Obstructive Airway Disease Flashcards
What are the 2 Obstructive Airway Diseases?
Asthma & COPD
Asthma:
Prevalence?
inc prevalence
Why is Asthma Prevalence increasing?
Hygiene hypothesis and inc in genetic hypersensitivity predisposition
What are the different classes of asthma?
Allergic, non-allergic, acute exacerbation
What is Asthma…
Reversible airway obstruction, inflammation of airways due to airway hyper-responsiveness
What is the pathophysiology of asthma?
Bronchoconstriction due to chronic airway inflammation & airway remodelling…
What drives inflammation in asthma pathophysiology?
TH1 & TH2 lymphocytes activate mast cells and eosinophils
- Mast Cells: release pro-inflam mediators which act on mucus secreting cells & ASM
- Eosinophils: release proteins that are toxic to epithelial cells
What does airway inflammation cause as a repercussion in asthma?
Airway remodelling; structural changes which alter airway physiology causing symptoms
Give 2 examples by which the airways are remodelled?
- depositions of proteins and cellular infiltration causing swelling of the submucosa resulting in airway narrowing
- swelling outside ASM layer causes a reduction in retractile forces of alveoli so airways close more
Asthma triggers (aetiology)?
atmospheric pollution, cold air, allergen, occupational sensitisers, drugs, irritants, viral, emotion, associated atopy (e.g. eczema), not using inhaler properly
Presenting symptoms of asthma…
wheezing, SOB, nocturnal exacerbations, non-productive cough
Asthma investigations…
blood test (eosinophilia >4%) PFTs (PEFR, spirometry) Exercise test, exhaled NO, skin test for allergen
Asthma treatment…
Avoid allergen
- SABA (occasional symptoms)
- SABA & Inh Corticosteroids (CS) + xanthine (e.g. theophylline)/ cromone (daily symptoms)
- LABA & Inh CS + CysLT1/ xanthine (severe)
- inc dose of inh CS & LABA & SABA/CysLT1/ xanthine (severe but not responding to 3)
- step 4 + oral CS (e.g. prednisolone) (severe and deteriorating)
- Hospital Admission
Presentation of acute exacerbation of asthma (AEoA)
progressive shortening of breath, accessory muscles engaged, tachypnoea
Grading of AEoA…
PEFR
Moderate: 75-50%
Severe: 50-30%, RR >25/min, HR> 100/min, can’t finish sentences
Threatening: <33%, stats <92%, CHEST criteria
What is the CHEST criteria?
Cyanosis Hypotension Exhausted Silent chest Tachycardic arrhythmias
Treatment of AEofA
Moderate: 100% O2, nebulised SAMA/SABA, CS (oral: prednisolone, IV: hydrocortisone)
Severe: O2, IV SABA, & ^
Threatening: intubation, IV Magnesium Sulphate Infusion
Prevalence of COPD…
10-20% of smokers develop COPD, dec in prevalence
Class of COPD…
chronic & acute exacerbation of COPD (AEoCOPD)
What is COPD…
chronic bronchitis and emphysema
What is Chronic bronchitis and how does it occur?
Inflammation of bronchi
- inflammation of airways resulting in ulceration & fibrosis of airways narrowing them
- also inc in mucus secreting goblet cells resulting in mucus hyper secretion and blockage of airways (COPD has dysfunctional mucociliary escalator)
What is emphysema and how does it occur?
Damaged alveoli
- abnormal permanent enlargement of alveoli due to destruction of their wall causing impaired gas exchange
- No bronchial support due to bronchitis so loss of lung recoil so small airways collapse and rapid closure of airways during expiration
What are the main points for the pathophysiology of COPD?
inflammation & scarring, loss of lung elasticity, inc mucus secretion= airway narrowing
air trapping= hyperinflation= inc work of breathing
COPD triggers…
smoking, long term exposure to toxins, not using inhaler properly
