*RONGGA MULUT DANTRACTUS GASTRO INTESTINALISDr.Resmi Kartini Ms

*Oral Soft tissueInflamasi : Et / H. Simplex tipe 1, HIV (human immunodeficiency vi) .Epstein- Barr Ulcus Aftosa Kandida , Glositis

Tumor dan Pre cancerous Lesions

Leukoplakia dan Erythroplakia Mempunyai nilai di Leukoplakia : Plaque putih pada mukosa dengan epitel mengalami hiperkeratosis dan penebalan epiteldengandasar terdiri dari sel spinosum - prolif epidermal 85-90 % -- Benign spi Malignant

*Plaque putih pada Membr. Mukosa mulut Tidak dpt diangkat dgn scrapingGambaran ; penebalan epitel, sitologi atipik - displasiaKarsinoma in situ prove prekankerMorfol : Mukosa bukal Dasar mulut Permuk ventral lidah Palatum durumHigh risk

*Soliter / multipleTebal , smooth , indurasi , wrinkled,corrugated / verrucose plaquesHistol : HiperkeratosisAcantosisDisplasia CISLesi displastik / Anaplastik --- infilt Limp,makrofa- Ganas 5-6 %

*Erythroplakia ( Dysplastic Leukoplakia )Erosi superfisial + Displasia -- CISEpitel atipik resiko yang tinggi tranformation malignanSpeckled leukoerythroplakiaMultifact origins Tobacco. Alkohol,chronic exposure - iritant

*Squamous Cell Ca95 %Tobacco ,alkohol Dasar mulut , lidah , palatum durum ,dasar lidahDiff baik sampai anaplastikMetast : KGB Mediastinum , paru ,hati, tulangProg : 5 Th 90% recurrent free:dsr lidah 20-30 %

*AmeloblastomaEpit odontogenic T Epit lining drpd dentigerous cystLamina dental ,enamel Lapisan basal dp mucosa mulutDekade 5 Folikuler dental epitplexiform

*Sel kolumner Pulau 2 sentral retikulum stellaeMetaplas skuamosa tipe akantomatousStroma jar ikat fibrousDentrigerous cistFoll Cyst

*Adenoma pleomorphikMixed tumor, Parotis ( 60 % )Elemen epitelial mucoid mixoid chondroidMorfol : Mass bulat , batas tegas 6 cm Encapsulated . Abu 2 putih mikoid Translusent biru

*HistologiElement Epit~cell duktal / mioepit glandulerAsini, ireg tubule , sheet tersebar pada jar miksoid . Khondroid , tulang.Sel epitel : duct sel kubis, kolumnerAsal ?RadiasiElemen noeplastik ( termasuk mesenkhimal Sel mio epitel ,ductal reserve cells. 2-3 % Ca

*WARTHINS TUMOR / pappillary cyst adenoma lymphomatosum

Parotis, 5 x Multifokal 10 % Bilat 10 %Morfol : bulat ,oval,encapsulated 2-5 cm bulat abu 2,kista kecil ,cleff like spaceSekresi serous,mucinous sel kolumnerLimpoid + germ centerMetaplasia squamousHistogenesis ? Small sarivatory gland rest kgb Aberant incorporation of similar inclutionlimfoid tissue in parotis

*Mukoepidermoid CaSel SkuamosaMucus secreting cells 60 -70 % parotisIntermediate hybrids- vacuol kecil / besar --- MusinMost Common Radiation induced neoplasmaMorfol :diameter 8 cm, circumscribed , lack well defined capsul , infiltratif. Abu 2 putih pucat kista kecil mucin Histol : cords, sheet ,kistik

*Low grade : largely of mucus secreting cells glanduler space. INV. Lok . Recur 15 % 5 th 90 % High grade : Largely of squamous cell + scattering mucus sekr .cellsIntermedRECUR 25 -30 % INVASSIVE ,5 TH 50 %. Adenoid cystic Ca :Morfol : kecil, poorly encap , infiltr . Lesi abu pinkHistol : sel kecil,kompak inti,sitopl.sdkt - tubuler solid / cribriform Lumen bahan hialinInvasi Perineural, 50 % tulang,hati, otak5 Th 60 -70 % 30 % ( 10 th ) 15 % ( 15 th )

*Acinic cell Ca normal serous cells of Sm glandParotisBilat / multi sentrikKecil, discrete , encapsHistol : - sel sheet ,micro kistik,gland,fol. PapilMeta KGB 10-15 %5 thn : 90 % , 20 thn : 60 %

*Kel Liur pada rongga mulutMayor : Parotis Submandibularis, sub lingualisMinor : Mukosa mulutInflamasi :Sialadenitis -- obstruksi kelenjar liur yg lamaPenyebab :Virus , Bakteri, Auto imun SJOGREN SYNDR DESTRUKSI MEDIATED IMUNOLOGI

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XEROSTOMIA Kerato Conjunctivitis siccaMikuliczs Syndrome : inflam lakrimalis salivary + xerostomiaSialolithiasis non specifik sialaoenitis DUCTAL OBSTRUCTION

*HISTOLOGIC classification and incidence of benign and malignant tumors of salifatory glandBENIGN MALIGNANT------------------------------------------------------1.Pleomorphic aden 45,4 % MUCOID.Ca 15,7 % low grade high grade

2.WARTHINS tumor 11 % Adenoid cystic Ca 8 %

3.Lympho epithelial lesion 0,6% Adeno Ca 8 %

*4.Oncocytoma 0,7 % Acinic cell Ca 3 %

5. Monomorphic Malignant Mixed T Adenoma 0,2 % ( 5,7 % )

6.Benign cyst 1 % Epid Ca ( 1,9 % ) Other Anaplastik Ca ( 1,3 % )

*ESOFAGUSAgenesis AtresiaFistula I. Stenosis - Defek perkembangan - Aqured cidra esof berat--dispepsia adult ( reflux gastro esof jar parut radiasi, skleroderma kaustic ) II Mucosal Ring WEB ( upper esof ) SCHATZIKIS RINGS ( dibwh squamo col junction )

*I. ACHALASIASEKUNDERNEUROPATI DM, INFILT (KANKER, AMILOIDOSIS, SARKOIDOSIS)TERJADI PROSES PATOLOGI CHAGASDISISPLEXUS MYENTERIK DESTRUKSIPRIMERPERUBAHAN DALAM INERVATION NEURAL (UNCERTAIN)

*II HERNIA HITAL - SLIDING - PARA ESOF ( ROLLING ) III DIVERTICULA : - ZENKERS ( pulsion ) - TRACTION - VARICES

*ESOFAGITISIran 80%Cina USA / Western Countries 10 -20 % 1. Reflux esofagitis, gastric content 2. Prologed gastric intubation 3. iritant 4. Sitostatika 5. Bakteremia / uremia

*6. Inf Jamur os dengan imunosupressed/ AB7. Uremua 8. Radiasi 9. Peny sistemik ( Hipotiroidism , Sklerosis sist )10. Desquamasi sitemik ( Pemfigoid, Epidermolisis Bullosa ) 11. Graft versus hits dis

*PATOGENESIS- Reflukx gastric contentMekanisme antifeflux - Clearance esof. ( BHN REFLUK ) lambat / inadekuatHernia hiatal slidingVol gastric Kapasitas penyembuhan mukosa esof Morfol : Tgtg causaRefluk esophagitis tanpa komplikasi :

*KHAS :Eosinofil ( Dengan / tanpa leukosit ) ( lapisan epithelial )Hiperplasia basalPapila lamina propia elongasi- Severe acute inflamasi : Nekrosis superfisial Ulcerasi , jar granulasi , debris purulen Fibrosis

*Klasifikasi histologik dan inciden dp tumor jinak dan ganas kel liurJinak Ganas1.Pleomorphic Adenoma 45,4% Mucoepid.Ca ( 15,7 % ) . Low dan High Grade2. Warthins tumor 11 % Adenoid Cystic Ca 10 % 3.Lymphoidepitelial lesion 0,6 % Adeno Ca 8 %

4. Oncocytoma 0,7 % Acinik cell Ca 9%5. Monomorphic Adenoma 0,2 % Malignant Mixed T 5,7 %6.Benign Cyct 1% Epid Ca 1,9 % Other anaplastik Ca 1,3 %

*ADENOMA PLEOMORPHIC* Mixed T* Parotis ( 60 % )Elemen epitelial mucoid Mixoid ChondroidMORFOL ; Masa bulat , batas tegas 6 cm Encapsulated , abu 2 putih mixoid Translucent Hondroid biruHislot ; elemen epit cell duktal / mio epit glanduler tersebar pd jar miksoid , khondroid, tulang. sel epit : Duct sel kuboid , kolumner

*Asal ?RadiasiElemen Neoplastik ( termasuk Mesenkhimal sel mioepit duktal reserve cells2 3 % - CaWARTHINS TUMOR / Pappillary Cyst adenoma lymphomatosumParotis 5 x Multifokal 10 % Bilat 10 %Morfol : bulat encap 2 -5 cm ,sekresi serous , musinous , limpoid + germ center, metaplasia squamousHistogenesis ? Small salivatory gland rest KGB - Aberrant incorporation of similar inclution limfoid tissue in parotid

*Mukoepidermoid Ca* Sel skuamosa* Mucus secreting cells 60 70 % Parotis* inter mediate Hybrids Vakuol kecil /besr --- Musin pd umumnya radiasi merngsang neoplasmPrimer pada Sal. GlandMORFOL : 8cm , circumscribed .capsule ,infilt kista kecil musinHistol : Cords, sheets,kistik Low Grade : banyak sel sekresi mukus gland space invasi lokal : recur 15 % 5 thn 90 % High Grade : Banyak sel squamosa + scattering mucus secr. cell Recur 25 30% , Invasive 5 THn ---50 % meta 30% Intermed

*ADENOID CYSTIK CA * Minor sal glandMORFOL : kecil , poorly encap , infilt ,lesi abu pinkHistol : Sel kecil , inti kompak , tubuler , solid / cribriformLumen bahan hialinInvasi peri neural 50 % Tulang ,hati otak 5 th 60 70 % 30 % ( 10 th ) 15 thn --. 15 %ACINIC Cell Ca ~ normal serous of sal .gland parotis bilat / multisentrik kecil, discrete, encap Histol : Sel Sheet, mikro kistik , Gland , Fol. Papil Meta KGB 10 15 % 5 thn : 90 % 20 thn : 60 %

*Barretts ESofagusKerusakan reflux gastroesofageal dalam waktu lama metaplasia kulumnerInflam, ulcerasi ep squamosa - reepiteliasasi Pluripotent stem cellUlcerasi lokal perdarahan--- strikturMikrosk : Displasia , lesi prekanker

*TUMORJinak : Leiomioma Mesenkhim T Fibrovaskuler polip / lipoma peduncula ted Squamous papiloma inflamatori polip / inflamatory peudotu mor

*GANAS : Ca skuamosa

: : 2 : 1 50 thnChina 100 / 100.000 20 %USA 2 8 / 100.000 Black : white 4 xEtiol ? Patogenesis carcinogen ; ter kontaminasi fungus nitrosamine alkohol Eropa,USA

Yg termsk alk ( fusel oil ,nitrosamine,polisiklik hidro karbon )Smoking

* 1/3 upper ---- 20 % KGB cervical 1/3 middle ---- 50 % -- Mediastinum Para traheal Tracheobroncheal1/3 lower ---- 30 % Gastric celial Morfol : 1. Protruded 60 % --- polipoid fungating 2. Flat 15 % --- difus, infilt tebal,rigid lumen sempit 3. Excavated 25 % --- Necr cancerous ulceration deeply - struktur sktr ---erosi respirasi

*Well Mod DIFSist Limfatik sub mucosa - spread : circum ferential / longitudinalIntra mural Cluster --- dapat beberapa cm dari tumorLokal extensi mediastinalPjln Peny : insidious onset - dispagia obstruksi,menelan sukar - BBUlcerasi - sepsis, hemorr.

*5 year survival rate : Ca Esof superfisial 75 % Advance 25 % Limph node metast 5 year surv Adeno Ca -------- Barrets Esof > 40 thn ( displasia ) surv. 5 thn < 15 % Diagnosa dini + Reseksi > 50 %

*SMALL AND LARGE INTESTINESKELAINAN Kongenital Divertikulum Meckel - Persisten Vitellin Duct - 30 cm dp iliocecall value - True Divertikel : Tdd semua tiga lapisan ( mukosa, sub mukosa , muskularis propia ) - Small Pouch / blind segmen 6 cm - Dapat heterotopik mukosa gaster Pancreas 50% kasus

*Komplikasi :Ulkus peptik - bleedingIntussusepsiInkaserasiPerforasi Congenital aganglionik Mega colon HIRSCHPRUNG DISMigrasi sel 2 neural crest tertahan prox sp anus segmen kolon distal agnglionik + obstr fungs. + dilatasi kolon prox kelainan- Meissner s submucosa - Auerbach s myenteric Pleannses lacks

*Koordinasi neuronal enterik loss ObstruksiDilatasi kolon proximal ( Affected segment )Morfol : Sel ganglion negatif dinding otot ,submucosa serat saraf nonmielin tebal , hipertropiKolon prox dil , hipertropi , distensi masif 15 20 cm - Megakolon1 5000 -8000 Live Birth : 4 : 1

*ACQUIRED MEGACOLON - Chagas DIS - Obstruksi ( Neoplasma , Striktura ) - Toxic MegaColon - Fungtional Psychosomatic DIS ATRESIA STENOSIS

*Vascular DISIschemic Bowel DIS oklusi akut : A. MESENT CELIAK SUP + INF - infark luas1. Infark Transmural P D besar2. Infark MURAl3. Mukosa Infark hipoperfusi akut / kronikFaktor predisposing TR ARTERI, Emboli, Tr VENOUS , ischaemia non occlusive. Angio Displasia -- 20 % bleeding Hemorrhoid

*TYPHOIDSEVERITY, UNTREARED , FATAL ( SERING ) , TO FOOD POISINING BIASA INFLAM KATARAK RINGAN DENGAN DIAREINGESTION 0F S. TYPHI ( KONTAMINASI H2O & MAKANAN )Fase IINVASION OF INTESTINAL LYMPHOID TISSUEAND PROLIFERATION OF BACTERIA. THIS PHASE LASTS FOR 2 WEEKS & IS VIRTUALLY ASYMPTOMATIC

*Fase IIDIAGNOSTC TEST( positive blood & urine cultures selama periode febril AB to S. TYPHI in blood + )INVASION OF BLOOD STREAM - BACTERIEMIA GENERAL TOXAEMIAIS CAUSED WITH RISE OF TEMPERATUREIMMUNOLOGICAL REACTION OCCURS LEADING TO THE NEXT PHASE IN 10 DAYS TIME ( widal test + at end of this phase )

*FASE III

LOCALISATION OF BACTERIA IN INTESTINAL LYMPHOID ----- ( widal test rising titre )TISSUE,MESENT NODES , CALL BLADDER, LIVER,SPLEEN, KDG 2 TULANG, LOKAL NEKROSIS, Rx hipersensitifitas AG AB lesi khas ( CULTURE OF FAECES )

*LESI INTESTINALTerutama Ileum ,yeyenum,kolon UlkusFol. Limph. Edem NekrosisInfilt MN, Sel plasmaMenyebar fever A. Endotoxin release myocardial deg nekrosis fokal M.abd Deg. Zenker Perub Deg . Hati & Ginj

*B. Lokalisasi bakteri Selama bakteriemia Kulit Rose Spot Splenomegali Endokarditis Meningitis Arthritis Peri kondritis Cartil CostaeNeutropeniaRelative lymphositosisJARANG

* Kompl : Ulkus jar. Parut minimal Ulkus dalam - Hemor Perforasi perito- nitis Carrier

*Mal absorptionSindrome primer Lesi patol mirip ( pada pada stadium ini) villi atropi reduksi tu yeyenum 1. Atropi villous partial Bbrp vili menjadi satu , ireg ridges villi pendek ,luas, lam propria sel plasma , regen 2. Atropi villous komplit Epietl kuboid , infilt sel palma mukosa flat & tipis

*Penyakit COELIACAnak Bhub dengan sensitivitas thdp glutenDewasa Villous atropi atropi lien gangguan respon immune N H LTropical SPRUE Negara 2 tropic , kec afrika An. Makrositik ( def Fe , B 12 , Folic acid )

*WHIPPLE DIS Jrg , dgn Limf adenopathi Arthropathi Pigmentasi kulitYeyenum khas : infil makrofag L. propria akumul lemak ok obstr ma krofagTerutama usia pertengahan

*Malabsorpsi sekunder :Sekunder akibat py digestion , absorption, transport nutrisi.A. Digestion 1. Destruksi mukosa intest pada regional enteritis, amiloidosis sklerosis sistemik , RD 2. Py Hepatik , Pancreas 3. Following resection of bowel 4.Cong.disach defect 5. Drug. ( Phenindione, neomisin )

*B.Absorption 1. Stasis intest ( dis , op ) 2. Obstruksi khronik terutama oleh baktC. GGN transport : 1. obstruk limfatik 2. Py ggn supply mesenterik 3. A BetalipoproteinemiaKLINIK : Diare bulky / fatty stuol

*Site of lesion Function Affected Clinical ManifestationDuod iron absorption anemiaYeyunum Prot . Digestion wasting Pancreatic stim fatty diare emulsif of fats def abs vit lrt dl lemak elektr & fluid abs dehidrasi def vit lrt air Vit B --- Pellagra C--- Scurvy Folic acid An. MakrositeIleum Abs B 12------- An. Makrositer Reabsor. Grm empedu ------ Thdp abs lemak

*IDIOPATIK INFLAMATORY BOWEL DESEASEETIOLOGI UNKNOWN CROHNS DISCOLITIS ULSERATIVAKRONIKRELAPSING INFLAMATORY DISORDER OF OBSCURE ORIGINGRANULOMATOSANY PARSION GITSMALL INTESTINE, KOLONNON GRANULOMATUSLIMITED KOLON

*Etiol dan Patogenesis1. Genetik2. Infeksious virus, klamidia , bakteri atipik, mikobakteria3.Perub mukosa intestin permeabilita intest Polietilen ggn musin gliokprot glikol4. Abnormal host immunoreactivity : - gg Fg sel ep sbg antigen presenting cell - cytokinen abn - induksi cytotoxic anti epith.antibody - Fg Nk limfosit abn5. Inflamasi