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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 scraping
Gambaran ; penebalan epitel, sitologi
atipik - displasia
Karsinoma in situ prove prekanker
Morfol :
Mukosa bukal
Dasar mulut
Permuk ventral lidah
Palatum durum
High risk
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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
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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
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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
SEKUNDER
NEUROPATI DM, INFILT
(KANKER, AMILOIDOSIS,
SARKOIDOSIS)
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 Ganas
1.Pleomorphic Adenoma 45,4% Mucoepid.Ca ( 15,7 % )
. Low dan High Grade
2. Warthins 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
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


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 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 Kulit Rose Spot
Splenomegali
Endokarditis
Meningitis
Arthritis
Peri kondritis
Cartil Costae
Neutropenia
Relative lymphositosis
J
A
R
A
N
G
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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 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 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 CROHNS 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. 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