Gastrointestinal Pathology

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thezidane
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Gastrointestinal Pathology
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2010-12-04 23:24:10
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Gastrointestinal pathology
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Gastrointestinal Pathology
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  1. What are inflammatory lesions of the salivary glands called?
    Symptoms?
    What is Sarcoidosis?
    • Inlammatory lesions of salivary glands = Sialadenitis
    • Symptoms: Dry mouth and/or gland swelling with pain.
    • Sarcoidosis: Mumps and salivary duct stones with obstruction.
  2. Are most tumors of the Salivary Gland benign or malignant?
    What are the Benign and malignant tumors of the salivary glands?
    • Benign.
    • Pleomorphic Adenoma, Wortin's Tumor: Benign
    • Mucoepidermoid Carcinoma: Malignant
  3. What is Sjogren's Disease?
    • Autoimmune disease causing salivary gland inflammation
    • affects mostly females in fifth generation.
    • Symptoms: xerostomia, dry eyes (keratoconjuctivitis sicca).
    • Intense lymphocytic infiltrate in salivary glands. Increased incidence of lymphoma.
  4. What's the most frequent site involved with salivary gland tumors? are they usually malignant?
    • Parotid gland is most frequently involved.
    • 80% benign
  5. What is a pleomorphic adenoma?
    Most common neoplasm of the salivary gland... it's a salivary gland tumor. Mixed tumor or mesenchymal and epithelial components. Usually in parotid gland, lobulated, variably encapsulated, can recur, can become malignant. Can affect facial nerve VII (motor for muscles of facial expression)
  6. Warthin's Tumor? What is it?
    Papillary cystandenoma lymphomatosum. Benign tumor of the salivary glands. Almost completely exclusive to parotid gland. Epithelium lining spaces of lymphoid tissue. Mal predilection, firm, cystic mass, oncocytes, lymphocytes infiltrate.
  7. Mucoepidermoid carcinoma? What is it?
    Malignant tumor of the salivary glands. Squamous and mucous cells in cords, sheets or lining cysts. Usually less than 8cm, lack well-defined capsule, mucin filled cysts. CN VII damage, paralysis, dysphagia and/or trismus.
  8. Esophagitis:
    Clinical symptoms:
    What's GERD?
    Extrinsic vs. intrinsic causes?
    • Inflammation of the esophagus.
    • Presents as dysphagia, retrosternal pain.
    • Reflux of gastric contents (GERD): Gastric esophageal reflex disorder.
    • Extrinsic causes: chemical(pill/radiation), infection (CMV/Herpes/Candida), trauma, iatrogenic (doctor induced)
    • INtrinsic: refulx
  9. What's Barrett's esophagus?
    • Metaplastic columnar epithelium with goblet cells.
    • This increases the risk of adenocarcinoma.
    • Barrett's esophagus is the single most important risk factor for esophageal adnocarcinoma.
  10. Gastroesophageal Reflux: What are the oral manifestations?
    Enamel erosion and loss over areas of teeth exposed to gastric contents. Generally, most affected area is the palatal surfaces of maxillary teeth (where the barf hits on the way out)
  11. Stomach:
    Gastritis: what is it?
    2 kinds... causes?
    • Gastritis: inflammation of stomach lining
    • Acute: environmental
    • Chronic: Autoimmune and environmental cause
  12. Acute Gastritis:
    What is it?
    Cells associated with it?
    Pathogenesis/causes?
    Pathology/affects/clinical manifestations?
    • Hyperemia of mucosa (variable). Occasional PMN's in lamina propria.
    • Cells associated = Neutrophil!
    • Etiologies: Tons of Cigarettes, alcohol intake. Stress, ischemia. NSAID's, aspirin, infection.
    • Asymptomatic until ulceration
    • Pathology: Punctate hemorrhage, EROSION (thinning of epithelium), edema, acute inflamation.
  13. Chronic Gastritis:
    What is it?
    Pathogenesis/how is it caused?
    Pathology/symptoms/clinical manifestations
    Clinical course:
    cells associated:
    main bacteria involved with infection:
    • Mononuclear inflammation of mucosa +/- gland atrophy.
    • Pathogenesis: 1. Autoimmune disease (pernicious anemia) antibodies to intrinsic factor and parietal cells.
    • 2. Infection (H. Pylori), chemical.
    • Pathology: flat epithelium, chronic inflammation, atrophy, intestinal metaplasia.
    • Clinical course: Ulceration (loss of continuity of epithelium), risk 2-4% (intestinal metaplasia)
    • cells associated: macrophages and lymphocytes (Antibodies)
    • Main bacteria: Helicobacter Pylori.
  14. Helicobacter pylori:
    cell morphology?
    Almost always seen in what disease/symptom?
    • S-shaped gram negative rod, flagellated.
    • Infects the gastric mucosa
    • Almost always seen in chronic active gastritis.
    • Present in 65% of gastric ulcers.
    • 85-100% duodenal ulcers.
    • May play a role in gastric cancers.
  15. Peptic Ulcer:
    What is it?
    Where does it occur?
    Type of defect?
    • Solitary ulcerations of mucosa secondary to aggressive unbalanced action of acid-pepsin secretion.
    • 98% in duodenum or stomach more common in duodenum.
    • Punched-out, round to oval defect.
  16. Peptic ulcer complications:
    Lifetime risk?
    What are four complications
    • lifetime risk is 10%
    • Complications:
    • Slow GI Bleed, can cause pernicious anemia (25% die)
    • Perforation (big holes): 2/3rds die.
    • Obstruction: cause edema, scarring 2%.
    • Intractable (hard to control/deal with) pain
  17. Small intestine:
    What structure of the GI tract is most susceptible to cancer/tumor, what is least?
    • Colon is the area where you get the most cancers!
    • Intestine: longest, biggest, most surface area and the LEAST likely location for cancer/tumors!
  18. Small Intestine Malabsorption
    Symptoms:
    Causes:
    • Symptoms: diarrhea, steatorrhea, weight loss, weakness
    • Causes: many ranging from defective intraluminal hydrolysis (i.e. cycstic fibrosis) to an abnormality of the mucosa (celiac disease)
  19. What are some examples of small intestine malabsorptions:
    • Celiac disease: gluton/wheat/ gliadin allergy
    • Tropical sprue: bacterial
    • Whipple's disease: block of lymphatic draining
    • Bacterial overgrowth
    • Disaccharidase deficiency
    • Abetalipoproteinemia.
  20. Celiac Disease:
    What is it?
    race prevalence?
    Hypersensitivity to what?
    Morphology of mucosa?
    Improved how?
    • Malabsorption/Hypersensitivity reaction to wheat or rye gluten. Hypersensitivity to GLIADIN
    • Caucasians 1:100-200
    • Morphology: Blunted villi, inflammatory infltrate.
    • Dramatically improves with withdrawal of wheat gliadin and related grain proteins from the diet.
  21. What are some clinical aspects of Malabsorption/symptoms or complications?
    • Anemia: iron, pyridoxine, folate or B12 deficiency. Bleeding from Vit K deficiency
    • Osteopenia, tetany: from defective Ca, Mg, Vit D and protein absorption.
    • Amenorrhea, impotence and infertility: from generalized malnutrition
    • Purpura, petechia
    • Deficiencies A and B12: peripheral neuropathy.
  22. Oral Manifestations of Malabsorption:
    What is the first oral manifestation?
    Common complaint?
    • Iron and vitamin B12 deficiency: atrophic glossitis (bald - red tongue), atchy or involvement of entire dorsum, glossopyrosis, angular cheilitis (cracking at angles/corners commisures of the mouth)
    • First oral manifestation: atrophic glossitis: bald, red tongue.
    • Common complant: burning sensation (glossophyrosis) sore tongue.
  23. Colon Polyps:
    Frequent?
    what are they?
    4 types?
    • Polyps found in 25-50% of older adults
    • Proliferations of mucosal glandular and surface epithelium to form a protrusion into the bowl lumen.
    • 1. hyperplastic: 90% of polyps
    • 2. Inflammatory
    • 3. Tubular adenoma: stalk
    • 4. Villous Adenomatous (neoplastic): No longer reactive, not going away on it's own. Typically larger and no stalk sessile, velvety occuring most commonly in rectum up to 40% have foci of cancer.
  24. Polyposis syndromes: Associated oral manifestations
    2 forms:
    • 1. Familial adenomatous polyposis (FAP)
    • 2. Peutz-Jeghers Syndrome
  25. Familial Adenomatous Polyposis (FAP)
    Common?
    Risk of cancer?
    Adenomas?
    Gardner's syndrome?
    Dental lesions?
    • Most common polyposis syndrome of the GI tract.
    • Risk of affected patients developing colon cancer approaches 100%
    • Adenomas throughout colorectum (average onset 16)
    • Gardner's syndrome : FAP + Extraintestinal lesions.
    • Dental Lesions: Unerupted teeth, supernumerary teeth, dentigerous and mandibular cysts, increased risk for odontomas.
  26. Familial Adenomatous Polyposis (FAP)
    Clinical features:
    penetrance?
    CHRPE?
    Untreated leads to what?
    • Estimated penetrance (% of population that carriers the gene for FAP alterations ) for adenomas is over 90%.
    • CHRPE may be present (congenital hyperplastic retinal pigmented epithelial cell)
    • Untreated polyposis leads to 100% risk of cancer.
  27. What are some extraintestinal manifestatins of FAP
    • Dental manifestations: Unerupted teeth (usually because of osteomas of the jaw)
    • Extraintestinal Tumors
    • Skin lesions
    • Thyroid Cancers
    • Desmoid Tumors (Major cause of morbidity and mortality after colectomy)
  28. Gardner's Syndrome: What is it?
    • A variant of FAP
    • Features of FAP plus extraintestinal lesions: desmoid tumors, CHRPE, JAW OSTEOMAs therefore failure of timely erruption of teeth.
  29. Peutz-Jeghers Syndrome:
    What is it?
    what is seen clinically?
    What's a key symptom (oral manifestation)
    • Second most common polyposis syndrome.
    • Gastrointestinal hamartomatous polyps and pigmented macules of mucous membranes and skin
    • MELANIN DEPOSITS AROUND NOSE, LIPS, BUCCAL MUCOSA, hands and feet, genitalia and perianal region.
  30. Idiopathic Inflammatory Bowel Disease:
    Crohn's disease:
    what are clinical symptoms?
    What is the pathology?
    • Clinical: Chronic intermittent diarrhea +/- blood, colicky abdominal pain, presents in young adulthood.
    • Pathology: Segmental transmural inflammation of bowel, particularly ileum. Frequently spares the rectum. Ulcerations, granulomas, thickened bowel wall with fat wraping, fissure and fistula formation.
  31. Chron's disease: Oral manifestations:
    • Multiofocal, linear, nodular, polypoid or diffuse mucosal thickening with predilection for labial and buccal mucosa and mucosal folds.
    • Can be confused with aphthous ulcers.
    • Subepithelial, noncaseating granulomatous inflammation identical to those seen in the bowel. Infections (fungal, TB) should be ruled out.
    • Typically persistent and remit and relapse over the years.
  32. Ulcerative Inflammatory disease:
    briefly describe Crohn's disease and Ulcerative colitis
    • Chron's disease: any portion of the GI tract! most often distal small bowel and colon. Transmural disease.
    • Ulcerative Colitis: COLON ONLY. Mucosal disease mainly.
  33. Tumors of the esophagus
    Benign:
    Malignant:
    • Benign: leiomyomas, squamous papillomas, lipomas
    • Malignant: squamous cell carcinoma, adenocarcinoma
  34. Esophageal Squamous Cell carcinoma: describe
    Esophageal Adenocarcinoma: describe
    • SCC: usually over 50 males, risk factors: esophagitis, smoking, drinking, MIDDLE 1/3rd of esophagus, presents as polypoid, fungating mass.
    • Adenoma: Barrett's esophagus is a precursor, occurs in DISTAL third of esophagus.
    • Both have really bad prognosis.
  35. Stomach Tumors: What re some benign ones?
    Hyperplastic, fundic gland polyps, adenomas and inflammatory polyps.
  36. Stomach Adenocarcinoma:
    two types
    incidene
    risk factors:
    less common malignant tumors
    • Malignant tumor, intestinal-type and diffuse type (litinis plastica)
    • Decreasing incidence of intestinal type.
    • 5 year survival 10%
    • Risk factors: Herediary factors, environmental factors, pernicious anemia, atrophic gastritis, adenomatous polyp
    • Less common tumors: Lymphoma and Gastrointestinal stromal tumor
  37. Gastric carcinoma:
    what is the usual kind of cancer?
    What is the main clinical manifestation
    • Adenocarcinoma of the stomach.
    • Metastasis: supraclavicular lymph node, liver, lung, and ovaries, very weird sites of spread are clue to gastric carcinoma.
  38. Risk factors for Colorectal cancer
    Main risk factor:
    Others:
    rank of cause of cancer death?
    • High fat, low fiber diet
    • Age is over 50,
    • personal history adenoma or colorectal carcinoma
    • A family history of CRC
    • Inflammatory bowel disease
    • Hereditary colon cancer syndromes.
    • 2nd cause of CANCER death (1st is lung)
  39. Colon: Malignant adenocarcinoma:
    Clinical:
    Risk factors:
    Pathology:
    • Clinical: peak incidence between ages 50-70, may present with spotty rectal bleeding.
    • Risk factors: high meat and animal fat consumption, high cholesterol lack of fiber, genetic: FAP
    • Pathology: 60-65% in descending colon and rectum. Annular, encircling "napkin-ring" shape on left side, polypoid in right colon.
  40. TNM staging of colon cancer
    What does it stand for?
    • T = Depth of Tumor invasion
    • N = Lymph Node involvment
    • M = presence of metastasis
  41. Oral Manifestations of GI tumors:
    Malignant neoplasms or liver and GI tract occasionally metastasize to the oral regoin, most commonly to the posterior mandible. They can present asymptomatic or with jaw or tooth pain, paresthesias or teeth loosening (unexplained).

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