GI
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| show | Highly dynamic epithelial cells
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| 2. What is the specialty of epithelial cell? | show 🗑
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| 3. What are two functions of epi cells? | show 🗑
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| show | In the lumen
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| 5. What is the absorptive surface regeneration time period? | show 🗑
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| show | It protects the absorptive surface from acute insults and the builds of mutagens
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| 7. Which part of the GI tract has accelerated turn over? | show 🗑
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| 8. What results in the slower turn over of the colon? | show 🗑
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| show | Predominantly viral
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| 10. What are the clinical presentations of gastroenteritis? | show 🗑
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| 11. Is medicine necessary for the treatment of gastroenteritis? | show 🗑
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| show | Oral rehydration followed by easily digestible diet and probiotic therapy (bacterial containing, Dr Robinson mentioned in the class that probiotic organisms in pateurized milk is not the real thing as pasteurization kills everything)
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| 13. What are the non bacterial causes of AGE? | show 🗑
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| show | EESSCC Enteropathogenic E. coli, Salmonella, Shigella, Cholera, Campylobacter
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| 15. What is the pathobiology of causative agents? | show 🗑
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| show | If there’s systemic symptoms
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| 18. What does antibiotic therapy do? | show 🗑
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| 19. What is a result of diarrhea? | show 🗑
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| 20. What is secondary lactose intolerance caused by? | show 🗑
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| show | Osmotic diarrhea
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| show | Osmotic diarrhea occurs when too much water is drawn into the bowels.
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| show | maldigestion (e.g., pancreatic disease or Coeliac disease, in which the nutrients are left in the lumen to pull in water).
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| 24. What is another cause of Osmotic diarrhea? | show 🗑
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| show | osmotic diarrhea and distention of the bowel.
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| show | difficulty absorbing lactose after an extraordinarily high intake of dairy products.
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| show | excess fructose intake can still cause diarrhea.
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| 28. What is less likely to cause diarrhea? | show 🗑
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| 29. What is difficult to absorb in the body? | show 🗑
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| 30. What is a distinguishing feature of osmotic diarrhea? | show 🗑
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| show | Unabsorbed CHO attract water into the lumen of the gut and causes diarrhea
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| show | Disaccharides for 7-10 days should be avoided
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| show | (Coeliac disease; celiac disease) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy.
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| 34. What are the symptoms of celiac disease? | show 🗑
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| 35. Who does the celiac disease affect? | show 🗑
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| show | by a reaction to gliadin, a gluten protein found in wheat (and similar proteins of the tribe Triticeae which includes other cultivars such as barley and rye).
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| 37. What happens upon exposure to gliadin? | show 🗑
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| 38. What does the exposure to gliadin lead to? | show 🗑
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| show | This interferes with the absorption of nutrients because the intestinal villi are responsible for absorption.
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| show | a lifelong gluten-free diet.
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| 41. Is wheat proteins and wheat allergy the same? | show 🗑
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| show | A chronic hereditary intestinal disorder in which an inability to absorb the gliadin portion of gluten results in the gliadin triggering an immune response that damages the intestinal mucosa
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| show | 10% in first degree relatives
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| show | Gluten, a rubbery mass that remains when dough is washed
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| show | Glutamine 35%, proline 15%, hydrophobic amino acid 15%
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| 46. What is the most reactive fraction of gluten? | show 🗑
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| show | Because it’s a valuable model for comprehension of a disease in which environmental, genetic and immunological factors interplay
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| show | Human leukocyte antigen
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| show | HLA DQA1 0501 and DQB1 0201
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| show | Peptide of gliadin
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| show | Gliadin need to bind to DQ heterodimer
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| 52. What are the primary lympocytes of Lamina propria? | show 🗑
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| show | TH1, TH2
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| show | Normal CD8TCRab+ whereas CD8TCRgd+ for gluten intolerance mucosa
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| 55. Is shift of lymphocyteCD8TC from Rab+ to Rgd+ make difference? | show 🗑
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| 56. What is the cause of tissue damage in celiac disease? | show 🗑
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| show | Unhappy blond child, with failure to thrive, bloating, diarrhea, vomiting, abdominal pain and growth delay.
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| show | And what happens as a result? Several months after introduction of cereal, sudden fall of growth cruve result
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| show | 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 abdominal pain
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| show | Dental enamel hypoplasia
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| show | IgA deficient children have a 10 fold risk of developing celiac disease compared to general population
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| show | Dermatitis herpetiformis, a condition characterized by clear vesicles or blood tinged vesicles distributed over the extensor area of the elbows, knees, buttocks, shoulder and scalp
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| show | The 8 hour stinging pruritic lesions that are pruritic tend to flare with consumption of gluten
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| 64. What allele is dermatitis herpetiformis associated with? | show 🗑
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| 65. Do all celiac patients present with dermatitis herpetiformis (DH)? No, 60% of pts with DH have celiac disease confirmed by biopsy | show 🗑
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| 66. What type of infiltrate is DH biopsy present? | show 🗑
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| 67. What does immunofluorescence demonstrate? | show 🗑
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| 68. What other diseases do DH patients present with? | show 🗑
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| show | Yes, young pts with alopecia have demonstrated to have celiac disease
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| show | Malabsorption, mild cases 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
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| show | Celiac disease cause occult blood loss and the cause of microcytic hypochromic anemia
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| 72. Why do most celiac dx pts have osteopenic bone dx? | show 🗑
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| 73. How is the celiac pts CNS is affected? | show 🗑
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| 74. What diseases are associated with allele DR3 in celiac pts? | show 🗑
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| show | Cystic fibrosis, and down syndrome
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| 76. What are the diagnostic tests for Celiac disease? | show 🗑
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| 77. What is the specificity of antiendomysial antibody test? | show 🗑
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| show | On patients with clinical symptoms and serological evidence of the disease, which will show short or absent villi, a mononuclear infiltrate, epithelial damage and hypertrophy of the crypts
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| show | Gluten free diet, rice, pure oats, treatment of anemia Fe, Folate, B12. Osteopenic bone disease treat with bone growth stimulators, seizure treated with dietary changes and antisezure medication, and specific diseases are treated accordingly such as diabe
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| 80. How is DH (dermatitis herpatiformis) treated? | show 🗑
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| show | GERD 15% affected
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| 82. What causes the symptoms of GERD? | show 🗑
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| 83. What is the normal antireflux mechanisms consists of? | show 🗑
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| show | When the gradient of pressure between the LES and stomach is lost which could be caused by transiet or loss of LES tone
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| show | Muscle weakness, scleroderma like illness, myopathy, pregnancy, smoking, drugs including anticholinergic agent, smooth muscle relaxants, Beta adrenergic agents, phosphodiesterase inhibitors, when gastric volume increases form meals, pyloric obstruction, g
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| show | Laryngopharyngeal reflux disease
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| 87. What is VCD? | show 🗑
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| show | 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, Laryngoepithelium is more susceptible to
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| show | Acid and pepsin are 100x more likely to cause injury to larynx than the esophagus that is protected by carbonate and peristalsis
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| show | Chronic dysphonia, clearing of the throat, dysphagia, chronic congestion of upper airways, dyspepsia and reflux
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| show | PPI therapy. Theophylline and beta 2 agonists decrease lower esophageal sphincter pressure
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| show | 50% of pH probes test positive
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| show | Pseudosulcus vocalis, ventricular obliteration, erythema, vocal fold edema, posterior glottic commisure hypertrophy, granuloma
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| show | 24 hour pH probe
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| show | It monitors patterns of reflux so that therapy can be monitored
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| show | 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 – nexium, prevacid
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| 97. What is reflux esophagitis? | show 🗑
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| 98. What infiltrates are seen in mild esophagitis? | show 🗑
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| 99. What is erosive esophagitis? | show 🗑
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| 100. What is basic pathophys of erosive esophagitis? | show 🗑
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| 101. What is the treatment of mild esophagitis? | show 🗑
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| show | The epi lining 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
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| show | Found in the oxyntic mucosa and contain mucous neck, parietal and cells
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| 104. What do pyloric glands contain? | show 🗑
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| show | In the antrum
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| show | HCL, pepsinogen/pepsin and bile salts, exogenous factors such as drugs, alcohol, and bacteria
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| show | Life style changes including decreasing your folk lifts, sleeping with head of the bed elevated, limit the intake of chocolate, fatty foods, coffee, alcohol, mint, orange juice, large meals particularly late at night, avoid anticholinergics, calcium chann
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| 108. What is the first line of defense of GI? | show 🗑
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| 109. What is mucin? | show 🗑
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| show | Bicarbonate secreted by the gastricduodenal cell forms a pH gradient
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| show | Calcium
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| show | Establishment and maintenance of intracellular pH
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| 113. What else form the defence mechanism of GI? | show 🗑
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| 114. What contains prostaglandins? | show 🗑
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| show | Regulate the release of mucosal bicarbonate and mucus, inhibit parietal cell secretion and are important regulators of mucous blood flow
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| show | It is the central metabolite for the formation of 2 isoforms COX 1 and 2
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| 117. What is the function of COX1? | show 🗑
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| show | It most specifically related to tissue inflammation
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| 119. What two secretory acids are capable of inducing mucosal injury? | show 🗑
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| show | At night
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| show | Cephalic, gastric, and intestinal
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| 122. When is cephalic secreted? | show 🗑
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| 123. What stimulates the gastric secretion? It is driven by amino acids and amines that stimulate the G cell to release gastrin | show 🗑
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| show | It is driven by luminal distention and nutrient assimilation
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| 125. What are inhibitory pathways? | show 🗑
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| 126. What does somatostatin effect? | show 🗑
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| 127. Where is the acid secreting parietal cell located? | show 🗑
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| show | Secrete intrinsic factor, has several receptors for H2, histamine, gastrin, M1
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| 129. What activates the histamine receptor? | show 🗑
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| 130. What activates the protein kinase pathway? | show 🗑
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| show | Yes
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| 132. What accounts for the decrease in ulcers? | show 🗑
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| show | H pylori and NSAIDs, increased gastric acid secretion is minor component
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| 134. What is H pylori? | show 🗑
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| 135. What does H. pylori produce? | show 🗑
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| show | Socioeconomic status
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| show | Chronic gastritis, but only 10-15% develop peptic ulcers
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| show | Urease that produce NH3 that sustains bacterial growth and concomitantly damage epithelial
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| 139. What are inflammatory mediators in H. pylori infection? | show 🗑
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| show | No
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| 141. What is NSAID pathophys in DU? | show 🗑
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| show | 15-30 years age peak, 60 years age peak, Jewish decent, cigarette smoking, oral contraceptive use
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| 143. What the genetic considerations of IBD? | show 🗑
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| 144. What are the 3 major organisms that have implicated in IBD? | show 🗑
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| show | Salmonella, Shigella, and Capylobacter. Psychosocial factor may also contribute
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| 146. What are some manifestations of IBD? | show 🗑
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| 147. What is mainstay treatment of IBD? | show 🗑
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| show | Glucocorticoids, infiximab is a monoclonal antibody agent aimed specifically in blocked TNF alpha, azatiprine, 6 mercapto purine and methotrexate
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