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1. What is the mucosal surface of the GI tract is composed of? Highly dynamic epithelial cells
2. What is the specialty of epithelial cell? Transmembrane absorption
3. What are two functions of epi cells? Secretion and absorption What do these functions facilitate? Digestive and nutrient absorption
4. Where do the harmful bacteria and mutagens? In the lumen
5. What is the absorptive surface regeneration time period? Every 24-72 hours
6. What is the function of rapid turn over? It protects the absorptive surface from acute insults and the builds of mutagens
7. Which part of the GI tract has accelerated turn over? The small intestine has a faster cell turn over while the colon has slower turn over
8. What results in the slower turn over of the colon? Foster mutagens and the increased rate of colonic cancer
9. Is gastroenteritis bacterial or viral? Predominantly viral
10. What are the clinical presentations of gastroenteritis? Transient, associated with vomiting and diarrhea and no fever
11. Is medicine necessary for the treatment of gastroenteritis? Can be treated without medication
12. What dietary changes are recommended for gastroenteritis? 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)
13. What are the non bacterial causes of AGE? GREE Giardia organ, rota virus, entero viruses, Entamoeba histolytica
14. What are the bacterial causes of AGE? EESSCC Enteropathogenic E. coli, Salmonella, Shigella, Cholera, Campylobacter
15. What is the pathobiology of causative agents? Preformed toxin producers (Staph aureus), Enterotoxin producers (Cholera, enterotoxigenic E.coli), Cytotoxin producers (Clostridium), Enteroadherent (Giardia, helminthes, entero-pathogenic E.coli, entero-adherent E.coli)
17. When is the specific therapy implicated? If there’s systemic symptoms
18. What does antibiotic therapy do? It prolongs carrier state
19. What is a result of diarrhea? Injury to the brush border of the SI and secondary lactose deficiency
20. What is secondary lactose intolerance caused by? Injury to absorptive surface of the SI
21. What is a result of lactose intolerance? Osmotic diarrhea
22. What is osmotic diarrhea? Osmotic diarrhea occurs when too much water is drawn into the bowels.
23. What is the result of osmotic diarrhea? maldigestion (e.g., pancreatic disease or Coeliac disease, in which the nutrients are left in the lumen to pull in water).
24. What is another cause of Osmotic diarrhea? by osmotic laxatives (which work to alleviate constipation by drawing water into the bowels).
25. In healthy individuals, too much magnesium or vitamin C or undigested lactose can produce what? osmotic diarrhea and distention of the bowel.
26. What difficulties can a person who has lactose intolerance have? difficulty absorbing lactose after an extraordinarily high intake of dairy products.
27. What happens in a person who does not have fructose malabsorption? excess fructose intake can still cause diarrhea.
28. What is less likely to cause diarrhea? High-fructose foods that also have a high glucose content are more absorbable.
29. What is difficult to absorb in the body? Sugar alcohols such as sorbitol (often found in sugar-free foods) and, in large amounts, may lead to osmotic diarrhea.
30. What is a distinguishing feature of osmotic diarrhea? it stops after the patient is fasted or stops consuming the poorly absorbed solute.
31. What are the steps of osmotic diarrhea? Unabsorbed CHO attract water into the lumen of the gut and causes diarrhea
32. What should be avoided during osmotic diarrhea? Disaccharides for 7-10 days should be avoided
33. What is celiac disease? (Coeliac disease; celiac disease) is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy.
34. What are the symptoms of celiac disease? chronic diarrhea, failure to thrive (in children), and fatigue, but these may be absent and symptoms in all other organ systems have been described.
35. Who does the celiac disease affect? 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 increased screening.
36. What is the cause of celiac disease? 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).
37. What happens upon exposure to gliadin? the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the bowel tissue, causing an inflammatory reaction.
38. What does the exposure to gliadin lead to? leads to flattening of the lining of the small intestine (called villous atrophy).
39. What does the flattening of the lining of small intestines interfere with? This interferes with the absorption of nutrients because the intestinal villi are responsible for absorption.
40. What is the effective treatment of celiac disease? a lifelong gluten-free diet.
41. Is wheat proteins and wheat allergy the same? While the disease is caused by a reaction to wheat proteins, it is not the same as wheat allergy.
42. What is wheat allergy? 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
43. What is the prevalence of celiac disease? 10% in first degree relatives
44. What is a precipitating factor of celiac disease? Gluten, a rubbery mass that remains when dough is washed
45. What are the components of gluten? Glutamine 35%, proline 15%, hydrophobic amino acid 15%
46. What is the most reactive fraction of gluten? Low molecular weight gliadin fractions are most biologically active component
47. Why is celiac disease important? Because it’s a valuable model for comprehension of a disease in which environmental, genetic and immunological factors interplay
48. What is HLA? Human leukocyte antigen
49. Which HLAs is celiac disease associated with? HLA DQA1 0501 and DQB1 0201
50. What does DQ heterodimer binds to? Peptide of gliadin
51. What is gliadin need to bind to in order for the CD4 to recognize it? Gliadin need to bind to DQ heterodimer
52. What are the primary lympocytes of Lamina propria? CD4
53. What cytokines are released in response to celiac disaease? TH1, TH2
54. What is the difference between the intraepithelial lymphocytes of normal intestinal mucosa vs. celiac mucosa? Normal CD8TCRab+ whereas CD8TCRgd+ for gluten intolerance mucosa
55. Is shift of lymphocyteCD8TC from Rab+ to Rgd+ make difference? Yes it is thought to cause the intolerance of gluten
56. What is the cause of tissue damage in celiac disease? Production of antiendomysial and antireticulum antibodies
57. What is the classic presentation of celiac disease in infancy? Unhappy blond child, with failure to thrive, bloating, diarrhea, vomiting, abdominal pain and growth delay.
58. What age of the infancy do symptoms present? And what happens as a result? Several months after introduction of cereal, sudden fall of growth cruve result
59. How do older children present with celiac disease? 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
60. What is a distinct sign of young children with celiac disease of HLA DR 3? Dental enamel hypoplasia
61. What is the importance of IgA deficiency in celiac disease? IgA deficient children have a 10 fold risk of developing celiac disease compared to general population
62. What is the clinical presentation of young adults with celiac disease? 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
63. What happens to young adults with celiac disease upon consumption of gluten? The 8 hour stinging pruritic lesions that are pruritic tend to flare with consumption of gluten
64. What allele is dermatitis herpetiformis associated with? HLA DR3, DQw2
65. Do all celiac patients present with dermatitis herpetiformis (DH)? No, 60% of pts with DH have celiac disease confirmed by biopsy
66. What type of infiltrate is DH biopsy present? Neutrophil rich infiltrate at the dermapapillae
67. What does immunofluorescence demonstrate? Granular deposits of IgA in the papillary dermis
68. What other diseases do DH patients present with? Achlorhydria, atropic gastritis, autoimmune throiditis, increased risk of non Hodgkins lymphoma which could be avoided gluten free diet
69. Is there any association between alopecia areata and celiac disease? Yes, young pts with alopecia have demonstrated to have celiac disease
70. How do older adults present with celiac disease? 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
71. How is anemia associated with celiac disease? Celiac disease cause occult blood loss and the cause of microcytic hypochromic anemia
72. Why do most celiac dx pts have osteopenic bone dx? Directly related to absorption of vitamin D, protein, and calicium malabsorption
73. How is the celiac pts CNS is affected? Epilepsy, intracranial calcification, serzures may be controlled by gluten free diet. Vitamin A deficient pts may have night blindness, B12 deficient pts have peripheral neuropathy.
74. What diseases are associated with allele DR3 in celiac pts? Diabetes mellitus, autoimmune thyroiditis, sjorgren’s syndrome, autoimmune thrombocytopenia
75. What conditions increases the risk of having celiac disease? Cystic fibrosis, and down syndrome
76. What are the diagnostic tests for Celiac disease? IgA antiendomysial antibody, IgA and IgG antigliadin antibodies, IgA tissue transglutaminase antibody
77. What is the specificity of antiendomysial antibody test? 95% specificity
78. When is biopsy performed? 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
79. How is celiac disease managed? 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
80. How is DH (dermatitis herpatiformis) treated? Strict diet, dapsone for lesions. Lesions DO NOT respond to steroids
81. What is the most prevalent GI disorder? GERD 15% affected
82. What causes the symptoms of GERD? Back flow of gastric acid into the esophagus
83. What is the normal antireflux mechanisms consists of? LES (lower esophageal sphincter/segment), crural diaphragm and gastroesophageal junction
84. When does reflux occur? When the gradient of pressure between the LES and stomach is lost which could be caused by transiet or loss of LES tone
85. What causes LES? 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
86. What is LPR? Laryngopharyngeal reflux disease
87. What is VCD? Vocal cord dysfunction
88. Compare and contrast GERD/LPR 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
89. What is the pathophys of GERD/LPR? Acid and pepsin are 100x more likely to cause injury to larynx than the esophagus that is protected by carbonate and peristalsis
90. What is clinical presentation of LRP/LRD? Chronic dysphonia, clearing of the throat, dysphagia, chronic congestion of upper airways, dyspepsia and reflux
91. What is LRP/LRD treated with? PPI therapy. Theophylline and beta 2 agonists decrease lower esophageal sphincter pressure
92. What tests do voice disorders test positive for? 50% of pH probes test positive
93. What are major findings of LRD diagnosis? Pseudosulcus vocalis, ventricular obliteration, erythema, vocal fold edema, posterior glottic commisure hypertrophy, granuloma
94. What is the gold standard for diagnosis of LRD? 24 hour pH probe
95. What does pH probe measure? It monitors patterns of reflux so that therapy can be monitored
96. How is LRD managed? 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
97. What is reflux esophagitis? It is the result of mucosal damage that occurs when mucosal defenses are unable to counteract the damage done by the acid
98. What infiltrates are seen in mild esophagitis? Infiltrations of granulocytes, hyperplasia of the basal cells
99. What is erosive esophagitis? A more progressive form of reflux related disease
100. What is basic pathophys of erosive esophagitis? More intensive including erythema, exudates, and ulcerations, strictures will occur with continuous damage
101. What is the treatment of mild esophagitis? 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, lansoprazol
102. What is gastric anatomy? 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
103. Where are the majority of gastric glands located? Found in the oxyntic mucosa and contain mucous neck, parietal and cells
104. What do pyloric glands contain? Mucous
105. Where are the endocrine cells found? In the antrum
106. GI mucosa is constantly attacked by what? HCL, pepsinogen/pepsin and bile salts, exogenous factors such as drugs, alcohol, and bacteria
107. What type of treatments are included for PUD? 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
108. What is the first line of defense of GI? Mucous bicarbonate layer which serves a physiochemical barrier, which is composed of water, lipids, and glycoprotein
109. What is mucin? It constituent glycoprotein and forms hydrophobic barrier
110. What forms the pH gradient in the stomach? Bicarbonate secreted by the gastricduodenal cell forms a pH gradient
111. What is bicarbonate secretion stimulated by? Calcium
112. What forms the second line of defense? Establishment and maintenance of intracellular pH
113. What else form the defence mechanism of GI? Growth factors EGF, TGF, FGF
114. What contains prostaglandins? Gastric mucosa
115. What is the function of prostaglandins? Regulate the release of mucosal bicarbonate and mucus, inhibit parietal cell secretion and are important regulators of mucous blood flow
116. What is arachidonic acid? It is the central metabolite for the formation of 2 isoforms COX 1 and 2
117. What is the function of COX1? Functions to prevent gastrointestinal integrity, platelet aggregation
118. What is the function of COX2? It most specifically related to tissue inflammation
119. What two secretory acids are capable of inducing mucosal injury? Hydrochloric acid and pepsinogen acid
120. When is the highest level of basal acids produced? At night
121. What are the three phase of gastric secretion stimulation? Cephalic, gastric, and intestinal
122. When is cephalic secreted? Sight, smell, and taste of food via vagus nerve
123. What stimulates the gastric secretion? It is driven by amino acids and amines that stimulate the G cell to release gastrin
124. What is intestinal secretion stimulated by? It is driven by luminal distention and nutrient assimilation
125. What are inhibitory pathways? Somatostatin is released to control HCl
126. What does somatostatin effect? Directly on the parietal cells and directly decreasing the release of histamine and gastric release
127. Where is the acid secreting parietal cell located? Oxyntic gland
128. What does the parietal cell do? Secrete intrinsic factor, has several receptors for H2, histamine, gastrin, M1
129. What activates the histamine receptor? Binding adenyl cyclase
130. What activates the protein kinase pathway? The gastric and M1 receptors
131. Is pathogenesis of DU and GU similar? Yes
132. What accounts for the decrease in ulcers? Decrease in pylori infection
133. What is the major etiologic agent in DU? H pylori and NSAIDs, increased gastric acid secretion is minor component
134. What is H pylori? Bacterium that is flagellated, g-, microaerophillic rod found most commonly in the deeper portion of the mucosal gel, it is designed to live in the rugged gastric environment
135. What does H. pylori produce? Urease, catalase, lipase, adehesins, PAF, and CagA
136. What is the epidemiology of H pylori? Socioeconomic status
137. What is H pylori always associated with? Chronic gastritis, but only 10-15% develop peptic ulcers
138. What product of H pylori damages the GI? Urease that produce NH3 that sustains bacterial growth and concomitantly damage epithelial
139. What are inflammatory mediators in H. pylori infection? Bacterial chemotatic factors, lipopolysaccharides, TNFa, II6, Gamma interferon, II 8, rantes
140. Is dyspepsia a prominent symptom of NSAIDs? No
141. What is NSAID pathophys in DU? The defect mediated through the inhibition of the COX 1 inhibition. Prostaglandin depletion leads to increased HCL, decreased mucin production, decreased bicarbonate production, decreased phospholipid secretion and decreased epi proliferation
142. What groups are more susceptible to inflammatory bowel disease IBD? 15-30 years age peak, 60 years age peak, Jewish decent, cigarette smoking, oral contraceptive use
143. What the genetic considerations of IBD? 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 commonly seen, uveitis, arthritis,
144. What are the 3 major organisms that have implicated in IBD? Mycobacterium paratuberculosis, paramyxovirus and helicobacter species
145. What other pathogens have been implicated in IBD? Salmonella, Shigella, and Capylobacter. Psychosocial factor may also contribute
146. What are some manifestations of IBD? Ankylosing sponylitis associated with HLA B27+, hepatic steatosis, and choleithiasis
147. What is mainstay treatment of IBD? Sulfaslazine which induces remission with mild to moderate IBD, Asacol, Pentasa
148. How is moderate/severe IBD treated? Glucocorticoids, infiximab is a monoclonal antibody agent aimed specifically in blocked TNF alpha, azatiprine, 6 mercapto purine and methotrexate
Created by: sap_213
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