GI 1 Flashcards
Barrett Esophagus
Where do adenocarcinomas of the esophagus occur?
What are some other risk factors?
What are adenocarcinomas?
What is it associated with?
Prognosis?
Majortiy arise in distal esophagus in association with Barrett esophagus
Risk Factors: smoking tobacco, obesity
Adenocarcinoma = gland-forming malignancy
Associated with dysplasia of adjacent glandular epithelium
Prognosis: Varies depending on stage, but overall 5yr survival
Normal Stomach
What is reflux esophagitis?
What is it characterized by?
Due to acid reflux; characterized by intra-epithelial inflammatory cells (esp. eosinophils), basal layer hyperplasia, spongiosis, and elongation of papillae of lamina propria
Gastric Ulcer
Adenocarcinoma of Esophagus
Esophageal Varices (ulceration that became thrombosed)
Normal Stomach (Antrum)
What is the change that happens in Barrett’s esophagus?
Intestinal metaplasia (goblet cell metaplasia) of distal esophagus in response to acid-reflux
What is the histology of gastritis?
Increased numbers of inflammatory cells within lamina propria, including lymphocytes, plasma cells, and neutrophils.
Neutrophils often infiltrate mucosal epithelium (“active” gastritis)
Gastric Ulcer
Adenocarcinoma of Esophagus
Herpes Esophagitis
Ground glass appearance
Acute Hemorrhagic Gastritis
Barrett Esophagus
Left side replaced by columnar glandular mucosa
Normal Stomach (fundus)
Chief cells - purple (Pepsinogen)
Parietal cells - pink (HCl, IF)
Gastric Adenocarcinoma
What is an erosion?
What is an ulcer?
Erosion: Partial thickness loss of mucosal tissue
Ulcer: Full-thickness loss of mucosa
What are the 2 main disorders of Hypertrophic Gastropathy?
Menetrier diseaes: hyperplasia of mucous neck cells due to elevated levels of TGF-alpha. Protein-losing enteropathy (diarrhea, edema). Associated with increased risk of gastric adenocarcinoma.
Zollinger Ellison Syndrome: Triad of gastrinoma (gastrin-secreting tumor usually in pancreas or duodenum due to hyperplasiz of oxyntic mucosa - parietal and chief cells), hypertrophic gastropathy and peptic ulcers due to hypersecretion of acid.
Candida Esophagitis
Herpes Esophagitis
(sharply demarcated lesions)
Gastric Adenocarcinoma
Signet Ring Cell Morphology
With stain for cytokeratin (ensures that it’s carcinoma, not macrophage)
Gastric Lymphoma
Gastric Ulcer
Adenocarcinoma of Esophagus
Normal Esophagus and stomach
Gastritis
Gastric Ulcer
Metastatic Gastric Carcinoma in liver
What is metaplasia?
Reversible change from one mature cell type into another. May represent adaptive (protective) change in response to injury
How is GIST treated?
Majority of GIST express CD117 (“c-kit”) which is the molecular target of tyrosine kinase inhibitor (Imatinib)
Hypertrophic gastropathy
Hyperplasia of mucus-secreting cells
Barrett’s esophagus
What are the different parts of the stomach?
Gastric Adenocarcinoma
Gastric Adenocarcinoma
Barrett Esophagus
Squamous Cell Carcinoma of Esophagus with keratin pearls
Herpes Esophagitis
Squamous Cell Carcinoma of Esophagus
Candida Esophagitis
What is the most common malignancy of th esophagus?
What are risk factors?
Where does it occur?
What is the prognosis?
What is the histology?
Squamous cell carcinoma
Risk factors: Alcohol, tobacco, consumption of hot beverages, dietary foods
Location: Upper 1/3 - 20%, Middle 1/3 - 50%, Lower 1/3 - 30%
Prognosis: usually advanced stage at time of Dx, poor prognosis, overall 5yr survival 20%
Histo: polygonal tumor cells with prominent intercellular bridges and foci and keratinization (Squamous pearls)
What is Adenocarcinoma of the stomach associated with?
H. pylori infection
Esophageal Varices
Gastrointestinal stromal tumor
Gastric Adenocarcinoma
Signet ring cell morphology
Esophagitis (acute)
-Intercellular edema (spongiosis) and inflammatory cells in lamina propria
Hypertrophic Gastropathy
Squamous Cell Carcinoma of Esophagus
50% mid-esophagus, 30% distal, 20% proximal
Gastric Adenocarcinoma
What are some copmlications of ulcers?
Bledding, performation, obstruction
Gastric Adenocarcinoma
Adenocarcinoma arising in Barrett Esophagus
Gastric Carcinoma
Signet Ring Cell Morphology
Reflux Esophagitis (increased eosinophils)
What are the damaging and defensive forces of the stomach?
What causes each?
Damaging: gastric acid, peptic enzymes
Caused by: H. pylori, NSAIDS, aspirin, cigarettes, alcohol, gastric hyperacidity, duodenal gastric reflux
Defensive: surface mucus secretion, HCO3 secretion into mucus, mucosal blood flow, apical surface membrane transport, epithelial regenerative capacity, elaboration of prostaglandins
Caused by: Ischemia, shock, delayed gastric emptying, and host factors
Gastrinoma Triangle
Describe a normal Esophagus
Gross: Pale esophageal mucosa (as compared with tan-brown gastric mucosa) and discrete gastro-esophageal junction
Histo: Squamous-lined mucosa of esophagus with submucosal glands and muscularis propria
Gastric Adenocarcinoma
What are some features that favor GIST malignancy?
Tumor size (>5 cm)
Increased mitotic rate (>5 mitotic figures/50 high power fields)
Presence of tumor necrosis
Mucosal invasion
Gastric Ulcer
Esophageal Varices
Herpes Esophagitis
Gastric Adenocarcinoma
Malignant Gastrointestinal stromal tumor
Adenocarcinoma of Esophagus
Barrett Esophagus
Compare and contrast Menetrier Disease (adult) and Zollinger-Ellison Syndrome
Both are examples of Hypertrophic gastropathy
Barrett Esophagus
Low grade dsyplasia
Esophageal Varices
Gastric Carcinoma (Polyploid/ulcerated)
What is the prognosis of stomach adenocarcinoma?
Depends on stage, overall 5 year survival about 30%
Describe a normal stomach
Gross: Tan brown mucosa and gastric rugae (folds)
Microscopic: gastric pits lined by mucous neck cells with glands lined by parietal (red-pink) and chief (pale) cells. Little/no inflammatory cells normally present in gastric mucosa.
Gastric Polyploid Carcinoma
Squamous Cell Carcinoma of Esophagus
Gastric Ulcer
Hypertrophic gastropathy
What are some associated findings of gastritis?
Erosion/ulceration
Intestinal metaplasia
Atrophy & fibrosis
Gastric Ulcer (Malignant)
Gastric Ulcer
Gastric Lymphoma
Squamous Cell Carcinoma of Esophagus
Herpes Esophagitis
Hypertrophic gastropathy
Barrett Esophagus
High grade dysplasia
Gastrointestinal stromal tumor
Can arise anywhere in GI tract, thought to be due to Cajal cells
What are the associated metastases of stomach adenocarcinoma?
Left supraclavicular lymph node (Virchow’s node) or both ovaries (Krukenberg tumor)
Metastatic Gastric Carcinoma in Lung
Squamous Cell Carcinoma of Esophagus
Adenocarcinoma of Esophagus
What is the difference between a malignant and benign ulcer?
Can’t absolutely distinguish between benign and malignant ulcers by macroscopic exam alone.
Benign: small, regular smooth edges
Malginant: large, irregular with “rolled” or “heaped up” borders
Gastric Adenocarcinoma
What are the different causes of gastritis?
Alcohol, drugs (NSAIDS), bile reflux, stress, radiation, chemotherapy
Malignant Gastrointestinal stromal tumor
Herpes Esophagitis
Loss of mucosa + exudate forming
Gastric Ulcer
Esophageal Varices (ulceration + hemorrhage)
What are some differences between H. pylori and autoimmune gastritis?
Location, inflammatory infiltrate, acid production, gastrin, other lesions, serology, sequelae, and associations
What is dysplasia?
Pre-malignant change involving abnormalities in nuclear size, shape, and (lack of) maturation
Metastatic Gastric Carcinoma
Virchow’s node
What is a GIST?
Gastrointestinal stromal tumor of stomach
Major of mesenchymal tumors of GI tract now classified as GISTs.
Thought to be dervied from interstitial cells of Cajal (pacemaker cells of GI tract).
Histo: Spindled (elongated) tumor cells
Gastric Ulcer
Candida Esophagitis
Gastric Adenocarcinoma
Signet ring cell morphology
What are esophageal varices?
Collateral, dilated veins which develop in response to portal hypertension. Tortuous dilated veins within submucosa that may cause massive upper GI bleeding
10-30% of upper GI hemorrhage
25-35% of cirrhotic patients
30% of initial bleeds fatal
Reflux Esophagitis
Gastrointestinal stromal tumor
Gastric Lymphoma
Hypertrophic gastropathy
Gastric Ulcer
What is the most common cause of chronic gastritis?
Helicobacter pylori. Spiral bacteria may be found in gastric biopsies
Gastritis
What is the clinical relevance of Barrett’s esophagus?
Increased risk of adenocarcinoma (dysplasia –> carcinoma)
Gastric Lymphoma
Normal esophagus by endoscopy
Candida Esophagitis
Pseudomembranes
Esophageal Varices
Gastritis with erosions
What are the gross and histologic patterns of adenocarcinoma of the stomach?
Gross: 1) Exophytic or polypoid, ulcerated mass
2) Diffuse thickening of stomach (linitis plastica “leather bottle” stomach)
Histologic: 1) “intestinal” type: cohesive, gland-forming tumor cells
2) “Diffuse” type: discohesive “signet” ring cells w/ intracytoplasmic mucin
Gastric Adenocarcinoma
Chronic Gastritis
Loss of glands + fibrosis
Gastric Adenocarcinoma
What is hypertrophic gastropathy characterized by?
Giant, “cerebriform” enlargement of rugal folds of gastric mucosa due to hyperplasia of epithelial cells
Gastrointestinal stromal tumor
Normal Stomach (Fundus)
Gastric Lymphoma
What are 2 types of infectious esophagitis?
Describe them.
Herpes esophagitis: Sharply “punched out” ulcers with multinucleated giant cells and intranuclear “ground glass” inclusions
Candida esophagitis: Gray-yellow exudates with yeast/pseudohyphae
Gastric Lymphoma
Normal Stomach
Gastrointestinal stromal tumor
How is Barrett’s esophagus diagnosed?
Combination of clinical & pathologic criteria
Clinical: Endoscopic presence of salmon-colored mucosa above GE junction
Pathologic: Histologic evidence of intestinal metaplasia (presence of goblet cells) within columnar epithelium biopsied
What is autoimmune gastritis?
What are some symptoms?
Autoantibodies against parietal cells, H/K ATPase, or IF
Chronic inflammation leads to mucosal injury and eventual atrophy.
Achlorhydria (low acid production) and hypergastrinemia
Pernicious anemia (B12 deficiency)
Increased risk for gastric cancer
Gastrointestinal stromal tumor
Normal
H. Pylori
Lymphomas of the stomach
What is the most common form?
Most common site of extranodal lymphomas
5% of gastric malignancies, 20% of all extranodal lymphomas
Most common form: low-grade B-cell lymphoma of MALT (mucosa-associated lymphoid tissue)
Associated with H. pylori infection
Composed of dense infiltrate of small lymphoid cells, often showing plasma cell differentiation and invasion of gastric glands (lymphoepithelial lesions)
