patologi anatomi colon

USUS BESAR (COLON)

 HIRCHSPRUNG DISEASE

                  Ada bagian colon yang tidak ada persarafan dari plexus Meissner dan Auerbach (aganglionosis), ……. 
          Congenetal aganglionic megacolon.

                  Tidak ada koordinasi gerakan peristaltik usus sehingga terjadi obstruksi fungsional.

                  Akibatnya terjadi dilatasi colon (megacolon) pada bagian proksimal dari colon yang kena.

         Hirschsprung disease.

  A.        Preoperative barium enema study showing constricted rectum and dilated sigmoid colon.

  B.        Corresponding intraoperative photograph showing constricted rectum and dilation of the sigmoid colon.

IRRITABLE BOWEL SYNDROME

•          Sakit perut kronis, hilang timbul, gangguan defikasi.

•          Tak ada kelainan patologis pada kolon.

•          Diduga faktor kejiwaan.

INFLAMATORY BOWEL DISEASE

        Kelainan kronis pada kolon akibat respon imun mukosa kolon tidak sepadan.

        Dua penyakit dalam kelompok ini yaitu Crohn Disease dan Colitis Ulcerosa.

        Ulcerative Colitis adalah ulcerating inflamatory disease yang terbatas mengenai kolon dan rektum dan inflamasinya hanya pada mukosa dan submukosa.

        Crohn Disease mengenai kolon dan ileum serta inflamasinya transmural (melawati lapisan muskularis propria)

PATOGENESIS IBD

        Genetik

        Mucosal Immune Responses

        Epithelial Defect

        Microbiota.

Gross pathology of Crohn disease.

         A.       Small-intestinal stricture.

         B.       Linear mucosal ulcers and thickened intestinal wall.

         C.        Perforation and associated serositis.

         D.       Creeping fat.

CROHN’S DISEASE

        Chronic Inflammatory disease of unknown etiology.

        Mainly involves the small intestinum, especially terminal ileum.

        Skip lesion of the intestine (normal intestine in between)

CROHN’S DISEASE

Histopathology:

        Marked oedema and inflammation of the submucosa º gross thickening of the intestinal wall.

        Between thickening º fissured ulcer º formation of the fistulae

        Chronic inflammatory changes are transmural º widespread fibrosis             bowel obstruction.

        Granuloma formation with giant cells.

ULCERATIVE COLITIS

        Chronic relapsing inflammatory disease

        Affecting the large bowel

        Unknown cause

Histopathology:

        Ulcerative process destroyed much of the mucosa and submucosa (crypts absceses).

        Non ulcerative mucosa º inflammatory pseudopolyps.
Gross pathology of ulcerative colitis.

                        A.        Total colectomy with pancolitis showing active disease, with red, granular mucosa in the cecum and smooth, atrophic mucosa     distally

                         B.        Sharp demarcation between active ulcerative colitis and normal

                         C.        Inflammatory polyps.

                         D.       Mucosal bridges.

Colitis-associated dysplasia.

A.       Dysplasia with extensive nuclear stratification and marked nuclear hyperchromasia.

B.       Cribriform glandular arrangement in high-grade dysplasia.

C.        Colectomy specimen with high-grade dysplasia on the surface and underlying invasive adenocarcinoma. A large cystic, neutrophil-filled space lined by invasive adenocarcinoma is apparent at the bottom beneath the muscularis mucosa, and is surrounded by small invasive glands.

COLLAGENOUS  COLITIS
(Chronic water non-bloody diarrhoea)

        Etiology is unknown (immunological cause?)

        Mainly in middle-aged and elderly women.

        Histopathology:

-          It is characterised by a band of collagen deposiet immediately below the epithelial

-          basment membrane.

-          Inflammation in the lamina propria.

-          Increase of intraepithelial lymphocytes in the surface epithelium

LYMPHOCYTIC COLITIS
(Chronic water non-bloody diarrhaea)

        Etiology is unknown (immunological cause?).

        Occurs in both man and women.

        Histopathology :

-          Marked increased of intraepithelial lymphocutes in both surface apithelium and gland.

-          Degenerative change in surface epithelium.

-          Inflammation in the lamina propria.

-          No collagen band.

Sigmoid diverticular disease.

          A.       Stool-filled diverticula are regularly arranged.

          B.       Cross-section showing the outpouching of mucosa beneath the muscularis propria.

C.                       Low-power photomicrograph of a sigmoid diverticulum showing protrusion of the mucosa and submucosa through            the muscularis propria.

ACUTE APPENDICITIS

Early Acute Appendicitis

        Ulceration of the mucosa with overlying acute fibrinopurulent inflammatory exudate.

        Purulent exudate within the lumen.

ACUTE APPENDICITIS

Later Acute Appendicitis

        The inflammation spreads throughout all layers af the wall of the appendix

        Mucosal ulceration more extensive.

        Large numbers of neutrophils have infiltrated through the submucosa and muscular layer to the serosa..

        One point of fibrinous exudate is beginning to form on the peritoneal surface (Peritonitis)

Established Acute Appendicitis

        The acute inflammatory infiltrate (mainly neutrophil) are shown in the muscular layer.

        The smooth muscle fibres are separated by inflammatory oedema.

GANGRENOUS APPENDICITIS

        Severe continuing inflammation of the appendix wall often leads to extensive necrosis of the muscle layer (gangren)

        Perforation is imminent.

        Pus (in the lumen) º peritoneal cavity º severe and extensive peritonitis

        Other complications: absces, septicaemia, shock & death.

HEMORRHOID
(ANAL VARICES)

        Pelebaran vena anal dan perianal plexus yang patogenesianya sama dgn varices esopagus, bisah disebabkan juga oleh hipertensi portal.

        Berlokasi dibawah batas anorectal disebut hemorrhoid interna, jika lebih rendah disebut hemorrhoid eksterna

MACAM2 POLIP DI KOLON

        Inflammatory Polyp.

        Juvenile Polyp

        Hyperplastic polyp

        Neoplatic polyp

COLONIC ADENOMATOUS POLYP

Tubular Adenoma (T)

        Displastic colonic epithelium arranged in straight tubular gland

        Solitary or multiple (familial polyposis coli)

COLONIC ADENOMATOUS POLYP

Dysplasia

1.        Cell are enlarged  and crowded with  large pleomorphic nuclei, 
2.      Increase neclear to cytoplamic ratio,

3.        Palisading of  nuclei

4.        Increased mitotic figures

Morphologic and molecular changes in the adenoma-carcinoma sequence.

         It is postulated that loss of one normal copy of the tumor suppressor gene APC occurs early. Individuals may be born with one mutant allele, making them extremely prone to develop colon cancer, or inactivation of APC may occur later in life. This is the "first hit" according to Knudson's hypothesis (Chapter 7). The loss of the intact copy of APC follows ("second hit"). Other mutations include those on KRAS, losses at 18q21 involving SMAD2 and SMAD4, and inactivation of the tumor suppressor gene p53, lead to the emergence of carcinoma, in which additional mutations occur. Although there seems to be a temporal sequence of changes, the accumulation of mutations, rather than their occurrence in a specific order, is most critical.

      Defects in mismatch repair genes result in microsatellite instability and permit accumulation of mutations in numerous genes. If these mutations affect genes involved in cell survival and proliferation, cancer may develop.