Asthma

Hyperresponsiveness & Reversible Obstruction

FreeMedSite USMLE STEP 1 REVIEW

Interactive Study:

Definition

Chronic inflammatory disorder causing hyperresponsive bronchi and reversible airway obstruction.

Presentation

Classic Findings

• • Episodic Wheezing & Cough
• • Prolonged expiration
• • Decreased I:E ratio (prolonged expiration)
• • Pulsus paradoxus (in severe attacks)

Triggers

• • Viral URIs (most common)
• • Allergens (Type I Hypersensitivity)
• • Stress, Cold Air, Exercise

Pathology

Microscopic Sputum Findings

• Curschmann spirals: Whorled mucus plugs.
• Charcot-Leyden crystals: Eosinophilic breakdown products.

Airway Remodeling

Smooth muscle hypertrophy and hyperplasia + Mucus plugging.

Diagnosis

Spirometry ↓ FEV1 (Reversible)

Methacholine Challenge Induces bronchoconstriction

DLCO Normal or mildly ↓

Special Phenotypes

NERD (Aspirin-Exacerbated Respiratory Disease)

Triad: Asthma + Nasal Polyps + NSAID use.
Mechanism: COX inhibition → Leukotriene overproduction.

1. What are the two classic microscopic findings in asthma sputum?

Answer: Curschmann spirals and Charcot-Leyden crystals.

2. What cell types are primarily involved in the chronic inflammation of asthma?

Answer: Eosinophils, Mast cells, and Th2 lymphocytes.

3. What does "reversibility" mean in the context of asthma diagnosis?

Answer: FEV1 increases significantly after bronchodilator administration.

4. Why do NSAIDs trigger bronchoconstriction in some asthma patients?

Answer: Inhibition of COX leads to shunting of arachidonic acid toward the leukotriene pathway.

5. What physical exam finding suggests a severe asthma attack?

Answer: Pulsus paradoxus (fall in systolic BP > 10mmHg during inspiration).

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1. Definition

“Hyperresponsive bronchi leading to reversible airway obstruction, with intermittent episodes of wheezing, coughing, dyspnea, and variable airflow limitation.”

• Airway obstruction is usually reversible spontaneously or with treatment.

2. Pathophysiology

• • Hyperresponsive bronchi → reversible bronchoconstriction
• • Chronic inflammation involves: Eosinophils, mast cells, T-helper 2 (Th2) lymphocytes
• • Cytokines → airway remodeling
• • Structural changes:
• - Smooth muscle hypertrophy and hyperplasia → airway narrowing
• - Mucus plugging → contributes to airflow limitation
• - Curschmann spirals → whorled mucus plugs from shed epithelium
• - Charcot-Leyden crystals → eosinophilic crystals from breakdown of eosinophils in sputum
• • Type I hypersensitivity reaction in allergen-mediated asthma

3. Clinical Features

Feature	Explanation
Asymptomatic at baseline	Patients may feel normal between episodes
Intermittent episodes	Wheezing, cough, tachypnea, dyspnea, hypoxemia
Prolonged expiration / ↓ I:E ratio	Due to airflow obstruction and air trapping
Pulsus paradoxus	Severe attacks → fall in systolic BP during inspiration
Triggers	Viral URIs, allergens, stress

4. Phenotypes

NERD (NSAID-exacerbated)

COX inhibition → leukotriene overproduction → bronchoconstriction. Associated with chronic sinusitis + nasal polyps + asthma symptoms.

5. Investigations

• • Spirometry: ↓ FEV1 during attack; reversible
• • Methacholine: Used to demonstrate hyperresponsiveness
• • DLCO: Usually normal or mildly ↓

6. Pathophysiology Notes

Obstruction: Airway hyperresponsiveness + inflammation → episodic obstruction.

Secretions: Mucus hypersecretion → airway plugging, contributes to wheezing and dyspnea.

Remodeling: Smooth muscle changes → persistent airway narrowing in chronic or severe asthma.

💡 Pearl for Exams / MCQs

Asthma = episodic, reversible airway obstruction + hyperresponsive bronchi + mucus plugging. Chronic remodeling (smooth muscle hypertrophy) occurs in persistent or severe asthma.