 Definition  Asthma is a chronic inflammatory disorder of the lung airways, characterised by reversible airway obstruction, airway hyper-responsiveness, and airway inflammation.

 Allergens bind to IgE, which is presented on the surface of Mast Cells  2 phases of initial response:  Early - Mast Cell activation, leading to degranulation of Histamine (etc.), causing smooth muscle contraction and airway obstruction (first 30min- 1hr).  Late - T cells (also IgE mediated) activate eosinophils and neutrophils, causing; further inflammation, mucus secretion, and vascular leakage.

 Poorly managed asthma can lead to Remodelling:  Smooth muscle hypertrophy  Smooth muscle & epithelial cell hyperplasia  Epithelial damage  Basement membrane thickening  Forms a vicious cycle of increasing frequency and severity of attacks

 Shortness of breath  Dyspnoea / chest tightness  Cough  Wheeze  Low O 2 sats.  Diurnal variation highly indicative  Other signs of Atopy

 FEV1/FVC ratio < 80%  Reversible: > 12% improvement after bronchodilator needed  Peak flow < 80% (either predicted value or patients base line)

 Act on the Beta-2 receptor for adrenaline, which is part of the sympathetic ‘fight-or-flight’ system  ß2-agonists bind to the receptor, activating adenyl cyclase via G-protein coupled mechanism  Adenyl cyclase increases cAMP levels, activating PKA (protein kinase A), leading to phosphorylation of downstream targets  Phosphorylation of MLCK (myosin light chain kinase) inactivates it, reducing smooth muscle contraction  Thus, results in relaxation of smooth muscle in airway

 Defintion  Chronic obstructive pulmonary disease  Combination of chronic bronchitis, emphysema and asthma

 Signs and symptoms  Productive cough  Wheeze  Dyspnoea  Frequent infective excaberations  Signs of respiratory failure

Pink pufferBlue bloater

Noxious gases and particles cause inflammation Small airway disease Airway inflammation producing exudate Disrupted alveolar attachments Thickened wall with inflammatory cells- macrophages, CD8 cells and fibroblasts Fibrosis Parenchymal destruction Alveolar wall destruction Decreased elastic recoil Destruction of pulmonary capillary bed Increased inflammatory cells- macrophages, CD8 lymphocytes

 SMOKING CESSATION  Bronchodilator SA B2 agonists- salbutamol, SA anticholinergic – ipratropium  Combination LA B2Ag- Salmeterol, LA anticholinergic- tiotropium Inhaled steroid- beclomethasone  Oral theophylline  Home Oxygen