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SALURAN CERNA
DEPARTEMEN PATOLOGI ANATOMIFAKULTAS KEDOKTERAN USU
MEDAN - 2010
Kuliah Keperawatan
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L I D A H
Kista tiroglosu
s
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Leukoplakia pada perokok
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Mikroskopik : Lesi dengan displasia berat Karsinoma sel skuamous
pada bagian posterior (lesi yang meninggi)
Penebalan epitel & hiperkeratosis
MULUT & GUSI
Normal : flora mulut (+)
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Tumor
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KELENJAR LIUR
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KELENJAR LIUR
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Neoplasma Kelenjar Liur
Faktor resiko kanker rongga :
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E S O F A G U S
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Achalasia
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Kardiospasmus syaraf simpatik (-) Otot sirkuler esogafus tidak bisa relaxSindroma dysphagia, nyeri menelan dan muntah2
O.k. esofagus terlalu pendek
O.k. bendungan susunan vena porta pd Cirrhosis Hepatis
Hernia Hiatus
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Varises Esofagus
Esophageal varices
Dilated submucosal veins (varices)
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Radang
Jenis tidak khas, ok: Zat korosif Uremia Reflux Makanan Anemia Bakteremi
Efek : • Hiperemia• Nekrosis• Fibrosis
Penyebab : • TBC• Actinomycosis
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Divertikulum Esofagus
Pelebaran setempat dari dinding esofagus ok tekanan dari dalam / dari luar
Striktura : Stenosis Esofagus
Spasme NeurogenJaringan parutTumor
Aneurisme aorta
Organik Fungsionil
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BARRETT ESOPHAGUS
♂ > ♀ (4:1) Whites > ras yang lain Refluks gastroesofageal kronik & berulang Metaplasia epitel kolumnar lebih resisten terhadap jejas refluks isi
lambung
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Mukosa Esofagus distal :epitel skuamous berlapis kolumnar
metaplastik yang mengandung sel goblet
(A) normal gastroesophageal junction and (B) the granular zone of Barrett esophagus (arrow). C, Endoscopic view showing red velvety gastrointestinal-type mucosa extending from the gastroesophageal orifice. Note paler squamous esophageal mucosa. (C, Courtesy of Dr. F. Farraye, Brigham and Women's Hospital, Boston, Massachusetts.)
Barrett esophagus
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Mikroskopik mukosa skuamous (left)
Intestinal-type columnar epithelial cells in glandular mucosa (right).
Barrett esophagus
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LAMBUNG
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Anatomi Dan Histologi Lambung
Junqueira L.C., Carneiro J., Digestive Tract. In: Basic Histology-Text&Atlas. 11th Ed. International Edition. McGraw-Hill.2005 :p.281-316.
KELENJAR KARDIA = ANTRUM
FOVEOLA : KELENJAR ( 1 : 1 )
KELENJAR FUNDUS = KORPUS
FOVEOLAR : KORPUS ( 1 : 4 )
G - CELL D - CELL
FUNDUS & CORPUS
PARIETAL (OXYNTIC) CELL
CHIEF CELL
MUCOUS CELL
ARGENTAFFIN CELL
ANTRUM-PILORIK
Fisiologi Lambung
Gambar 3. Gambaran sekresi asam oleh sel parietal.27
KELAINAN LAMBUNG
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Radang (Gastritis)
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Highlighted by the dark digested blood in their bases.
Multiple stress ulcers of the stomach
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Showing partial replacement of the gastric mucosal epithelium by intestinal metaplasia (upper left), and inflammation of the lamina propria containing lymphocytes and plasma cells (right).
Chronic gastritis
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Coloured scanning electron micrograph of H.pylori on surface of gastric cell
Gram (-), 2-3μm, Aerobic / microaerophilic, Spiral-shaped bacilli, Motile (flagella)
Lokalisasi H. pylori (dalam lambung)
H.pylori : Lumen (-) Mucous (+)
Produksi musinase : Melisis mukus Viskositas ↓
Koloni : Melekat di sel epitel (pH ~ netral)
H. pylori (lambung)
Strain H.pylori
Faktor berpengaruh :
Perbedaan genetik
vacA cag PAI (Pathogeneicity islands)
Polimorfik host
Mutasi TP53
menimbulkan radang
Faktor lingkungan
Mempromosi tampilan kuat
IL-1b
Mengapa sebagian besar penderita carrier tidak menimbulkan gejala penyakit ?
Faktor Virulensi (untuk kolonisasi mukosa lambung)
Motilitas & daya kemotaksis
Enzim urease
Perlekatan bakteri
vac-A & cag-A
(Faktor virulensi yang dikirim dari luar)
Sistem sekresi tipe-4
(Disekresi langsung ke sitosol)
Dalam Lumen Lambung
Urea AmoniaFungsi
Lumen mukosa kolonisasi (permukaan sel epitel)
Melindungi sekeliling sel H.Pylori
Produk urease ↑↑(untuk me↑↑ pertumbuhan organisme)
Bentuk (heliks) & motilitas
Memudahkan bakteri
Metode Konvensional
Invasif Non-invasif
EndoskopikBiopsi (HP)KulturRapid Urease TestsPCR / DNATest cairan lambungKadar urea / amonium IgA
Urea Breath Test (UBT)H.pylori stool antigen (HpSA)Serologi (IgG, IgA)PCR air liurSerum C-bicarbonate* Ekskresi urin NH4*
(* tidak digunakan dalam klinis)
Diagnosa Infeksi Helicobacter pylori
Steiner silver stain, darkly stained Helicobacter organisms along the luminal surface of the gastric epithelial cells. There is no tissue invasion by bacteria.
(Courtesy of Dr. Melissa Upton, Department of Pathology, University of Washington, Seattle, Washington.)
Helicobacter pylori gastritis
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Tukak lambung (Ulcus Ventriculi)
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Komplikasi tukak
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Pathogenesis Peptic Ulcers
Aggravating causes of, and defense mechanisms against, peptic ulceration. The right panel shows the basis of a nonperforated ulcer, demonstrating necrosis (N), inflammation (I), granulation tissue (G), and fibrosis (S).
Tukak kecil (2 cm) with a sharply punched-out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base is clean (compare with the ulcerated carcinoma in Fig. 15-19). (Courtesy of Dr. Robin Foss, University of Florida, Gainesville, Florida).
Tukak Peptik Duodenum
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Demonstrating the layers of necrosis (N), inflammation (I), granulation tissue (G), and scar (S) moving from the luminal surface at the top to the muscle wall at the bottom.
Medium-power detail of the base of a nonperforated peptic ulcer
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TUMOR LAMBUNG
Tumor GIT asal dari mukosa > tumor mesenkim
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PARADIGMA KARSINOGENESIS LAMBUNG MARSHALL & WARREN (AUSTRALIA - 1983)
MUKOSA LAMBUNG NORMAL
GASTRITIS KRONIK
GASTRITIS ATROFI MULTIFOKAL
METAPLASIA INTESTINAL
DISPLASIA
NEOPLASIA INVASIF(KANKER LAMBUNG)
MUTASI :GENOMIK & FENOTIP
H.pylori
H.pylori
Antisecretory RxGastric pH ↑
Ascorbic acid ↓
pH ↑
Diet, rokok
Genetik
Medscape@
http://www.medscape.com
Gastric Carcinoma
Among the malignant tumors that occur in the stomach, carcinoma is overwhelmingly the most important and the most common (90% to 95%).
Next in order of frequency are lymphomas (4%), carcinoids (3%), and stromal tumors (2%).
This discussion of gastric tumors focuses on gastric carcinomas, with only a brief mention of the other types.
Gastrointestinal stromal tumors, carcinoids, and lymphomas are discussed later in this chapter, after the presentation of intestinal tumors.
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Risk Factors for Gastric Carcinoma
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Hirayama (Klass. Histopatologi)
Karsinoma lambung
The ulcer is large with irregular, heaped-up margins. There is extensive excavation of the gastric mucosa with a necrotic gray area in the deepest portion.
Ulcerative gastric carcinoma
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A, H&E stain demonstrating intestinal type of gastric carcinoma with gland formation by malignant cells that are invading the muscular wall of the stomach. B, Diffuse type of gastric carcinoma with signet-ring tumor cells.
Gastric cancer.
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TRAKTUS INTESTINAL
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TRAKTUS INTESTINALIS (Saluran usus )
Cacat bawaan : Malrotasi Reduplikasi Aplasia Atresia & Stenosis Dilatasi usus (Hisch sprung) Diverticulum :
Diverticulitis Mecheli Fistula
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Meckel diverticulum. The blind pouch is located on the antimesenteric side of the small bowel.
Hirschsprung Disease: Congenital Megacolon
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VASCULAR DISORDERS Acute Ischemic Bowel Disease
Note the three levels of severity, represented for the small intestine
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Secondary to acute thrombotic occlusion of the superior mesenteric artery
Infarcted small bowel
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The mucosa is hemorrhagic, and there is no epithelial layer. The remaining layers of the bowel are intact.
Mucosal infarction of the small bowel
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A, Section through the sigmoid colon showing multiple saclike diverticula protruding through the muscle wall into the mesentery. The muscularis between the diverticular protrusions is markedly thickened. B, Low-power micrograph of diverticulum of the colon showing protrusion of mucosa and submucosa through the muscle wall. A dilated blood vessel at the base of the diverticulum was a source of bleeding; some blood clot is present within the diverticular lumen.
COLONIC DIVERTICULOSIS
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BOWEL OBSTRUCTION
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Major Causes of Intestinal Obstruction
Empat penyebab utama obstruksi usus
(1) Herniation of a segment in the umbilical / inguinal regions
(2) Adhesions between intestinal loops
(3) Intussusception,
(4) volvulus.
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ENTRITIS REGIONALIS
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CROHN disease = Ileitis terminalis
Merupakan peradangan penebalan & fibrosis dinding usus secara segmental dengan
bagian-bagian yang normal.
CROHN disease = Ileitis terminalis
Etiologi :• Alergy intestinal • Emosi • Limfedema
Morfologi :• Submucosa (Radang & edema) • Fibrosis usus (lead pipe)• Lumen usus menyempit (String sign)• Ulkus berbagai bentuk
Klinis :• Nyeri perut bawah kanan • Diare• Obstipasi • Sering relaps
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Colitis Ulcerative/diapathica
Etiologi : Tidak diketahui Emosional stress Antoimmune
Morfologi : Perdarahan mukosa Mikroabsces Ulcus lender antar ulcus ikut meradang
Klinis : Nyeri perut Diare Melena Degenerasi maligna
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TBC Usus :
Infeksi : Minum susu terkontaminasi Sekunder dari paru
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TUMORS OF THE SMALL AND LARGE INTESTINES
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Two forms of sessile polyp (hyperplastic polyp and adenoma) and of two types of adenoma (pedunculated and sessile). There is only a
loose association between the tubular architecture for pedunculated adenomas and the villous architecture for sessile polyps.
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The surface is carpeted by innumerable polypoid adenomas. (Courtesy of Dr. Tad Wieczorek, Brigham and Women's Hospital, Boston, Massachusetts.)
Familial adenomatous polyposis
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Familial Polyposis Syndromes
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showing a fibrovascular stalk covered by normal colonic mucosa and a head that contains abundant dysplastic epithelial glands-hence the blue color. B, A small focus of adenomatous epithelium in an otherwise normal (mucin-secreting, clear) colonic mucosa, showing how the dysplastic columnar epithelium (deeply stained) can populate a colonic crypt ("tubular" architecture).
Tumor
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Morphologic & molecular changes in the adenoma-carcinoma sequence
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Defects in mismatch repair genes result in microsatellite instability and permit the accumulation of mutations in numerous genes. If these mutations affect genes involved in cell survival and proliferation, cancer may develop.
Morphologic & molecular changes in the mismatch repair pathway of colon
carcinogenesis
Stage kanker kolon
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The exophytic carcinoma projects into the lumen but has not caused obstruction.
Carcinoma of the cecum
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This circumferential tumor has heaped-up edges and an ulcerated central portion. The arrows identify separate mucosal polyps.
Carcinoma of the descending colon
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Showing malignant glands infiltrating the muscle wall.
Invasive adenocarcinoma of colon
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Gastrointestinal stromal tumor
(GIST).
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A, GIST from the stomach wall.
B, Histology of the tumor showing spindle cells with elongated nuclei with fine chromatin, and eosinophilic fibrillar cytoplasm.
C, KIT stain showing strong and uniform reactivity of the tumor cells. Note KIT staining of mast cells in the adjacent normal muscle wall.
(Courtesy of Dr. Brian Rubin, Department of Pathology, University of Washington, Seattle, Washington.)
Carcinoid tumor
A, Multiple protruding tumors are present at the ileocecal junction. B, The tumor cells show a monotonous morphology, with a delicate intervening fibrovascular stroma. (H&E). C, Electron micrograph showing dense-core bodies in the cytoplasm.
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