Systemic Pathology - GI - Galan

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  1. Layers of the esophagus
    • From the lumen
    • Mucosa
    • - Epithelium (squamous)
    • - Lamina propria
    • - Muscularis mucosa (thin layer of muscle)
    • Submucosa
    • Muscularis Propria
    • - inner circumferential
    • - outer longitudinal
  2. Gastroesophageal junction
    • squamous epithelium esophagus -> glandular epithelium stomach
    • “Z-line”
    • important pathology occurs here
  3. Tracheo-Esophageal Fistula
    • Most common congenital anomaly
    • Associated with esophageal atresia in 90% of cases (usually the middle 3rd)
    • Presents in neonatal period
    • Can lead to death by causing aspiration pneumonia
  4. Development of foregut
    • Tracheobronchial diverticulum forms on foregut anterior wall
    • Esophagotracheal septum and the pouch develop
    • Septum completes, pharynx, trachea, esophagus form, lung buds are developing at the end of the extending pouch
  5. Types of Tracheo-Esophageal Fistula
    • Type A - espophageal atresia forms w/o the fistula, causes vomiting
    • Type B, C, D - Esophageal atresia w/ fistula. B has proximal fistula (proximal part of esophagus connected to trachea via fistula; least common); C has distal fistula (most common); D has proximal and distal fistula
    • Type E - Fistula w/o atresia (H-type)
  6. Hernias
    • Congenital, stomach goes up the diaphragm; can compress and impair lungs.
    • Hiatal (sliding) Hernia - The entire proximal stomach protrudes into the mediastinum
    • Paraesophageal (rolling) Hernia - Only part of the fundus protrudes into the mediastinum
  7. Esophagitis
    • Reflux: most important cause; distal 1/3
    • Certain foods or drugs (NSAIDs, Fe iron pill sticks to the wall and causes irritation)
    • Caustic bases (NaOH) or acids - rare but serious
    • Hypersensitivity reaction
    • Nasogastric tubes
    • Infections: e.g. Herpes, Candida, CMV (esp. in immunosuppressed individuals)
    • Complications: Erosions, ulcers, perforation, Barrett’s metaplasia (reflux), strictures (mostly result of caustic exposure, eg ly, becoming fibrotic)
  8. Reflux Esophagitis
    • Passage of gastric/duodenal contents back up through the lower esophageal sphincter
    • Most common cause of esophagitis
    • Incidence in the US is ~30-40%
    • More common in adults >40 and babies
  9. reflux esophagitis - micro - Classic elements
    • Elongation of rete
    • Basal cell hyperplasia
    • Intraepithelial eosinophils (which are also seen in hypersensitivity esophagitis)
  10. reflux esophagitis - gross
    Endoscopically, described as “feline” esophagus, aka “trachealization”, whereas normal esophagus should be smooth.
  11. Reflux Esophagitis - Consequences
    • Repeated injury -> glandular-type epithelium of the stomach to move into the esophagus.
    • Glandular epithelium then become “intestinalized”, aka Barrett’s Esophagus
    • Barrett’s Esophagus gives rise to adenocarcinoma
  12. Barrett’s Esophagus against normal - Gross Pathology
    • up-tick (finger-like) border vs regular zigzag
    • red, velvety, salmon-colored vs pale pink
  13. Barrett’s Esophagus - Micro
    • Glandular, gastric-type epithelium moving upward
    • Intestinalization (goblet cells)
  14. Goblet cells + glandular epithelium =
    Barrett's esophagus
  15. Most common causes of infectious esophagitis
    • #1 - Candida; Usually C. albicans or C. tropicalis
    • #2 - Herpes Simplex Virus (HSV)
  16. Candida - Associations/risk factors:
    • Immunosuppression
    • • HIV, bone marrow transplant, immunosuppressive tx, bone marrow disorders
    • Acid-suppression tx
    • Diabetes
    • Esophageal motility disorders
    • Rheumatic diseases
  17. Candida - Presentation:
    • Dysphagia
    • Gross - characteristic white plaques seen on endoscopy
    • Micro - spike in neutrophils; filaments, the fungal hyphae, bright red w/ PAS stains
  18. Candida - Treatment:
    Antifungals (like fluconazole)
  19. Herpes Simplex Virus (HSV)
    • Affects immunosuppressed people and immunocompetent children
    • Superinfection w/ bacteria and fungi can happen
    • Causes esophageal ulcers -> perforations
    • The infection can also become disseminated
    • Treat with antivirals (like acyclovir)
  20. HSV esophagitis - micro hallmarks
    • Multinucleation
    • Margination - chromatin marginates to the periphery
    • Molding - nuclei mold against each other
  21. Cytomegalovirus (CMV) Infection
    • Immunocompromised patients
    • – Up to ~30% of HIV patients not on HAART have CMV, HSV, or Candida esophagitis
    • Ulcers grossly resembling HSV ulcers
    • Therapy:
    • – Antivirals
    • – Modulation of immunosuppression
    • – Treat the underlying cause (as with HAART in HIV patients)
  22. CMV infected cells - micro hallmark
    • famous “owl’s eye” nucleus
    • - large cells (hence "megalo”)
    • - very dark nucleus w/ inclusions
  23. Mallory-Weiss Syndrome
    • Most commonly seen in alcoholics
    • Complication of violent vomiting -> Longitudinal tears in the lower esophagus and superficial blood vessels, possibly extending into the upper stomach (across GE junction) -> hematemesis, can be serious
    • Usually superficial, do not lead to perforation
    • – A transmural perforation due to violent vomiting is known as Boerhaave Syndrome
  24. Esophageal Varices
    • #1 cause - Alcohol
    • Complication of portal hypertension, occurs in 90% of cirrhotic patients
    • Portal hypertension -> shunts blood into associated veins (can't withstand high pressure; A major player is the left gastric vein, aka the cardiac vein) -> massive hematemesis, death if not treated immediately
    • #1 cause of death in cirrhotics
  25. Esophageal Carcinoma - Two Main Types:
    • Squamous cell carcinoma
    • Adenocarcinoma
  26. Epidemiologic differences worldwide between the two main types of esophageal carcinoma:
    • Worldwide - SCC about 90% of esophageal cancers
    • USA - SCC and adenocarcinoma roughly comparable
    • Environmental and genetic factors are believed to be the reasons
  27. Squamous Cell Carcinoma of the Esophagus - epidemiology
    • M>F (About 4:1)
    • In America, the main causes are EtOH and tobacco
    • (which work synergistically)
    • Other factors
    • • Environmental
    • • Food - processed, nitrite
    • • HPV
    • • Corrosives and thermal injury
    • • RTX for other mediastinal tumors
    • • Celiac disease
  28. High-grade dysplasia, or carcinoma in-situ (CIS) - micro
    • Significantly thickened basal cell layer w/ high N/C ratio
    • No gradual maturation profile from basal cell layer to the lumen, organization of cells become random
    • Eventually develops into invasive carcinoma
  29. 95% Adenocarcinoma of the Esophagus arise in a background of __________, the presence of which confers an estimated ________ risk.
    • Barrett’s esophagus (only a small portion of it)
    • 30-125x
  30. The Road to Adenocarcinoma
    repeated injury to intestinalized esophagus (Barrett’s) -> mutations -> increasing grades of glandular dysplasia -> carcinoma in-situ -> invasive carcinoma
  31. Anatomy of stomach
    • Cardia - mucous cells
    • Fundus - Parietal cells (acid, intrinsic factor), chief cells (pepsin)
    • Body - Parietal cells (acid), chief cells (pepsin)
    • Antrum - Mucous cells, G cells (neuroendocrine, gastrin)
    • Pylorus
    • (Duodenum)
  32. Layers of stomach wall
    • The same as esophagus
    • From the lumen
    • Mucosa - types of cell depends on the location in the stomach
    • - Epithelium (squamous)
    • - Lamina propria
    • - Muscularis mucosa (thin layer of muscle)
    • Submucosa
    • Muscularis Propria
    • - inner circumferential
    • - outer longitudinal
  33. Congenital Pyloric Stenosis
    • M:F=4:1, usually in first born
    • Rare in AAs & Asians
    • etiology - Unknown, genetic?
    • Presents in middle to end of 1st month w/ projectile vomiting
    • Enlarged pylorus, thickened muscle; aka Hypertrophic pyloric stenosis
    • Treatment - pyloromyotomy
  34. Gastritis
    • Acute and Chronic, overlap a lot
    • Acute - Characterized by neutrophils; Caused by - NSAIDS, EtOH, Smoking, Chemo TX, Uremia, Systemic infection, Ischemia, Caustics, Hypersensitivities (allergies), Mechanical (NG tubes)
    • Chronic - Characterized by plasma cells and lymphocytes; Caused by - H. pylori, Autoimmune, Toxins (EtOH, smoking), Mechanical, Radio TX
  35. Acute Gastritis - Gross
    dark spots - punctate areas of mucosal erosion, bleeding
  36. Acute Gastritis - Micro
    Erosive - show erosion
  37. Eosinophilic (Allergic) Acute Gastritis
    • Children or young adults
    • Also seen in esophagus, but more common in stomach
    • A hypersensitivity reaction
    • Presents with
    • • Vomiting
    • • Diarrhea
    • • Failure to thrive
    • Treatment - Steroids, diet modification
    • Histologic hallmark - marked tissue eosinophils
  38. Chronic Gastritis
    • Hallmark - Plasma cells, lamina propria is loaded with; characteristic large cells with comet-like large nuclei
    • Common consequence - Intestinal metaplasia, goblet cells
  39. The most important type of chronic gastritis is due to ___________.
    • Helicobacter pylori infection
    • Present ~90% of cases of chronic gastritis in the antrum.
    • Colonization is very common - most would show gastritis histologically
    • The most common cause of peptic ulcers
  40. H. pylori
    • Curved G(-) rod
    • Uses flagella to swim through viscous mucus
    • Uses urease to generate acid-neutralizing ammonia
  41. H. pylori gastritis - micro
    • under low power - lamina propria loaded w/ plasma, the pits are pushed out
    • high power - filament can be seen; can be visualized by silver stain or immunohisto stain
  42. Autoimmune Atrophic Gastritis
    • A special type of chronic gastritis caused by auto-antibodies to parietal cells, which produce both HCl and intrinsic factor
    • Losing parietal cells - fundus look like antrum
    • Loss of intrinsic factor -> compromised VitB12 absorption -> pernicious anemia
  43. Gastropathies
    • Gastritis w/o inflammatory cells
    • various etiologies
    • The most important one is chemical gastropathy
  44. Chemical Gastropathy can be caused by
    • Bile reflux from duodenum
    • GERD
    • NSAIDS
    • EtOH
  45. Chemical Gastropathy - pathogenesis
    • Stomach mucosa injury -> exfoliation of epithelium -> reactive/regenerative changes
    • – Tortuous, dilated pits
    • – Epithelial mucin depletion
    • – Fibrosis of lamina propria
    • – Mitotic activity in pits
  46. Peptic Ulcer Disease
    • Chronic ulcer of the first part of the duodenum and/or distal (antral/pyloric) stomach.
    • Major cause - H. pylori
    • Contributed by hyperacidity, NSAIDS, smoking and other factors
    • – H. pylori causes nearly all of duodenal ulcers, and ~90% of gastric ulcers not caused by NSAIDS or Zollinger-Ellison Syndrome
    • Happens when damaging factors overwhelm the defense causing increased damage or decreased defense, which eventually leads to peptic ulceration
    • Eats through the epithelium, blood, fibrin, neutrophils at the base.
  47. Zollinger-Ellison Syndrome
    • Pancreatic islet cell tumors, in pancreas or elsewhere of GI
    • -> secrete gastrin
    • -> stomach secretes more acid
    • -> promotes ulcer formation
  48. Gastric Cancer - most common types
    • 1. Adenocarcinoma (glandular epithelial cells)
    • 2. Lymphoma (lymphoid tissue in the stomach)
    • 3. Gastrointestinal Stromal Tumor (GIST)
  49. Gastric Cancer - causes
    • Virtually anything injuring stomach, most commonly:
    • - H. pylori
    • - Dietary factors
    • - Environmental factors
    • - Genetics
  50. Gastric cancer - Genetic factors
    • Hereditary Non-Polyposis Colon Cancer (HNPCC)
    • - genetic syndrome
    • - defective replication of DNA
    • -> adenocarcinoma in many organ systems, including stomach (most famous for colon cancer)
    • Familial Adenomatous Polyposis (FAP)
    • - genetic syndrome
    • - deactivated tumor suppressor genes
    • -> cancer, mainly colon cancers, gastric cancers sometimes
  51. Pathogenesis of adenocarcinoma
    • H. pylori or other risk factors
    • -> chronic active gastris; + dietary factors + host factors
    • -> intestinal metaplasia
    • -> dysplasia, precancer
    • -> high grade dysplasia, carcinoma in situ
    • -> adenocarcinoma, invasive
  52. Adenocarcinoma - gross
    • ulcerating, with irregular and raised edges, not seen in PUD
    • Serosal/omental nodules, inoperatable
  53. Signet ring-cell carcinoma
    • Special gastric adenocaricinoma
    • Grows in a diffuse manner, vs conventional ones growing as discrete masses
    • Forming mechanism poorly understood
    • Micro - Diffused cells with enlarged mucin globules, pushing the nucleus to the side - signet ring look
    • Gross - cancer cells line the gastric wall, make it stiff, hence linitis plastica, aka leather bottle stomach
  54. Gastric Lymphoma
    • Either the same lymphomas as anywhere else in the body
    • Or more specific to the GI tract
  55. Lymphoma of mucosal-associated lymphoid tissue (MALT)
    • aka MALToma
    • Common to GI tract
    • B-cell lymphoma
    • MALT - aggregate of lymphoid along GI mucosa, including esophagus, stomach, small intestine, colon. Also found in Bronchi, BALT.
  56. MALT lymphoma - micro
    • Enormous proliferation of lymphocytes, pushing the gastric pits apart or obliterating them.
    • Mono-morphic cells vs differentiated look in normal lymphoid tissue, major red flag for lymphoma
  57. Gastrointestinal Stromal Tumor (GIST)
    • Arises from the interstitial cells of Cajal, the pacemaker cells of GI tract.
    • Anywhere in GI tract, most commonly in stomach
    • Micro - spindle cells w/ spindled nuclei
    • Not malignant by definition, but all have malignant potential, increase with size, mitotic activity level, necrosis
    • Therapy (Gleevec) available for the majority, which have a specific mutation.

Card Set Information

Author:
neopho
ID:
325008
Filename:
Systemic Pathology - GI - Galan
Updated:
2016-11-11 10:39:44
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SystemicPathology
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SystemicPathology
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Systemic Pathology - GI - Galan
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