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If your not sure what answer should be entered, press the space bar and the next missing letter will be displayed. When you are all done, you should look back over all your answers and review the ones in red. These ones in red are the ones which you needed help on. Question: 1. What is the mucosal of the GI tract is composed of?Answer: Highly dynamic cells Question: 2. What is the specialty of cell?Answer: Transmembrane Question: 3. What are two functions of epi ?Answer: Secretion and What do these functions facilitate? Digestive and nutrient absorption Question: 4. Where do the bacteria and mutagens?Answer: In the Question: 5. What is the absorptive surface regeneration time ?Answer: Every 24-72 Question: 6. What is the of rapid turn over?Answer: It protects the absorptive surface from acute insults and the of mutagens Question: 7. Which part of the GI has accelerated turn over?Answer: The small intestine has a cell turn over while the colon has slower turn over Question: 8. What results in the slower turn over of the ?Answer: Foster mutagens and the rate of colonic cancer Question: 9. Is gastroenteritis bacterial or ?Answer: Predominantly Question: 10. What are the clinical presentations of ?Answer: Transient, with vomiting and diarrhea and no fever Question: 11. Is necessary for the treatment of gastroenteritis?Answer: Can be treated medication Question: 12. What dietary changes are for gastroenteritis?Answer: Oral rehydration followed by easily digestible diet and therapy (bacterial containing, Dr Robinson mentioned in the class that probiotic organisms in pateurized milk is not the real thing as pasteurization kills everything) Question: 13. What are the non bacterial of AGE?Answer: GREE organ, rota virus, entero viruses, Entamoeba histolytica Question: 14. What are the causes of AGE?Answer: EESSCC Enteropathogenic E. coli, , Shigella, Cholera, Campylobacter Question: 15. What is the pathobiology of agents?Answer: Preformed toxin producers (Staph aureus), Enterotoxin producers (Cholera, enterotoxigenic E.coli), Cytotoxin (Clostridium), Enteroadherent (Giardia, helminthes, entero-pathogenic E.coli, entero-adherent E.coli) Question: 17. When is the therapy implicated?Answer: If systemic symptoms Question: 18. What does therapy do?Answer: It prolongs state Question: 19. What is a of diarrhea?Answer: Injury to the brush border of the SI and lactose deficiency Question: 20. What is secondary intolerance caused by?Answer: Injury to absorptive surface of the Question: 21. What is a of lactose intolerance?Answer: Osmotic Question: 22. What is diarrhea?Answer: Osmotic diarrhea occurs when too much is drawn into the bowels. Question: 23. What is the of osmotic diarrhea?Answer: maldigestion (e.g., pancreatic disease or Coeliac disease, in which the nutrients are left in the lumen to pull in ). Question: 24. What is cause of Osmotic diarrhea?Answer: by laxatives (which work to alleviate constipation by drawing water into the bowels). Question: 25. In individuals, too much magnesium or vitamin C or undigested lactose can produce what?Answer: osmotic diarrhea and of the bowel. Question: 26. What can a person who has lactose intolerance have?Answer: difficulty absorbing lactose after an extraordinarily high of dairy products. Question: 27. What happens in a person who does not have malabsorption?Answer: excess fructose can still cause diarrhea. Question: 28. What is less likely to diarrhea?Answer: High-fructose foods that also have a high glucose are more absorbable. Question: 29. What is difficult to in the body?Answer: alcohols such as sorbitol (often found in sugar-free foods) and, in large amounts, may lead to osmotic diarrhea. Question: 30. What is a distinguishing feature of diarrhea?Answer: it stops after the patient is fasted or stops the poorly absorbed solute. Question: 31. What are the of osmotic diarrhea?Answer: Unabsorbed CHO attract water into the lumen of the gut and causes Question: 32. What should be avoided osmotic diarrhea?Answer: for 7-10 days should be avoided Question: 33. What is disease?Answer: (Coeliac disease; celiac disease) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle . Question: 34. What are the symptoms of disease?Answer: chronic diarrhea, failure to thrive (in children), and fatigue, but these may be absent and in all other organ systems have been described. Question: 35. Who does the celiac disease ?Answer: It is estimated to affect about 1% of all Indo-European populations, but is thought to be significantly under diagnosed. A growing portion of diagnoses are being made in asymptomatic persons as a result of screening. Question: 36. What is the cause of disease?Answer: by a reaction to gliadin, a gluten protein found in wheat (and similar proteins of the tribe Triticeae which other cultivars such as barley and rye). Question: 37. What upon exposure to gliadin?Answer: the enzyme tissue transglutaminase the protein, and the immune system cross-reacts with the bowel tissue, causing an inflammatory reaction. Question: 38. What does the to gliadin lead to?Answer: leads to flattening of the lining of the intestine (called villous atrophy). Question: 39. What does the of the lining of small intestines interfere with?Answer: This interferes with the absorption of nutrients because the intestinal villi are responsible for . Question: 40. What is the effective of celiac disease?Answer: a gluten-free diet. Question: 41. Is proteins and wheat allergy the same?Answer: While the disease is caused by a reaction to wheat proteins, it is not the same as allergy. Question: 42. What is allergy?Answer: A chronic hereditary intestinal disorder in which an inability to absorb the gliadin portion of gluten results in the gliadin an immune response that damages the intestinal mucosa Question: 43. What is the prevalence of disease?Answer: 10% in first degree Question: 44. What is a factor of celiac disease?Answer: Gluten, a rubbery mass that remains when dough is Question: 45. What are the components of ?Answer: Glutamine 35%, 15%, hydrophobic amino acid 15% Question: 46. What is the most fraction of gluten?Answer: Low molecular weight gliadin are most biologically active component Question: 47. Why is disease important?Answer: it’s a valuable model for comprehension of a disease in which environmental, genetic and immunological factors interplay Question: 48. What is HLA?Answer: Human leukocyte Question: 49. Which HLAs is disease associated with?Answer: HLA DQA1 0501 and DQB1 Question: 50. What does DQ binds to?Answer: Peptide of Question: 51. What is need to bind to in order for the CD4 to recognize it?Answer: Gliadin need to bind to DQ Question: 52. What are the primary of Lamina propria?Answer: CD4 Question: 53. What cytokines are released in response to disaease?Answer: TH1, Question: 54. What is the between the intraepithelial lymphocytes of normal intestinal mucosa vs. celiac mucosa?Answer: Normal CD8TCRab+ whereas CD8TCRgd+ for gluten mucosa Question: 55. Is of lymphocyteCD8TC from Rab+ to Rgd+ make difference?Answer: Yes it is thought to the intolerance of gluten Question: 56. What is the cause of tissue damage in disease?Answer: Production of antiendomysial and antireticulum Question: 57. What is the classic presentation of celiac in infancy?Answer: Unhappy blond child, with failure to thrive, bloating, , vomiting, abdominal pain and growth delay. Question: 58. What age of the do symptoms present?Answer: And what as a result? Several months after introduction of cereal, sudden fall of growth cruve result Question: 59. How do older children with celiac disease?Answer: Children older than 2 years of age Extra-intestinal symptoms such as growth failure, hepatitis, epilepsy, angular cheilitis. Recurrent aphothous stomatitis may be the only symptom associated with pain Question: 60. What is a distinct sign of children with celiac disease of HLA DR 3?Answer: Dental hypoplasia Question: 61. What is the importance of IgA in celiac disease?Answer: IgA deficient have a 10 fold risk of developing celiac disease compared to general population Question: 62. What is the clinical presentation of young adults with disease?Answer: Dermatitis , a condition characterized by clear vesicles or blood tinged vesicles distributed over the extensor area of the elbows, knees, buttocks, shoulder and scalp Question: 63. What happens to young adults with celiac disease upon of gluten?Answer: The 8 hour stinging pruritic lesions that are tend to flare with consumption of gluten Question: 64. What is dermatitis herpetiformis associated with?Answer: HLA DR3, Question: 65. Do all celiac patients present with dermatitis herpetiformis (DH)? No, 60% of pts with DH have disease confirmed by biopsyAnswer: Question: 66. What type of is DH biopsy present?Answer: Neutrophil rich at the dermapapillae Question: 67. What does immunofluorescence ?Answer: Granular deposits of IgA in the dermis Question: 68. What diseases do DH patients present with?Answer: Achlorhydria, atropic gastritis, autoimmune throiditis, increased risk of non Hodgkins lymphoma which be avoided gluten free diet Question: 69. Is there any association between alopecia and celiac disease?Answer: Yes, young pts with alopecia have demonstrated to have disease Question: 70. How do older present with celiac disease?Answer: Malabsorption, mild of malabsorption are frequently asymptomatic. As the disease progresses the stool become greasy, bulky, foul smelling. The GI symptoms can be associated with nutritional or vitamin deficiencies including visual disturbances, neur Question: 71. How is anemia associated with disease?Answer: Celiac disease cause blood loss and the cause of microcytic hypochromic anemia Question: 72. Why do most dx pts have osteopenic bone dx?Answer: related to absorption of vitamin D, protein, and calicium malabsorption Question: 73. How is the pts CNS is affected?Answer: , intracranial calcification, serzures may be controlled by gluten free diet. Vitamin A deficient pts may have night blindness, B12 deficient pts have peripheral neuropathy. Question: 74. What are associated with allele DR3 in celiac pts?Answer: Diabetes mellitus, thyroiditis, sjorgren’s syndrome, autoimmune thrombocytopenia Question: 75. What increases the risk of having celiac disease?Answer: Cystic fibrosis, and down Question: 76. What are the diagnostic tests for disease?Answer: IgA antiendomysial , IgA and IgG antigliadin antibodies, IgA tissue transglutaminase antibody Question: 77. What is the specificity of antibody test?Answer: 95% Question: 78. When is performed?Answer: On patients with symptoms and serological evidence of the disease, which will show short or absent villi, a mononuclear infiltrate, epithelial damage and hypertrophy of the crypts Question: 79. How is celiac managed?Answer: Gluten free diet, rice, pure oats, treatment of anemia Fe, Folate, B12. bone disease treat with bone growth stimulators, seizure treated with dietary changes and antisezure medication, and specific diseases are treated accordingly such as diabe Question: 80. How is DH (dermatitis herpatiformis) ?Answer: Strict diet, for lesions. Lesions DO NOT respond to steroids Question: 81. What is the most GI disorder?Answer: GERD 15% Question: 82. What the symptoms of GERD?Answer: Back flow of gastric acid into the Question: 83. What is the normal antireflux mechanisms of?Answer: LES (lower esophageal sphincter/segment), crural diaphragm and junction Question: 84. When does occur?Answer: When the gradient of pressure between the LES and stomach is lost could be caused by transiet or loss of LES tone Question: 85. What LES?Answer: Muscle weakness, scleroderma like illness, myopathy, pregnancy, smoking, drugs including anticholinergic , smooth muscle relaxants, Beta adrenergic agents, phosphodiesterase inhibitors, when gastric volume increases form meals, pyloric obstruction, g Question: 86. What is LPR?Answer: Laryngopharyngeal disease Question: 87. What is VCD?Answer: cord dysfunction Question: 88. Compare and GERD/LPRAnswer: GERD (Supine nocturnal reflux, Prolonged acid exposure, Lower esophageal dysfunction) and LPR (Daytime reflux, Short but extensive damage phenomenon <40% heart burn, <25% esophagitis, Upper esophageal dysfunction, is more susceptible to Question: 89. What is the of GERD/LPR?Answer: Acid and pepsin are 100x more to cause injury to larynx than the esophagus that is protected by carbonate and peristalsis Question: 90. What is presentation of LRP/LRD?Answer: Chronic dysphonia, clearing of the throat, , chronic congestion of upper airways, dyspepsia and reflux Question: 91. What is LRP/LRD with?Answer: PPI . Theophylline and beta 2 agonists decrease lower esophageal sphincter pressure Question: 92. What do voice disorders test positive for?Answer: 50% of pH probes test Question: 93. What are major findings of LRD ?Answer: Pseudosulcus vocalis, obliteration, erythema, vocal fold edema, posterior glottic commisure hypertrophy, granuloma Question: 94. What is the gold for diagnosis of LRD?Answer: 24 hour pH Question: 95. What does pH measure?Answer: It monitors patterns of reflux so that can be monitored Question: 96. How is LRD ?Answer: Elevate the head of the bed, weight loss, don’t lie down until 3 hours after eating, avoid tobacco, fatty foods, alcohol, caffeine, Ca blockers, nitrates, and sedatives, PPI – , prevacid Question: 97. What is esophagitis?Answer: It is the of mucosal damage that occurs when mucosal defenses are unable to counteract the damage done by the acid Question: 98. What infiltrates are seen in mild ?Answer: Infiltrations of granulocytes, hyperplasia of the cells Question: 99. What is esophagitis?Answer: A more progressive form of related disease Question: 100. What is basic pathophys of esophagitis?Answer: More intensive including erythema, exudates, and ulcerations, strictures will with continuous damage Question: 101. What is the treatment of mild ?Answer: H2 blockers such as cimitidine and ranitidine for 2-3 months. Pts non responsive to H2 are antagonists are treated with proton pump inhibitors. Omperazole, Question: 102. What is gastric ?Answer: The epi consists of rugae that contain microscopic pits. The majority of gastric glands are found in the oxyntic mucosa and contain mucous neck, parietal and cells. Pyloric glands contain mucous and endocrine cell are found in the antrum Question: 103. Where are the of gastric glands located?Answer: Found in the oxyntic mucosa and contain mucous neck, and cells Question: 104. What do glands contain?Answer: Mucous Question: 105. Where are the cells found?Answer: In the Question: 106. GI mucosa is attacked by what?Answer: HCL, /pepsin and bile salts, exogenous factors such as drugs, alcohol, and bacteria Question: 107. What type of are included for PUD?Answer: Life style changes including decreasing your folk lifts, sleeping with head of the bed elevated, limit the intake of chocolate, foods, coffee, alcohol, mint, orange juice, large meals particularly late at night, avoid anticholinergics, calcium chann Question: 108. What is the first line of of GI?Answer: Mucous bicarbonate layer which a physiochemical barrier, which is composed of water, lipids, and glycoprotein Question: 109. What is ?Answer: It glycoprotein and forms hydrophobic barrier Question: 110. What the pH gradient in the stomach?Answer: Bicarbonate secreted by the gastricduodenal cell forms a pH Question: 111. What is secretion stimulated by?Answer: Question: 112. What forms the line of defense?Answer: Establishment and maintenance of pH Question: 113. What else form the mechanism of GI?Answer: Growth factors EGF, TGF, Question: 114. What prostaglandins?Answer: mucosa Question: 115. What is the of prostaglandins?Answer: Regulate the release of mucosal bicarbonate and mucus, inhibit parietal cell secretion and are regulators of mucous blood flow Question: 116. What is acid?Answer: It is the central metabolite for the formation of 2 isoforms COX 1 and Question: 117. What is the of COX1?Answer: Functions to prevent gastrointestinal integrity, aggregation Question: 118. What is the of COX2?Answer: It most specifically to tissue inflammation Question: 119. What two secretory acids are of inducing mucosal injury?Answer: Hydrochloric acid and acid Question: 120. When is the level of basal acids produced?Answer: At night Question: 121. What are the phase of gastric secretion stimulation?Answer: , gastric, and intestinal Question: 122. When is secreted?Answer: Sight, smell, and of food via vagus nerve Question: 123. What stimulates the gastric secretion? It is driven by amino acids and that stimulate the G cell to release gastrinAnswer: Question: 124. What is secretion stimulated by?Answer: It is by luminal distention and nutrient assimilation Question: 125. What are pathways?Answer: Somatostatin is to control HCl Question: 126. What does effect?Answer: Directly on the parietal cells and directly the release of histamine and gastric release Question: 127. Where is the acid parietal cell located?Answer: gland Question: 128. What does the cell do?Answer: Secrete intrinsic factor, has several receptors for H2, , gastrin, M1 Question: 129. What activates the histamine ?Answer: Binding cyclase Question: 130. What the protein kinase pathway?Answer: The gastric and M1 Question: 131. Is pathogenesis of DU and GU ?Answer: Question: 132. What accounts for the in ulcers?Answer: Decrease in pylori Question: 133. What is the etiologic agent in DU?Answer: H pylori and NSAIDs, gastric acid secretion is minor component Question: 134. What is H ?Answer: Bacterium that is , g-, microaerophillic rod found most commonly in the deeper portion of the mucosal gel, it is designed to live in the rugged gastric environment Question: 135. What does H. produce?Answer: Urease, catalase, lipase, , PAF, and CagA Question: 136. What is the epidemiology of H ?Answer: Socioeconomic Question: 137. What is H pylori associated with?Answer: Chronic gastritis, but only 10-15% develop ulcers Question: 138. What of H pylori damages the GI?Answer: Urease that produce NH3 that sustains bacterial and concomitantly damage epithelial Question: 139. What are inflammatory mediators in H. infection?Answer: Bacterial chemotatic , lipopolysaccharides, TNFa, II6, Gamma interferon, II 8, rantes Question: 140. Is a prominent symptom of NSAIDs?Answer: Question: 141. What is pathophys in DU?Answer: The defect mediated through the inhibition of the COX 1 inhibition. Prostaglandin depletion leads to increased HCL, decreased mucin production, decreased bicarbonate , decreased phospholipid secretion and decreased epi proliferation Question: 142. What are more susceptible to inflammatory bowel disease IBD?Answer: 15-30 age peak, 60 years age peak, Jewish decent, cigarette smoking, oral contraceptive use Question: 143. What the considerations of IBD?Answer: It is a polygenic disorder; UC (Characterized by gross blood, mucus, fever, anemia pain, increased sed rate, pANCA +, HLA DR2 allele, Manifested erythema nodosum 10-15%, pyoderma gangernosum and peripheral athritis more seen, uveitis, arthritis, Question: 144. What are the 3 organisms that have implicated in IBD?Answer: Mycobacterium paratuberculosis, and helicobacter species Question: 145. What pathogens have been implicated in IBD?Answer: Salmonella, , and Capylobacter. Psychosocial factor may also contribute Question: 146. What are some of IBD?Answer: sponylitis associated with HLA B27+, hepatic steatosis, and choleithiasis Question: 147. What is treatment of IBD?Answer: Sulfaslazine which remission with mild to moderate IBD, Asacol, Pentasa Question: 148. How is moderate/severe IBD ?Answer: Glucocorticoids, infiximab is a monoclonal antibody agent aimed specifically in TNF alpha, azatiprine, 6 mercapto purine and methotrexate |
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