GI MTM Patho for PUD, GERD, and Pancreatitis

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GI MTM Patho for PUD, GERD, and Pancreatitis
2012-10-08 18:35:08

Patho GI
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  1. 5 Functions of the stomach
    • 1.  Temporary Food Storage
    • 2. Control the rate at which food enters the duodenum
    • 3. Acid secretion and antibacterial action
    • 4. Fluidisation of stomach contents
    • 5. Prelim digestion with pepsin, lipases, ect.
  2. What occurs in the fundus of the stomach?
    Collects digestive gases and produces pepsinogen
  3. What do perietal cells secrete?
  4. G cells release _____ which leads to perietal cells releasing____
    gastrin, acid
  5. Antrum and foveolar cells release
  6. What is the lower esophageal sphincter?
    Transition from the esophagus to the gastric mucosa
  7. Presentation of GERD
    • 1. Dysphagia (difficulty swallowing)
    • 2.heartburn/chestpain
    • 3. pain after meals, when lying down or bending over
  8. Patient population most likely to exp. GERD
    • age >40
    • overweight
    • pregnant
    • those who use tobacco or drink alcohol
  9. Pathology (causes) of GERD
    • 1. LES pressure: spontaneous relaxation
    • 2. delayed gastric emptying and/or increased gastric volume
    • 3.decreased esophageal clearance:  (acid stays in esophagus)---decreased mucous with age increases this issue
    • 4. Mucosal resistance: acid damage over time
    • 5. refluate composition: concentration of the acid, pepsin, or bile
  10. Epidemiology of PUD
    • 1. common
    •     a. Gastric: H. pylori, nsaids, older patients
    •     b. duodenal: h. pylori, younger patients, type O blood
  11. Defensive forces in the gut
    • 1. prostaglandins
    • 2. mucosal blood flow
    • 3. bicarb secretions
    • 4. mucous secretion
  12. Presentation of PUD
    • Epigastric pain, iron def. anemia (due to bleeding)
    • Gastric ulcer: increased pain with meals
    • Duodenal: decreased pain with meals
  13. H. pylori induced PUD presentation
    • 1. 80-90% asymptomatic
    • 2. Mild: epigastric pain, N&V
    • 3. Severe: mucosal erosion, ulceration, hemorrhage, blood loss
    • 4. Stomach and duodenal ulcers
  14. Epidemiology of H. pylori induced PUD
    • 1. increased incidence with age
    • 2. poverty
    • 3. household crowding
    • 4. minority population
    • 5.rural areas
  15. Causes of PUD
    H. pylori (helix shaped gram negative bacteria that move away from acid).  They burrow into the mucosal layer to get away from the acid
  16. Patho of H. pylori duodenal ulcers
    • 1. Occurs mostly in children
    • 2. Occurs in individuals with increased acid levels
    • 3.Infection causes G cells to secrete gastrin which causes the parietal cells to secrete more acid  (this causes the bac to burrow deeper) over time the # of periatal cells increases which causes an increase in acid secretion (leads to damage)
  17. Patho of H. pylori stomach ulcers
    • 1. Occurs mostly in elderly who have decreased acid levels
    • 2. Body of the stomach colonization
    • 3. This causes damage and loss of protection and atrophy of the stomach
    • 4. Ulcer forms as you lose cells
  18. Patho behind mucosal injury in PUD ulcers
    • 1. H. pylori secretes urease whose biproduct is ammonia
    • 2. ammonia and acid produce ammonium which would normally neutralize acid however it is also damaging to the epithelium itself
    • 3. More urease in produced in stomach ulcers
  19. Presentation of NSAID induced PUD
    • Mild: shallow erosions w/ superficial epithelial damage
    • Moderate-Severe: erosions that penetrate hte depth of the mucosa
  20. Epidemeology of NSAID PUD
    NSAID users w/in 6 months of use, age > 65, previous PUD, high dose NSAID, h. pylori infection, alcohol
  21. How do NSAIDS cause damage?
    Block prostaglandins which would normally inhibit acid secretion, stimulate mucus, stimulate bicarb, and increase mucosal blood flow
  22. Two categories of IBS
    • 1. Crohn Disease: transmural inflammation of the GI tract (mouth-anus)
    • 2. Ulcerative colitis: mucosal inflammation of the GI tract (colon-rectum)
  23. Epidemiology of IBS
    • 1. Nothern latitudes
    • 2. teens-20s or 60-80 yo
    • 3. women> men
    • 4. Caucasion
    • 5. Hygeine hypothesis
  24. Crohn Disease
    • 1. Discontinous skip lesions throught intestines
    • defects in intestinal tight junctions and treansepithelial transport of paneth cells
  25. Presenation of Crohn Dx
    • Intermittent attacks of mild diarrhead
    • lower right quadrant pain, bloody diarrhea, fever
    • Fibrous strictures can form
  26. Ulcerative colitis
    • 1. Superfical continous colonic inflammation
  27. Ulcerative colitis presentation
    intermittent attacks of urge to defacate, chronic bloody diarrhea with mucoid material (HALLMARK), lower abdominal pain, and cramps
  28. Presentation of IBS
    • 1. Chronic, relapsing abdominal pain, bloating, changes in bowel habits
    • 2. 3days/month for 3 months, improvement in pain with defecation
    • 3. Change in stool frequency or form
  29. Epi. of IBS
    • 20-40 yo
    • F>M
  30. Causes of IBS
    Triggers: stress, diet, abnormal GI motility, enteric sensory function
  31. Presentation of acute pancreatitis
    • 1. severe abdominal pain that can be referred to upper back and left shoulder
    • 2. anorexia, N&V
    • 3. Elevated amylase and lipase
    • 4. Shock
    • 5. Infection from necrosis
  32. Epidemiology of Acute Pancreatitis
    Fairly common, 80% associated with billary tract disease F>M, and alcoholism, 30-60% related to gallstones
  33. Causes of acute pancreatitis
    • 1. Pancreatic duct obstruction: intestinal backup which causes local inflammation, edema, and lack of blood flow
    • 2.  Direct acinar cell injury by alcohol, drugs, trauma, ischemia, and viruses
    • 3. Inappropriate delivery of proenzymes within acinar cells leading to activation of digestive enzymes w/in acinar cells
  34. Presenation of Chronic Pancreatitis
    • 1. Asymptomatic until diabetes mellitus or pancreatic insufficiency develops
    • 2. epigastric pain, jaundice, and indigestion, mild fever, increase in serum lipase/amylase
    • 3. malabsorption and chronic pain
  35. Epi of Chronic Pancreatitis
    most commonly middle aged alcoholic men

    If 20-25yo 50% mortality
  36. Causes of Chronic Pancreatitis
    Mild inflammation-> tissue destruction -> inflammation resolves -> damaged pancreatic tissue is replaced by scar tissue -> progressive destuction of pancrease