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42 Cards in this Set
- Front
- Back
Hematochezia
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Bright Red Stool
Usually associated as Distal GI Bleed or bleeding too quickly to not be broken down |
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Melana
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Dark Stool
Digestion/Oxidation of hemoglobin Upper GI Bleed or small amounts of blood |
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Congenital Anorectal malformations
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Anorectal Agenesis
Rectal Atresia Imperforate Anus Anal Stenosis Fistulas |
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Hirschsprung's Disease
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-'Congenital Megacolon' or 'Congenital Aganglionosis'
-intestinal obstruction -Constipation/Stenosis -Rectal Biopsy -Absence of Submucosal Enteric Ganglion Cells -Compensatory HYPERTROPHY of non-enteric PSNS nerve fibers -RET gene loss-of-function mutations |
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What is the most common Functional GI tract disorder?
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Irritable Bowel Syndrome
-ROME III criteria (must present >3 months with symptoms) -Bristol Stool Chart -Unknown pathophys |
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Diverticulosis vs Diverticulitis... etiology?
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-osis: d/t prolonged intralumenal pressure (low dietary fiber)
-itis: inflammation of the diverticula |
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Complications of Diverticulitis?
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-can destroy/weaken wall of colon
-Abscess formation (contains neutrophils) |
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Location of diverticular disease?
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can be all through GI tract but occurs mostly in the distal colon d/t the reabsorption of water --> hard stool forms --> pressure on wall of colon
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Pseudomembranous colitis..presentation on colonoscopy?
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mucosal surface is hyperemic and partially covered by YELLOW-GREEN EXUDATE
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Most likely pathogen for Pseudomembranous Colitis?
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C difficile (post Abx therapy when normal colonic flora is inhibited and C difficile can grow rapidly)
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Inflammatory Bowel Disease has one vague overlying cause ....
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-pronounced inflammatory process is occurring (persistent inappropriate immunologic response to GI lumenal Ag's)
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Name of IBD where you cannot distinguish between Crohn's disease and Ulcerative colitis...
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Indeterminant colitis
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Major characteristics of Crohn's disease..
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-very high C reactive protein levels
-anywhere within GI tract (mouth --> anus) -Skip lesions -'cobblestoning' mucosal pattern -'creeping fat' -NON-caseating granuloma with multinucleated giant cells -Transmural inflammation (Full thickness of the gut wall) -Perianal Fistulas -Th1 cells are active -'string sign' found by radiologist -Nephrolithiasis may occur (along with other extra-intestinal manifestations) -Colonic carcinoma is less of a risk than UC |
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Major characteristics of Ulcerative colitis..
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-elevated C reactive protein (less severe than CD though)
-Begins at the Rectum and moves proximally (more definite location --> can tx surgically) -continuous lesions -smoking PREVENTS UC -Partial thickness of gut wall -Crypt Abscesses -'lead pipe' (radiology) -inflammatory pseudopolyps -higher risk of colonic carcinoma!!! compared to CD |
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Which is more apt to have systemic inflammatory processes - UC or CD?
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UC
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Important aspect to Microscopic colitis?
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It appears normally but if you look at microscopically --> increase in inflammatory cells
-Collagenous colitis -Lymphocytis colitis |
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Are Sporadic (isolated) Juvenile Polyps malignant?
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NO!
-most common childhood polyp |
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Does Hereditary Juvenile Polyposis Syndrome have a risk for GI carcinoma?
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Yes!
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Extra-GI manifestations of Cowden's disease?
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Mucocutaneous Lesions
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Extra-GI manifestations of Peutz-Jeghers polyposis?
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Mucosal Pigmentation (on buccal mucosa, lips)
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What do Cowden's disease and Peutz-Jeghers Polyposis have in common?
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-have increased risk of malignancy (Cowden = breast, thyroid; Peutz-Jeghers = gastric, small intestines, CRC, pancreas, breast, lung, ovary)
-Autosomal Dominant -pt < 15 yo at presentation (Peutz-Jeghers is 10-15 yo; Cowden's is <15 yo) |
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Characteristics of Hyperplastic Polyps..
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-pts > 50 yo
-Asymptomatic -do NOT grow and get larger -usually benign with little malignant potential -Hyperplastic + Adenomatous features = Serrated Adenoma |
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Tubular Adenoma
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Neoplastic (benign, pre-invasive)
ROUND! Lower risk of dev into invasive Adenocarcinoma |
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Villous Adenoma
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Higher risk of developing into Invasive Adenocarcinoma
Large Villous Adenomas = Watery, Secretory Diarrhea |
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What is the genetic component to Familial Adenomatous Polyposis?
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APC gene is inactivated
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When is FAP usually diagnosed or found (with colonoscopy)?
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10-20 yo
NOTE: when younger and family hx of FAP --> genetic testing for APC gene |
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Important aspect to FAP...
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hundreds --> thousands of polyps form
Polyps themselves have malignant potential May develop into malignancy by 30s-40s Tx: prophylactic colectomy 1% of Colorectal Carcinomas = d/t FAP |
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Gardner's Syndrome =
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FAP + osteomas, desmoid tumors
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Turcot's Syndrome =
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FAP + CNS tumors
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HNPCC =
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Hereditary Non-Polyposis Colon Cancer
5-15% of Colorectal Carcinomas = d/t HNPCC Genetics = DNA mismatch repaid genes with MSI (microsatellite instability); MSH2 and MLH1 Lynch Syndrome |
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Adenocarcinoma sequence
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-The accumulation of mutations is more important than their actual sequence
-APC Gene is mutated FIRST (birth or later in life) --> K-RAS --> p53 |
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Where else is K-RAS gene effected (beyond Adenocarcinoma sequence)?
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Pancreatic Ductal Carcinoma
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Left-sided colon cancer..location/size/shape?
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-nearer to rectum
-SMALLER (d/t smaller diameter of bowel wall) -usually develops as a ring |
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Rigth-sided colon cancer..size/shape?
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-LARGER (d/t larger bowel diameter size)
-Polypod shape |
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Which has more bleeding..left or right sided colon cancer?
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Right-sided colon cancer has MORE bleeding --> pt can have Melana in feces and may develop Iron Def Anemia
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Where do Left-sided colon cancers and Right-sided colon cancers metastasize to?
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LIVER, Lungs, Brain, Bone
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Three common forms of Anorectal Neoplasms?
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Basaloid Carcinoma
Adenocarcinoma Squamous Cell Carcinoma (HPV 16 and 18) |
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External Hemorrhoids
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PAINFUL!
-Inferior Rectal Vein |
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Internal Hemorrhoids
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PainLESS!
-Superior Rectal Vein -may lead to External Thrombosis |
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Appendiceal Mucocele.. characteristics?
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Dilated, mucin-filled Appendix
May be Mucinous Cystadenoma or Mucinous Cystadenocarcinoma (difficult to tell the difference) |
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Appendiceal Carcinoids
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Neuroendocrine Tumor
TIP if Appendix Good Prognosis |
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What can develop between Taenia coli?
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Diverticula
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