Flow chart for pathophysiology of asthma
asthma pathophysiology flowchart mechanism 2024
A detailed medical flowchart showing the pathophysiology of asthma with two main pathways: Atopic (Allergic) Asthma and Non-Atopic Asthma. The chart flows top to bottom with the following structure: TOP ROW - Two trigger boxes side by side: Left box: "ATOPIC ASTHMA - Triggers: Allergens (dust mites, pollen, animal dander, mold)" Right box: "NON-ATOPIC ASTHMA - Triggers: Viral infections, Air pollutants, Cold air, Exercise, Stress" Both arrows point down to: "AIRWAY SENSITIZATION - Dendritic cells present antigen → Th2 cell activation" Arrow down to: "Th2 CYTOKINE RELEASE - IL-4 → promotes IgE synthesis - IL-5 → eosinophil recruitment & activation - IL-13 → goblet cell metaplasia, mucus" Arrow down splits into two boxes side by side: Left: "IgE binds to mast cells → Re-exposure to allergen → Mast cell degranulation" Right: "Eosinophil activation → Release of major basic protein, ECP → Airway epithelial damage" Both arrows converge to: "EARLY PHASE REACTION (0–30 min) - Histamine, Leukotrienes (LTC4/D4), Prostaglandins, PAF - Bronchoconstriction + Vasodilation + Edema" Arrow down to: "LATE PHASE REACTION (4–12 hrs) - Cytokines, Chemokines - Influx of eosinophils, neutrophils, T-cells - Sustained inflammation" Arrow down to large central box: "AIRFLOW OBSTRUCTION (Triple mechanism): ① Bronchial smooth muscle contraction (bronchoconstriction) ② Inflammation & edema of bronchial wall ③ Hypersecretion of mucus" Arrow down splits into two parallel outcomes: Left: "ACUTE SYMPTOMS - Wheezing - Dyspnea - Chest tightness - Cough" Right: "IF UNTREATED → AIRWAY REMODELING - Sub-basement membrane fibrosis - Smooth muscle hyperplasia - Goblet cell hyperplasia - Bronchial gland hypertrophy → Irreversible obstruction" Both arrows converge at bottom: "AIRWAY HYPERRESPONSIVENESS → Exaggerated bronchoconstriction to further triggers → Risk of future exacerbations" Use clean medical diagram style with color coding: blue for triggers, orange for immune response, red for inflammatory mediators, dark red for obstruction, purple for remodeling. White background, clear arrows, readable fonts.
Pathophysiology of Asthma — Summary
Two Main Types
| Atopic (Allergic) | Non-Atopic | |
|---|---|---|
| Trigger | Allergens (dust mites, pollen, mold, animal dander) | Viral infections, pollutants, cold, exercise |
| Mechanism | IgE / Th2-mediated | Poorly understood; neurogenic or direct irritant |
Key Steps
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Sensitization — Antigen-presenting cells (dendritic cells) activate Th2 lymphocytes, which release:
- IL-4 → stimulates B cells to switch to IgE production
- IL-5 → recruits and activates eosinophils
- IL-13 → goblet cell metaplasia and mucus hypersecretion
-
Early Phase (0–30 min) — Re-exposure to allergen cross-links IgE on mast cells → degranulation → release of histamine, leukotrienes (LTC4/D4/E4), prostaglandins, and PAF → rapid bronchoconstriction, vasodilation, edema
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Late Phase (4–12 hrs) — Chemokines recruit eosinophils, neutrophils, and T cells → sustained cytokine-driven inflammation → prolonged airflow limitation
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Triple Mechanism of Airflow Obstruction
- Bronchial smooth muscle contraction
- Inflammation and edema of the bronchial wall
- Mucus hypersecretion plugging the lumen
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Airway Hyperresponsiveness — Heightened bronchoconstrictor response to stimuli; eosinophil-derived major basic protein damages the epithelium, lowering the threshold for further responses
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Airway Remodeling (if untreated):
- Sub-basement membrane fibrosis
- Smooth muscle hyperplasia
- Bronchial gland hypertrophy
- Goblet cell metaplasia → Adds an irreversible component to obstruction