RONGGA MULUT

DAN

TRACTUS GASTRO INTESTINALIS

Dr.Resmi Kartini Ms

Oral Soft tissue

Inflamasi : Et / H. Simplex tipe 1 Ulcus Aftosa Kandida , Glositis

Tumor dan Pre cancerous Lesions

Leukoplakia dan Erythroplakia

Leukoplakia : Plaque putih - prolif epidermal 85-90 % -- Benign spi Malignant
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 Plaque putih pada Membr. Mukosa mulut Tidak dpt diangkat dgn scraping Gambaran ; penebalan epitel, sitologi atipik - displasia Karsinoma in situ prove prekanker Morfol : Mukosa bukal Dasar mulut High risk Permuk ventral lidah Palatum durum
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 Soliter / multiple Tebal , smooth , indurasi , wrinkled,corrugated / verrucose plaques Histol : Hiperkeratosis Acantosis Displasia CIS Lesi displastik / Anaplastik --- infilt Limp,makrofa - Ganas 5-6 %
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Erythroplakia ( Dysplastic Leukoplakia )

Erosi superfisial + Displasia -- CIS Epitel atipik resiko yang tinggi tranformation malignan Speckled leukoerythroplakia Multifact origins Tobacco. Alkohol,chronic exposure - iritant

Squamous Cell Ca

95 % Tobacco ,alkohol Dasar mulut , lidah , palatum durum ,dasar lidah Diff baik sampai anaplastik Metast : KGB Mediastinum , paru ,hati, tulang Prog : 5 Th 90% recurrent free:dsr lidah 20-30 %
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Ameloblastoma

Epit odontogenic T Epit lining drpd dentigerous cyst Lamina dental ,enamel Lapisan basal dp mucosa mulut Dekade 5 Folikuler dental epit plexiform
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Sel kolumner Pulau 2 sentral retikulum stellae

Metaplas skuamosa tipe akantomatous Stroma jar ikat fibrous Dentrigerous cist Foll Cyst

Adenoma pleomorphik

Mixed tumor, Parotis ( 60 % ) Elemen epitelial mucoid mixoid chondroid Morfol : Mass bulat , batas tegas 6 cm Encapsulated . Abu 2 putih mikoid Translusent biru
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Histologi
Element Epit~cell duktal / mioepit glanduler Asini, ireg tubule , sheet tersebar pada jar miksoid . Khondroid , tulang. Sel epitel : duct sel kubis, kolumner Asal ? Radiasi Elemen noeplastik ( termasuk mesenkhimal Sel mio epitel ,ductal reserve cells. 2-3 % Ca
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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 space Sekresi serous,mucinous sel kolumner Limpoid + germ center Metaplasia squamous Histogenesis ? Small sarivatory gland rest kgb Aberant incorporation of similar inclutionlimfoid tissue in parotis
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Mukoepidermoid Ca
Sel Skuamosa Mucus secreting cells 60 -70 % parotis Intermediate hybrids- vacuol kecil / besar --- Musin Most Common Radiation induced neoplasma Morfol :diameter 8 cm, circumscribed , lack well defined capsul , infiltratif. Abu 2 putih pucat kista kecil mucin Histol : cords, sheet ,kistik
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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 .cells Intermed
RECUR 25 -30 % INVASSIVE ,5 TH 50 %.

Adenoid cystic Ca : Morfol : kecil, poorly encap , infiltr . Lesi abu pink Histol : sel kecil,kompak inti,sitopl.sdkt - tubuler solid / cribriform Lumen bahan hialin Invasi Perineural, 50 % tulang,hati, otak 5 Th 60 -70 % 30 % ( 10 th ) 15 % ( 15 th )
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Acinic cell Ca
normal serous cells of Sm gland Parotis Bilat / multi sentrik Kecil, discrete , encaps Histol : - sel sheet ,micro kistik,gland,fol. Papil Meta KGB 10-15 % 5 thn : 90 % , 20 thn : 60 %
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Kel Liur pada rongga mulut

Mayor : Parotis Submandibularis, sub lingualis Minor : Mukosa mulut Inflamasi : Sialadenitis -- obstruksi kelenjar liur yg lama Penyebab :Virus , Bakteri, Auto imun SJOGREN SYNDR DESTRUKSI
MEDIATED IMUNOLOGI
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XEROSTOMIA Kerato Conjunctivitis sicca Mikuliczs Syndrome : inflam lakrimalis salivary + xerostomia Sialolithiasis non specifik sialaoenitis DUCTAL OBSTRUCTION

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HISTOLOGIC classification and incidence of benign and malignant tumors of salifatory gland

BENIGN MALIGNANT -----------------------------------------------------1.Pleomorphic aden 45,4 % MUCOID.Ca

15,7 %

low grade high grade 2.WARTHINS tumor 11 % 8% Adenoid cystic Ca

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

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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 % )

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ESOFAGUS
Agenesis Atresia Fistula 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 )
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I. ACHALASIA
NEUROPATI DM, INFILT (KANKER, AMILOIDOSIS, SARKOIDOSIS) SEKUNDER TERJADI PROSES PATOLOGI CHAGASDISIS PLEXUS MYENTERIK DESTRUKSI

PRIMER

PERUBAHAN DALAM INERVATION NEURAL (UNCERTAIN)

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II HERNIA HITAL

- SLIDING - PARA ESOF ( ROLLING ) III DIVERTICULA : - ZENKERS ( pulsion ) - TRACTION - VARICES

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

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6. Inf Jamur os dengan imunosupressed/ AB 7. Uremua 8. Radiasi 9. Peny sistemik ( Hipotiroidism , Sklerosis sist ) 10. Desquamasi sitemik ( Pemfigoid, Epidermolisis Bullosa )

11. Graft versus hits dis

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PATOGENESIS - Reflukx gastric content

- Mekanisme antifeflux - Clearance esof. ( BHN REFLUK ) lambat /

inadekuat Hernia hiatal sliding Vol gastric Kapasitas penyembuhan mukosa esof Morfol : Tgtg causa Refluk esophagitis tanpa komplikasi :
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KHAS :

Eosinofil ( Dengan / tanpa leukosit ) ( lapisan epithelial ) Hiperplasia basal Papila lamina propia elongasi - Severe acute inflamasi : Nekrosis superfisial Ulcerasi , jar granulasi , debris purulen Fibrosis
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Klasifikasi histologik dan inciden dp tumor jinak dan ganas kel liur
Jinak
1.Pleomorphic Adenoma 45,4%
2. Warthins tumor 11 % 3.Lymphoidepitelial lesion 0,6 % 4. Oncocytoma 0,7 % 5. Monomorphic Adenoma 0,2 % 6.Benign Cyct 1%

Ganas
Mucoepid.Ca ( 15,7 % ) . Low dan High Grade Adenoid Cystic Ca 10 % Adeno Ca 8 %
Acinik cell Ca 9% Malignant Mixed T 5,7 % Epid Ca 1,9 % Other anaplastik Ca 1,3 %
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ADENOMA PLEOMORPHIC * Mixed T

* Parotis ( 60 % ) Elemen epitelial mucoid Mixoid Chondroid MORFOL ; Masa bulat , batas tegas 6 cm
Encapsulated , abu 2 putih mixoid Translucent Hondroid biru Hislot ; elemen epit cell duktal / mio epit glanduler tersebar pd jar miksoid , khondroid, tulang. sel epit : Duct sel kuboid , kolumner
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Asal ? Radiasi Elemen Neoplastik ( termasuk Mesenkhimal sel mioepit duktal reserve cells 2 3 % - Ca WARTHINS TUMOR / Pappillary Cyst adenoma lymphomatosum Parotis 5 x Multifokal 10 % Bilat 10 % Morfol : bulat encap 2 -5 cm ,sekresi serous , musinous , limpoid + germ center, metaplasia squamous Histogenesis ? Small salivatory gland rest KGB - Aberrant incorporation of similar inclution limfoid tissue in parotid
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Mukoepidermoid Ca
* Sel skuamosa
* Mucus secreting cells 60 70 % Parotis * inter mediate Hybrids Vakuol kecil /besr --Musin pd umumnya radiasi merngsang neoplasm Primer pada Sal. Gland MORFOL : 8cm , circumscribed .capsule ,infilt kista kecil musin Histol : 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

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ADENOID CYSTIK CA * Minor sal gland

MORFOL : kecil , poorly encap , infilt ,lesi abu pink Histol : Sel kecil , inti kompak , tubuler , solid / cribriform
Lumen bahan hialin Invasi 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 %
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Barretts ESofagus

Kerusakan reflux gastroesofageal dalam waktu lama metaplasia kulumner Inflam, ulcerasi ep squamosa - reepiteliasasi Pluripotent stem cell
Ulcerasi lokal perdarahan--- striktur Mikrosk : Displasia , lesi prekanker
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TUMOR
Jinak : Leiomioma Mesenkhim T Fibrovaskuler polip / lipoma peduncula ted Squamous papiloma inflamatori polip / inflamatory peudotu mor

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GANAS : Ca skuamosa

: : 2 : 1 50 thn China 100 / 100.000 20 % USA 2 8 / 100.000 Black : white 4 x Etiol ? Patogenesis carcinogen ; ter kontaminasi fungus nitrosamine alkohol Eropa,USA
Smoking

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

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1/3 upper ---- 20 % KGB cervical

1/3 middle ---- 50 % -- Mediastinum Para traheal Tracheobroncheal 1/3 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
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Well Mod DIF

Sist Limfatik sub mucosa - spread : circum ferential / longitudinal Intra mural Cluster --- dapat beberapa cm dari tumor Lokal extensi mediastinal Pjln Peny : insidious onset - dispagia obstruksi,menelan sukar - BB
Ulcerasi - sepsis, hemorr.
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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 %

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SMALL AND LARGE INTESTINES

KELAINAN 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
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Komplikasi :

Ulkus peptik - bleeding Intussusepsi Inkaserasi Perforasi Congenital aganglionik Mega colon HIRSCHPRUNG DIS Migrasi 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
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Koordinasi neuronal enterik loss Obstruksi

Dilatasi kolon proximal ( Affected segment ) Morfol : Sel ganglion negatif dinding otot ,submucosa serat saraf nonmielin tebal , hipertropi Kolon prox dil , hipertropi , distensi masif 15 20 cm - Megakolon 1 5000 -8000 Live Birth : 4 : 1

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ACQUIRED MEGACOLON

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

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Vascular DIS

Ischemic Bowel DIS oklusi akut : A. MESENT CELIAK SUP + INF

- infark luas 1. Infark Transmural P D besar 2. Infark MURAl 3. Mukosa Infark hipoperfusi akut / kronik Faktor predisposing TR ARTERI, Emboli, Tr VENOUS , ischaemia
non occlusive. Angio Displasia -- 20 % bleeding Hemorrhoid

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TYPHOID
SEVERITY, UNTREARED , FATAL ( SERING ) , TO FOOD POISINING BIASA INFLAM KATARAK RINGAN DENGAN DIARE INGESTION 0F S. TYPHI ( KONTAMINASI H2O & MAKANAN ) Fase I INVASION OF INTESTINAL LYMPHOID TISSUE AND PROLIFERATION OF BACTERIA. THIS PHASE LASTS FOR 2 WEEKS & IS VIRTUALLY ASYMPTOMATIC
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Fase II
DIAGNOSTC TEST ( positive blood & urine cultures selama periode febril AB to S. TYPHI in blood + ) INVASION OF BLOOD STREAM - BACTERIEMIA GENERAL TOXAEMIA IS CAUSED WITH RISE OF TEMPERATURE IMMUNOLOGICAL REACTION OCCURS LEADING TO THE NEXT PHASE IN 10 DAYS TIME ( widal test + at end of this phase )
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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 )

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LESI INTESTINAL
Terutama Ileum ,yeyenum,kolon
Ulkus Fol. Limph. Edem Nekrosis Infilt MN, Sel plasma Menyebar fever A. Endotoxin release myocardial deg nekrosis fokal M.abd Deg. Zenker Perub Deg . Hati & Ginj
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B. Lokalisasi bakteri
Selama bakteriemia
Neutropenia Relative lymphositosis Kulit Rose Spot Splenomegali Endokarditis Meningitis Arthritis Peri kondritis Cartil Costae

J A R A N G

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Kompl : Ulkus jar. Parut minimal Ulkus dalam - Hemor Perforasi peritonitis Carrier

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Mal absorption
Sindrome 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

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Penyakit COELIAC
Anak Bhub dengan sensitivitas thdp gluten Dewasa Villous atropi atropi lien gangguan respon immune N H L

Tropical SPRUE
Negara 2 tropic , kec afrika An. Makrositik ( def Fe , B 12 , Folic acid )

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WHIPPLE DIS Jrg , dgn Limf adenopathi

Arthropathi

Pigmentasi kulit Yeyenum khas : infil makrofag L. propria akumul lemak ok obstr ma krofag Terutama usia pertengahan
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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 )
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B.Absorption 1. Stasis intest ( dis , op )

2. Obstruksi khronik terutama oleh bakt C. GGN transport : 1. obstruk limfatik 2. Py ggn supply mesenterik 3. A Betalipoproteinemia KLINIK : Diare bulky / fatty stuol

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Site of lesion
Duod Yeyunum Ileum

Function Affected
iron absorption Prot . Digestion Pancreatic stim emulsif of fats

Clinical Manifestation

anemia wasting fatty diare def abs vit lrt dl lemak elektr & fluid abs dehidrasi def vit lrt air Vit B --- Pellagra C--- Scurvy Folic acid An. Makrosite Abs B 12------An. Makrositer Reabsor. Grm empedu ------ Thdp abs lemak

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IDIOPATIK INFLAMATORY BOWEL DESEASE

CROHNS DIS

ETIOLOGI UNKNOWN

KRONIK RELAPSING INFLAMATORY DISORDER OF OBSCURE ORIGIN

COLITIS ULSERATIVA

GRANULOMATOS ANY PARSION GIT SMALL INTESTINE, KOLON

NON GRANULOMATUS LIMITED KOLON

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Etiol dan Patogenesis

1. Genetik 2. Infeksious virus, klamidia , bakteri atipik,
mikobakteria
3.Perub mukosa intestin permeabilita intest Polietilen ggn musin gliokprot glikol 4. Abnormal host immunoreactivity : - gg Fg sel ep sbg antigen presenting cell - cytokinen abn - induksi cytotoxic anti epith.antibody - Fg Nk limfosit abn 5. Inflamasi
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