week 6- asthma Flashcards
Asthma
Chronic inflammatory disorder of airways, with acute episodes of airway obstruction due to:
-Bronchospasm
-Mucosal oedema
-Excess mucus production
Overreact to various stimuli, leading to recurrent episodes of coughing and chest tightness and wheezing.
Extrinsic (atopic) asthma:
begins in childhood; sensitivity to external allergens (typically on inhalation)
-Genetic predisposition to develop IgE response
Intrinsic (non-atopic) asthma:
reaction to internal non-allergic factors
No obvious role of allergen in inflammatory response
However, IgE synthesis occurs; subsequent inflammation similar to extrinsic asthma
whats different about asthma and anaphalaxisis t-cells
As with anaphylaxis, T-cell differentiation is skewed to pro-inflammatory T2H response.
-This is instead of T1H- IgM or IgG
mast cell degranulation in asthma
releases histamine, Cytokines: (major component of inflammatory response, attracting more inflammatory mediators to increase the response)
Leukotrienes: (increase mucus secretion, further obstructing airway, & cause more histamine release)
histamine
Histamine increases nitric oxide production, relaxes vascular smooth muscle, increases permeability of capillaries and venules, and causes smooth muscle contraction and bronchial constriction.
acute phase asthma- inhalation
histamine- vasodilation and bhronchspasm
leukotrines-mucous secretion
cytokines mucous secretion and airway constriction.
-narrowed bronchial lumen can expand slightly, so air reaches alveoli
late phase asthma
- Hyperinflation due to air trapping in occluded & narrowed airways
- Air trapped in alveoli so inspiration at higher residual lung capacity
- More energy required to overcome tension in lungs
- Accessory muscles utilised to maintain ventilation & gas exchange
- results in ventalation-perfusion mismatch
astmha exhalation
increased intrathoracic pressure closes bronchial lumen completely- prolonged expiration due to progressive airway obstruction.
