Bronchial Asthama 10 marks long answer question 4 th year mbbs

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Bronchial Asthma - Long Answer (10 Marks)

Definition

Bronchial asthma is a chronic inflammatory disorder of the airways characterized by three key elements:

Reversible airway obstruction (partially or fully reversible, spontaneously or with treatment)
Airway inflammation (involving multiple cells - mast cells, eosinophils, T-lymphocytes)
Airway hyperresponsiveness (AHR) - increased airway responsiveness to a variety of stimuli

Clinically, it presents with recurrent episodes of wheezing, breathlessness, chest tightness, and cough - particularly nocturnal or early morning.

(Murray & Nadel's Textbook of Respiratory Medicine; Textbook of Family Medicine 9e)

Epidemiology

Affects >300 million people worldwide; most common chronic disease of childhood
Causes >15 million disability-adjusted life-years (DALYs) annually
Prevalence is rising globally; in the United States, ~20 million adults and 6.1 million children are affected
Higher rates in low-income, uninsured, and minority populations
Hospitalization rates are 3.3x higher in Black patients vs. White patients (disparity condition)

Etiology and Risk Factors

Extrinsic (Allergic/Atopic) Asthma

Most common type; IgE-mediated hypersensitivity
Triggers: pollens, house dust mites, cockroach excreta, animal dander, mold spores
Usually begins in childhood; family history of atopy common

Intrinsic (Non-Allergic) Asthma

Triggered by non-immunologic stimuli
Infections (viral URIs - commonest trigger of acute exacerbations)
Exercise-induced bronchospasm (EIB)
Cold air, fog, weather changes
Drugs: NSAIDs, aspirin (Samter's triad = asthma + nasal polyposis + aspirin sensitivity), beta-blockers, ACE inhibitors
Occupational exposures: isocyanates, flour dust, latex
GERD, emotional stress

Strongest risk factors:

Household smoke exposure
Family history of asthma or atopy

Pathogenesis

Phase 1 - Sensitization

In atopic individuals, inhaled allergens are processed by antigen-presenting cells (APCs/dendritic cells) -> activate Th2 lymphocytes -> release IL-4, IL-5, IL-13 -> class switching in B-cells to produce IgE -> IgE binds to high-affinity receptors (FcεRI) on mast cells and basophils.

Phase 2 - Early Phase Reaction (0-60 min)

On re-exposure to allergen, cross-linking of IgE on mast cells causes degranulation, releasing:

Histamine - bronchospasm, mucosal edema
Leukotrienes (LTC4, LTD4, LTE4) - potent bronchospasm and mucus secretion
Prostaglandin D2 - bronchoconstriction
Platelet-activating factor (PAF) - airway inflammation

Result: acute bronchospasm within minutes.

Phase 3 - Late Phase Reaction (4-8 hours)

Recruitment of eosinophils (by IL-5 and eotaxin), neutrophils, Th2 cells to airway:

Eosinophil degranulation releases major basic protein (MBP) and eosinophil cationic protein (ECP) -> epithelial damage
Mucus hypersecretion, mucosal edema, inflammatory infiltrate
Mediators released sustain AHR

Airway Remodeling (Chronic Disease)

With repeated episodes:

Sub-epithelial fibrosis (collagen deposition beneath basement membrane)
Smooth muscle hypertrophy and hyperplasia
Goblet cell metaplasia and mucus gland hypertrophy
Angiogenesis and neural remodeling
Results in fixed (irreversible) airflow limitation

Pathophysiology

The three hallmarks - bronchospasm, mucosal edema, mucus plugging - cause:

Airflow obstruction predominantly in expiration -> air trapping -> hyperinflation
Increased airway resistance -> increased work of breathing
V/Q mismatch -> hypoxemia initially (PaO2 falls)
In mild-moderate attack: hypocapnia (compensatory hyperventilation)
In severe/near-fatal attack: rising PaCO2 (normocapnia then hypercapnia) = respiratory failure - ominous sign

Clinical Features

Symptoms (classic triad):

Paroxysmal wheezing (expiratory)
Breathlessness (dyspnea)
Chest tightness
Cough (often nocturnal, productive of thick mucus)
Symptoms typically worse at night/early morning and with triggers

Signs during attack:

Tachypnea, tachycardia
Use of accessory muscles (sternocleidomastoid, scalene)
Hyperinflated chest, reduced air entry
Prolonged expiration; diffuse bilateral expiratory wheeze
Pulsus paradoxus (>10 mmHg fall in systolic BP on inspiration) in severe attack

Signs of life-threatening attack (Status Asthmaticus):

Silent chest (no wheeze despite severe obstruction)
Cyanosis
Altered consciousness/exhaustion
Bradycardia, hypotension
Inability to speak in full sentences

Classification by Severity (NAEPP / GINA Guidelines)

Feature	Intermittent	Mild Persistent	Moderate Persistent	Severe Persistent
Daytime symptoms	≤2 days/week	>2 days/wk (not daily)	Daily	Throughout the day
Nighttime awakenings	≤2x/month	3-4x/month	>1x/week	Often nightly (7x/wk)
SABA use	≤2 days/wk	>2 days/wk	Daily	Several times/day
Activity limitation	None	Minor	Some	Extremely limited
FEV1 (% predicted)	>80%	>80%	60-80%	<60%
FEV1/FVC	Normal	Normal	Reduced 5%	Reduced >5%
Step therapy	Step 1	Step 2	Step 3	Step 4 or 5

Investigations

1. Spirometry (most important)

FEV1/FVC ratio <0.7 confirms obstruction
FEV1 <80% predicted
Reversibility test: ≥12% AND ≥200 mL increase in FEV1 after bronchodilator (salbutamol 400 mcg) = diagnostic of asthma

2. Peak Expiratory Flow Rate (PEFR)

Portable, inexpensive monitoring tool
Diurnal variation >20% is diagnostic
Used for monitoring and action plans

3. Bronchial Provocation Test

Methacholine or histamine challenge
PC20 (concentration causing 20% fall in FEV1) <8 mg/mL = AHR
Used when spirometry is normal but asthma suspected

4. Chest X-ray

Usually normal between attacks
During attack: hyperinflation (flattened diaphragm, increased AP diameter, increased intercostal spaces)
Excludes: pneumothorax, consolidation, foreign body

5. Blood tests

CBC: eosinophilia (>400/mm3) suggests atopic disease
Total serum IgE - elevated in atopic asthma
Arterial Blood Gas (ABG) in acute severe attack:
- Mild/moderate: hypoxemia + hypocapnia (respiratory alkalosis)
- Severe/near-fatal: normocapnia or hypercapnia + acidosis

6. Skin prick tests / RAST (Radioallergosorbent test)

Identify specific allergens causing IgE-mediated sensitization

7. FeNO (Fractional exhaled Nitric Oxide)

25 ppb indicates eosinophilic airway inflammation
Guides ICS therapy

Treatment

Step-Up Pharmacotherapy (NAEPP Stepwise Approach)

Step 1 - Intermittent Asthma:

SABA (Short-Acting Beta-2 Agonist) PRN only: Salbutamol (albuterol) 100-200 mcg inhaled

Step 2 - Mild Persistent:

Daily Inhaled Corticosteroid (ICS) (first-line controller): Beclomethasone, Budesonide, Fluticasone (low dose)
Alternative: Leukotriene Receptor Antagonist (LTRA) - Montelukast

Step 3 - Moderate Persistent:

Low-dose ICS + LABA (Long-Acting Beta-2 Agonist): Salmeterol or Formoterol
Or medium-dose ICS alone

Step 4 - Severe Persistent:

Medium-to-high dose ICS + LABA
Add LTRA or theophylline if needed

Step 5 - Very Severe:

High-dose ICS + LABA + oral corticosteroids
Consider anti-IgE therapy: Omalizumab (monoclonal antibody) for severe allergic asthma
Consider bronchial thermoplasty

Drug Classes:

Drug Class	Examples	Mechanism	Use
SABA	Salbutamol, Terbutaline	Beta-2 agonist -> bronchodilation	Acute relief
LABA	Salmeterol, Formoterol	Long-acting beta-2 agonism	Add-on to ICS
ICS	Budesonide, Fluticasone	Suppress eosinophilic inflammation	Daily controller
LTRA	Montelukast, Zafirlukast	Block CysLT1 receptors	Add-on; exercise-induced
Theophylline	Aminophylline	Phosphodiesterase inhibitor -> bronchodilation; anti-inflammatory	Add-on; IV in acute severe
Anti-cholinergic	Ipratropium	Block muscarinic receptors	Acute attack adjunct
Systemic corticosteroids	Prednisolone	Anti-inflammatory	Acute exacerbations; severe persistent
Anti-IgE	Omalizumab	Binds free IgE	Severe allergic asthma

Management of Acute Severe Asthma (Status Asthmaticus)

Immediate (Emergency) Management - "ABOS":

Oxygen: High-flow via face mask to maintain SpO2 >94%
Nebulized SABA: Salbutamol 5 mg via oxygen-driven nebulizer every 20 min x 3 (or continuous)
Nebulized Ipratropium: 0.5 mg with salbutamol (additive bronchodilation)
Systemic corticosteroids: Oral prednisolone 40-50 mg OR IV hydrocortisone 200 mg
IV Magnesium sulfate: 2 g IV over 20 min (bronchodilator; for severe attacks not responding to initial therapy)
IV Aminophylline: Loading dose 5 mg/kg (if not on theophylline) then infusion
Heliox (helium-oxygen mixture): Reduces airway resistance in very severe cases
Mechanical ventilation (ICU): For respiratory failure (rising CO2, exhaustion, altered consciousness)

Monitoring: ABG, peak flow (PEFR), SpO2 continuous

Non-Pharmacological Management

Trigger avoidance: House dust mite control (mattress covers), HEPA filters, avoiding known allergens
Smoking cessation: Most important environmental intervention
Patient education: Inhaler technique, action plans, PEFR self-monitoring
Allergen immunotherapy (AIT): Subcutaneous or sublingual; for allergic asthma unresponsive to standard therapy
Breathing exercises: Buteyko technique, yoga
Weight loss: Obesity worsens asthma
Control of GERD and rhinitis: Both worsen asthma control

Differential Diagnosis

Children	Adults
Viral bronchiolitis	COPD
Foreign body aspiration	Congestive cardiac failure ("cardiac asthma")
Cystic fibrosis	Pulmonary embolism
GERD	Vocal cord dysfunction
Heart disease	ACE inhibitor-induced cough

Key point: "Not all that wheezes is asthma, and not all asthma wheezes."

Complications

Acute: Status asthmaticus, pneumothorax, respiratory failure, death
Chronic: Fixed airflow limitation (remodeling), cor pulmonale, growth retardation (children), side effects of long-term corticosteroids (osteoporosis, cataracts, adrenal suppression)
Aspergilloma/ABPA: Allergic bronchopulmonary aspergillosis - complication of severe asthma

Prognosis

Most patients achieve good control with appropriate therapy
About 50% of children with mild asthma go into remission by adulthood
Severe persistent asthma with fixed obstruction carries significant morbidity
Risk factors for death: previous near-fatal attack, poor adherence, over-reliance on SABAs, underuse of ICS, low socioeconomic status, psychiatric comorbidity

Summary Table

Aspect	Key Points
Definition	Chronic airway inflammation + reversible obstruction + AHR
Cells involved	Mast cells, eosinophils, Th2 cells, basophils
Key mediators	Histamine, leukotrienes (LTC4/D4/E4), IL-4, IL-5, IL-13
Hallmarks	Bronchospasm + mucosal edema + mucus plugging
Diagnosis	FEV1/FVC <0.7, reversibility >12%, PEFR variability >20%
First-line controller	Inhaled corticosteroid (ICS)
Acute reliever	SABA (salbutamol)
Severe attack Rx	O2 + SABA + Ipratropium + systemic steroids + MgSO4
Bad signs	Silent chest, rising PaCO2, cyanosis, altered consciousness

Sources: Textbook of Family Medicine 9e (Rakel); Murray & Nadel's Textbook of Respiratory Medicine; Fishman's Pulmonary Diseases and Disorders

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