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 OBSTRUCTION Paralytic 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

Gmbrn Histologik

C2 D.

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

*Strangulasi usus *

CYST .
T : Primer Mesotel Sekunder