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101 Cards in this Set
- Front
- Back
Difficulty in swallowing
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dysphagia
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retrosternal burning pain, regurgitation of gastric contents
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heartburn
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blood in stools
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melena
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vomiting of blood
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hematamesis
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lower gi bleeds
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hematochezia
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dilated tortous veins protrude into esophagus
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esophageal varices
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esophageal varices is result of what?
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portal hypertension and chronic alcoholism
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injury to the esophageal mucosa with subsequent inflammation.
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esophagitis
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esophagitis has been correlated strongly with this
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esophageal carcinoma
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narrow of esophagus
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stricture
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due to chronic GI reflux, this is the replacement of normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells
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barrett esophagus
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significant clinical outcome of barrett esophagus
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dev. of adenocarcinoma, thus screening recommended
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90% of esophageal cancers but in US not so much.
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Squamous cell carcinoma
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dominant esophageal cancer in US
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adenocarcinoma
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only recognized precursor to esophageal adenocarcinoma
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barret esophagus
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1. iron deficiency anemia
2. atrophic glossitis (bald tongue) 3. dysphagia (dif. swallowing) |
plummer-vinson syndrome, common in swedish women who also have atrophic gastritis and esophageal webs.
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chronic inflammation of stomach
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atrophic gastritis
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overused term, inflammation of the gastric mucosa
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gastritis
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chronic mucosal inflammatory changes leading to muscosal atrophy and epi. dysplasia
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chronic gastritis
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most important etiologic association for chronic gastritis
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H. pylori
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autoantibodies to the gastric gland parietal cells
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autoimmune gastritis
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name two types of chronic gastritis
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1. H. Pylori
2. autoimmune |
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h. pylori induced proliferations of lymphoid tissue w/in gastric mucosa can lead to
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gastric lymphomas
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patients with peptic ulcer often have what?
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h. pylori infection
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acute mucosal inflammatory process of transient nature
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acute gastritis (NOT ASSOCIATED WITH H. PYLORI)!!
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major cause of hematameses (throwing up blood), complicated by NSAID use
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acute gastritis (NOT ASSOCIATE WITH H. PYLORI)!!
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breach in epi. of mucosa only.
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erosion
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a breach in the mucosa of the GI that extends through the musc. mucosa into the submucosa or deeper.
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ulcer
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chronic, usually solitary lesions that occur in any portion of the GI exposed to the aggressive action of acid-peptic juices.
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peptic ulcers
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ratio of peptic ulcers in duodenum to stomach
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4:1
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remitting, relapsing lesions with no racial or genetic influence
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peptic ulcers
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name the two key facts regarding peptic ulcers
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1. fundamental requisite is mucosal exposure to gastric acid and pepsin
2. strong causal assoc. w/ H. Pylori (70% of cases) |
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Other major cause of peptic ulcers (besides H. pylori)
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NSAIDs, ^ w/ age, dose of NSAID & prolonged usage. Suppression of prostaglandin synthesis is key to nsaid indused peptic ulceration
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extremely common condition in peptic ulcer disease patients
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chronic gastritis
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what do NSAID associated peptic ulcer disease pts + H. pylori results in
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Chronic gastritis, without H. Pylori, won't have chron. gastritis
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Multiple peptic ulcerations in the stomach, duodenum and even jejunum due to excess gastrin by a tumor (a paraneoplastic syndrome)
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Zollinger-Ellison Syndrome
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focal, acutely developing gastric mucosal defects due to stresses
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Acute Gastric Ulcerations
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acute gastric ulcerations due to trauma defined as:
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major surgery, sepsis
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ulcers due to extensive burns
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Curling ulcers
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ulcers due to trauma or surgical injury to the CNS or intracerebral hemorrhage
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Cushing ulcers
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final type of acute gastric ulcerations, do to irritants:
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NSAIDs and corticosteroids, typically.
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leading gastric cancer, has intestingal and diffuse types
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Gastric carcinoma
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malignancy that arises from gastric mucous cells having undergone metaplasia due to chronic gastritis. Well differentiated, form neoplastic intestinal glands, declining in US
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Intestinal type gastric carcinoma
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arrises de novo from native gastric mucous cells, not assoc. w/ chronic gastritis, poorly differentiated, no glands, permeate mucosa and infiltrative growth pattern, 1/2 of GC in the US
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Diffuse type gastric carcinoma
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metastasis involving supraclavicular lymph node
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Virchow's node
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metastatic invasion to ovaries
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Krukenberg tumor
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predisposing factors to adenocarcinoma:
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1.chronic gastritis associated w/ H. Pylori
2. diet |
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distension of colon greater than 6-7 cm, congenital and acquired disorder
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Hirschsprung disease, congenital megacolon
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cause of hirschsprung/megacolon
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caudad migration of neural crest-derived cells along GI arrests before reaching anus
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variceal dilations of anal and perianal submucosal venous plexuses
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hemorrhoids (straining or chronic constipation or pregnancy)
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increased stool mass, frequency or fluidity
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diarrheal disease
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viral, bacterial, parasitic or protozoal GI infection
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enterocolitis
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bacterial diarrhea due to toxins
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bacterial enterocolitis, an example of a toxin would be C. Botulinum
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enteric pathogen that adheres to mucosal epi.
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bacterial enterocolitis, incubation of several hours to days before onset
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suboptimal absorption of any or all ocmponents of normal diet
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malabsorption syndromes
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defective intraluminal digestion
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pancreatic insufficiency, undigested nutrients ^ osmotic pressure, result in diarrhea
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mucosal cell abnormalities
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lactose intolerance, a deficiency of disaccharidase
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reduced small intestinal surface area
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gluten sensitive enteropathy, aka celiac disease
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prototypical noninfectious malabsorption due to reduced absorptive surface area
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celiac disease
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sensitivity to gliadin
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celiac disease, leads to total flattening of mucosal villi and loss of absorptive surf. area due to immune response
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malabsorption due to intestinal infection
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tropical sprue
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Crohn disease an dulcerative colitis, collectively known as
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idiopathic inflammatory bowel disease
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affects any level of GI, mouth to anus, mostly small intestine and colon. a systemic inflammatory diesaes w/ predominant GI involvement.
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Regional Enteritis (Crohn Disease)
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skip lesions
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sharply delimited and typically transmural involvement of the bowel by an inflammatory process with mucosal damage (Crohn Disease)
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Granulomas in alimentary tract
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presence of non-caseating granuloma in 40-50% of cases of Crohn Disease
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fistula formation
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the 3rd characteristic of CD
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ulceroinflammatory disease affecting the colon but limited to the mucosa and submucosa except in the most sever cases. Begins in rectum and extends proximally in continuous fashion
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Ulcerative colitis
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well formed granulomas are absent
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UC
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no skip lesions
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UC
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mucosal ulcers rarely extend below submucosa and serosal surface typically normal
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UC
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much greater risk for carcinoma than Crohn Disease
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Ulcerative Colitis - think inflammation = predisposition to cancer
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blind pouch leading off GI tract
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colonic diverticulosis
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most common location for diverticula
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colon
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2 causes of diverticula
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1. exaggerated peristaltic contractions with abnormal elevation of intraluminal pressure
2. focal defects peculiar to the normal musculature of colonic wall |
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weakness or defect in wall of peritoneal cavity, protrusion of pouch like sac of peritoneum
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hernial sac
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adhesions between bowel segments or abdominal wall, often post surgery
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intestinal adhesions
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telescoping of proximal segment of bowel into immediately distal segment
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intussusception
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twisting of a loop of bowel about its base or attachment
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volvulus
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tumorous mass that protrudes into lumen of gut
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polyps
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90% of all epi. polyps, no malig. potential
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non-neoplastic polyps
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most common type of non-neoplastic polyp, small and multiple
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hyperplastic polyps
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normal tissue, all jumbled around
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hamartoma
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juvenile or peutz-jeghers
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examples of hamartomatous polyps
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hamartomatous proliferation occurs most freq in kids
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juvenile polyps
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a familial polyposis syndrome, hamartomatous polyps. does not develop colonic carcinomas but is assoc. w/ ^ risk of malignancy
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Peutz-Jephers Syndrome
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500 to 2500 colonic adenomas that carpet mucosa, due to mutation in APC gene. min of 100 polyps for dx. colonic cancer 100% by midlife
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familial adenomatous polyposis FAP
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APC mutation, has several extraintestinal tumors, hundreds of thousands of adenoma, colon cancer 100% by midlife
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Gardener's syndrome
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Two polyp syndrome related to mutated APC gene
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Familial adenomatous polyposis (FAP) and Gardener's Syndrome
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hamartomatous polyps in GI, does not develop colonic carcinomas, but is associated with ^ risk of malignancy
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Cowden syndrome
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Two syndromes, both w/ hamartomatous polyps, don't becme carcinomas, but are associated w/ ^ risk of malignancy
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1. Peutz-Jephers Syndrome
2. Cowden Syndrome |
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2 pathways for colon cancer development
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1. APC/Beta catenin pathway
2. MSI microsatellite instability pathway |
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loss of APC tumor supressor gene is believed to be the earliest event in the formation of adenomas. Chromosomal instability.
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APC/Beta Catenin pathway *most colon cancers*
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germline mutations in APC gene giving rise to hundreds of adenomas that progress to form cancers
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adenoma-carcinoma sequence, part of APC/b catenin pathway
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defective *DNA repair* caused by inactivation of DNA mismatch repair genes
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MSI microsatellite instability. *non polyps*
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MSI pathway gives rise to this type of cancer
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hereditary nonpolyposis colon carcinoma
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unique tumor from enterochromaffin cells of gut
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Carcinoid tumors, mainly small intestine
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problem with GI carcinoids
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often have secratory products, ex: zollinger-ellison (excess gastrin) cushing syndrome (ACTH secretion).
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GI carcinoids that have metastasized to liver
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Carcinoid Syndrome
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w/ GI carcinoids, what must be present for development of syndrome?
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hepatic dysfunction due to metastases from other sites.
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chronic gastritis and H. Pylori predispose to what lymphatic cancer?
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gastrointestinal lymphoma
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result of fecalith
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acute appendicitis.
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