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56 Cards in this Set
- Front
- Back
a. What is Hirschsprung disease?
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i. Defective relaxation and peristalsis of rectum and distal sigmoid colon
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b. What are the clinical features of Hirschsprung disease?
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a. What is the most common cause of pseudomembranous colitis?
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a. What is the most common cause of pseudomembranous colitis?
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i. C. dif
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a. Where does Chron disease present? With what type of lesions?
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i. Anywhere from mouth to anus
ii. Skip lesions |
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b. What are the symptoms of Chron disease?
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i. RLQ pain
ii. Non-blood diarrhea |
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c. What type of inflammation is in Chron disease?
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i. Lymphoid aggregates with granulomas
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d. What is the gross appearance of Chron disease?
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i. Cobblestone mucosa
ii. Creeping fat iii. Strictures |
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e. What are the complications of Chron disease?
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i. Malabsorption with nutritional deficiency
ii. Carcinoma if colonic disease is present iii. Fistula formation |
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a. Where does UC present?
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i. Begins in rectum and can extend proximally up to cecum
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b. What are the symptoms of UC?
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i. LLQ pain
ii. Blood diarrhea |
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c. What type of inflammation is in UC?
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i. Crypt abscesses with neutrophils
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d. What are the complications of UC?
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i. Toxic megacolon
ii. Carcinoma |
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a. What is acute appendicitis caused by?
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i. Children→ Lymphoid hyperplasia
ii. Adults→ fecalith |
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b. What are the symptoms of acute appendicitis?
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i. Periumbilical pain
ii. Fever iii. Nausea iv. RLQ pain |
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a. What are colonic diverticula?
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i. Outpouchings of mucosa and submucosa through the lamina propria
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b. What causes colonic diverticula?
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i. Constipation
ii. Straining iii. Low-fiber diet |
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c. Where do colonic diverticula arise?
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i. Where vasa recta traverse the lamina propria
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d. What are the symptoms of colonic diverticula?
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i. Hematochezia
ii. Diverticulitis iii. Fistula |
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a. What are colonic polyps?
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i. Raised protrusions of colonic mucosa
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b. What are the two types of colonic polyps?
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i. Hyperplastic
ii. Adenomatous |
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c. What are hyperplastic polyps? What is their malignant potential?
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i. Due to hyperplasia of glands
ii. Benign with no malignant potential |
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d. Where do hyperplastic polyps arise?
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i. Left side-- colon
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e. What are adenomatous polyps? What is their malignant potential?
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i. Neoplastic proliferation of glands
ii. Benign but premalignant |
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f. How do you screen for polyps?
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i. Colonoscopy
ii. Testing for fecal occult blood |
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g. What are the greatest progression risk factors for colonic polyps?
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i. Size >2 cm
ii. Sessile growth iii. Villous histology |
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a. What is FAP?
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i. Autosomal dominant disorder characterized by 100s to 1000s of adenomatous polyps
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b. What causes FAP?
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i. Inherited APC mutation
ii. Increases propensity to develop adenomatous polyps throughout colon and rectum |
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c. What is the tx for FAP?
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i. Prophylactic removal of colon and rectum
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d. How many polyps typically present in FAP? What is the minimum?
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i. 500-2500
ii. 100 is the minimum |
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e. How can you prevent cancer in FAP?
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i. Early detection
ii. Prophylactic colectomy |
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f. What is Gardner syndrome?
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i. FAP with fibromatosis and osteomas
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g. What is fibromatosis?
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i. Non-neoplastic proliferation of fibroblasts
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h. What is an osteoma?
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i. Benign tumor of bone
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i. For what other conditions does HNCC put you at risk?
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1. Colorectal cancer
2. Extraintestinal cancer-- endometrium |
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ii. What is the typical presentation of HNCC?
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1. Right-sided tumors
2. More likely to be poorly differentiated 3. Present at a younger age |
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iii. What is stage T1S cancer?
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1. Penetration into the mucosa
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iv. What is state T1 cancer?
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1. Penetrates full thickness of mucosa and muscularis mucosae into submucosa
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v. What is stage T2 cancer?
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1. Penetrates down to serosa
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vi. What is stage T3 cancer?
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1. Penetrates through serosa
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vii. What causes HNCC?
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1. Mutations in genes encoding proteins responsible for detections, excision, and repair of DNA replication errors
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viii. What genes are mutated in HNCC?
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1. MSH2
2. MLH1 |
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1. What is the most common GI malignancy?
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a. Adenocarcinoma
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2. What are the risk factors for colonic adenocarcinoma?
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a. Diets high in fat and refined carbohydrates
b. Diets low in vegetable fiber and antioxidants c. Alterations in GI flora d. FAP, HNCC |
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3. What causes colonic adenocarcinoma?
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a. APC/beta-catenin pathway→ activation of genes that promote epithelial proliferation
b. Microsatellite instability results in increased proliferation and decreased apoptosis c. Late K-RAS and P53 mutations promote growth and prevent apoptosis d. SMAD mutations reduce TGF-beta signaling and promote cell cycle progression |
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4. What will a colonic adenocarcinoma look like upon gross examination?
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a. May be polypoid and exophytic
b. Distal colon→ napkin ring mass encircling the bowel c. May be ulcerated |
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5. What will the microscopic appearance of colonic adenocarcinoma be?
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a. Tall columnar cells arranged in haphazard glands
b. Similar to adenomatous polyps |
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6. What is a dx for iron deficiency anemia in a post-menopausal female or adult male without any eating disorder or malabsorption syndrome?
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a. Colon cancer until proven otherwise
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1. With what is squamous cell carcinoma of the anal canal associated?
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a. HPV
b. Condyloma accuminatum |
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1. From where to carcinoid tumors arise?
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a. Neuroendocrine cells of the gut
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2. What is the most common tumor of the appendix?
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a. Carcinoid tumor
b. Most often near tip |
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1. What are the sx of carcinoid syndrome?
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a. Cutaneous flushing
b. Bronchospasm c. Increased bowel motility-- projectile diarrhea d. Right-sided cardiac valve thickening |
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4. How do you cure foregut carcinoids? What is their metastatic potential?
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a. Excision
b. Rarely metastasize |
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1. What is the metastatic potential of midgut carcinoids?
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a. Multiple and aggressive
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6. What are the characteristics of hindgut carcinoids?
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a. Usually found incidentally
b. Very indolent c. Excision is curative |
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7. What is the gross morphology of a carcinoid?
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a. Tan-yellow polypoid lesions
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8. What is the microscopic morphology of a carcinoid?
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a. Nests and cords or islands and sheets of uniform, small, round to oval cells
b. Nuceli are oval |