01 git esofagus rev1

1

RONGGA MULUT DAN

TRACTUS GASTRO INTESTINALIS

Dr.Resmi Kartini Ms

2

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

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

4

Soliter / multipleTebal , smooth , indurasi ,

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

Limp,makrofa- Ganas 5-6 %

5

Erythroplakia ( Dysplastic Leukoplakia )

Erosi superfisial + Displasia -- CISEpitel atipik resiko yang tinggi

tranformation malignanSpeckled leukoerythroplakiaMultifact origins Tobacco. Alkohol,chronic

exposure - iritant

6

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 %

7

Ameloblastoma

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

8

Sel kolumner Pulau 2 sentral retikulum stellae

Metaplas skuamosa tipe akantomatousStroma jar ikat fibrousDentrigerous cistFoll Cyst

9

Adenoma pleomorphik

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

10

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

11

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

12

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

13

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 )

14

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 %

15

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

16

XEROSTOMIA Kerato Conjunctivitis siccaMikulicz’s Syndrome : inflam lakrimalis salivary +

xerostomiaSialolithiasis non specifik sialaoenitis ↓↓ DUCTAL OBSTRUCTION

17

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 %

18

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 % )

19

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

23

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