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Asthma: Notes, PPT and PYQs for MBBS

Asthma (bronchial asthma) is a chronic inflammatory disease of the airways that causes recurrent wheeze, breathlessness, chest tightness and cough, with variable and often reversible airflow limitation. It is examined in Physiology in 1st Year, Pathology and Pharmacology in 2nd Year, and General Medicine and Paediatrics in Final Year.

SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and notes.

Quick Summary: What You Need to Know for University Exams

  • Asthma is a heterogeneous disease with chronic airway inflammation and variable expiratory airflow limitation.
  • Symptoms vary over time and are often worse at night or early morning.
  • The main mechanism is Th2-driven inflammation with mast cells, eosinophils, IgE and airway hyperresponsiveness.
  • Spirometry with bronchodilator reversibility supports the diagnosis.
  • Inhaled corticosteroids (ICS) are the cornerstone of long-term control; current Global Initiative for Asthma (GINA) guidance does not recommend reliever-only treatment with a short-acting beta-agonist (SABA) for adults and adolescents.
  • A "silent chest" in an acute attack is a life-threatening sign.
  • Inhaler technique and adherence are central to good control.

Asthma Across MBBS Subjects

MBBS Year

1st Year

Subject

Physiology

What Is Usually Asked

Airway resistance, lung function tests, spirometry

MBBS Year

2nd Year

Subject

Pathology

What Is Usually Asked

Pathogenesis, morphology, Curschmann spirals, Charcot-Leyden crystals

MBBS Year

2nd Year

What Is Usually Asked

Classification of drugs for bronchial asthma, salbutamol, corticosteroids, montelukast, theophylline

MBBS Year

Final Year

What Is Usually Asked

Diagnosis, stepwise management, acute severe asthma

MBBS Year

Final Year

What Is Usually Asked

Childhood asthma and wheezing

Definition and Classification

Definition (GINA): Asthma is a heterogeneous disease, usually characterised by chronic airway inflammation. It is defined by a history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation.

Types (Phenotypes)

Type

Allergic (extrinsic) asthma

Key Features

Often begins in childhood; associated with atopy, allergic rhinitis, eczema and raised IgE

Type

Non-allergic (intrinsic) asthma

Key Features

Often adult onset; no evident allergy

Type

Exercise-induced bronchoconstriction

Key Features

Symptoms triggered by exercise

Type

Occupational asthma

Key Features

Caused by agents at work

Type

Aspirin-exacerbated respiratory disease

Key Features

Asthma, aspirin or NSAID sensitivity and nasal polyps (Samter's triad)

Type

Cough-variant asthma

Key Features

Chronic cough as the main symptom

Asthma Versus COPD

Feature

Age at onset

Asthma

Often childhood or young adulthood

COPD

Usually after 40 years

Feature

Smoking history

Asthma

Not essential

COPD

Usually significant

Feature

Symptoms

Asthma

Variable, episodic

COPD

Persistent, slowly progressive

Feature

Reversibility

Asthma

Marked reversibility with bronchodilator

COPD

Limited reversibility

Feature

Main inflammatory cells

Asthma

Eosinophils, mast cells, Th2 cells

COPD

Neutrophils, macrophages, CD8 cells

Aetiology (Triggers and Risk Factors)

Risk factors:

  • Family history of asthma or atopy
  • Personal atopy (allergic rhinitis, eczema)
  • Exposure to tobacco smoke, including in pregnancy and childhood
  • Obesity
  • Occupational exposures

Common triggers:


Trigger Type

Allergens

Examples

House dust mite, pollen, animal dander, cockroach, moulds

Trigger Type

Infections

Examples

Viral respiratory infections

Trigger Type

Irritants

Examples

Tobacco smoke, air pollution, strong odours

Trigger Type

Physical

Examples

Exercise, cold air

Trigger Type

Drugs

Examples

Aspirin and NSAIDs in sensitive people, non-selective beta-blockers

Trigger Type

Others

Examples

Emotional stress, gastro-oesophageal reflux

Pathophysiology

Immunological Mechanism (Flowchart)

  1. Genetic predisposition and allergen exposure
  2. Dendritic cells present allergen to Th2 cells
  3. Th2 cells release IL-4 (IgE production), IL-5 (eosinophil activation) and IL-13 (mucus production and hyperresponsiveness)
  4. IgE binds to mast cells; re-exposure to allergen causes mast cell degranulation
  5. Early phase: histamine, leukotrienes and prostaglandins cause bronchoconstriction, oedema and mucus secretion within minutes
  6. Late phase: eosinophils and other cells cause sustained inflammation hours later
  7. Repeated inflammation leads to airway remodelling

Airway Remodelling

  • Thickening of the basement membrane (subepithelial fibrosis)
  • Smooth muscle hypertrophy and hyperplasia
  • Goblet cell hyperplasia and submucosal gland enlargement
  • Increased vascularity

Pathology Findings

Finding

Curschmann spirals

Description

Spiral mucus plugs from small airways

Finding

Charcot-Leyden crystals

Description

Crystals formed from eosinophil proteins

Finding

Creola bodies

Description

Clusters of shed epithelial cells

Finding

Lungs in fatal asthma

Description

Overinflated, with mucus plugs in bronchi

(Examiner may ask you to draw the pathogenesis flowchart.)


Clinical Features

Symptoms:

  • Episodic wheeze
  • Breathlessness
  • Chest tightness
  • Cough, often worse at night or early morning
  • Symptoms triggered by allergens, exercise, cold air or infections

Signs:

  • Prolonged expiration
  • Polyphonic expiratory wheeze
  • Use of accessory muscles in severe attacks
  • Examination may be normal between attacks

Assessing an Acute Attack

Severity

Mild to moderate

Features

Talks in phrases, prefers sitting, not agitated, respiratory and heart rates raised

Severity

Severe

Features

Talks in words, sits hunched forward, agitated, marked tachypnoea and tachycardia, accessory muscle use, low peak flow

Severity

Life-threatening

Features

Drowsiness or confusion, silent chest, cyanosis, poor respiratory effort, exhaustion, bradycardia or hypotension

Pulsus paradoxus (an exaggerated fall in systolic pressure during inspiration) may be present in severe asthma.


Diagnosis

Investigation

Spirometry

Findings or Purpose

Reduced FEV1/FVC ratio (obstructive pattern)

Investigation

Bronchodilator reversibility

Findings or Purpose

Improvement in FEV1 of more than 12% and more than 200 mL after a bronchodilator supports asthma

Investigation

Peak expiratory flow (PEF) variability

Findings or Purpose

Diurnal variation supports the diagnosis; useful for monitoring

Investigation

Bronchial challenge test

Findings or Purpose

Methacholine or histamine challenge shows airway hyperresponsiveness

Investigation

Fractional exhaled nitric oxide (FeNO)

Findings or Purpose

Marker of eosinophilic airway inflammation

Investigation

Blood eosinophils and total IgE

Findings or Purpose

Support allergic or eosinophilic asthma

Investigation

Skin prick tests

Findings or Purpose

Identify specific allergens

Investigation

Chest X-ray

Findings or Purpose

Usually normal; hyperinflation in acute attacks; excludes other causes and pneumothorax

Investigation

Arterial blood gas

Findings or Purpose

In acute severe asthma; a normal or rising PaCO2 in a breathless patient is a warning sign

Management

Goals

  1. Good symptom control
  2. Prevention of attacks (exacerbations)
  3. Normal activity and lung function
  4. Minimal side effects of treatment

Drugs Used in Asthma

Drug Class

Short-acting beta-2 agonists (SABA)

Examples

Salbutamol, terbutaline

Role

Quick relief of symptoms

Drug Class

Long-acting beta-2 agonists (LABA)

Examples

Salmeterol, formoterol

Role

Add-on to ICS; never used alone in asthma

Drug Class

Inhaled corticosteroids (ICS)

Examples

Budesonide, beclomethasone, fluticasone

Role

Main anti-inflammatory controller

Drug Class

ICS-formoterol combination

Examples

Budesonide-formoterol

Role

Used as reliever and controller in current GINA tracks

Drug Class

Long-acting muscarinic antagonists (LAMA)

Examples

Tiotropium

Role

Add-on in more severe asthma

Drug Class

Short-acting muscarinic antagonist

Examples

Ipratropium

Role

Add-on in acute severe attacks

Drug Class

Leukotriene receptor antagonists

Examples

Montelukast

Role

Add-on controller; useful in aspirin-exacerbated and exercise-induced asthma

Drug Class

Methylxanthines

Examples

Theophylline

Role

Less used because of a narrow therapeutic index

Drug Class

Systemic corticosteroids

Examples

Prednisolone, hydrocortisone

Role

Acute attacks and severe asthma

Drug Class

Biologics

Examples

Omalizumab (anti-IgE), mepolizumab (anti-IL-5), dupilumab (anti-IL-4 receptor)

Role

Severe asthma under specialist care

Stepwise Treatment (Principles)

  • Treatment is stepped up or down according to symptom control and risk of attacks.
  • Current GINA guidance for adults and adolescents prefers low-dose ICS-formoterol as the reliever, with maintenance ICS added at higher steps.
  • At higher steps, doses are increased and add-on drugs such as LAMA are used; severe asthma is referred for phenotyping and biologic therapy.
  • Always check inhaler technique, adherence and triggers before stepping up.

Use your current textbook and the latest GINA report for step details, since recommendations are updated regularly.

Acute Severe Asthma (MBBS Level)

  1. Sit the patient up and give controlled oxygen to maintain adequate saturation
  2. Repeated inhaled or nebulised SABA
  3. Add nebulised ipratropium in severe attacks
  4. Systemic corticosteroids early (oral prednisolone or intravenous hydrocortisone)
  5. Intravenous magnesium sulphate in severe attacks not responding to initial treatment
  6. Monitor peak flow, oxygen saturation and blood gases
  7. Intensive care for life-threatening features, exhaustion or rising PaCO2

Non-Drug Measures

  • Avoid known triggers and tobacco smoke
  • Correct inhaler technique; spacers for children and during attacks
  • Written asthma action plan
  • Vaccination against influenza as advised
  • Regular review

Complications

  • Acute severe asthma (status asthmaticus) and respiratory failure
  • Pneumothorax and pneumomediastinum
  • Lobar collapse from mucus plugging
  • Side effects of long-term steroids
  • Fixed airflow obstruction from remodelling
  • Death in poorly controlled or untreated severe attacks

Prognosis

Most people with asthma achieve good control with regular inhaled corticosteroid-containing treatment and correct inhaler use. Childhood asthma often improves with age, but may return later. Poor adherence, frequent attacks and previous life-threatening episodes predict worse outcomes.


Quick Viva Questions

Q: What is the main controller drug in asthma? A: Inhaled corticosteroids.

Q: Why should LABA never be used alone in asthma? A: LABA relieves bronchoconstriction but does not treat inflammation, and LABA monotherapy is associated with an increased risk of severe attacks.

Q: What are Curschmann spirals? A: Spiral-shaped mucus plugs from small airways, seen in the sputum of asthmatic patients.

Q: What is a "silent chest"? A: Very little air movement on auscultation in a severe attack; it is a life-threatening sign.

Q: What is Samter's triad? A: Asthma, aspirin sensitivity and nasal polyps.

Q: What spirometry finding supports reversibility? A: An increase in FEV1 of more than 12% and more than 200 mL after a bronchodilator.


How Asthma Appears in MBBS University Exams

Typical question styles (not attributed to specific papers or years):

  1. "Define bronchial asthma. Discuss the aetiology, pathogenesis, clinical features and management." (Long essay, General Medicine)
  2. "Classify drugs used in bronchial asthma. Write a note on inhaled corticosteroids." (Long essay, Pharmacology)
  3. "Discuss the management of acute severe asthma." (Short note, Medicine)
  4. "Describe the pathogenesis and morphology of bronchial asthma." (Short note, Pathology)
  5. "Write a short note on montelukast." (Short note, Pharmacology)

Frequently Asked Questions

What is the difference between asthma and COPD?

Asthma usually starts earlier, has variable symptoms and shows marked reversibility with bronchodilators. COPD usually follows long-term smoking, progresses slowly and shows limited reversibility.

Is salbutamol alone enough for asthma?

For adults and adolescents, current GINA guidance does not recommend treatment with a short-acting beta-agonist alone, because it does not treat airway inflammation. An inhaled corticosteroid-containing treatment is recommended.

Can I download the asthma PPT for my presentation?

Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.

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