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RONGGA MULUT

DAN

TRACTUS GASTRO
INTESTINALIS
Dr.Resmi Kartini Ms

Oral Soft tissue


Inflamasi :
Et / H. Simplex tipe 1, HIV (human immunodeficiency
.Epstein- Barr

Ulcus Aftosa

Kandida , Glositis

vi)

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 scraping
Gambaran ; penebalan epitel, sitologi
atipik - displasia
Karsinoma in situ prove prekanker
Morfol :
Mukosa bukal
Dasar mulut
High risk
Permuk ventral lidah
Palatum durum
3

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
7

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 %

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 )
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
J
Meningitis
A
R
Arthritis
A
N
Peri kondritis
G
Cartil Costae

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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

Function Affected

Clinical Manifestation

iron absorption
Prot . Digestion
Pancreatic stim
emulsif of fats
elektr & fluid abs

Makrosite

Ileum

Abs B 12------Reabsor. Grm empedu ------

anemia
wasting
fatty diare
def abs vit
lrt dl lemak
dehidrasi
def vit lrt air
Vit B --- Pellagra
C--- Scurvy
Folic acid An.
An. Makrositer
Thdp abs lemak

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IDIOPATIK INFLAMATORY BOWEL DESEASE


ETIOLOGI UNKNOWN

CROHNS DIS

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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