Hamart. Mutiple tsebar GIT
Melatonik mukosa
Pigmentasi kutis ( bibir , mukosa oral ,
muka , genetalia , telapak tgn
Histol / Morfol :
Pedunculated , Besar , lobulated
Jar.penyokong / otot polip
Dikel. Kel. N. Dilap ep intest . N. , sel goblet >>
Gaster 25 %, kolon 30%, Small Bowel 100 %
Pot. Malig ( - ), ttp increase risk Develop. Ca of
Pankreas,Mammae, Pr , Ovarium, Uterus.

Lesi Epit Neoplastik

ADENOMA :
Polip Adenoma Neopl
Kecil : Bsr SESSILE
ll
Pedunculated
20 -30% < 40 th
40 -50 % > 60 %
Predisp . Familial Aden. Sporadik
Ade. Tub Kel Tub >>> ( kecil , Bsr Pedunculated )
Ade. Villosa Villousa 1% ( Besar , Sessile )
Ade. TubVillous 5 10 %
Over lap Tub 75% , tubulovillous 50 % , Vill 25 -50 %
ADENOMA Prol Epit displastik Mild Severe CIS

POLIP ADENOMAYTOUS resiko Malig.~ dgn : *

ukuran * histol * severity of epit. displ
1.Kanker jrg pd aden. Tub < 1 cm
2. Resiko kanker ^^( > 40 % ) Pd adn. Vill > 4 cm
3.Severe Displ. Biasanya pd dhr villous
4. Periode Aden ukuran 2 x kira 2 10 th
Pertumbuhan lambat spi tdeteksi
Morfol :
Ad. Tub : * pada kolon 90 % 1/ 2 nya pd
rektosig ,dpt pd gaster usus halus , singel
kecil smooth
sessile lobulated kasar , tungkai luas

Histol :
Tgkai jar fibromusk P.D >>(sub mukosa )
Dilap mukosa non neopl. normal
Ep Adenomatous ke tgkai,mukosa
Raspberry like head tdd epit neopl
Kel bercabangdilap.sel kolumner, hiperkrom
Sekr. Musin + / Aden. Tub benign kel bcab di pisah L.prop
Displ RGN severe
Severe Dyspl ( CIS ) - intramukosa
Invasi karsinomatous invasi tungkai polip Adeno
Ca

Aden. Villous
Rektum

sigmoid
Sessile 10 cm
Cauliflower 1 3 cm, papiler dilap. Epit
kolumner displ
Inti variasi , hiperkr. Der Displ ringan
berat
40 % Ca invasif ~ ukuran & der disp
Aden.Tubulovillous

Klinik
Tubuler kolorectal ( tub . Villous ) Aden.Asimptomatik
( / anemia occult bleeding )
Aden. Villous Bleeding
Aden. Usus halus Anemia
Obstruksi
jrg biasanya ke
Intussusepsi
betulan Ro/
Autopsi
Klinikal prub maligna tgtg :
I. Displ brt ( CIS ) Ksanggupan metast --- masih lesi
benigna
II. Sal limfatik mukosa kolon << Ca intra mural potentik
metastase
III.Mukosa muskularis sub muc . Space Adeno Ca invasive
Potensial metas

ADEKUAT Exsisi ( Endoskopic Removal)

histo ditemukan
Adeno

Ca superfisial , batas sayatan ( Stalk )

(-)
Invasi Vask / limfatik ( - )
Ca diferensiasi jelek
IV. Adeno Ca Polip sessile

Polipektomi Surgery
V. Ca pada adenoma pedunkulated / sessile
op

Ca invasive dpt ditemukan sec PA jar

Adenomatous Residu Tdk dpt ditemukan dgn
PA. Histol dari bahan resected Portion

Poliposis Adenomatous Familial :

* Jarang Autosomal dominant

Tdd : I. Peutz Jeghers Synd

- Polip Hamartomatous
TU bila extra GIT resiko Ca
II. Poliposis Aden. Familial ( F A P)
Polip Adenoma >> Ca ham,pir 100 %
100 -150
Histol : Polip Tub >> , kdg Villous
D / ditegakan sdh Ca kolon / Rectum

III SINDR Gardner .

Variasi FAD + osteoma multyiple ( terutama mandibula ,
Tengkorak , Tl Panj )
Kista epidermal
Fibromatosis
Jrg pd Gigi abn ( un erupted / supernumery teeth )
Sering Ca Tiroid , Ca Duod , Adeno Ca
IV. SINDR TURCOT btk kombinasi dp Poliposis
Adenomatoid kolon dan T. CNS Glioma
Polip dekade II III diikuti kanker dlm wkt 10 -15 th

Adenoma Carcinoma Sequence

Perkemb Ca dari adenoma Carcinoma sequence
-

berdsr kan observasi brkt ini :

Polpulasi prenalensi aden , Ca kolorectal
Distribusi adenoma kolorectal dpt dibandingkan Ca
kolorekt
Puncak incidevce polip aden . mendahului beberapa
thn dr puncak Ca kolorekt
Fokus Ca kecil berhub relatif dg aden polip, ttp fokus yg
sama muncul langsung dr mukosa non polip sgt
jarang
Resiko Ca jumlah aden. os FAP
Follow up pkb aden. Dan OP. suspect incidence Ca
kolorerektal

Karcinoma kolorektal
Adeno

Ca 98 %

Dari Polip
Symtome relatif early
Curable reseksi
USA : kasus baru / th i50.000 58 ooo
mrp 15 % ke
Epid, Etiol, patogenesis : peak inc 60 -70 th 20 % , <
50 th
Orang muda U C / Sindr poliposis
Rectum : : 2 : 1
USA , CANADA,Austr, Swedia : Jepang ,Am Sel , Afrika

FAKTOR DIET INCIDENENCE

*

SAYUR Serat

* KH DIHALUSKAN ( Vit A, C, E ) O 2 radikal

* Fat
* intake Mikronutrient protektif
MORFOL :Kolon Ca tu pd orang tua
25 % : Cecum / colon ASC rectum , sigmoid distal
25 % kolon desc , sigm. Prox: sisa tersebar
T. Kolon Prox Polipoid,Fungating Extensi DD
Cecum , kolon Asc. Obstruksi Jarang
T. Kolon Distal Annular, Encircling mrpkan Ring
Kontruction

Histol :

Klinik : Asimp. ber thn 2 Kdg + bln / th sblm D / : tegak

Ca Cecum
fatique
Kolon kanan
lemah , anemia def Fe
Kolon kiri occult bleeding
kebiasaan defikasi berubah
kram kwadran bawah kiri
melena , diare, kontsipasi
Rektum
Sigmoid
infiltr . D / prog > buruk
Manifestasi sistemikextensi
METASTASE : extensi lgs limfogen , hematogen
KGB , Hati , Pr , Tl , Serosa Kavum Perit. , Otak

Stadium tumor
A
B1
B2
C1

C2
D.

Gmbrn Histologik

Terbatas mukosa
Muskul. Propria
Nodes ( - )
Penetrasi muskul.Prop
Nodes ( - )
Extensi Muskul.Propria
Penetrasi ( - )
Nodes ( + )
Penetrasi muskul. Prop
Nodes ( + )
Metast jauh
ASTLER COLLER CLASS ( Modif. Duke )

Neoplasma Small Intestine :

75 % dari py GIT 3 5 % T GIT
Benign T >>
Adeno Ca
Napkin Ring
Polipoid Fungating
T. Carcinoid : Maligna
Agresifitas tgtg
site
Depth lokal penetrasi
size
App, rektum metast ( - )
Ileum, gaster , kolon metast ( + )

PATOGENESIS ; Morfol

Soliter ? Multiswentrik
Solid , kuning
Histol :

Limfoma
T. Mesenchimal

Clinical Features of Carcinoid Syndr

Vasomotor disturbances
. Cutaneous flushes and apparent
( most patients )

Cyanosis

Intestinal Hypermotility :
D, Cramps , N, V ( most patients )
Asthmatic Bronchoconstrictive attacks
Cough, wheezing , dyspnea ( 2 / 3 os )
Hepatomegaly
Nodular, hepatic metast(some cases)
Systemic Fibrosis : Cardial, Pnebal katub tricuspid,
pulmonal, stenosis fibrosis endo cardial ( VD )
( bronchial carcinoid left side )
* Fibrosis retro peritoneal , pelvik
* Collagenous pleural and intimal aortic plaque

Appendik
Appendisitis

Akut
50 -80 % obstruksi ( fecolith, Batu , T / cacing )
Mucin tek intra lumen dranage vena
-- ischemik Prol. Bakteri
Morfol : Appendicitis akut early

Supp

Gangrenous
Histol : Akut PMN muskularis
Appendicitis chronik :

Mucocele
Sekresi

musin
Prol. Epit :
1. Non neoplastic Epit . Hyperpl tdk
dapat dibedakan dari polip hiperpla. Kolon.
2. Musinous cyst adenoma
3.Musinous cyst adeno Ca
MORFOL :
Dil.App - sekr . Mucin
Peudo Myxoma Peritonei

Peritoneum

Infeksi :
* App is * Ruotured Peptic Ulcer
* Cholecystitis * Diverticulitis * *
Acut Salphingitis
* Trauma Abdomen * Peritoneal dialisis
E. Colitaf Aureus
Clostridium Perfringen
Morfol : Tgtg lama nya
sub hepatik / sub diaf. Abses
- fibrosis Sklerosing

CYST

.
T : Primer Mesotel
Sekunder

*Strangulasi usus *