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