Patho Exam 2 Upper GI

  1. What are the hostile aggressive factors in PUD?
    • Gastric Acid
    • H. pylori
    • NSAIDS
    • Pepsin
  2. What are the protective factors in PUD?
    • Prostaglandins
    • Mucus
    • Bicarbonate
    • Blood flow to mucosa
  3. Define PUD
    Group of upper GI tract ulcerative disorders that develop whne GI tract is exposed to acid and pepsin secretions
  4. What is the underlying problem in PUD?
    • Imbalance in aggressive and protective factors
    • - Increased gastric acidity (Oversecretion)
    • - Decreased prostaglandin production (NSAIDS)
    • - Interference with mucous layer (H. pylori infection)
  5. What damages the mucosal layer?
    Increased histamine secretion
  6. Why is histamine released?
    Released in response to damage done to organ wall
  7. What does histamine release result in?
    • Increased pepsin and acid secretion (causing injury)
    • Local vasodilation (increasing capillary permeability- resulting in mucosal edema)
  8. How does H. pylori survive?
    Produces urea-splitting enzyme called urease, which breaks up urea into ammonia and bicarbonate forming a cloud
  9. What diseases are attributed to H. pylori?
    • Peptic ulcer
    • Chronic gastritis
    • some Stomach cancers
  10. What is the pathology behind H. pylori?
    • H. pylori secretes protease
    • Breaks through mucosal gel barrier
    • Colonizes mucosa
    • Triggers inflammatory response
    • Activation of inflammatory mediators

    Resulting in: Inflammation-based Damage
  11. What is the mechanism of injury for H. pylori?
    Inflammation response
  12. What are the risk factors for NSAID-Induced PUD?
    • Advanced age r/t higher does longer
    • Higher doses of NSAIDS
    • Concomitant use of corticosteroids and anticoagulants (harm GI tract)
    • Serious systemic disorders (chronic comorbidities)
    • H. pylori infection
  13. What is Cyclo-oxygenase (COX), that NSAIDS target?
    Enzyme responsible for production of important biological mediators
  14. What does COX 1 do (which NSAIDS inhibit)?
    • Protects the GI tract
    • produces gastric prostaglandins- PGE

    therefore NSAIDS harm the GI tract inhibiting production of PGE
  15. What does COX 2 do (which NSAIDS inhibit)?
    Proinflammatory- causing pain

    therefore NSAIDS inhibit pain and inflammation (why we take them)
  16. What age group gets duodenal ulcers?
  17. What age group gets Gastic ulcers and why?
    • Age 55 to 70
    • High doses of NSAIDS
  18. Define Erosion
    • Superficial damage to mucosa and submucosa layers
    • known as "stress ulcers"
  19. Define Acute Ulcer
    • Penetration into muscle layer
    • if it eats through vascular- more bleeding
  20. Define Perforating Ulcer
    • Approaching penetration of the wall
    • at this point- through the muscular and deep, it hurts
  21. List the S&S of PUD
    • Asymptomatic until deeper
    • N/V, anorexia
    • Weight loss r/t not eating from fear of inflammation
    • Bleeding (Hematemesis or melena)
    • Pain
  22. Describe the pain associated with PUD
    • Burning, chewing pain
    • Located in the epigastric and back
    • Gastric- 1 to 2 hrs following meals
    • Duodenal- 2 to 4 hrs following meals
    • Relief: antacids and sometimes eating (seen as a buffer)
  23. What are the complications of PUD?
    • Hemorrhage
    • Obstruction
    • Perforation and Peritonitis
  24. What are the causes of Hemorrhage r/t PUD?
    • Bleeding granulation tissue (which sweeps away granulation tissue which could heal the ulcer)
    • Further erosion
  25. What are the causes of Obstruction r/t PUD?
    • Edema
    • Spasm
    • Contraction of scar tissue
  26. What does Obstruction r/t PUD do?
    Can interfere with passage of GI contents (causing symptoms) (as the scar tissue develops it strinks causing smaller passageways)
  27. What is Perforation r/t PUD?
    Erosion through all layers of tract ex. GI contents through peritoneum causing peritonitis or can attach to other organs causing damage from gastric juices
  28. List two types of Stress Ulcers and characteristics
    • Curling ulcer
    • Cushing ulcer
    • painless upper GI bleed
    • Melena
  29. Describe a Curling ulcer and cause
    • Cause: physiologic stress- seen in critical care, top priority (must be corrected within 24 hours)
    • It is the shunting of blood
    • GI tissue becomes ischemia resulting in tissue acidosis
  30. Describe Cushing ulcer and cause
    • Cause: Increased intracranial pressure
    • More severe than curling ulcer
    • Compromised brain causes hypersecretion of gastric acid
  31. Define GERD
    • Backflow (reflux) of gastric contents into esophagus
    • due to weakened or incompetent valve or physiological (feeding or NG tube)
  32. List the sequence of events r/t GERD
    • Transient relaxation of esophagus
    • Reflux (from increased gastric volume and increased gastric/ abdominal pressure)
    • Esophageal mucosal exposure to gastric refluxate
    • Symptoms of GERD
  33. What is the normal physiological response to reflux?
    • Rapid Neutralization
    • esophageal peristalsis
    • salivary bicarbonate
  34. What is abnormal (GERD) response to reflux?
    • Reflux esophagitis
    • mucosal injury
    • hyperemia (increased blood to organ)
    • inflammation
  35. What are the contributing factors to abnormal (GERD) response?
    • Increased exposure time
    • Highly acidic refluxate
  36. What happens in Barrett's Esophagus (chronic GERD)?
    • Metaplasia condition- normal stratified squamous epithelium replaced by abnormal columnar epithelium
    • can result in esophageal cancer
  37. List the clinical manifestations of Heartburn
    • Onset: following meals and while lying down or bending over
    • Regurgitation of "sour" material
    • Atypical chest pain
  38. Define acute gastritis
    Transient gastric mucosal inflammation with the introduction of gastric irritants
  39. List the 3 Major gastric irritants
    • Drugs or chemicals- common irritants (caffeine, NSAIDS, ETOH) and suppressed gastric PGE
    • Bacterial endotoxins (food poisoning)
    • H. pylori bacteria
  40. List the Acute Gastritis Sequence of Events
    • Exposure to Gastric Irritant
    • Gastric inflammation caused by ETOH, Histamine, Metabolic disorders, and certain drugs
    • Mucosal injury
    • Focal or Generalized Erosion of surface epithelium (superficial)
  41. List clinical manifestations of Acute Gastritis
    • Anorexia (from not wanting to eat from pain)
    • N/V (from pain in stomach)
    • Abdominal discomfort
    • Hematemesis (vomitting frank blood) and or melena (black tarry stool)
  42. Describe Chronic Gastritis
    • Slow, progressive disorder (initally asymptomatic)
    • Begins with superficial inflammation
    • Gradually leads to destroyed functional cells

    Stomach can atrophy and take on a diff appearance
  43. What group is targeted with Chronic Gastritis?
  44. What are the two types of Chronic Gastritis?
    • Type A (Atrophic Gastritis)- autoimmune
    • Type B (H. pylori)- slow destruction
  45. Describe Chronic Gastritis: Type A (Atrophic)
    Progressive Gastric Mucosa Degeneration from autoimmune disorder
  46. What does Chronic gastritis type A reult in?
    • Loss of chief cells- decrease in pepsin (breakdown protein)
    • Loss of parietal cells- decreased HCL and intrensic factor (needed to absorb B12- resulting in pernicious anemia) and increase in Gastrin
  47. List the characteristics of Chronic Gastritis: Type A
    • Disappearance of gastric folds (causing smooth pale non-functional stomach)
    • Visualization of submucosal blood vessels
    • Total or partial loss of mucosal lining
  48. Describe Chronic Gastritis: Type B (H. pylori)
    • Chronic inflammation
    • Cause: Thinning and atrophy of mucosal layer
    • Resulting in decreased protection from autodigestive substances
  49. List the clinical manifestations of Chronic Gastritis
    • Asymptomatic until advanced disease
    • Vague gastric distress
    • Ulcer-like symptoms
    • Pain from erosion
    • Type A: sx of anemia, sx of vit B12 deficiency
  50. Define Hiatal Hernia
    Portion of upper stomach slips up or passes (herinates) through hiatus and into chest
  51. Cause and potential contributing factors of Hiatal Hernia
    • Structural Defect
    • Cause: Larger than normal esophageal hiatus
    • Permanent shortening of esophagus
    • Abnormally loose attachment of esophagus to diaphragm
  52. List the clinical manifestations of Hiatal Hernia
    • Asymptomatic then...
    • GERD-like
    • Worsens with certain activities (like lying down after eating)
  53. How you treat H. pylori?
    Combination therapy with 2 antibiotics for 2 weeks
  54. How can you treat Upper GI disorders?
    • Increasing protective factors- antacids, sucralfate, Misoprostol
    • Decresing aggressive factors- Histamine 2 blockers, proton pump inhibitor, protectants, Cholingergic-Blockers
  55. Why are antacids taken in combination?
    The two drugs do the same thing, but balance out the others side effects
  56. What are the major purposes of Antacids?
    • Reduce acid indigestion
    • Relief of Sx (heartburn, gastric distress)
    • Help protect mucosal layer
  57. What is the MOA of large-dose Antacids?
    Neutralizes acid through a chemical reaction in which the end product is water instead of acid
  58. What is the MOA of small-dose Antacids?
    Promote gastric mucosal defense mechanisms by increasing production of protective secretions (mucous and prostaglandins)
  59. List the side effects of Antacids
    • Acid-Base Imbalance
    • Diarrhea or constipation
    • Rebound hypersensitivity (symptomatic when therapy stopped)
    • Chelation (binds to other drug to prevent absorption)
    • Altered stomach pH (other drug cannot break up)
    • Metabolic alkalosis
  60. Describe the antacid, Alginic acid and its MOA
    • Seaweed base makes it hydrophobic
    • Physical buffer
    • Floats on top of chyme as a protectant when backflow present
  61. What is the MOA of Sucralfate (Carafate)?
    • MOA: alters when exposed to gastric acid, becomes sticky thick gel and adheres to ulcer crater as a protective barrier
    • Therefore is a mucosal protectant and promotes healing
  62. List route, SE, and interactions of Sucralfate (Carafate)
    • PO- tablet or suspension
    • No major SE- works locally on active ulcer
    • Decreases other drugs absorption, take 2 hours apart
  63. What is the MOA of Misoprostol (Cytotec)?
    • PGE replacement that is lost with NSAIDS (through stimulating COX 1)
    • Increases mucosal protective factors through being a synthetic PGE
  64. State the therapeutic use of Misoprostol (Cytotec)
    Approved for gastric ulcer secondary to NSAID therapy
  65. List the side effects and contraindication of Misoprostol (Cytotec)
    • Diarrhea
    • Abdominal discomfort
    • Contraindicated in Pregnancy (stimulates contractions)
  66. What is gastric acid secretion stimulated by?
    • Histamine
    • Acetylcholine (ACh)
    • Gastrin
    • (body preparing acids for food)
  67. What is the prototype Histamine type 2 receptor antagonists?
    • Cimetidine (Tagamet)
    • look for "-idine" endings
  68. What is the MOA of cimetidine (Tagamet)?
    • Block H2 receptors
    • Reduces gastric acid secretions (blocks 90% of acids being formed)
  69. List the SE and interactions for cimetidine (Tagamet)
    • SE: well tolerated
    • Slight increased risk for pneumonia in elderly (acids are in the stomach to fight bacteria, if chyme is aspirated without acids there is a risk for bacterial infection)
    • Interactions: smoking
  70. What is the final stage of gastric acid secretion?
    • Proton pump
    • H+ is a proton
    • If the pump is stopped then histamine and other acids are blocked from releasing
  71. What is the prototype drug for Proton Pump Inhibitors?
    • omeprazole (Prilosec)
    • look for "-prazole" suffix
  72. What is the MOA of omeprazole (Prilosec)?
    • Prodrug
    • Blocks final production step
    • PPI binds to H+/K+ ATPase
    • Prevents release of HCl
    • highly effective (targets exiting cells, not entering)
  73. List the SE and adverse effects of omeprazole (Prilosec)
    • Safe when taken short term
    • Slight increased risk for pnemonia when aspirated gastric contents by elderly resulting in bacterial infections
    • Interaction: Other PO drugs require acid pH to break down
  74. List the nursing implications of omeprazole (Prilosec)
    • Limit use to 2 weeks- not permanent
    • Drug of choice when H2RA (Tagament) not effective
    • More expensive therefore insurance companies require proof of H2RA failure
  75. Describe metoclopramide (Reglan) and its MOA
    • Prokinetic agent, antiemetic
    • MOA: Stimulates gastric muscle contraction, and relaxation of pyloric and duodenal segments (helps peristalsis in the stomach)
    • Does not increase secretions
  76. List the drug effects and SE of metoclopramide (Reglan)
    • Drug effects: promotion of movement of substances through GI tract (temporarily move GI tract)
    • SE: many! Sedation or restlessness, Extrapyramidal reactions (involuntar limb, facial, or eye movements)
  77. List the nursing implications of metoclopramide (Reglan)
    • Short term therapy
    • Check pt drug regimen therapy before initiating
    • Teach regaring possible side effects
Card Set
Patho Exam 2 Upper GI
Urinary, Endocrine, GI, Hepatobilary