ASTHMA AND COPD
ASTHMA Definition
Asthma is a chronic inflammatory disorder of the lung airways, characterised by reversible airway obstruction, airway hyper-responsiveness, and airway inflammation.
PATHOPHYSIOLOGY 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.
HYPERSENSITIVITY REACTIONS
TRIGGERS
LONG-TERM CHANGES Poorly managed asthma can lead to
Remodelling:Smooth muscle hypertrophySmooth muscle & epithelial cell hyperplasiaEpithelial damageBasement membrane thickening
Forms a vicious cycle of increasing frequency and severity of attacks
SIGNS + SYMPTOMS Shortness of breath Dyspnoea / chest tightness Cough Wheeze Low O2 sats.
Diurnal variation highly indicative Other signs of Atopy
INVESTIGATIONS FEV1/FVC ratio < 80%
Reversible: > 12% improvement after bronchodilator needed
Peak flow < 80% (either predicted value or patients base line)
MANAGEMENT OF ASTHMA
SABA MOA 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
COPD Defintion
Chronic obstructive pulmonary diseaseCombination of chronic bronchitis,
emphysema and asthma
COPD Signs and symptoms
Productive coughWheezeDyspnoeaFrequent infective
excaberationsSigns of respiratory
failure
Pink puffer Blue bloater
PATHOPHYSIOLOGYNoxious 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
MANAGEMENT SMOKING CESSATION Bronchodilator• SA B2 agonists- salbutamol,• SA anticholinergic – ipratropium
Combination LA B2Ag- Salmeterol, LA anticholinergic- tiotropium Inhaled steroid- beclomethasone
Oral theophylline Home Oxygen
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