Pathology Gastrointestinal

System I

Yuni prastyo kurniati, Dr, SpPA

FK UMS
 Patology GI tract
Esophagus

• Kelainan  kongenital

Stomach

• Infeksi

Intestinal & bowell

• Tumors
Anatomi Sistem Gastrointestinal
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
 KONGENITAL
Atresia Esofagus
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
 (Gangguan Anatomik & Motorik)
(1) Achalasia
Hilangnya
Oleh Karena
Inervasi PRIMER SEKUNDER
Penyakit Lain,
inhibitor LES
Ex : Chagas
intrinsik
3 Kondisi : disease
(1) Aperistaltik (T cruzi), Polio,
(2) Relaksasi LES parsial Neuropati DM,
/ inkomplet saat Malignansi, dll
dilewati bolus
(3) Peningkatan tonus
LES
 (Gangguan Anatomik & Motorik)
(1) Achalasia
OBSTRUKSI Dilatasi Esofagus Dinding esofagus
Proksimal menipis

Inflamasi & Ulkus

pada dinding Stasis bolus
esofagus

Insidensi : 1 / 100.000 orang / tahun

Prevalensi Usia : 25 – 60 tahun
 (Gangguan Anatomik & Motorik)
(1) Achalasia
Disfagia (Solid &
Liquid)
90%
Nyeri dada Berkembang
lambat, dan sering
Heartburn
terlambat dibawa
Regurgitasi 60% ke dokter
Penurunan berat
badan

5% Berkembang menjadi
Squamous karsinoma
(Gangguan Anatomik & Motorik)
(2) Hiatal Hernia
Displacement dari segmen
gaster memasuki kavum toraks
melalui crura Diafragma

Gastroesofageal Reflux

GEJALA
Nyeri epigastrium pain,
postprandial fullness,
substernal fullness, nausea, and
retching
 (Gangguan Anatomik & Motorik)
(2) Hiatal Hernia
Tipe : sliding hernia (95%) & paraesophageal
hernia (5%)
(Gangguan Anatomik & Motorik)
(2) Hiatal Hernia

Komplikasi :
1. Ulserasi mukosa
2. Perdarahan & perforasi
3. GERD, Strangulasi,
obstruksi -- dyspneu
 (Gangguan Anatomik & Motorik)
(3) Mallory Weiss Syndrome
Laserasi / sobekan Longitudinal pada
segmen bawah esofagus
(esophagogastric junction)

• Laki : Perempuan = 1 : 1
• Usia : 40 – 60 Thn
• UGIB : 47-116
kasus/100.000 populasi
 (Gangguan Anatomik & Motorik)
(3) Mallory Weiss Syndrome
Risk factor :
• Hiatal hernia (> 75%)
Gastroesophageal
• Hiperemesis
Reflux
gravidarum
• Alkoholism
• Bulimia Nervosa
Iritasi Mukosa /
• Muntah hebat
radang
karena suatu sebab
• Peningkatan tekanan
intragastric / distensi
Laserasi Mukosa

Sign & symptom : Hematemesis (~ 100%), Melena (10%), Nausea,

vomiting, Upper abdominal pain (40%)
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
VARICES ESOPHAGUS

Varises Plexus vena

Esofagus esofagus

Obstruksi aliran Hipertensi Portosistemik

darah v.porta portal shunting
 VARICES ESOPHAGUS

Peningkatan
tekanan
intraabdomen
Ruptur
Varises Peningkatan tekanan
Muntah Varises
Esofagus intravaskuler vena
Esofagus
esofagus
Erosi
Silent Perdarahan

Shock Hipovolemik
 VARICES ESOPHAGUS
> 65% dari pasien
Sirosis Hepatis

Ketika ruptur, 20% - Sign : asimptomatik

30% pasien hingga ruptur,
meninggal dalam Hematemesis
serangan pertama (< 50%)

Ketika ruptur, jika survive, 70%

ruptur lagi dalam 1 Thn
 Gangguan – Achalasia
Kongenital Anatomik & – Hiatal Hernia
Motorik – Laceration
– Other disorder

Varises Esofagus ESOPHAGUS

PENYAKIT PADA
ESOFAGUS

Esofagitis & Karsinoma – Adenokarsinoma

Barrett’s Esofagus – Karsinoma
Esofagus Squamous Cell
Kelainan kongenital
esophagus
Esophageal obstruction Achalasia
Nutcracker esophagus : lack coordination (outer Increased tone of the lower
before inner) esophageal sphincter/ LES  impaired
Difuse esofageal spasm : motor disorder smooth muscle relaxation  esof
obstruction
Zenker divertikulum / pharyngoesophageal Primer : neural innervation
divertikulum : small mucosal outpouching  Sekunder Chagas ds, trypanosoma
accumulate food  mass  regurgitation cruzi infection,failure of peristalsis,
esof dilatation.
Stenosis : passage of food  k/ thickening fibrous Triad incomplete : LES relaxation,
of the submucosa, atrofi propia  inflamasi, increased tone, aperistalsis esofagus.
scarring.
Esophageal mucosal webs : protrusion of mucosa ,
>40s , upper >>, dysfagia g-eso reflux-chronic
graft/ blistering skin ds, fibrovascular connective
tissue & overlying epthelium.
Esophageal rings/ schatzki rings = webs,
circumferential, thicker  hipertrofi muscularis
propia
DIVERTIKULUM (200x)
Infeksi pada esophagus
Esophagitis
Laceration : near gastroesophageal junction (Mallory-Weiss tears)
, hematemesis if in superficial esophagus
Chemical & infectious esophagitis : pil-induced esofagitis, herpes
simplex, CMV, fungal, aspergilosis & mucormycosis; skin : bullous
pemfigoid-epidermolisis bullosa-Chron ds
Dysfagia-hemorhage-striktur-perforasi
Dense infiltrat netrofil, ulceration & granulation  fibrosis,
irradiasi : intimal proliferation, luminal narrowing of submucosal
& mural blood vessels.
Candidiasis  gray-white pseudomembran, dense fungal hyphae.
Herpes  punched out ulcers, nuclear viral inclusions, deg ept
cell in the margin of the ulcer
CMV  shallower ulcerations, nuclear & cytoplasmic incl within
capilar endotelium & stromal
Graft-versus host ds  basal ept cell apoptosis, mucosal atrophy,
submucosal fibrosis
Esophagitis

Reflux esophagitis : reflux gastric into the lower esof  decrease

tone spincter lower esof / increased abd pressure ( alk & tobbco,
obesity, central nerv depresant, pregnancy, hiatal hernia) ; > 40s/
infant & children; disfagia-heartburn-regurgitation
Simple hiperemi  redness, eosinofil sd mukosa, basal zone
hiperplasia
Komplikasi : ulserasi esof-hematemesis-melena-striktur-barrett
Eosinophilic esophagitis : food impaction-disfagia-feeding
intolerance in children, eosinofil intraept >>, absence of acid
reflux , atopic >>  dermatitis, alergi rhinitis, asma
Barrett Esophagus Esophageal varices
Complication of chronic GERD  intestinal k/ portal hipertension 
metaplasia within the esophageal sq congested subepitelial &
mucosa increased risk to adenoca submucosa in distal esof.
esophagus, male, 40-60s k/ sirrhosis, hepatic
schistosomiasis
Several tongues/patches of red, velvety Tortous dilated veins in the
mucosa, pale sq mucosa, light brown submucosa esof distal & prox
colummnar gastric mucosa ; long & short stomach, mucosa is intact
segment (= 3cm) ; goblet cell (distinc mucous Massive hematemesis
vacuoles that stain pale blue  a wine
goblet)
Displasia : increased ept prolif, atypical
mitosis, nuclear hiperchromasia &
stratification, irregularly clumped chromatin,
n/c ratio >>, failure of ept cell mature; gland
architecture  budding, irregular shape,
cellular crowding
Makroskopis Esophagus
Mikroskopis Esophagitis

• Eosinofil didalam
squamous epithelium
• Papila lamina propia yang
memanjang
• Hiperplasia zona basal
Barret esophagus, squamous mucosa and
Squamous cell carcinoma, invasion into
intestinal-type collumnar ept cell/ goblet
the submucosa
cells in a glandular mucosa
Tumors esophagus
Adenocarcinoma
Arises in barrett esophagus & long
standing GERD  dysplasia &
invasive , associated with
Helicobacter pylori , caucasians &
men >>, 60s,
C-ERB-B2, cyclin D1,cyclin E,
p16/INK4a  contribute neoplastic
progression
Pain/ difficulty in swallowing,
weight loss>>, hematemesis, chest
pain, vomiting
Distal third of the esof, flat/raised
patches, mucosa intact, produce
mucin, intestinal & diffuse infiltratif
signet-ring sel
Squamous cell carcinoma
<45s, male >>, risk fact : tobacco-alkohol-
achalasia, very hot beverages
Nutritional deff : polycyclic hidrokarbon,
nitrosamines, mutagenic , HPV, p16/INK4a
Middle third esof, insitu : sq displasia, small-
gray white-plaque like thickening,
polypoid/exophytic/ protrude into lumen,
thickening-rigidity-luminal narrowing.
Well diff>>, verrucous-spindle cell-basaloid,
very large  invade the esof wall, lymp
node metastase
Transition Barrett esophagus to adenocarcinoma
 Uncommon esophageal tumors

Undiff-carcinoid-melanoma-lymphoma-sarcoma
Benign  mesenchymal origin : leiomyoma, fibroma, lipoma,
hemangioma, neurofibroma, lymphangioma
Fibrovascular polip/ pedunculated lipoma
Sq papiloma : HPV
A mass of inflamed granulation tissue : infl polip  infl
pseudotumors
 Large
ulcerated cell
carcinoma of
the esophagus
STOMACH
Struktur Stomach
Infeksi pada stomach
Acut gastritis Acut gastric ulceration
Surface ept is intact, Stress ulcers : shock, sepsis, trauma
netrofil>>, if above the Curling ulcers : burn & trauma
basement membran & duodenum prox
ept cells is abnormal Cushing ulcers :
 active inflammation gastric,duodenal,esophageal 
perforasi >>
Bleeding >>  transfusi
Erosi : loss of ept Shallow erosion, <1cm,brown to black
superfic, netrofil in by acid digestion of extravasasi blood,
mucosa & fibrin normal gastric rugal fold , sharply
purulent exudate in demarcated & normal mucosa;
the lumen; if erosi & If chronic : scarring & thickening of
hemoragi  acute blood vessel, healing with complete re-
erosive hemorhagic ept.
gastritis
Acut gastritis
Helicobacter pylori gastritis
Spiral-shaped/curved baccili, duodenal ulcers + gastric ulcers/
chronic gastritis ,most common cause chronic gastritis (90%)
4 features : flagella, urease, adhesins, toxins.
Within the superficial mucus overlying ept cells in the surface &
neck, anthrum stomach  erythematous & coarse nodular,
accumulate neutrophil in lumen intraepithelial  pit abscesses ,
large numbers of plasma cells + lymphocyt + macrophages.
Lymphoid agregates  mucosa-associated lymphoid tissue /
MALT  transform lymphoma
Characteristic : intraepithelial neutrophil + subepithelial plasma
cells
Autoimun gastritis
Diffuse mucosal damage of the
oxyntic (acid producing ) within body
& fundus, rugal fold (-)
Small surface elevations  intestinal
metaplasia  presence goblet cells &
collumnair absorptive cells;
hypergastrin stimulate endokrin cells
hyperplasia  low grade
neuroendokrin/ carcinoid tumor
Klinik : antibodies to parietal cells &
intrinsic factor ; associated
autoimmune disease ( hasimoto, DM
tipe 1, grave’s, addison ds)
Uncommon forms of gastritis
Reactive gastropathy ( foveolar
hiperplasia- glandular reg change-
mucosal edema )  coz NSAID, bile
reflux, trauma  gastric antral vascular
ectasia (GAVE)
Eosinophlic  cow’s milk & soy protein
Lymphocytic  celiac ds , increased
lymphosit T withi surface & pit
Granulomatous  tissue macrophage (
Chron ds, sarcoidosis, mycobacteria,
fungi, CMV, H. Pylori )
 Complication of chronic gastritis
Peptic ulcer ds/ PUD Mucosal atrophy & intestinal
metaplasia

Associated H.pylori-induced Long standing chronic gastritis 

hyperchlorhydric chronic gastritis, HP & oxyntic atrophy  intestinal metaplasia
NSAID is primary underlying causes of ( goblet cells + )  gastric adeno ca >>
PUD  parietal cells hiperplasia ,
malignant transformation >>

Imbalance of mucosal defences & Achlorhydria  overgrowth bacteria 

damaging forces  chronic gastritis  produce carsinogenic nitrosamines
PUD , prox duodenum >>, soliter, less <
0,3 cm , round to oval, sharply
punched-out defect, hemorhage &
fibrin deposition on gastric serosa ,
perforation  RO : free air under the
diagram on upright abd , base of petic is
smooth & clean,
 Complication of chronic gastritis

Dysplasia Gastritis cystica

Chronic gastritis  inflamation ept Exuberant reactive
 free radical damaged & epithelial proliferation :
proliferative stimuli  pre-invasive -submucosa/ polyposa
insitu lesions -deep layer/ profunda
Variation in epithelial size,
shape,orientation – coarse
chromatin, hyperchromasia, nuclear
enlargment
Peptic ulcerations
Menetrier disease
A rare ds coz excessesive secretion of
TGF-alfa , difuse hyperplasia foveolar
ept of the body & fundus +
hipoproteinemia  protein-losing
enteropathy ;
Weight loss-diare-edema perifer
Irregular enlargment of the gastric
rugae, hiperplasia foveolar mucous
cells, elongated glands with a cork-
screw like app & cystic dilation, difuse
& patchy glandular atrophy 
hipoplasia of parietal & chief cells
Zollinger-ellison syndrome
Syndrome coz gastrin-secreting
tumor/ gastrinomas , small intestine
& pancreas >>, duodenal ulcers &
chronic diare, malignant, 25% with
multiple endokrin neoplasia tipe I ,
soliter
Doubling of oxyntic mucosal
thickness  increased parietal cells
>>,
gastrin : hiperplasia of mucous neck
cells- mucin hiper production-
proliferasi endokrin cells within
oxyntic mucosa
Menetrier disease
20A. GASTRITIS KRONIK 20B. GASTRITIS KRONIK
HELICOBACTER PYLORI HELICOBACTER PYLORI
Tumors stomach
Inflamatory & hyperplastic Fundic gland polyps Gastric adenoma
polip
75% inflamatory & Familial adenomatous Increased with FAP, on a
hiperplastic polip , polyposis (FAP)  background chronic
assosiation with chronic increased gastrin gastritis with atrophy &
gastritis secretion, reduced intestinal metaplasia,
gastric acidity, glandular
hiperplasia
Smaller < 1cm, multiple, Nausea-vomiting- Soliter, < 2 cm, antrum
a smooth surface, erosi epigastric pain, womwn >>, intestinal-type,
>>, kistik, elongated >>, body & fundus, well epithelial dysplasia,
foveolar glands sircumscribed, smooth enlargement-elongated-
surface, kistik, iregular hyperchromasia-
glands lined by flattened crowding-
parietal & chief cells pseudostratification
Polip gaster
Gastric adenocarcinoma
Dispepsia, disfagia, nausea, weight loss,
anorexia, anemia, hemorhage
Multifocal mucosa atrophy & intestinal
metaplasia >> , related to Barrets esofagus
Intestinal-type : bulky tumor, glandular
structure, exophytic mass/ ulcerated tumors,
contain apical mucin vacuoles & abundant
mucin in gland lumen, anthrum
Difuse –type : signet ring cells, discohesive
cells, large mucin vacuoles  large mucin
lake, nucleus in periphery, infiltratif  a
desmoplastic reaction, if large area  a
leather bottle linitis plastica
Lymphoma
Most common, EBV – positif B
cells-deficit in T cell function, in
gut : MALTomas, translokasi,
dispepsia-epigastric pain-
hematemesis-melena-weight
loss
A dense lymphocytic infiltrate in
the lamina propia, in gastric
gland  lymphoepithelial
lesion, accumulate large of pale
cytoplasma : monocytoid
change, express the B-cell
marker CD19 & 20
 Gastric adenocarcinoma
Ulcerative type Polypoid type
ADENOKARSINOMA GASTER ADENO KARSINOMA GASTER
Makroskopis lymphoma
lymphoma
Carcinoid tumor
Arise from the diffuse component of the endocrine system : GI
tract & small intestine, endokrin cells hiperplasia-cronic atrophic
gastritis-zollinger Ellison syndrom, best considered to be welldiff
neuroendokrin ca  release peptide & non pepetide hormon,
cutaneus flashing-sweating-bronchospasm-colicky abd pain-
diarhhea-right side cardiac valvular fibrosis , important
prognostic fc is location (fore-mid-hind gut)
Intramural & submucosal mass, yellow-very firm-an intense
desmoplastic reaction kinking of the bowel & obstruction ,
uniform cells with scant-pink granular cytoplasm-a round to oval
stippled nucleus, minim pleomorphism-anaplasia-mitotic –
necrosis, positif synaptophysisn & chromogranin A
KARSINOID TUMOR
Gastrointestinal stromal tumors
Mesenchymal neoplasma in the stomach, male >>, mutation the
tyrosine kinase c-Kit, Cajal cells express c-KIT/ CD117 &
CD34,mucosa ulceration  blood loss, anemia, prognosis :
tumor size,mitotic index,location (less agresive than in small
intestine)
Large (> 30 cm), soliter, well sircumscribed, fleshy mass,
composed of thin elongated cells(spindel cell type)
Epithelial app cells (epitheloid type)
SMALL INTESTINE
AND COLON
 KONGENITAL
Atresia & Stenosis
• Atresia : Kegagalan perkembangan usus.
(Atresia duodeni >>)
• Stenosis : Penyempitan lumen usus (o.k
tebalnya dinding usus / hipertrofi sfingter /
kelainan persarafan usus)  obstruksi
 KONGENITAL
Divertikulum Meckel
kegagalan involusi dari Penonjolan buntu
duktus omfalomesenterik persisten lumen usus
saat dalam kandungan sepanjang 5-6 cm

Umumnya terjadi pada

ileum 80 cm dari
valvula iliocaecal,
dinding = dinding usus

Asimptomatik
 KONGENITAL
Omphalocele & Gastroschisis
Omphalocele : Gastroschisis :
Defek dinding abdomen Defek dinding abdomen
dari kulit hingga otot, dari kulit hingga otot dan
periumbilikal, namun tidak peritonum, daerah
sampai peritoneum. periumbilikal

Herniasi isi
abdomen
 KONGENITAL
HIRSCHSPRUNG DISEASE (congenital megacolon)
Berhentinya migrasi sel krista
neuralis sebelum mencapai anus 
segmen aganglionic (Meissner &
Auerbach)
OBSTRUKSI
segmen aganglionik

DILATASI Segmen Proksimal

(stercoral ulcers)

1 in 5000 to 8000 Kelahiran hidup

Laki-laki: Perempuan = 4 : 1
 KONGENITAL
HIRSCHSPRUNG DISEASE (congenital megacolon)
Gejala Klinis : (Sesuai panjangnya segmen
aganglionik) :
• Pengeluaran mekonium terlambat, diikuti
muntah dalam 48 - 72 jam.
• Superimposed enterocolitis
• Perforation

Acquired Megacolon
1. Chagas disease (T cruzi)
2. Neoplasma, striktur radang
3. Ulcerative colitis or Crohn disease
4. Psychosomatic disorder
 GANGGUAN VASKULER
Ischemic Bowel Disease

Transmural infarct : o.k oklusi akut

arterimesenterika
 GANGGUAN VASKULER
Ischemic Bowel Disease
Trombosis Atherosclerosis, vasculitis, aneurysm,
Arteri hypercoagulable, oral contraceptives

Vegetasi cardiac, prosedur angiografi,

Emboli Arteri aortic Atheroembolism

FAKTOR Trombosis hypercoagulable, neoplasma

PREDISPOSISI vena vaskular, sirosis, trauma abdomen

Iskemi non- Cardiac failure, shock, dehydration,

oklusif vasoconstrictive drugs

Miscellaneous Radiation, volvulus, striktur, hernia

 GANGGUAN VASKULER
Ischemic Bowel Disease
Infark Transmural Infark Mukosa & Mural
1. Edema 1. Edema
2. Perdarahan 2. Perdarahan
3. Nekrosis 3. Nekrosis
4. Infeksi bakteri MORFOLOGI 4. Pseuomembran (Infeksi
gangren (24 jam) sekunder)
5. Perforasi 5. Radang kronik & ulkus

1. Nyeri abdomen 1. abdominal discomfort

mendadak 2. Diare darah
GEJALA
2. Diare darah 3. Perbaikan, jika sebab
3. Shock hipovolemik dihilangkan
 GANGGUAN VASKULER
/’=;-5
Angiodysplasia
Tekanan dinding Obstruksi aliran Dilatasi pembuluh
usus >> vena submukosa darah

Perdarahan Ruptur

1. self-limited
2. Kronik 0.8% pada orang
3. Recurrent sehat > 50 Th
4. Life threatening
Lokasi : caecum, kolon ascenden proximal
GEJALA : Perdarahan (30-40% dari perdarahan GI yang tidak jelas),
melena, hematochezia, darah samar feses, anemia
 GANGGUAN VASKULER
Hemorrhoid
Tekanan vena >> Dilatasi variseal

Internal Hemorrhoid
Diatas linea anorectal, tercover
mukosa

External Hemorrhoid
Dibawah linea anorectal, tercover
mukosa anus / kulit

Faktor predisposisi : konstipasi, kehamilan, Hipertensi porta

GANGGUAN VASKULER
Hemorrhoid
Gejala Klinis:
Internal :
• Perdarahan (Melena)
• Prolaps keluar anus (> Stage II)
External :
• Perdarahan (darah segar)
• Prolaps keluar anus (> Stage II)
• Nyeri, strangulation
• Dapat trombosis
 Divertikulosis Kolon
Diverticulum :
Kantong buntu yang berhubungan dengan lumen usus

Congenital Acquired
Meckel diverticulum (mucosa,
(mucosa, submucosa, submucosa, lack
muscularis propria) muscularis propria)

Common site : sigmoid (95%)

 Divertikulosis Kolon

1. Defek fokal pada

Perlemahan tunika
muskularis dinding kolon.
muskulais – locus
2. Adanya perstaltik kolon &
minoris resistensia
peningkatan tekanan
intralumen kolon

Lokasi Pontesial
herniasi
Prevalensi : 50% pd > 50 y.o
Faktor resiko : konsumsi low fiber
diet
Diverticulum
 Divertikulosis Kolon

Clinical Features :
• asymptomatic
• Abdominal pain/discomfort
• Unsatisfactory defecation
• Fever (diverticulitis)
• Bleeding or peforation (complcation)
 OBSTRUKSI USUS

Obstruksi Mekanik Penyebab lain

1. Hernias 1. Tumors
2. Adhesions 2. Inflammatory
3. Intussusception strictures
4. Volvulus 3. Obstructive
gallstones, fecaliths,
foreign bodies
4. Congenital stricture,
PENYEBAB atresias
5. Imperforate anus
OBSTRUKSI USUS
 Enterocolitis
(Diarrheal Diseases)
• Diare : Peningkatan masa feses, frekuensi, dan atau
fluiditasnya
• More than 14 L/day of fluid may be lost in severe
cases of diarrhea equivalent to the circulating blood
volume!
• Often Accompanied by pain, urgency,
perianal discomfort, and incontinence
• Dysentery : stool containing blood & mucus;
abdominal cramp/pain; rectal tenesmus
Struktur intestinal & colon
 Intestinal obstruction
Hernia Adhesions Volvulus Intussusception
Protusion of a Fibrous bridge  Complete twisting When a segment
serosa-lined pouch closed loops of a loop of bowel of the intestine
of peritoneum through other  feature of constricted by a
(hernia sac) viscera  internal obstruction & wave of peristalsis,
herniation infarction telescope into the
immediately distal
segment
Leading to Colon sigmoid, May progress to
permanent cecum, small intestinal
entrapment/ bowel, stomach obstruction,
incarceration & compression
strangulation mesenteric vessel,
infarction
 Ischemia bowel disease
• Mucosa & mural infarction
• Mucosa is hemorrhagic, ulcerated, luminal
hemorrhage  thickened bowel wall, rubbery
• Coagulative necrosis musc propia within 1-4 days
• Ischemic intestine : atrophy/ sloughing of surface
epithelium, crypt hiperproliferative
• Clinical : sudden, severe abd pain, tenderness,
nausea, vomiting, bloody diarhea/ groosly
melanositic stool
 Malabsorption & diarhea
Celiac ds Tropical sprue Lactase deficiency A
betalipoproteinemia
Celiac sprue- gluten Malabsorptio In the apical brush- Rare autosomal
sensitive enteropathy n syndrome in border membran of resesive ds (mutasi
the tropics the villous absorptive MTP)
epithelial
Triggered by the ingestion of Similar celiac 2 type : an inability to secrete
gluten-containing cereals but total Kongenital  mutasi triglyserida-rich
villous Dapatan  down lipoprotein
atrophy regulation of lactat acumulate in
uncommon gene expresion epithelial cells (lipid
vacuolization )
Duodenum/ proximal Deficiency Abd fullness, diare, Failure to thrive,
jejunum, increased CD8+ T folate & vit flatulence diarrhea, steatorhea
lymphosit (intraepithelial B12 /
lymphositosis), crypt megaloblastic
hiperplasia & villous atrophy
 increased plasma cells,
mast cells, eosinofil
 Infectious enterocolitis
Cholera Campylobacter Shigellosis Salmonellosis
enterocolitis
Abrupt onset of Travellers diare, Gram-negatif baccili, Enterobacter, baccili
watery diare & unpasteurized milk/ unencapsulated- gram negatif, typhi &
vomiting, incubasi 1- contaminated water, nonmotile- fakultatif nontyphi / enteridis ,
5 ds, stools resemble flagela motil, HLA- anaerob, related to transfering bacterial
rice water, a fishy B27, Influenza-like enteroinvasiv E. Coli, protein into M cells
odor, dehidrasi- prodrome, watery resistant to the harsh & enterocyt , flagelin
hipotensi-shock- diare, acidic of the activate TLR5 on host
death stomach,watery cells  inflamasi ,
diare – fever- abd ept release
pain eicosanoid hepoxilin
A3  netrofil
Hemaglutinin/ Comma shaped, Left colon >>, Non spesific, similar
metalloproteinase  flagelated, gram abundance M cells in camphy & shigella ,
bacterial detachment negatif, mucosal & ept over the Peyer’s stool culture
& shedding in the intraepithelial patches, mucosa
stool, netrophil infiltrated hemorhagic &
 cryptitis/ kripta, ulcerated &
abses/ lumina pseudomembran
Thyphoid fever Yersinia
Salmonella thyphi & parathyphi  taken up M cells Invade M cells &
engulfed by mononuclear cells  reactive hiperplasia adhesin to bind host
of fagositosis & lymphoid , anorexia- abd pain- cells B1 integrin ,
bloating- nausea- vomiting- bloody diare
Peyer patches in terminal ileum to enlarge into involve the ileum-
sharply delineated, plateau=like elevations up 8 cm, appendix-right colon,
netrofil accumulate within the superficial lamina lymp node & peyer
propia & macrophage containing bacteria- rbc- patches hiperplasia ,
nuclear debris- lymphosit- sel plasma, mucosal bowel wall thickening
shedding  oval ulcers, along the axis of the ileum,
spleen : soft, enlarged, uniform pale red pulp,
obliterasi folikular, prominent fagosit hyperplasia ,
typhoid nodule : necrosis parenchym, hepatocyt
replaced by macrofag in liver
Pseudomembranous colitis
Clostridium difficile,
Formation pseudomembran 
adherent layer of infl cells & debris
at side of colonic mucosal injury,
superficial damaged crypt
distended by a mucopurulent
exudat  eruption reminiscent of
a volcano
Whipple ds
Multivisceral chronic ds, intestinal
lipodistrophy, malabs-
lymphadenopathy- arthritis
A dense accumulation of distended,
foamy macrofag in small intestine lamina
propia (acid-fast satin : positif in
mycobacteria) , intact rod-shaped
baccili, lymphatic dilatation & mucosal
lipid deposition, bacteria laden makrofag
accumulate in mesenteric lymp nodes-
synovial membran of afacted joint ,
cardiac valve, the brain.
Intestine’s Disorder
Tumor
 Intestine’s Disorder
Tumor
NON-NEOPLASTIC POLYPS
• 90% of all epithelial polyps, > 50% of all
persons age 60 y.o
• Most are hyperplastic polyps (single/multiple,
nipple like, < 5 mm diameter)
• Common site : rectosigmoid
 Intestine’s Disorder
Tumor
JUVENILE POLYPS
• hamartomatous proliferations, mainly of the
lamina propria
• most frequently in children < 5 y.o
• 1-3 cm diameter, single
• source of rectal bleeding, painful infarction
(Torsio of polyps)
 Intestine’s Disorder
Tumor
ADENOMA
• 20-30% (before 40 y.o), 40-50% (after 60 y.o)
• Usually sessile
• result of epithelial proliferation and dysplasia
• Geater risk become carcinoma (4X)
• Sign : asymptomatic, occult bleeding
 Intestine’s Disorder
Tumor
FAMILIAL POLYPOSIS SYNDROMES
• Autosomal dominant disorders
• Typically develop 500-2500 colonic adenomas
• The risk of colonic cancer is virtually 100% by
midlife , unless a prophylactic colectomy is
performed
• Mutation in APC gene
 Intestine’s Disorder
Tumor
Peutz-Jeghers syndrome
• Hamartomatous polyps + melanotic mucosal +
cutaneous pigmentation
• Mutations in the LKB1 gene

Major CAUSES of diarrheal diseases

COWDEN SYNDROME
• Hamartomatous polyps + increased risk of
neoplasms : thyroid, breast, uterus, and skin
• Mutations in the PTEN gene
 Intestine’s Disorder
Colorectal Carcinoma
• 2nd cancer killer in USA after pulmonary Ca
• 5% of USA population will develop this Ca
• Adenocarcinoma : 70% of all malignancies in
GI Tract
Major CAUSES & diseases
of diarrheal 98% of all Ca in large intestine
• 134,000 new cases & 55,000 deaths/year
• Almost always arise in adenomatous polyps
• 80% in > 60 y.o & 20% in < 50 y.o
• Male > female
 Intestine’s Disorder
Colorectal Carcinoma
Risk Factor :
1. Genetic
• Individuals with hereditary nonpolyposis
Major CAUSES colorectal cancer syndrome (HNPCC/Lynch
of diarrheal diseases

syndrome, caused by germ-line mutations

of DNA mismatch repair genes)
• preexisting ulcerative colitis or one
of the polyposis syndromes
(in young patient)
 Intestine’s Disorder
Colorectal Carcinoma
Risk Factor :
2. Environment
a. Low content of unabsorbable vegetable
Major CAUSES of diarrheal diseases
fiber
b. High content of refined carbohydrates
c. High fat content
d. Decreased intake of protective
micronutrients
 Intestine’s Disorder
Colorectal Carcinoma (CRC)
Molecular Genetic Pathways / Carcinogenesis of CRC

Major CAUSES of diarrheal diseases

 Intestine’s Disorder
Colorectal Carcinoma (CRC)
Clinical Features
• Asymptomatic for years
• Fatigue, weakness, and iron deficiency anemia
(right lession)
• Occult bleeding, changes in bowel habit, or
Major CAUSES of diarrheal diseases
crampy left lower quadrant discomfort (Left
lession)
• Spread : direct extension, lymphatic & Blood
(liver, lung, bone)
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