ASTHMA AND COPD Flashcards
(28 cards)
What are the main causes of asthma?
Genetic predisposition (linked to atopy)
Environmental exposure in early life
Tobacco smoke, allergens, air pollution, viral infections, low microbial exposure
Name precipitating factors for asthma.
Allergen exposure
Infections
Cold air
Exercise
Medications (e.g., aspirin)
Pollutants
List asthma phenotypes.
Allergic asthma
Non-allergic asthma
Adult-onset asthma
Asthma with persistent airflow limitation
Describe the early inflammatory cascade in allergic asthma.
IgE binds mast cells → allergen exposure → mast cell degranulation
Release of histamine, leukotrienes (LTC4, LTD4), PGD2
Bronchoconstriction, edema, mucous secretion
Describe the late-phase reaction.
3–6 hours later: Infiltration of eosinophils, T2 lymphocytes (IL-4, IL-5, IL-13)
Increases IgE, mucus, reactivity
What is used to assess asthma?
Spirometry (FEV1, PEF)
Symptom control (frequency, night symptoms)
Reliever use
Risk of exacerbation
What are the goals of asthma therapy?
No symptoms or night waking
Normal activity
Normal lung function
Prevent exacerbations and side effects
Chronic asthma treatment in adults (5 steps)?
Low-dose ICS-formoterol as needed
Daily low-dose ICS
Low-dose ICS + LABA
Medium/high-dose ICS + LABA
Refer, add-on therapy (tiotropium, biologics)
Chronic asthma treatment in children (6–11)?
Low-dose ICS
Daily low-dose ICS
ICS + LABA or LTRA
Medium-dose ICS + LABA
Specialist referral
What’s the role of β2 agonists in asthma?
Relieve bronchoconstriction
Prevent mast cell degranulation
Increase mucociliary clearance
SABAs vs LABAs — onset & duration?
SABAs (e.g., salbutamol): Rapid onset, short duration
LABAs (e.g., formoterol): Long duration, some fast onset
Adverse effects of β2 agonists?
Tachycardia
Tremor
Hypokalemia
Headache (usually with systemic absorption)
ICS mechanism of action in asthma?
Nuclear receptor activation → ↓ IL-2, ↓ eosinophils
Upregulate β2 receptors
↓ IgE, ↓ mucus, ↓ edema
ICS safety profile?
Local: Oral thrush, hoarseness
Systemic: Adrenal suppression, growth retardation (rare)
Montelukast mechanism and uses?
CysLT1 receptor antagonist
↓ bronchoconstriction, ↓ mucus
Use: Add-on in allergic asthma, EIB, aspirin sensitivity
Theophylline mechanism and uses?
Inhibits PDE → ↑ cAMP
Adenosine receptor antagonist
Use: Add-on in persistent asthma
Theophylline risks?
Narrow therapeutic index
Side effects: seizures, arrhythmia, GI upset
What are the causes of COPD?
Smoking (most common)
Air pollution, biomass fuel
TB, infections
Genetic: α-1 antitrypsin deficiency
Describe COPD pathophysiology.
Airflow obstruction from chronic bronchitis/emphysema
↓ gas exchange, V/Q mismatch
Chronic hypoxia → cor pulmonale
COPD presentation?
Cough, sputum, wheeze, dyspnea
Increased chest size
Exertion-related breathlessness
Spirometry in COPD?
↓ FEV1
FEV1/FVC < 70% post-bronchodilator confirms obstruction
How to differentiate asthma and COPD?
Asthma: Early onset, reversible, atopy
COPD: Later onset, progressive, irreversible, smoking history
Role of muscarinic antagonists in COPD?
M1/M3 antagonism: Bronchodilation
M2 antagonism: Unwanted (blocks autoregulation)
Ipratropium vs Tiotropium? (COPD)
Ipratropium: Non-selective, short-acting
Tiotropium: Long-acting, M3 selective (preferred for maintenance)
