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GASTROINTESTINAL DISORDERS Fe A. Bartolome, MD, FPASMAP Department of Pathology Our Lady of Fatima University
Signs & Symptoms of Small Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Signs & Symptoms of Large Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meckel Diverticulum ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meckel Diverticulum ,[object Object],[object Object],[object Object]
Meckel Diverticulum The specimen is a portion of small intestine with a diverticulum protruding out 25 mm in length.
Meckel Diverticulum Meckel diverticulum.  Photomicrograph (original magnification, ×16; hematoxylin-eosin [H-E] stain) shows the diverticulum composed of all layers of the intestinal wall. Normal small intestinal mucosa and a focus of gastric mucosa (arrow) line the diverticulum.
Large Bowel Pulsion Diverticulum ,[object Object],[object Object],[object Object],[object Object]
Large Bowel Pulsion Diverticulum ,[object Object],[object Object],[object Object],[object Object],[object Object]
Extensive diverticulosis of sigmoid colon with segmentation and shortening of bowel. Openings of diverticula can be clearly seen. Circular muscle is thick and corrugated.
Whole mount of colon with diverticular disease. Whole-mount view of colonic diverticulosis. One of the diverticula shows marked chronic peridiverticulitis. Note hypertrophy of the muscle wall.
Hirschsprung Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hirschsprung Disease
Hirschsprung Disease ,[object Object],[object Object],[object Object],[object Object]
Hirschsprung Disease ,[object Object],[object Object],[object Object]
Hirschsprung Disease Gross specimen of Hirschsprung's disease. The proximally dilated segment of bowel has been resected. Colonic mucosa stained for acetylcholinesterase from a patient with Hirschsprung's disease. There is a marked increase in the number of nerve fibers in the lamina propria.
Hirschsprung Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Intestinal Obstruction ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object]
Route of a direct hernia. The hernia sac passes directly through Hesselbach's triangle and may disrupt the floor of the inguinal canal.
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object]
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object],Route of an indirect hernia. Note that the hernia sac passes outside of the boundaries of Hesselbach's triangle and follows the course of the spermatic cord.
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],Route of an indirect hernia. Note that the hernia sac passes outside of the boundaries of Hesselbach's triangle and follows the course of the spermatic cord.
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Umbilical hernia exacerbated by refractory ascites. Advanced liver disease precluded operative repair in this case.
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object],[object Object]
Intestinal Obstruction: Hernias ,[object Object],[object Object],[object Object]
 
Incarcerated umbilical hernia Strangulated inguinal hernia
Intestinal Obstruction: Adhesions ,[object Object],[object Object],[object Object]
 
Intestinal Obstruction: Volvulus ,[object Object],[object Object],[object Object]
A volvulus is a twisting of the bowel on itself. It is one cause of intestinal obstruction.
Intestinal Obstruction: Intussusception ,[object Object],[object Object],[object Object]
 
Intestinal Obstruction: Intussusception ,[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object]
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Ischemic colitis. The lesion is typically located in the splenic flexure. The mucosa is markedly hyperemic and covered by a fibrinopurulent exudate. Ischemic colitis with hyalinized lamina propria and gland dropout
Ischemic Bowel Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Autopsy of infant showing abdominal distension, intestinal necrosis and hemorrhage, and peritonitis due to perforation.
Necrotizing enterocolitis. Gross appearance. The mucosa is necrotic. Numerous small gas-filled cysts are present in the wall. Low-power microscopic appearance showing extensive ulceration, necrosis, and hemorrhage.
Angiodysplasia ,[object Object],[object Object],[object Object],[object Object],[object Object]
An angiodysplasia in the cecum, explaining the patients iron deficiency anaemia
Angiodysplasia ,[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption ,[object Object],[object Object],[object Object]
Malabsorption ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Cystic Fibrosis Absent epithelial cystic fibrosis transmembrane conductance regulator Defective intestinal chloride ion secretion Impaired bicarbonate, sodium, and water secretion Defective luminal hydration Formation of intraductal concretions in pancreatic ducts Exocrine pancreatic insufficiency Failure of intraluminal phase of nutrient absorption
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object]
Malabsorption: Celiac Disease Some gliadin peptides Induce epithelial cell expression of IL-15 Activation and proliferation of NKG2D+ CD8+ intra-epithelial T lymphocytes No recognition of gliadin Cross the epithelium Deaminated by tissue trans-glutaminase Interact with HLA-DQ2 or HLA-DQ8 on APCs  Presented to CD4+ T cells (+) Immune reaction
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
This is an endoscopic biopsy of celiac disease that shows total crypt hyperplastic villous atrophy with complete flattening of the mucosal surface.  Note the intense lymphoplasmacytic inflammation in the lamina propria.
The surface epithelium of this biopsy contains numerous intraepithelial lymphocytes.
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Dermatitis herpetiformis on the forearm
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Celiac Disease ,[object Object],[object Object],[object Object],[object Object]
Whipple Disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Whipple Disease Outer aspect of mesenteric lymph nodes massively involved by Whipple's disease. Cut surface of mesenteric lymph nodes massively involved by Whipple's disease.
Whipple Disease Jejunal mucosa in Whipple's disease. The lamina propria is packed with histiocytes and empty round spaces. The latter contained lipid material that has been extracted during tissue processing.
Celiac Disease Whipple Disease Characteristic Clinical Autoimmune: Abs vs gliadin Female dominant; usually begins in infancy Primarily involves  duodenum & jejunum Flattened villi Hyperplastic glands w/ chronic inflammation Strong association with dermatitis herpetiformis (autoimmune vesicular disease) May produce T-cell  lymphoma of stomach and/or small intestines Restrict or eliminate gluten from diet Best screening test: anti- gliadin antibodies Male dominant disease Caused by  Tropheryma whippelii  bacilli (only visible by EM) Blunting of villi Foamy PAS-positive macrophages in lamina propria    obstruct lymphatics & reabsorption of chylomicrons Fever, recurrent polyarthritis, generalized LAD, increased skin pigmentation Treat with antibiotics
Malabsorption: Tropical Sprue ,[object Object],[object Object],[object Object],[object Object],[object Object]
Tropical sprue showing lymphoplasmacytic infiltrate and villous blunting
Malabsorption: Lactase Deficiency ,[object Object],[object Object],[object Object],[object Object],[object Object]
Malabsorption: Lactase Deficiency ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diarrhea ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diarrhea ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diarrhea ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diarrhea ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Cholera Cholera Toxin B subunit A subunit Binds GM1 ganglioside (surface of epithelial cells) Carried to ER (retrograde transport) Endocytosis  Reduced by protein disulfide isomerase in ER Cytosol  Unfolding  Refolding  Interact with cytosolic ADP ribosylation factors Activate G protein Stimulate adenylate cyclase Inc. cAMP Open CFTR Cl released in lumen; secretion of HCO 3  , Na +  & water MASSIVE DIARRHEA
Infectious Enterocolitis: Shigellosis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Shigellosis MOT M (microfold) cells Intracellular proliferation Escape into lamina propria Phagocytosed by macrophages Induce apoptosis and inflammation
Infectious Enterocolitis: Shigellosis ,[object Object],[object Object],[object Object]
Infectious Enterocolitis: Shigellosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Salmonellosis ,[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Salmonellosis Salmonella  Virulence genes Encode type III secretion system Transfer of bacterial proteins into M cells and enterocytes Activation of host cell Rho GTPases (+) actin rearrangement and bacterial uptake Bacterial growth within phagocytes
Infectious Enterocolitis: Salmonellosis Salmonella  Induce epithelial release of eicosanoid hepoxilin A3 Attract neutrophils into intestinal lumen Mucosal damage
Infectious Enterocolitis: Salmonellosis Salmonella  Flagellin  Activation of TLR4 in host cells Bacterial LPS Acute Inflammation +  ulceration PG synthesis Enterotoxins  Cytokines  Activation of adenyl cyclase Inc. cAMP Fluid production (SI and LI) DIARRHEA
Infectious Enterocolitis: Typhoid Fever Salmonella typhi  Small intestines Engulfed by mononuclear cells in underlying lymphoid tissue M cells Blood and lymphatic dissemination Reactive hyperplasia of phagocytes and lymphoid tissue
Infectious Enterocolitis: Typhoid Fever ,[object Object],[object Object],[object Object]
Infectious Enterocolitis: Typhoid Fever Seen here: Salmonella, isolated from infected macrophages. (Mildly color-enhanced.)
Infectious Enterocolitis: Typhoid Fever ,[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Typhoid Fever Histopathology of a lymph node in a case of Typhoid Fever. Typhoid nodules (microgranulomas) in ileal wall.
Infectious Enterocolitis: Escherichia coli – ETEC  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Escherichia coli – EHEC  ,[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Escherichia coli – EHEC  Lethal enterohemorrhagic E. coli O-157 infection (8 y-o F). Massive and diffuse hemorrhage in the autopsied colon (gross findings)
Infectious Enterocolitis: Escherichia coli – EHEC  Lethal enterohemorrhagic E. coli O-157 infection (8 y-o F). Marked hemorrhagic destruction of the autopsied colonic mucosa (HE)
Infectious Enterocolitis: Escherichia coli – EIEC  ,[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Escherichia coli – EAEC  ,[object Object],[object Object],[object Object],[object Object],[object Object]
Infectious Enterocolitis: Escherichia coli – EAEC  Numbers of rods attached to the crypt epithelium in the region of active inflammation (HE, high power) Numbers of rods attached to the crypt epithelium (HE, oil immersion)
Pseudomembranous Colitis ,[object Object],[object Object],[object Object]
Pseudomembranous Colitis Antibiotic intake Disruption of normal colonic flora Overgrowth of  C. difficile Toxin release Ribosylation of small GTPAses (Rho) Disruption of epithelial cytoskeleton Tight junction barrier loss Cytokine release Apoptosis
Pseudomembranous Colitis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Pseudomembranous Colitis There are multiple, discrete white plaques of purulent exudate on the mucosal surface. The patient was taking ampicillin. (Courtesy of Dr. RA Cooke, Brisbane, Australia; from Cooke RA, Stewart B: Colour Atlas of Anatomical Pathology. Edinburgh, Churchill Livingstone, 2004).
Pseudomembranous Colitis Fully developed pseudomembrane
Pseudomembranous Colitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral Gastroenteritis: Norovirus ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral Gastroenteritis: Rotavirus ,[object Object],[object Object],[object Object]
Viral Gastroenteritis: Rotavirus Marked infiltration of lymphoid cells both in the lamina propria and within the surface epithelium (HE)
Irritable Bowel Syndrome (IBS) ,[object Object],[object Object],[object Object],[object Object],[object Object]
Irritable Bowel Syndrome (IBS) ,[object Object],[object Object],[object Object],[object Object]
Inflammatory Bowel Disease: UC and CD ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Fever Ulcerative colitis Crohn’s disease Epidemiology Whites > black Americans No sex predilection Young adults Whites > black Americans; Jews > non-Jews Women > men Young adults Extent Mucosal & submucosal Transmural Location Mainly rectum Extends continuously into left colon (may involve entire colon) Does not involve other  areas of GIT 30% - terminal ileum alone 50% - ileum and colon 20% - colon alone Involves other areas of GIT (mouth to anus) Gross feature Bowel region Distribution Stricture Wall appearance Colon only Diffuse  Rare Thin  Ileum  +  colon Skip lesions Yes Thick
Fever Ulcerative colitis Crohn’s disease Microscopic Inflammation Pseudopolyps Ulcers Lymphoid rxn Fibrosis Serositis Granulomas Fistula/sinus Limited to mucosa Marked Superficial, broad-based Moderate Mild to none Mild to none No No  Transmural Moderate Deep, knife-like Marked Marked Marked Yes (~35%) Yes  Clinical findings Perianal fistula Malabsorption Malignant potential Recurrence after surgery Toxic megacolon No No Yes No Yes Yes (in colonic disease) Yes With pancolitis, early age onset, duration > 10  years Common No  Radiography “ Lead pipe” appearance in chronic disease “ String” sign in terminal ileum from luminal narrowing by inflam-mation, fistulas
Ulcerative colitis.  Chronic form, showing mucosal ulceration with residual foci of elevated and hyperemic mucosa. Ulcerative colitis.  Acute form with marked hyperemia.
Pseudopolyps in ulcerative colitis.
 
Gross appearance of Crohn's disease. Note the segmental nature of the inflammation, and rigidity of the wall, and flattening of the mucosa are characteristic. So-called ‘aphthous ulcers’, an early feature of Crohn's disease.
Gross appearance of Crohn's disease.  Example of cobblestone appearance.
Whole mount specimen of Crohn's disease showing transmural inflammation with predominance of the inflammation in the mucosa and submucosa. Crohn's disease showing marked inflammatory changes and the formation of a fissure.
Inflammatory Bowel Disease: Diverticulitis ,[object Object],[object Object],[object Object]
Inflammatory Bowel Disease: Diverticulitis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Acute inflammatory infiltrates near the base of the diverticulum Acute diverticulitis
Small and Large Bowel Polyps ,[object Object],[object Object],[object Object]
 
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gross appearance of inflammatory fibroid polyp. Inflammatory fibroid polyp showing myofibroblast-like cells, eosinophils, and other inflammatory cells in a sclerotic background.
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Juvenile polyposis. The markedly hyperemic quality is a characteristic feature of these lesions. Whole-mount view of a juvenile (retention) polyp.
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Duodenal polyp in a Peutz-Jeghers syndrome patient. Medium power microscopic view of a PJS-type jejunal polyp with pseudo-invasion. Arrows indicate hamartomatous small intestine mucosa in the intestinal wall.
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gross appearance of multiple hyperplastic polyps. The lesions are characteristically small, sessile, and pale. Microscopic appearance of hyperplastic polyp. The individual glands show a typical serration of their mid portion.
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object]
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
A small adenomatous polyp (tubular adenoma) is seen here. This lesion is called a "tubular adenoma" because of the rounded nature of the neoplastic glands that form it. It has smooth surfaces and is discreet. Such lesions are common in adults. Small ones are virtually always benign. Those larger than 2 cm carry a much greater risk for development of a carcinoma, having collected mutations in APC, DCC, K-ras, and p53 genes over the years.
A microscopic comparison of normal colonic mucosa on the left and that of an adenomatous polyp (tubular adenoma) on the right is seen here. The neoplastic glands are more irregular with darker (hyperchromatic) and more crowded nuclei. This neoplasm is benign and well-differentiated, as it still closely resembles the normal colonic structure.
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Tubulovillous adenoma
Small and Large Bowel Polyps: Types ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gross appearance of villous adenoma. The lesion is characteristically large and flat and has an arborescent architecture. Low-power microscopic appearance of villous adenoma. Long villi are arranged in parallel, perpendicularly to the mucosa.
Familial Syndromes ,[object Object],[object Object],[object Object],[object Object],[object Object]
Familial Syndromes ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Familial polyposis The colon is covered in a carpet of adenomatous polyps.
Familial Syndromes ,[object Object],[object Object],[object Object],[object Object],[object Object]
Small Bowel Malignancy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
This low power section shows the typical histologic appearance of a submucosal carcinoid tumor. Histologically, carcinoids typically grow as multiple solid nests of tumor cells.
Colon Cancer ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
The malignant transformation is evident through different grades of cellular alterations (dysplasia).
Colon Cancer ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Colon Cancer ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
Colon Cancer ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Colon Cancer ,[object Object],[object Object],[object Object],[object Object],[object Object]
Duke’s Staging:  Stage A tumors  - limited to the wall (not extending beyond muscularis propria),  stage B  - extending through the wall (into subserosa and/or serosa, or extra-rectal tissues), and  stage C  - those having lymph node metastasis (C1 when only perirectal nodes were positive and C2 when nodes at the point of mesenteric blood vessel ligature, called apical nodes, were involved.
Astler-Coller Staging:  The original scheme had five stages,  A  was limited to the mucosa,  B1  involved muscularis propria but did not penetrate it,  B2  penetrated the muscularis propria, and  C1 and C2  were counterparts of B1 and B2 with nodal metastases. Since then, later modifications have added three more stages.  B3  represents involvement of adjacent structures,  C3  is B3 with nodal metastasis, and  D  signifies presence of distant metastasis. 6
 
Acute Appendicitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute Appendicitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute Appendicitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Swollen appendix due to acute appendicitis
 
Signs and Symptoms of Anorectal Disease ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Internal hemorrhoids ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
External hemorrhoids ,[object Object],[object Object]
Anal Carcinoma ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Gross appearance of carcinoma of anal canal. The tumor involves the dentate line and is exophytic with a central ulceration.
Invasive well-differentiated squamous cell carcinoma of the anal canal. Low-power view of basaloid carcinoma of the anal canal.

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Gastrointestinal disorders 2

  • 1. GASTROINTESTINAL DISORDERS Fe A. Bartolome, MD, FPASMAP Department of Pathology Our Lady of Fatima University
  • 2.
  • 3.
  • 4.
  • 5.
  • 6. Meckel Diverticulum The specimen is a portion of small intestine with a diverticulum protruding out 25 mm in length.
  • 7. Meckel Diverticulum Meckel diverticulum. Photomicrograph (original magnification, ×16; hematoxylin-eosin [H-E] stain) shows the diverticulum composed of all layers of the intestinal wall. Normal small intestinal mucosa and a focus of gastric mucosa (arrow) line the diverticulum.
  • 8.
  • 9.
  • 10. Extensive diverticulosis of sigmoid colon with segmentation and shortening of bowel. Openings of diverticula can be clearly seen. Circular muscle is thick and corrugated.
  • 11. Whole mount of colon with diverticular disease. Whole-mount view of colonic diverticulosis. One of the diverticula shows marked chronic peridiverticulitis. Note hypertrophy of the muscle wall.
  • 12.
  • 14.
  • 15.
  • 16. Hirschsprung Disease Gross specimen of Hirschsprung's disease. The proximally dilated segment of bowel has been resected. Colonic mucosa stained for acetylcholinesterase from a patient with Hirschsprung's disease. There is a marked increase in the number of nerve fibers in the lamina propria.
  • 17.
  • 18.
  • 19.
  • 20.  
  • 21.
  • 22. Route of a direct hernia. The hernia sac passes directly through Hesselbach's triangle and may disrupt the floor of the inguinal canal.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27. Umbilical hernia exacerbated by refractory ascites. Advanced liver disease precluded operative repair in this case.
  • 28.
  • 29.
  • 30.  
  • 31. Incarcerated umbilical hernia Strangulated inguinal hernia
  • 32.
  • 33.  
  • 34.
  • 35. A volvulus is a twisting of the bowel on itself. It is one cause of intestinal obstruction.
  • 36.
  • 37.  
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
  • 43.
  • 44.
  • 45.
  • 46.
  • 47.
  • 48.
  • 49.  
  • 50.  
  • 51.  
  • 52.
  • 53.
  • 54.
  • 55. Ischemic colitis. The lesion is typically located in the splenic flexure. The mucosa is markedly hyperemic and covered by a fibrinopurulent exudate. Ischemic colitis with hyalinized lamina propria and gland dropout
  • 56.
  • 57. Autopsy of infant showing abdominal distension, intestinal necrosis and hemorrhage, and peritonitis due to perforation.
  • 58. Necrotizing enterocolitis. Gross appearance. The mucosa is necrotic. Numerous small gas-filled cysts are present in the wall. Low-power microscopic appearance showing extensive ulceration, necrosis, and hemorrhage.
  • 59.
  • 60. An angiodysplasia in the cecum, explaining the patients iron deficiency anaemia
  • 61.
  • 62.
  • 63.
  • 64. Malabsorption: Cystic Fibrosis Absent epithelial cystic fibrosis transmembrane conductance regulator Defective intestinal chloride ion secretion Impaired bicarbonate, sodium, and water secretion Defective luminal hydration Formation of intraductal concretions in pancreatic ducts Exocrine pancreatic insufficiency Failure of intraluminal phase of nutrient absorption
  • 65.
  • 66. Malabsorption: Celiac Disease Some gliadin peptides Induce epithelial cell expression of IL-15 Activation and proliferation of NKG2D+ CD8+ intra-epithelial T lymphocytes No recognition of gliadin Cross the epithelium Deaminated by tissue trans-glutaminase Interact with HLA-DQ2 or HLA-DQ8 on APCs Presented to CD4+ T cells (+) Immune reaction
  • 67.
  • 68. This is an endoscopic biopsy of celiac disease that shows total crypt hyperplastic villous atrophy with complete flattening of the mucosal surface.  Note the intense lymphoplasmacytic inflammation in the lamina propria.
  • 69. The surface epithelium of this biopsy contains numerous intraepithelial lymphocytes.
  • 70.
  • 71.
  • 72.
  • 73.
  • 75.
  • 76.
  • 77.
  • 78. Whipple Disease Outer aspect of mesenteric lymph nodes massively involved by Whipple's disease. Cut surface of mesenteric lymph nodes massively involved by Whipple's disease.
  • 79. Whipple Disease Jejunal mucosa in Whipple's disease. The lamina propria is packed with histiocytes and empty round spaces. The latter contained lipid material that has been extracted during tissue processing.
  • 80. Celiac Disease Whipple Disease Characteristic Clinical Autoimmune: Abs vs gliadin Female dominant; usually begins in infancy Primarily involves duodenum & jejunum Flattened villi Hyperplastic glands w/ chronic inflammation Strong association with dermatitis herpetiformis (autoimmune vesicular disease) May produce T-cell lymphoma of stomach and/or small intestines Restrict or eliminate gluten from diet Best screening test: anti- gliadin antibodies Male dominant disease Caused by Tropheryma whippelii bacilli (only visible by EM) Blunting of villi Foamy PAS-positive macrophages in lamina propria  obstruct lymphatics & reabsorption of chylomicrons Fever, recurrent polyarthritis, generalized LAD, increased skin pigmentation Treat with antibiotics
  • 81.
  • 82. Tropical sprue showing lymphoplasmacytic infiltrate and villous blunting
  • 83.
  • 84.
  • 85.
  • 86.
  • 87.
  • 88.
  • 89.
  • 90. Infectious Enterocolitis: Cholera Cholera Toxin B subunit A subunit Binds GM1 ganglioside (surface of epithelial cells) Carried to ER (retrograde transport) Endocytosis Reduced by protein disulfide isomerase in ER Cytosol Unfolding Refolding Interact with cytosolic ADP ribosylation factors Activate G protein Stimulate adenylate cyclase Inc. cAMP Open CFTR Cl released in lumen; secretion of HCO 3 , Na + & water MASSIVE DIARRHEA
  • 91.
  • 92. Infectious Enterocolitis: Shigellosis MOT M (microfold) cells Intracellular proliferation Escape into lamina propria Phagocytosed by macrophages Induce apoptosis and inflammation
  • 93.
  • 94.
  • 95.
  • 96. Infectious Enterocolitis: Salmonellosis Salmonella Virulence genes Encode type III secretion system Transfer of bacterial proteins into M cells and enterocytes Activation of host cell Rho GTPases (+) actin rearrangement and bacterial uptake Bacterial growth within phagocytes
  • 97. Infectious Enterocolitis: Salmonellosis Salmonella Induce epithelial release of eicosanoid hepoxilin A3 Attract neutrophils into intestinal lumen Mucosal damage
  • 98. Infectious Enterocolitis: Salmonellosis Salmonella Flagellin Activation of TLR4 in host cells Bacterial LPS Acute Inflammation + ulceration PG synthesis Enterotoxins Cytokines Activation of adenyl cyclase Inc. cAMP Fluid production (SI and LI) DIARRHEA
  • 99. Infectious Enterocolitis: Typhoid Fever Salmonella typhi Small intestines Engulfed by mononuclear cells in underlying lymphoid tissue M cells Blood and lymphatic dissemination Reactive hyperplasia of phagocytes and lymphoid tissue
  • 100.
  • 101. Infectious Enterocolitis: Typhoid Fever Seen here: Salmonella, isolated from infected macrophages. (Mildly color-enhanced.)
  • 102.
  • 103. Infectious Enterocolitis: Typhoid Fever Histopathology of a lymph node in a case of Typhoid Fever. Typhoid nodules (microgranulomas) in ileal wall.
  • 104.
  • 105.
  • 106. Infectious Enterocolitis: Escherichia coli – EHEC Lethal enterohemorrhagic E. coli O-157 infection (8 y-o F). Massive and diffuse hemorrhage in the autopsied colon (gross findings)
  • 107. Infectious Enterocolitis: Escherichia coli – EHEC Lethal enterohemorrhagic E. coli O-157 infection (8 y-o F). Marked hemorrhagic destruction of the autopsied colonic mucosa (HE)
  • 108.
  • 109.
  • 110. Infectious Enterocolitis: Escherichia coli – EAEC Numbers of rods attached to the crypt epithelium in the region of active inflammation (HE, high power) Numbers of rods attached to the crypt epithelium (HE, oil immersion)
  • 111.
  • 112. Pseudomembranous Colitis Antibiotic intake Disruption of normal colonic flora Overgrowth of C. difficile Toxin release Ribosylation of small GTPAses (Rho) Disruption of epithelial cytoskeleton Tight junction barrier loss Cytokine release Apoptosis
  • 113.
  • 114. Pseudomembranous Colitis There are multiple, discrete white plaques of purulent exudate on the mucosal surface. The patient was taking ampicillin. (Courtesy of Dr. RA Cooke, Brisbane, Australia; from Cooke RA, Stewart B: Colour Atlas of Anatomical Pathology. Edinburgh, Churchill Livingstone, 2004).
  • 115. Pseudomembranous Colitis Fully developed pseudomembrane
  • 116.
  • 117.
  • 118.
  • 119. Viral Gastroenteritis: Rotavirus Marked infiltration of lymphoid cells both in the lamina propria and within the surface epithelium (HE)
  • 120.
  • 121.
  • 122.
  • 123. Fever Ulcerative colitis Crohn’s disease Epidemiology Whites > black Americans No sex predilection Young adults Whites > black Americans; Jews > non-Jews Women > men Young adults Extent Mucosal & submucosal Transmural Location Mainly rectum Extends continuously into left colon (may involve entire colon) Does not involve other areas of GIT 30% - terminal ileum alone 50% - ileum and colon 20% - colon alone Involves other areas of GIT (mouth to anus) Gross feature Bowel region Distribution Stricture Wall appearance Colon only Diffuse Rare Thin Ileum + colon Skip lesions Yes Thick
  • 124. Fever Ulcerative colitis Crohn’s disease Microscopic Inflammation Pseudopolyps Ulcers Lymphoid rxn Fibrosis Serositis Granulomas Fistula/sinus Limited to mucosa Marked Superficial, broad-based Moderate Mild to none Mild to none No No Transmural Moderate Deep, knife-like Marked Marked Marked Yes (~35%) Yes Clinical findings Perianal fistula Malabsorption Malignant potential Recurrence after surgery Toxic megacolon No No Yes No Yes Yes (in colonic disease) Yes With pancolitis, early age onset, duration > 10 years Common No Radiography “ Lead pipe” appearance in chronic disease “ String” sign in terminal ileum from luminal narrowing by inflam-mation, fistulas
  • 125. Ulcerative colitis. Chronic form, showing mucosal ulceration with residual foci of elevated and hyperemic mucosa. Ulcerative colitis. Acute form with marked hyperemia.
  • 127.  
  • 128. Gross appearance of Crohn's disease. Note the segmental nature of the inflammation, and rigidity of the wall, and flattening of the mucosa are characteristic. So-called ‘aphthous ulcers’, an early feature of Crohn's disease.
  • 129. Gross appearance of Crohn's disease. Example of cobblestone appearance.
  • 130. Whole mount specimen of Crohn's disease showing transmural inflammation with predominance of the inflammation in the mucosa and submucosa. Crohn's disease showing marked inflammatory changes and the formation of a fissure.
  • 131.
  • 132.
  • 133. Acute inflammatory infiltrates near the base of the diverticulum Acute diverticulitis
  • 134.
  • 135.  
  • 136.
  • 137. Gross appearance of inflammatory fibroid polyp. Inflammatory fibroid polyp showing myofibroblast-like cells, eosinophils, and other inflammatory cells in a sclerotic background.
  • 138.
  • 139.
  • 140.
  • 141. Juvenile polyposis. The markedly hyperemic quality is a characteristic feature of these lesions. Whole-mount view of a juvenile (retention) polyp.
  • 142.
  • 143. Duodenal polyp in a Peutz-Jeghers syndrome patient. Medium power microscopic view of a PJS-type jejunal polyp with pseudo-invasion. Arrows indicate hamartomatous small intestine mucosa in the intestinal wall.
  • 144.
  • 145. Gross appearance of multiple hyperplastic polyps. The lesions are characteristically small, sessile, and pale. Microscopic appearance of hyperplastic polyp. The individual glands show a typical serration of their mid portion.
  • 146.
  • 147.
  • 148.
  • 149. A small adenomatous polyp (tubular adenoma) is seen here. This lesion is called a "tubular adenoma" because of the rounded nature of the neoplastic glands that form it. It has smooth surfaces and is discreet. Such lesions are common in adults. Small ones are virtually always benign. Those larger than 2 cm carry a much greater risk for development of a carcinoma, having collected mutations in APC, DCC, K-ras, and p53 genes over the years.
  • 150. A microscopic comparison of normal colonic mucosa on the left and that of an adenomatous polyp (tubular adenoma) on the right is seen here. The neoplastic glands are more irregular with darker (hyperchromatic) and more crowded nuclei. This neoplasm is benign and well-differentiated, as it still closely resembles the normal colonic structure.
  • 151.
  • 153.
  • 154. Gross appearance of villous adenoma. The lesion is characteristically large and flat and has an arborescent architecture. Low-power microscopic appearance of villous adenoma. Long villi are arranged in parallel, perpendicularly to the mucosa.
  • 155.
  • 156.
  • 157. Familial polyposis The colon is covered in a carpet of adenomatous polyps.
  • 158.
  • 159.
  • 160.  
  • 161. This low power section shows the typical histologic appearance of a submucosal carcinoid tumor. Histologically, carcinoids typically grow as multiple solid nests of tumor cells.
  • 162.
  • 163.  
  • 164. The malignant transformation is evident through different grades of cellular alterations (dysplasia).
  • 165.
  • 166.
  • 167.  
  • 168.  
  • 169.
  • 170.  
  • 171.
  • 172. Duke’s Staging: Stage A tumors - limited to the wall (not extending beyond muscularis propria), stage B - extending through the wall (into subserosa and/or serosa, or extra-rectal tissues), and stage C - those having lymph node metastasis (C1 when only perirectal nodes were positive and C2 when nodes at the point of mesenteric blood vessel ligature, called apical nodes, were involved.
  • 173. Astler-Coller Staging: The original scheme had five stages, A was limited to the mucosa, B1 involved muscularis propria but did not penetrate it, B2 penetrated the muscularis propria, and C1 and C2 were counterparts of B1 and B2 with nodal metastases. Since then, later modifications have added three more stages. B3 represents involvement of adjacent structures, C3 is B3 with nodal metastasis, and D signifies presence of distant metastasis. 6
  • 174.  
  • 175.
  • 176.
  • 177.
  • 178. Swollen appendix due to acute appendicitis
  • 179.  
  • 180.
  • 181.
  • 182.  
  • 183.
  • 184.
  • 185. Gross appearance of carcinoma of anal canal. The tumor involves the dentate line and is exophytic with a central ulceration.
  • 186. Invasive well-differentiated squamous cell carcinoma of the anal canal. Low-power view of basaloid carcinoma of the anal canal.