The Oral Cavity And Gastrointestinal System June 08 Xition

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  • The Oral Cavity And Gastrointestinal System June 08 Xition

    1. 1. Karl Robstad, M.D. Pathology Department
    2. 2. Ulcerative and inflammatory lesions Disease associated with systemic infection Pre-cancerous lesions and malignancy
    3. 3. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Aphthous Ulcers (Canker Sore) </li></ul><ul><ul><li>Superficial ulcerations of the oral mucosa (< 5 mm) covered by a gray/white exudate, with an erythematous rim </li></ul></ul><ul><ul><li>Can be single or multiple </li></ul></ul><ul><ul><li>40 % of population affected </li></ul></ul><ul><ul><li>Common in first two decades of life </li></ul></ul>
    4. 4. The Oral Cavity: Ulcerative and Inflammatory Lesions
    5. 5. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Herpes Simplex Virus 1: </li></ul><ul><li>Groups of small vesicles (1-3 mm) on lips, buccal mucosa, and around nasal orifices </li></ul>
    6. 6. The Oral Cavity: Ulcerative and Inflammatory Lesions Intercellular Edema
    7. 7. The Oral Cavity: Ulcerative and Inflammatory Lesions Eosinophilic intranuclear viral inclusions forming mulitnucleated polykaryons Tzanck prep is the diagnostic stain of choice
    8. 8. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Initial infection : may take 3- 4 weeks to clear up entirely. Virus hangs out in the local ganglia (Trigeminal, etc) until…. </li></ul><ul><li>Reactivation of infection : usually lasts 6- 10 days. Triggers include upper respiratory infections, sunlight, cold weather, allergies, stress. </li></ul><ul><li>Acute gingivostomatitis : severe form with diffuse involvement of oropharyngeal mucosa occurring in children. </li></ul>
    9. 9. The Oral Cavity: Ulcerative and Inflammatory Lesions
    10. 10. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Oral Candidiasis (Thrush): </li></ul><ul><ul><li>Superficial curd-like plaque/membrane on mucous membranes </li></ul></ul>
    11. 11. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Oral Candidiasis : Population affected </li></ul><ul><ul><li>Immunocompromised individuals especially HIV/AIDS patients </li></ul></ul><ul><ul><li>Diabetics </li></ul></ul><ul><ul><li>Patients with malignancy </li></ul></ul><ul><ul><li>Immunosuppressed individuals </li></ul></ul>
    12. 12. The Oral Cavity: Ulcerative and Inflammatory Lesions <ul><li>Oral Candidiasis: Histolopathology: </li></ul><ul><ul><li>Plaque consists of a fibrinosuppurative exudate containing enmeshed Candida organisms </li></ul></ul>
    13. 13. The Oral Cavity: Diseases Associated with Systemic Infection <ul><li>Kaposi’s Sarcoma: </li></ul><ul><li>Multifocal systemic disease characterized by purpuric discolorations or violaceous raised nodular masses. </li></ul>
    14. 14. The Oral Cavity: Diseases Associated with Systemic Infection <ul><li>Kaposi’s Sarcoma: </li></ul><ul><li>Histology: </li></ul><ul><ul><li>Dilated irregular blood vessels lined by endothelial cells. Surrounding infiltrate of macrophages, lymphocytes, plasma cells. </li></ul></ul>
    15. 15. The Oral Cavity: Precancerous Lesions <ul><li>Leukoplakia: </li></ul><ul><li>White well-defined plaque/patch on mucous membranes secondary to epidermal thickening or hyperkeratosis </li></ul><ul><li>CANNOT be removed by scraping </li></ul>
    16. 16. The Oral Cavity: Leukoplakia
    17. 17. The Oral Cavity: Precancerous lesions <ul><li>Leukoplakia: </li></ul><ul><li>Occurs twice as often in men, ages 40-70 years </li></ul><ul><li>STRONGLY associated with tobacco use (smoking and smokeless) </li></ul><ul><li>3-6 % transform into malignancy </li></ul>
    18. 18. The Oral Cavity: Precancerous Lesions <ul><li>Erythroplakia: </li></ul><ul><li>Red velvety granular area on mucosa that is AT LEVEL with the surrounding mucosa </li></ul><ul><li>Marked dysplasia is evident </li></ul><ul><li>50 % transform into malignancy </li></ul>
    19. 19. The Oral Cavity: Erythroplakia
    20. 20. The Oral Cavity: Neoplasms <ul><li>Squamous Cell Carcinoma: </li></ul><ul><li>Comprises 95 % of oral cancers and 3 % of ALL cancers </li></ul><ul><li>Risk Factors: </li></ul><ul><ul><li>Leukoplakia/erythroplakia </li></ul></ul><ul><ul><li>Tobacco use </li></ul></ul><ul><ul><li>EtOH abuse </li></ul></ul><ul><ul><li>HPV 16, 18, 33 </li></ul></ul>
    21. 21. The Oral Cavity: Squamous Cell Carcinoma <ul><li>Raised, pearly plaques or irregular verrucous areas of mucosal thickening </li></ul>
    22. 22. The Oral Cavity: Squamous Cell Carcinoma <ul><li>Variable histology: In situ components, keratinizing areas, anaplastic, and invasive/infiltrating areas. </li></ul>
    23. 23. The Oral Cavity <ul><li>Squamous Cell Carcinoma: </li></ul><ul><li>Prognosis: </li></ul><ul><ul><li>Lip lesions have 90 % 5 year survival rate </li></ul></ul><ul><ul><li>Floor of mouth lesions have a 20-30 % 5 year survival rate </li></ul></ul>
    24. 24. The Oral Cavity : Salivary Gland Disease <ul><li>Salivary Gland Inflammation (Sialadenitis): </li></ul><ul><li>Causes: </li></ul><ul><ul><li>Bacterial– related to sialolithiasis and usually due to S. aureus or S. viridans </li></ul></ul><ul><ul><li>Viral-- usually caused by paramyxovirus (e.g. mumps) </li></ul></ul><ul><ul><li>Autoimmune-- seen in Sjogren’s syndrome (associated with xerostoma, keratoconjunctivitis sicca) </li></ul></ul>
    25. 25. The Oral Cavity: Sialadenitis
    26. 26. The Oral Cavity: Salivary Gland Neoplasms
    27. 27. The Oral Cavity: Salivary Gland Neoplasms <ul><li>Benign Neoplasms: </li></ul><ul><li>Pleomorphic Adenoma </li></ul><ul><li>Warthin tumor </li></ul>Pleomorphic Adenoma
    28. 28. The Oral Cavity: Salivary Gland Neoplasms <ul><li>Pleomorphic Adenoma (mixed tumor): </li></ul><ul><li>90 % of all benign salivary gland tumors </li></ul><ul><li>Superficial parotid </li></ul><ul><li>Can undergo malignant transformation (Carcinoma ex pleomorphic adenoma) </li></ul>
    29. 29. The Oral Cavity: Salivary Gland Neoplasms (Benign) <ul><li>Pleomorphic Adenoma: </li></ul><ul><li>Epithelial and myxoid connective tissue stroma. </li></ul><ul><li>May contain bone or chondroid elements. </li></ul><ul><li>Well demarcated from normal gland </li></ul>
    30. 30. The Oral Cavity: Carcinoma ex Pleomorphic Adenoma
    31. 31. The Oral Cavity: Salivary Gland Neoplasms (Benign) <ul><li>Warthin Tumor (Papillary cystadenoma lymphomatosum): </li></ul><ul><li>Round encapsulated masses in the superficial parotid gland </li></ul><ul><li>Often bilateral </li></ul><ul><li>Always benign </li></ul>
    32. 32. The Oral Cavity : Warthin Tumor <ul><li>Cystic spaces lined by double layer of epithelial cells, resting on a dense lymphoid stroma </li></ul><ul><li>Epithelial columnar cells are palisading and have abundant granular cytoplasm </li></ul>
    33. 33. The Oral Cavity: Salivary Gland Neoplasms (Malignant) <ul><li>Mucoepidermoid Carcinoma: </li></ul><ul><li>15 % of all salivary gland tumors and the most common malignant one </li></ul><ul><li>Parotid gland most common site </li></ul><ul><li>Well-circumscribed, encapsulated mass </li></ul>
    34. 34. The Oral Cavity: Salivary Gland Neoplasms (Malignant) <ul><li>Mucoepidermoid Carcinoma: </li></ul><ul><li>Cords, sheets and cystic arrangement of squamous cells, mucous cells, or intermediate cells </li></ul><ul><li>Low grade tumors have more mucoid elements and high grade tumors have more squamous elements. </li></ul>
    35. 35. The Oral Cavity: Salivary Gland Neoplasms (Malignant)
    36. 38. The Upper GI Tract: Esophagus <ul><li>Normal Esophagus: </li></ul><ul><li>Averages 23-25 cm in length in adults </li></ul>
    37. 39. The Upper GI Tract: Esophagus Congenital Anomalies <ul><li>Atresia and tracheoesophageal fistula </li></ul><ul><li>Stenosis </li></ul><ul><li>Webs, rings </li></ul><ul><li>Diverticula </li></ul>
    38. 40. The Upper GI Tract: Esophagus <ul><li>Atresia and TE fistulas: </li></ul>
    39. 41. The Upper GI Tract: Esophagus Atresia and Tracheoesophageal Fistulas
    40. 42. The Upper GI Tract: Esophagus Congenital Anomalies <ul><li>Stenosis: fibrous </li></ul><ul><li>thickening </li></ul><ul><li>of esophageal wall, </li></ul><ul><li>especially submucosa </li></ul>
    41. 43. The Upper GI Tract: Esophagus Congenital Anomalies <ul><li>Mucosal Webs and Rings: </li></ul><ul><li>Ledgelike protrusions of the mucosa into the lumen of the esophagus. </li></ul>Distal Proximal
    42. 44. The Upper GI Tract: Esophagus Congenital Anomalies <ul><li>Diverticula: outpouchings of the GI tract that contain all visceral layers </li></ul>Epiphrenic: Immediately above LES
    43. 45. The Upper GI Tract: Esophagus Motor Disorders <ul><li>Achalasia: failure of the LES to relax, aperistalsis, and increased LES tone </li></ul><ul><ul><li>Results in progressive dilation of the esophagus above the LES </li></ul></ul><ul><ul><li>SCCA occurs in 5 % </li></ul></ul><ul><ul><li>of these patients </li></ul></ul>
    44. 46. The Upper GI Tract: Esophagus Motor Disorders <ul><li>Hiatal hernias : </li></ul><ul><li>Sliding </li></ul><ul><li>Paraesophageal (rolling) </li></ul>
    45. 47. The Upper GI Tract: Esophagus Motor Disorders <ul><li>Sliding Hiatal Hernia: </li></ul><ul><li>90 % of cases </li></ul><ul><li>Stomach pulled through diaphragm </li></ul><ul><li>No vascular compression </li></ul><ul><li>Can lead to chronic reflux esophagitis </li></ul>
    46. 48. The Upper GI Tract: Esophagus Motor Disorders <ul><li>Paraesophageal Hernia: </li></ul><ul><li>10 % of cases </li></ul><ul><li>Gastric fundus supply may be compromised </li></ul><ul><li>May see ischemia and perforation of herniated portion </li></ul><ul><li>Immediate surgical intervention </li></ul>
    47. 49. The Upper GI Tract: Esophagus <ul><li>Mallory Weiss Syndrome (lacerations): </li></ul><ul><li>Longitudinal tears at the GE junction </li></ul><ul><li>Secondary to severe retching (alcoholics) </li></ul><ul><li>May lead to significant upper GI bleed </li></ul>
    48. 50. The Upper GI Tract: Esophagus <ul><li>Esophageal Varices: </li></ul><ul><li>Natural point of communication between portal and systemic circulation </li></ul><ul><li>Veins become dilated and tortuous from long term portal hypertension (related to cirrhosis) </li></ul>
    49. 51. The Upper GI Tract: Esophagus Esophagitis <ul><li>Esophagitis: Inflammation of the esophageal mucosa </li></ul><ul><li>Reflux symptoms occur monthly in up to 44% of Americans. </li></ul><ul><li>GERD found on 23% of endoscopies. </li></ul><ul><li>Reflux esophagitis diagnosed in only 0.5% of the US population. </li></ul>
    50. 52. The Upper GI Tract: Esophagus <ul><li>Esophagitis: Histologic Findings </li></ul>
    51. 53. The Upper GI Tract: Esophagus Barrett’s Esophagus <ul><li>Complication of long term GERD </li></ul><ul><li>“ Salmon colored” mucosa, usually around the GEJ </li></ul>
    52. 54. The Upper GI Tract: Esophagus Barrett’s Esophagus <ul><li>Normal squamous epithelium replaced by metaplastic columnar epithelium containing goblet cells </li></ul>
    53. 55. The Upper GI Tract: Esophagus Adenocarcinoma <ul><li>Barrett’s esophagus increases the risk for development of adenocarcinoma , 30-40 fold. </li></ul><ul><li>Adenocarcinoma of the esophagus occurs at the distal aspect and may involve the gastric cardia </li></ul><ul><li>Prognosis: 30 % 5 year survival rate </li></ul>
    54. 56. The Upper GI Tract: Esophagus Adenocarcinoma
    55. 57. The Upper GI Tract: Esophagus Squamous Cell Carcinoma <ul><li>90 % of esophageal cancers worldwide </li></ul><ul><li>Risk factors: Smoking and EtOH, etc </li></ul><ul><li>50 % occur in the middle 1/3 of the esophagus </li></ul>
    56. 58. The Upper GI Tract: Esophagus Squamous Cell Carcinoma <ul><li>Small, gray plaques on mucosa that may be polypoid, uclerated, or infiltrative </li></ul>
    57. 60. The Upper GI Tract: Stomach <ul><li>Normal gastric physiology: facilitates secretion of hydrochloric acid </li></ul><ul><li>Mucosal protection from the gastric acid: </li></ul><ul><ul><li>Mucus secretion </li></ul></ul><ul><ul><li>Bicarbonate secretion </li></ul></ul><ul><ul><li>Epithelial barriers </li></ul></ul><ul><ul><li>Mucosal blood flow </li></ul></ul>
    58. 61. The Upper GI Tract: Stomach Congenital Anomalies <ul><li>Pyloric stenosis: hypertrophy of the pyloric smooth muscle wall </li></ul><ul><li>Diaphragmatic hernia </li></ul><ul><li>Gastric heterotopia : gastric mucosa in areas outside the actual stomach e.g. esophagus, SI </li></ul>
    59. 62. The Upper GI Tract: Stomach Gastritis <ul><li>Gastritis: Inflammation of the gastric mucosa </li></ul>
    60. 63. The Upper GI Tract: Stomach Gastritis <ul><li>Acute Gastritis : </li></ul><ul><li>Associated with NSAIDs, smoking, EtOH, systemic infection, stress, ischemia, trauma, etc </li></ul><ul><li>Related to increased acid secretion, decreased bicarb, reduced blood flow, damage to the epithelium </li></ul>
    61. 64. The Upper GI Tract: Stomach Gastritis <ul><li>Acute Gastritis : </li></ul><ul><li>Proliferation of polys </li></ul><ul><li>in the epithelium </li></ul><ul><li>Erosion of the epithelium </li></ul><ul><li>Hemorrhage in the lamina propria </li></ul>
    62. 65. The Upper GI Tract: Stomach Chronic Gastritis <ul><li>Chronic mucosal inflammation leading to mucosal atrophy and epithelial metaplasia </li></ul>
    63. 66. The Upper GI Tract: Stomach Chronic Gastritis <ul><li>STRONG association with H. Pylori organisms (gm negative coccobacilli) </li></ul>
    64. 67. The Upper GI Tract: Stomach Chronic Gastritis <ul><li>H. Pylori gastritis: </li></ul><ul><li>Intestinal metaplasia </li></ul><ul><li>Active inflammation denoted by poly’s in the epithelial and glandular layer </li></ul><ul><li>Dysplasia in long term chronic gastritis can lead to carcinoma in situ </li></ul>
    65. 68. The Upper GI Tract: Stomach Gastritis <ul><li>Autoimmune gastritis: autoantibodies to parietal cells; decreased intrinsic factor leads to B12 deficiency and sequelae </li></ul><ul><li>Leads to mucosal atrophy and hyperplasia of the G cells in antrum (gastrin-producing cells) </li></ul>
    66. 69. The Upper GI Tract: Stomach Ulcers <ul><li>Peptic Ulcers : chronic, solitary breaches in the mucosa that extend into submucosa or deeper </li></ul><ul><ul><li>4 times more common in duodenum than stomach </li></ul></ul><ul><ul><li>Risk factors: H. pylori, NSAID use, tobacco use, steroids, Zollinger-Ellison syndrome </li></ul></ul><ul><ul><li>Complications include bleeding and perforation </li></ul></ul><ul><ul><li>Commonly recur </li></ul></ul>
    67. 70. The Upper GI Tract: Stomach Peptic Ulcers <ul><li>Zones of histologic changes: </li></ul><ul><li>Necrotic fibrinoid debris at base </li></ul><ul><li>Active nonspecific inflammation, polys predominate </li></ul><ul><li>Granulation tissue </li></ul><ul><li>Fibrous scar that fans out from the ulcer </li></ul>
    68. 71. The Upper GI Tract: Stomach Peptic Ulcers
    69. 72. The Upper GI Tract: Stomach Peptic Ulcers <ul><li>Acute Gastric Ulcers: “stress ulcers” </li></ul><ul><li>Associated with severe trauma, extensive burns, injury to the CNS, and chronic exposure to gastric irritants, sepsis </li></ul>
    70. 73. The Upper GI Tract: Stomach Neoplasms <ul><li>Gastric Polyps—nodule or mass projecting above the level of the surrounding mucosa </li></ul><ul><li>Hyperplastic (80 %) </li></ul><ul><li>Fundic gland type (10 %) </li></ul><ul><li>Adenomatous (5 %) </li></ul>
    71. 74. The Upper GI Tract: Stomach Neoplasms <ul><li>Gastric Carcinoma: </li></ul><ul><li>Common in Japan, Columbia, Costa Rica, Hungary </li></ul><ul><li>5 year survival = 20 % </li></ul><ul><li>Lesser curvature </li></ul><ul><li>Risk Factors: H. pylori, autoimmune gastritis, raw fish ingestion </li></ul>
    72. 75. The Upper GI Tract: Stomach <ul><li>Gastric Carcinomas: Two types </li></ul><ul><li>Intestinal—arises from metaplastic gastric mucous cells; often well differentiated; occurs in older population with male preponderance </li></ul><ul><li>Diffuse—arises de novo from native gastric mucous cells; usually poorly differentiated; occurs at earlier age </li></ul>
    73. 76. The Upper GI Tract: Stomach <ul><li>Gastric Carcinoma : Three macroscopic growth patterns </li></ul>Exophytic Flat Ulcerating
    74. 77. The Upper GI Tract: Stomach Neoplasms <ul><li>Gastric Carcinoma: Histology </li></ul><ul><ul><li>Intestinal variant: malignant cells forming glands resembling adenocarcinoma </li></ul></ul><ul><ul><li>Diffuse variant: gastric-type cells that penetrate the mucosa and wall as signet rings </li></ul></ul>
    75. 78. The Upper GI Tract: Stomach Neoplasms
    76. 80. The Lower GI Tract <ul><li>Normal Histology : </li></ul><ul><li>Small bowel: </li></ul><ul><ul><li>Comprised of villi and crypts lined by epithelial cells </li></ul></ul><ul><li>Large bowel: </li></ul><ul><ul><li>No villi, just tubular crypts </li></ul></ul><ul><li>Lymphoid tissue </li></ul><ul><li>Neuromuscular function (extrinsic and intrinsic) </li></ul>
    77. 81. Small Bowel Large Bowel
    78. 82. The Lower GI Tract: Congenital Anomalies <ul><li>Duplication </li></ul><ul><li>Malrotation </li></ul><ul><li>Omphalocele </li></ul><ul><li>Gastroschisis </li></ul><ul><li>Atresia/Stenosis </li></ul><ul><li>Meckel Diverticulum </li></ul><ul><li>Hirschsprung Disease </li></ul>
    79. 83. The Lower GI Tract: Congenital Anomalies <ul><li>Meckel Diverticulum : Rule of 2’s </li></ul><ul><ul><li>Failed involution of the vitelline duct </li></ul></ul><ul><ul><li>Contains all 3 layers of bowel wall—”true” </li></ul></ul>
    80. 84. The Lower GI Tract: Congenital Anomalies <ul><li>Hirschsprung’s Disease: </li></ul><ul><ul><li>Absence of ganglion cells in the large bowel leading to functional obstruction </li></ul></ul><ul><ul><li>1 in 5000 children </li></ul></ul><ul><ul><li>4:1 male predominance </li></ul></ul><ul><ul><li>Variable lengths </li></ul></ul><ul><ul><li>Complication = </li></ul></ul><ul><ul><li>MEGACOLON </li></ul></ul>
    81. 85. The Lower GI Tract: Hirschsprung’s Disease
    82. 86. The Lower GI Tract: Vascular Disorders <ul><li>Normal Vascular supply : </li></ul><ul><li>Superior mesenteric artery supplies the proximal jejunum to the proximal transverse colon </li></ul><ul><li>Inferior mesenteric artery supplies the remainder of the colon </li></ul>
    83. 87. The Lower GI Tract: Vascular Disorders <ul><li>Ischemic bowel disease: </li></ul>Major artery Hypoperfusion
    84. 88. The Lower GI Tract: Vascular Disorders <ul><li>Transmural: Hemorrhagic, edematous, necrosis of all the bowel wall layers. </li></ul><ul><li>Mural: epithelial sloughing of the villi and crypts. Acute and chronic inflammation </li></ul>
    85. 89. The Lower GI Tract: Vascular Disorders <ul><li>Ischemic Bowel Disease: </li></ul><ul><li>Chronic ischemia may lead to fibrosis of tissue due to inflammation and stricture </li></ul><ul><li>High risk of perforation—results in 50-75% death rate </li></ul>
    86. 90. The Lower GI Tract: Vascular Disorders <ul><li>Hemorrhoids: Variceal dilations of anal/perianal submucosal venous plexi </li></ul><ul><ul><li>Internal when occurring above anorectal line and covered by rectal mucosa </li></ul></ul><ul><ul><li>External when below the anorectal line, usually squamous mucosa </li></ul></ul>
    87. 92. The Lower GI Tract: Diarrheal Diseases <ul><li>Diarrhea can be characterized by and increased stool mass, stool frequency, and stool fluidity </li></ul><ul><li>Causes: Secretory, osmotic, exudative, malabsorptive </li></ul>
    88. 95. The Lower GI Tract: Enterocolitis <ul><li>Infectious Enterocolitis: </li></ul><ul><li>Causes 2.9 million deaths worldwide annually </li></ul><ul><li>Cause of 50 % of deaths in children under age 5 years </li></ul><ul><li>May be viral, bacterial, protozoal </li></ul>
    89. 96. The Lower GI Tract: Enterocolitis <ul><li>Viral enterocolitis: </li></ul><ul><li>Common causes: </li></ul><ul><ul><li>Rotavirus: children 6-24 months; watery diarrhea and vomiting for several days </li></ul></ul><ul><ul><li>Norwalk : older children and adults; 12-60 hours of watery diarrhea, vomiting, abdominal pain </li></ul></ul><ul><ul><li>Others : enteric adenoviruses, astroviruses </li></ul></ul>
    90. 97. The Lower GI Tract: Enterocolitis <ul><li>Viral enterocolitis: </li></ul><ul><li>Histologically appears as blunting of villi, and infiltration of the lamina propria by lymphocytes </li></ul>
    91. 98. The Lower GI Tract: Enterocolitis <ul><li>Bacterial Enterocolitis: </li></ul><ul><li>Organisms must adhere to the mucosa to produce disease </li></ul><ul><li>Pathogenic mechanisms: </li></ul><ul><ul><li>Ingested preformed toxin e.g. S. aureus, V. cholera </li></ul></ul><ul><ul><li>Infection by toxigenic organisms e.g. secrete polypeptides </li></ul></ul><ul><ul><li>Infection by enteroinvasive organisms e.g. EIEC, Shigella </li></ul></ul>
    92. 99. The Lower GI Tract: Enterocolitis <ul><li>Histologic changes depend on organism, but generally: </li></ul><ul><li>Damage of surface epithelium </li></ul><ul><li>Decreased epithelial maturation </li></ul><ul><li>Hyperemia and edema of lamina propria </li></ul><ul><li>Villus blunting in small bowel </li></ul><ul><li>Progression may be evidenced by erosion, ulceration and submucosal inflammation </li></ul>
    93. 100. The Lower GI Tract: Entercolitis <ul><li>Bacterial enterocolitis: </li></ul><ul><li>Clinical presentation: </li></ul><ul><ul><li>Ingested preformed toxins: sx occur in hours, with explosive diarrhea. 1 day </li></ul></ul><ul><ul><li>Enteric pathogen ingested: may take hours to days to develop; diarrhea and dehydration; 2-3 days </li></ul></ul>
    94. 101. Clostridium Enterocolitis
    95. 102. Shigella Colitis
    96. 103. The Lower GI Tract: Enterocolitis <ul><li>Necrotizing enterocolitis: </li></ul><ul><li>Acute necrotizing inflammation of small and large bowel </li></ul><ul><li>Premature neonates (2-4 days old) </li></ul><ul><li>Usually affects terminal ileum and ascending colon </li></ul><ul><li>Mucosal edema, hemorrhage and necrosis can progress to transmural changes </li></ul>
    97. 104. The Lower GI Tract: Enterocolitis <ul><li>Pseudomembranous Colitis : </li></ul><ul><li>acute colitis characterized by inflammatory exudate over the mucosal injury. </li></ul>
    98. 105. The Lower GI Tract: Enterocolitis <ul><li>Other Causes of enterocolitis: </li></ul><ul><li>Parasites and protozoa: </li></ul><ul><ul><li>Nematodes, flatworms, entamoeba histolytica, giardia lamblia </li></ul></ul><ul><li>AIDS-associated enteropathy </li></ul><ul><li>Complication of transplantation </li></ul><ul><li>Drug induced </li></ul><ul><li>Radiation enterocolitis </li></ul>
    99. 106. The Lower GI Tract: Enterocolitis GIARDIA LAMBIA CRYPTOSPORIDIUM
    100. 107. The Lower GI Tract: Malabsorptive Syndromes <ul><li>Malabsorption : </li></ul><ul><li>suboptimal absorption of fat, vitamins, proteins, carbs, electrolyetes, minerals, water. </li></ul><ul><li>Caused by disturbances in: </li></ul><ul><ul><li>Intraluminal digestion </li></ul></ul><ul><ul><li>Terminal digestion </li></ul></ul><ul><ul><li>Transepithelial transport </li></ul></ul>
    101. 108. The Lower GI Tract: Malabsorptive Syndromes <ul><li>Celiac Sprue (Gluten sensitive enteropathy): </li></ul><ul><li>Small bowel mucosal lesion resulting in impaired nutrient absorption </li></ul><ul><li>Associated with anti-gliadin antibodies </li></ul><ul><li>Sx’s improve with withdrawal of gluten from diet </li></ul>
    102. 109. The Lower GI Tract: Malabsorptive Syndromes <ul><ul><li>Blunting and atrophy of villi </li></ul></ul><ul><ul><li>Increase in chronic inflammatory cells in lamina propria </li></ul></ul>
    103. 110. Normal Sprue
    104. 111. The Lower GI Tract: Malabsorptive Syndromes <ul><li>Tropical Sprue: celiac-like disease that occurs in people of the tropics (post infectious) </li></ul><ul><li>Whipple Disease : caused by infection from Trophyrema whippelii ; characteristic foamy histiocytes in the lamina propria causing expansion of villi </li></ul>
    105. 113. The Lower GI Tract: Malabsorptive Syndromes <ul><li>Lactose intolerance : lactase deficiency with resulting inability to digest lactose and watery diarrhea, abdominal distension and gaseousness </li></ul><ul><li>Abetalipoproteinemia: inability to synthesize apolipoprotein B </li></ul><ul><ul><li>Intestinal mucosal cells cannot export lipoproteins and cells hang onto lipids causing vacuolation </li></ul></ul>
    106. 114. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Crohn disease and Ulcerative Colitis: </li></ul><ul><li>Chronic, relapsing inflammatory disorders of unclear origin </li></ul><ul><ul><li>Destructive mucosal immune response </li></ul></ul><ul><ul><li>Genetic predisposition </li></ul></ul><ul><ul><li>Deranged mucosal immunity </li></ul></ul>
    107. 115. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Crohn’s Disease: </li></ul><ul><li>Small bowel involved </li></ul><ul><li>Skip lesions </li></ul><ul><li>Granuloma formation </li></ul><ul><li>Transmural inflammation </li></ul><ul><li>Strictures and fistulas </li></ul><ul><li>Ulcerative Colitis: </li></ul><ul><li>Rectum involved and disease extends proximally </li></ul><ul><li>Continuous lesions </li></ul><ul><li>No granulomas </li></ul><ul><li>Mucosal and submucosal inflam. </li></ul><ul><li>Toxic megacolon </li></ul>
    108. 116. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Crohn’s Disease: </li></ul><ul><li>Gross cobblestone appearance of mucosa, with fissure and fistula formation </li></ul><ul><li>Luminal narrowing (string sign) due to wall edema </li></ul>
    109. 117. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Crohn’s Disease : </li></ul><ul><li>Histologic changes: neutrophils in crypts and crypt abscesses </li></ul>
    110. 118. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Chronic changes: </li></ul><ul><li>Crypt/villus distortion </li></ul><ul><li>non-caseating granulomas </li></ul><ul><li>fibrosis of submucosa </li></ul><ul><li>muscularis propria </li></ul>
    111. 120. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Crohn’s Disease : </li></ul><ul><li>Clinically: intermittent attacks of diarrhea, fever, abdominal pain </li></ul><ul><li>Extraintestinal manifestations: migratory polyarthritis, ankylosing spondylitis, erythema nodosum </li></ul>
    112. 121. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Ulcerative Colitis: </li></ul><ul><li>Gross: Hyperemic with pseudopolyp formation in areas of regenerating mucosa; no mural thickening </li></ul>
    113. 122. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Ulcerative Colitis: </li></ul><ul><li>Mononuclear inflammation of lamina propria; crypt abscesses; ulceration of mucosa </li></ul>
    114. 124. The Lower GI Tract: Inflammatory Bowel Disease <ul><li>Ulcerative Colitis: </li></ul><ul><li>Clinically: presents as relapsing bloody diarrhea persisting for days-months </li></ul><ul><li>May see overgrowth of normal flora </li></ul><ul><li>Complications: </li></ul><ul><ul><li>Risk for Toxic Megacolon </li></ul></ul><ul><ul><li>Increased risk for Adenocarcinoma </li></ul></ul>
    115. 125. The Lower GI Tract: Diverticular Disease <ul><li>Diverticula: Mucosally lined outpouching of </li></ul><ul><li>Usually occur in sigmoid colon due to increased intraluminal pressure and focal weakness in the colonic </li></ul><ul><li>wall </li></ul>
    116. 126. The Lower GI Tract: Diverticular Disease <ul><li>Diverticulosis: Multiple diverticula </li></ul><ul><li>Diverticulitis: Inflammation of diverticula </li></ul><ul><ul><li>May result in perforation </li></ul></ul>
    117. 127. Causes of Intestinal Obstruction
    118. 128. The Lower GI Tract: Tumors of the Small Bowel <ul><li>Small Bowel Adenocarcinoma: </li></ul><ul><li>VERY rare </li></ul><ul><li>Duodenum most commonly (Ampulla of Vater) </li></ul><ul><li>Usually extensive disease at diagnosis, but 5 year survival of 70 % </li></ul>
    119. 129. The Lower GI Tract: Tumors of the Small Bowel <ul><li>Carcinoid Tumor: </li></ul><ul><ul><li>Site of origin correlates with behavior </li></ul></ul><ul><ul><li>Most common sites: appendix > ileum > rectum > stomach > colon </li></ul></ul><ul><ul><li>May be asx or associated with “carcinoid syndrome” </li></ul></ul><ul><ul><ul><li>Flushing Diarrhea/vomiting </li></ul></ul></ul><ul><ul><ul><li>Cough/dyspnea Systemic fibrosis </li></ul></ul></ul><ul><ul><ul><li>Hepatomegaly Elevated blood 5 HT </li></ul></ul></ul>
    120. 130. The Lower GI Tract: Tumors of the Small Bowel <ul><li>Carcinoid Tumors: </li></ul><ul><li>Excellent prognosis </li></ul><ul><ul><li>90 % 5 year survival </li></ul></ul><ul><ul><li>50 % 5 year survival with liver metastasis </li></ul></ul>
    121. 131. Carcinoid Tumor
    122. 132. The Lower GI Tract: Tumors of the Small Bowel <ul><li>Gastrointestinal Lymphoma: </li></ul><ul><ul><li>Can affect any segment of GI tract, most common in stomach and small intestine </li></ul></ul><ul><ul><li>MALT lymphomas arise in the B cells of the lymphoid tissue </li></ul></ul>
    123. 133. The Lower GI Tract: Large Bowel Tumors <ul><li>Polyps: Tumorous mass protruding into the lumen of the gut </li></ul><ul><ul><li>Pedunculated: on a stalk </li></ul></ul><ul><ul><li>Sessile: no stalk </li></ul></ul><ul><ul><li>Adenoma vs. Hyperplastic </li></ul></ul>
    124. 134. The Lower GI Tract: Large Bowel Tumors <ul><li>Non-neoplastic Polyps: </li></ul><ul><li>VERY common </li></ul><ul><ul><li>Hyperplastic—proliferation and maturation of normal goblet cells leading to crowding and serration </li></ul></ul><ul><ul><li>Juvenile Polyp—cystically dilated glands in lamina propria </li></ul></ul><ul><ul><li>Peutz-Jeghers polyps </li></ul></ul>
    125. 136. The Lower GI Tract: Large Bowel Tumors <ul><li>Familial Syndromes: </li></ul><ul><li>Autosomal dominant </li></ul><ul><ul><li>Familial Adenomatous Polyposis </li></ul></ul><ul><ul><li>Hereditary Non Polyposis Colorectal CA </li></ul></ul><ul><ul><li>Gardner Syndrome </li></ul></ul>
    126. 138. The Lower GI Tract: Large Bowel Tumors <ul><li>Neoplastic Polyps </li></ul><ul><li>Tubular Adenoma </li></ul><ul><li>Villous Adenoma </li></ul><ul><li>Tubulovillous Adenoma </li></ul>
    127. 139. The Lower GI Tract: Large Bowel Tumors <ul><li>Adenomatous Polyps: </li></ul><ul><li>Characterized by variable epithelial dysplasia </li></ul><ul><li>High grade dysplasia = carcinoma in situ </li></ul><ul><li>Invasion of stalk (or into submucosa) = Invasive adenocarcinoma </li></ul>
    128. 140. The Lower GI Tract: Large Bowel Tumors <ul><li>Colorectal Adenocarcinoma: </li></ul><ul><li>Ages 60 – 80 years </li></ul><ul><li>Site prevalence: Cecum/ascending colon > sigmoid > transverse > descending </li></ul><ul><li>Clinical s/sx: anemia, weakness, heme + stool </li></ul>
    129. 141. The Lower GI Tract: Large Bowel Tumors Proximal Distal – Apple core
    130. 142. The Lower GI Tract: Large Bowel Tumors
    131. 143. The Lower GI Tract: Large Bowel Tumors
    132. 144. The Lower GI Tract: Appendix <ul><li>Acute appendicitis: </li></ul>
    133. 145. The Lower GI Tract: Appendix <ul><li>Acute Appendicitis: </li></ul>
    134. 146. The Lower GI Tract: Appendix <ul><li>Tumors: </li></ul><ul><li>Carcinoids are most common tumor </li></ul><ul><li>Mucinous neoplasms e.g. mucinous cystadenoma and mucinous cystadenocarcinomas </li></ul>
    135. 147. <ul><li>www.maxillofacialcenter.com </li></ul><ul><li>Mspis.medsci.indiana.edu </li></ul><ul><li>www.dentistry.leeds.ac.uk </li></ul><ul><li>www.tmd.ac.jp/dent/opat </li></ul><ul><li>www.afip.org/…/vgi </li></ul><ul><li>www.icare.org </li></ul><ul><li>www.contessamotel.com </li></ul><ul><li>www.phil.muni.cz </li></ul><ul><li>www.edu.rcsid.ac.uk </li></ul><ul><li>www.oralpatho.dent.chula.ac.th </li></ul><ul><li>Ajoupath.ajou.ac.kr </li></ul><ul><li>www.nuh.com.sg…/images gastrointestinal.jpg </li></ul><ul><li>w.3.uokhsc.edu/histology </li></ul>Owen et al. Atlas of Gastrointestinal Pathology. 1994. W.B. Saunders co, Philadelphia. Kumar et al. Robbins Basic Pathology, 7 th Edition. 2003. Saunders, Philadelphia. P. 543-590 Cotran et al. Robbins Pathologic Basis of Disease, 6 th Ed. 1999. W.B. Saunders Company, Philadelphia. P.756-844. www.drpstokes.com www.postgradmed.com www.faculty.plattsburgh.edu www.yale path.org www.kotan.ec.hokudai.ac.jp www.vascular.surgeon.co.uk www.colorado.edu www.vh.org/…/GIAtlas www.medlib.med.utah/edu/Webpath
    136. 148. <ul><li>Questions?  robstak@mail.amc.edu </li></ul>

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