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RONGGA MULUT DAN

TRACTUS GASTRO INTESTINALIS

Dr.Resmi Kartini Ms

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Oral Soft tissue Inflamasi : 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

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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 durum

High risk

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Soliter / multipleTebal , smooth , indurasi ,

wrinkled,corrugated / verrucose plaquesHistol : HiperkeratosisAcantosisDisplasia CISLesi displastik / Anaplastik --- infilt

Limp,makrofa- Ganas 5-6 %

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Erythroplakia ( Dysplastic Leukoplakia )

Erosi superfisial + Displasia -- CISEpitel atipik resiko yang tinggi

tranformation malignanSpeckled leukoerythroplakiaMultifact origins Tobacco. Alkohol,chronic

exposure - iritant

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Squamous Cell Ca

95 %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 %

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Ameloblastoma

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

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Sel kolumner Pulau 2 sentral retikulum stellae

Metaplas skuamosa tipe akantomatousStroma jar ikat fibrousDentrigerous cistFoll Cyst

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Adenoma pleomorphik

Mixed tumor, Parotis ( 60 % )Elemen epitelial mucoid mixoid chondroidMorfol : 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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WARTHIN’S 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 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

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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 glandParotisBilat / multi sentrikKecil, discrete , encapsHistol : - sel sheet ,micro kistik,gland,fol.

PapilMeta KGB 10-15 %5 thn : 90 % , 20 thn : 60 %

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Kel Liur pada rongga mulut

Mayor : 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 siccaMikulicz’s Syndrome : inflam lakrimalis salivary +

xerostomiaSialolithiasis 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.WARTHIN’S tumor 11 % Adenoid cystic Ca 8 %

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 )

SCHATZIKI’S RINGS ( dibwh

squamo col junction )

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I. ACHALASIA

SEKUNDER

NEUROPATI DM, INFILT (KANKER, AMILOIDOSIS, SARKOIDOSIS)

TERJADI PROSES PATOLOGI CHAGASDISIS

PLEXUS MYENTERIK DESTRUKSI

PRIMERPERUBAHAN DALAM INERVATION NEURAL (UNCERTAIN)

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II HERNIA HITAL

- SLIDING - PARA ESOF ( ROLLING ) III DIVERTICULA : - ZENKER’S ( 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/ AB7. 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 basalPapila 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 Ganas1.Pleomorphic Adenoma 45,4% Mucoepid.Ca ( 15,7 % )

. Low dan High Grade

2. Warthin’s 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 %

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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 WARTHIN”S 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 : Ø 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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Barrett’s ESofagus

Kerusakan reflux gastroesofageal dalam waktu lama metaplasia kulumner

Inflam, ulcerasi ep squamosa - reepiteliasasi Pluripotent stem cell↑

Ulcerasi lokal perdarahan--- strikturMikrosk : 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

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

Smoking

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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 mediastinalPjln 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 -------- Barret’s 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 , hipertropiKolon prox dil , hipertropi , distensi masif 15

– 20 cm - Megakolon1 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 DISIschemic 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 IIDIAGNOSTC 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 INTESTINALTerutama 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 Kulit Rose Spot Splenomegali Endokarditis Meningitis Arthritis Peri kondritis Cartil Costae Neutropenia Relative lymphositosis

JARANG

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

nitis 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 kulitYeyenum khas : infil makrofag L. propria akumul lemak ok obstr ma krofagTerutama ♂ 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 Function Affected Clinical Manifestation

Duod iron absorption anemia Yeyunum 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.

Makrosite

Ileum Abs B 12------- An. Makrositer Reabsor. Grm empedu ------ Thdp abs lemak

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IDIOPATIK INFLAMATORY BOWEL DESEASE

ETIOLOGI UNKNOWN CROHN’S DIS

COLITIS ULSERATIVA

KRONIK RELAPSING

INFLAMATORY DISORDER OF OBSCURE ORIGIN

•GRANULOMATOS•ANY PARSION GIT•SMALL INTESTINE, KOLON •NON GRANULOMATUS

•LIMITED KOLON

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Etiol dan Patogenesis

1. 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