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1
RONGGA MULUT DAN
TRACTUS GASTRO INTESTINALIS
Dr.Resmi Kartini Ms
2
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
3
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 )
20
I. ACHALASIA
SEKUNDER
NEUROPATI DM, INFILT (KANKER, AMILOIDOSIS, SARKOIDOSIS)
TERJADI PROSES PATOLOGI CHAGASDISIS
PLEXUS MYENTERIK DESTRUKSI
PRIMERPERUBAHAN DALAM INERVATION NEURAL (UNCERTAIN)
21
II HERNIA HITAL
- SLIDING - PARA ESOF ( ROLLING ) III DIVERTICULA : - ZENKER’S ( pulsion ) - TRACTION - VARICES
22
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
24
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 :
25
KHAS :
Eosinofil ( Dengan / tanpa leukosit ) ( lapisan epithelial )Hiperplasia basalPapila lamina propia elongasi- Severe acute inflamasi : Nekrosis superfisial Ulcerasi , jar granulasi , debris purulen Fibrosis
26
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 %
27
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
28
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
29
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
30
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 %
31
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
32
TUMOR
Jinak : Leiomioma Mesenkhim T Fibrovaskuler polip / lipoma peduncula ted Squamous papiloma inflamatori polip / inflamatory peudotu mor
33
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
34
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
35
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.
36
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 %
37
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
38
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
39
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
40
ACQUIRED MEGACOLON
- Chagas ‘ DIS - Obstruksi ( Neoplasma , Striktura ) - Toxic MegaColon - Fungtional Psychosomatic DIS ATRESIA STENOSIS
41
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
42
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
43
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 )
44
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 )
45
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
46
B. Lokalisasi bakteri Selama bakteriemia Kulit Rose Spot Splenomegali Endokarditis Meningitis Arthritis Peri kondritis Cartil Costae Neutropenia Relative lymphositosis
JARANG
47
Kompl : Ulkus jar. Parut minimal Ulkus dalam - Hemor Perforasi perito-
nitis Carrier
48
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
49
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 )
50
WHIPPLE DIS Jrg , dgn Limf adenopathi Arthropathi Pigmentasi kulitYeyenum khas : infil makrofag L. propria akumul lemak ok obstr ma krofagTerutama ♂ usia pertengahan
51
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 )
52
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
53
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
54
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
55
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