Nursing Pharmacology Chapter 27: Gastrointestinal Drugs
Peptic ulcer disease appears to result from an imbalance between aggressive factors (including gastric acid, pepsin and Helicobacter pylori) and protective factors including gastric mucus, bicarbonate, prostaglandins.
Helicobacter pylori: the principal role in peptic ulcer pathogenesis
H. pylori:
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Causes active, chronic gastritis
Bacterial protein products appear damaging
Proteases and phospholipases produced by H. pylori degrade glycoprotein-lipid mucus layer complex
H. pylori is proinflammatory
Management of H. pylori infection: clinical consequences
15% relapse rate for duodenal ulcer (DU) following H. pylori eradication
75% relapse rate for duodenal ulcer following treatment with H2 receptor blockers only
Possible genetic factor in duodenal ulcer
Cigarette smoking
Increased incidence of DU
Decreased therapeutic response
Increased mortality rate from DU
Chronic renal failure |
Renal transplantation |
Systemic mastocytosis |
Alcoholic cirrhosis |
Hyperparathyroidism |
Chronic obstructive pulmonary disease (COPD) |
Friedman, L. S. and Peterson, W.L. Peptic Ulcer and Related Disorders In Harrison's Principles of Internal Medicine 14th edition, (Isselbacher, K.J., and Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L., eds) McGraw-Hill, Inc (Health Professions Division), 1998, pp. 1597-1616.