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Which of the following medications, if used consistently, would prevent these pathological change?
Dr. Shoaib Ahmad Baig
December 21, 2024
π Question
A 32-year-old woman presents to the emergency department with severe shortness of breath that has progressively worsened over the past few hours. She denies chest pain, recent infections, or significant travel history. She has a known history of asthma but admits to poor compliance with her prescribed medications. She does not smoke or consume alcohol.
On examination:
β’ Temperature: 36.8Β°C (98.2Β°F)
β’ Heart rate: 112/min
β’ Blood pressure: 128/76 mm Hg
β’ Respiratory rate: 32/min
β’ Oxygen saturation: 88% on room air
On auscultation:
β’ Diffuse bilateral wheezing
β’ Prolonged expiratory phase
Her condition deteriorates during the examination, requiring emergency intubation due to acute respiratory failure. Despite resuscitation efforts, she experiences cardiac arrest and succumbs.
Autopsy Findings:
β’ Hyperinflated lungs
β’ Airway mucus plugging
β’ Cellular infiltration of bronchial walls, including eosinophils
Which of the following medications, if used long-term, would have best prevented the pathological airway changes seen in this patient? |
Correct Answer π―: Fluticasone
π§ Fluticasone is the best long-term therapy because it directly targets the underlying inflammatory cascade (β IL-4, IL-5, IL-13) β Prevents structural changes (e.g., mucus plugging, bronchial wall thickening). Other options are either acute therapies or adjuncts.
βοΈ
Trigger Event
Chronic asthma exacerbation
β¬
Exposure to Trigger (e.g., allergens, irritants)
β¬
Immune Activation
π§ Antigen exposure β Activation of Th2 cells
β¬
Th2 Cell Cytokine Release
π§ IL-4, IL-5, IL-13 β
β¬
Effects of Cytokines
IL-4, IL-13 β IgE class switching β Mast cell sensitization
IL-5 β Eosinophil recruitment β
β¬
Mast Cell Degranulation
π§ Histamine, leukotrienes, prostaglandins β
β¬
Acute Inflammatory Response
π§ Bronchial smooth muscle contraction β Bronchoconstriction
β Mucus secretion β Airway obstruction
β¬
Chronic Inflammatory Response (due to Noncompliance)
Eosinophil activation β Bronchial epithelial damage
π§ β Goblet cells β Mucus hypersecretion
β¬
Bronchial Wall Remodeling
π§ β Fibrosis, smooth muscle hypertrophy
β¬
Acute Respiratory Failure
β¬
Intubation Failure β Cardiac Arrest
Image Source: NEJM
Differential Diagnosis Table ποΈ
Condition | Key Features | Reason for Exclusion |
|---|---|---|
Acute Asthma Exacerbation | π§ Wheezing, dyspnea, hyperinflated lungs, mucus plugging | Fits scenario; however, focus on chronic inflammation prevention |
Pulmonary Embolism | π Sudden onset dyspnea, chest pain, hypoxemia | No chest pain or risk factors (e.g., immobility, DVT) |
Heart Failure (HF) | π Dyspnea, orthopnea, pulmonary edema | No evidence of cardiomegaly or fluid overload |
Chronic Obstructive Pulmonary Disease (COPD) | π Chronic cough, history of smoking, hyperinflation | Patient is young and non-smoker |
Anaphylaxis | π Acute onset of dyspnea, urticaria, hypotension | No history of allergen exposure or hypotension |
βοΈ Explanation of Other Differentials
Differential βοΈ | Mechanism βοΈ | Why Incorrect? π΄ |
|---|---|---|
Albuterol | Short-acting bronchodilator (β Ξ²2 receptor agonist β cAMP) | π§ Only provides temporary relief; no long-term anti-inflammatory effects |
Ipratropium | Blocks acetylcholine (β muscarinic receptor antagonist) | π§ Improves airflow acutely but no effect on chronic inflammation |
Magnesium Sulfate | Calcium channel blocker (β smooth muscle relaxation) | π§ Reserved for acute severe asthma; no role in prevention |
Montelukast | Leukotriene receptor antagonist (β leukotrienes β) | π§ Useful adjunct but less potent than corticosteroids for airway inflammation |
Theophylline | PDE inhibitor (β cAMP β) | π§ Minimal anti-inflammatory effect; limited role in chronic asthma |
π Flashcards
π° What'd you think of today's Newsletter ? |
Stay Hungry, Stay Curious!
Your Brother In This Struggle
Dr. Shoaib Ahmad
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