CROHNS Disease1932 Py idiopatik terminal ileitis Skip area regional enteritis any level GIT Crohns DisPatol Khas :1. Sharply delimited - Trasmural ----- Pr inflam + kerusakkan mucosa2.Non Caseating granulomatous3. Fissure , fistula4. Mainfest, SistemikEpid : Any age - anak 2 s/d usia lanjut. Peak decade 6 - 7 IDIOPHATIC !NFLAMATORY BOWEL DISEASE

MorfolSmall 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 - ReduplikasiTebal, ireg, fibrosis StrikturaLimfangiektasis, saraf hipertrop, vaskulitis fokalKLINIK : Diare,demam ,abdominal pain feses + darahKomplikasi : Fibrosis , fistula Protein losing enteropathy General mal absorption B12 , bile salt Manifestasi extra intes poli artritis migrans,sacroilietis, ankylos spondilitis,eritem nodosum

Kolitis ulseratifaUlsero inflammatory disKolon Mukosa Submukosa severe CASEBerbd dgn CD,K UExtends in a Continuous fashion prox.from RectumPy ImunMorfol Rectum retrograde fashion kolon pancolitis continuity,mukosa merah , granuler , pdrh,ulcerasi ,pseudo polip ,serosa normalDapat toxic mega kolon ( gangren )Displasia Ca ( low + high grade )Klinik : Diare + Pdrh

Colonic DiverticulosisBlind Pouch dilapisi mukosaIleum yeyenum divert. Multipel jrgKolon --- sering multipel divertikulosisMorfol : Small flask like , sferikal 0,5 1 cm kolon sigmoidHistol : 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 obstructionMechanikal obstruction AdhesionsHernia , internal / externalVolvulusIntussusceptionTUMORSInflam . StrikObstruction gall stone , fecolith, Bd asingCong. Stricture , AtresiaCong. BandMeconeum in mucoviscidosis ( Cystic fibrosis )Imperforate anus

PSEUDO OBSTRUCTION

Paralytic ileus ( Post OP )Vascular infarkMiopathi, neuropati ( HIRSCHSPRUNGS DIS )

Tumours of the SMALL and large intestinalisNon neoplastic polyps Hyperplasia polyps Hamartomatous polyp juvenile polyp Peutz jegher polyp Inflam. Polyp Lymphoid Polyp

Neoplastik Epithelial LesionsBenign Polyp Tub. Adenoma _ Tub. Villous Adenoma Villous AdenomaMalignant Lesions Adenoma Ca 70 % KGNS GIT - Carcinoid T - Anal Zone CaMesenchymal Lesions Benig lesions: Leiomio,lipoma,neuroma,angiomaMalignant : leiomio sarcoma, Liposarc, Malignant spindle cell kaposi sarcLimfoma

Polip Masa T dalam lumen - Polip pedunculated - Sessile dpt sbg akibat * Maturasi abnormal ( Mukosa ) * Inflamasi Non Neoplastik spt polip hiperplPolip Epitelial Akbt Prol. Displ Polip Adenoma / Adenoma True Neoplasia ( New Growth ) precusor CaPolipoid Lesions Tumor Submucosa / Mural

Polip Non neoplastikSporadikTu kolon~ UsiaLarge intest 90 % Polip hiperpl > 50 % 60 thPolip inflam ( Pseudo Polip ) disekitar inflam mukosa Yg regenerasi ulcerasi tu UC / CDPolip limfoid normal Tdd jar limpoid intra mukosa

Morfol :Polip hiperplastik : Polip epit, kecil < 5 mmSegala gol usia ( dekade 5,7 )Diatas fold mukosa , nipple like , hemisferik , smooth singel / multipleHistol : Well formed glands / crypt dilapisi sel non neopl ( mature goblet / absorptive cells )L. propria < > Gaster 25 %, kolon 30%, Small Bowel 100 % Pot. Malig ( - ), ttp increase risk Develop. Ca of Pankreas,Mammae, Pr , Ovarium, Uterus.

Lesi Epit NeoplastikADENOMA :Polip Adenoma NeoplKecil : Bsr SESSILE llPedunculated20 -30% < 40 th 40 -50 % > 60 %Predisp . Familial Aden. SporadikAde. 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. displ1.Kanker jrg pd aden. Tub < 1 cm2. Resiko kanker ^^( > 40 % ) Pd adn. Vill > 4 cm3.Severe Displ. Biasanya pd dhr villous4. Periode Aden ukuran 2 x kira 2 10 th Pertumbuhan lambat spi tdeteksiMorfol :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. normalEp Adenomatous ke tgkai,mukosaRaspberry like head tdd epit neoplKel bercabangdilap.sel kolumner, hiperkromSekr. Musin + / -Aden. Tub benign kel bcab di pisah L.propDispl RGN severeSevere Dyspl ( CIS ) - intramukosaInvasi karsinomatous invasi tungkai polip AdenoCa

Aden. VillousRektum sigmoidSessile 10 cmCauliflower 1 3 cm, papiler dilap. Epit kolumner displInti variasi , hiperkr. Der Displ ringan berat40 % Ca invasif ~ ukuran & der disp

Aden.Tubulovillous

KlinikTubuler kolorectal ( tub . Villous ) Aden.Asimptomatik ( / anemia occult bleeding )Aden. Villous BleedingAden. Usus halus Anemia Obstruksi jrg biasanya ke Intussusepsi betulan Ro/ AutopsiKlinikal prub maligna tgtg : I. Displ brt ( CIS ) Ksanggupan metast --- masih lesi benigna II. Sal limfatik mukosa kolon

ADEKUAT Exsisi ( Endoskopic Removal) histo ditemukanAdeno Ca superfisial , batas sayatan ( Stalk ) ( - )Invasi Vask / limfatik ( - )Ca diferensiasi jelekIV. Adeno Ca Polip sessile Polipektomi SurgeryV. 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 dominantTdd : 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 epidermalFibromatosisJrg pd Gigi abn ( un erupted / supernumery teeth )Sering Ca Tiroid , Ca Duod , Adeno CaIV. 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 SequencePerkemb Ca dari adenoma Carcinoma sequence berdsr kan observasi brkt ini : Polpulasi prenalensi aden , Ca kolorectal Distribusi adenoma kolorectal dpt dibandingkan Ca kolorektPuncak incidevce polip aden . mendahului beberapa thn dr puncak Ca kolorektFokus Ca kecil berhub relatif dg aden polip, ttp fokus yg sama muncul langsung dr mukosa non polip sgt jarangResiko Ca jumlah aden. os FAPFollow up pkb aden. Dan OP. suspect incidence Ca kolorerektal

Karcinoma kolorektalAdeno Ca 98 %Dari Polip Symtome relatif early Curable reseksiUSA : kasus baru / th i50.000 58 ooo mrp 15 % ke Epid, Etiol, patogenesis : peak inc 60 -70 th 20 % , < 50 thOrang muda U C / Sindr poliposisRectum : : 2 : 1USA , CANADA,Austr, Swedia : Jepang ,Am Sel , Afrika

FAKTOR DIET INCIDENENCE * SAYUR Serat * KH DIHALUSKAN ( Vit A, C, E ) O 2 radikal* Fat * intake Mikronutrient protektifMORFOL :Kolon Ca tu pd orang tua 25 % : Cecum / colon ASC rectum , sigmoid distal25 % kolon desc , sigm. Prox: sisa tersebarT. Kolon Prox Polipoid,Fungating Extensi DD Cecum , kolon Asc. Obstruksi JarangT. Kolon Distal Annular, Encircling mrpkan Ring Kontruction

Histol :Klinik : Asimp. ber thn 2 Kdg + bln / th sblm D / : tegak Ca Cecum fatiqueKolon kanan lemah , anemia def FeKolon kiri occult bleeding kebiasaan defikasi berubah kram kwadran bawah kiri melena , diare, kontsipasiRektum Sigmoid infiltr . D / prog > burukManifestasi sistemikextensi

METASTASE : extensi lgs limfogen , hematogen KGB , Hati , Pr , Tl , Serosa Kavum Perit. , Otak

Stadium tumor Gmbrn Histologik A Terbatas mukosa B1 Muskul. Propria Nodes ( - ) B2 Penetrasi muskul.Prop Nodes ( - ) C1 Extensi Muskul.Propria Penetrasi ( - ) Nodes ( + ) C 2 Penetrasi muskul. Prop Nodes ( + ) D. Metast jauh ASTLER COLLER CLASS ( Modif. Duke )

Neoplasma Small Intestine :75 % dari py GIT 3 5 % T GITBenign T >>Adeno Ca Napkin Ring Polipoid Fungating

T. Carcinoid : Maligna Agresifitas tgtg site Depth lokal penetrasi sizeApp, rektum metast ( - )Ileum, gaster , kolon metast ( + )

PATOGENESIS ; Morfol Soliter ? MultiswentrikSolid , kuningHistol :

LimfomaT. Mesenchimal

Clinical Features of Carcinoid SyndrVasomotor disturbances . Cutaneous flushes and apparent Cyanosis ( most patients )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

AppendikAppendisitis Akut 50 -80 % obstruksi ( fecolith, Batu , T / cacing )Mucin tek intra lumen dranage vena -- ischemik Prol. BakteriMorfol : Appendicitis akut early Supp GangrenousHistol : Akut PMN muskularisAppendicitis chronik :

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

Peritoneum Infeksi : * App is * Ruotured Peptic Ulcer * Cholecystitis * Diverticulitis * * *Strangulasi usus * Acut Salphingitis * Trauma Abdomen * Peritoneal dialisis E. Colitaf Aureus Clostridium PerfringenMorfol : Tgtg lama nya sub hepatik / sub diaf. Abses - fibrosis SklerosingCYST . T : Primer Mesotel Sekunder