PHA 3112 Study Guide - Final Guide: Wheeze, Shortness Of Breath, Mast Cell

• School: University of Ottawa
• Department: Pharmacology
• Course: PHA 3112
• Professor: Frank Feiner

Document Summary

Asthma pathophysiology: allergen binds via ige to mast cell & activates it. Inflammatory mediators (histamine, leukotrienes, prostaglandins, interleukins) released: result: airway bronchoconstriction & inflammation. Inflammation: edema, mucus plug, muscle hypertrophy, bronchial hyperreactivity to mild trigger factors (cold air, cigarette smoke, exercise, rx: bronchodilators + antiinflammatory drugs, allergen known in 50% children/some adults. In other, unknown or may not be allergen that triggers. Antiinflammatory: glucocorticoids: most effective drugs, suppress inflammation, do not alter natural course (even when given in childhood) ** not cures. Inhaled: first-line therapy for asthma (ex. beclomethasone, prophylaxis/ fixed daily schedule: prn/abort ongoing attack, quick -relief: 3-10 days at start of rx/ gradual deterioration. Long- term systemic use gives rise to severe side effects: Leukotriene modifiers: (suppress inflammatory mediators: zileuton, zafirlukast montelukast n/a, omalizumab, monoclonal antibody. Ige antagonist: blocks allergens: 2nd- line agent, not prn, modest benefit, sq, ses: anaphylaxis, cancer, $ 10k/yr. Long-term safety: cromolyn, suppress bronchial inflammation, 2nd- line agent, not prn.