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PH-RS01

Asthma

How type 2 inflammation makes the airways narrow too easily, why the narrowing is variable and reversible, why wheeze is loudest on breathing out, and how long-standing asthma can remodel the airway wall.

By the end, you can

  • Describe the normal bronchiole, its smooth muscle and its control.
  • Explain how Th2 cytokines, IgE and mast cells produce early and late airway responses.
  • Relate bronchospasm, wall oedema and mucus to wheeze, air trapping and V/Q mismatch.
  • Explain why a normal or rising PaCO2 in a severe attack is a warning sign.
  • Distinguish reversible obstruction from the fixed component that remodelling can leave.
  • Recognise the classic appearances, severity grades and tests of asthma, and explain how each main drug class acts on its mechanism.

What it is

Asthma is a chronic inflammatory disease of the airways in which hyperresponsive airways narrow in episodes, causing variable airflow obstruction that reverses, fully or largely, on its own or with a bronchodilator. Most asthma involves type 2 inflammation (often allergic); some does not.

2 types to tell apart
Type 2 (T2-high) asthma
Driven by Th2 cytokines (IL-4, IL-5, IL-13), with eosinophils, IgE and mast cells; often allergic and starting in childhood.
T2-low asthma
Fewer eosinophils and more neutrophils or few inflammatory cells; often adult-onset and linked with obesity or smoking. It responds less to treatments aimed at type 2 inflammation.

US spelling: fibres → fibers, adrenaline → epinephrine.

Normal function

Conducting airways and their smooth muscle

Air reaches the alveoli through a branching tree of conducting airways. Bronchi are held open by cartilage; the , under about 1 mm across, have none. A sheet of wraps the walls of both, and in the bronchioles it alone sets the width of the lumen. The terminal bronchioles open into , where gas exchange begins.

Parasympathetic (vagal) fibres release acetylcholine, which contracts the muscle; adrenaline acting on β2-adrenoceptors relaxes it. The larger airways are lined by a ciliated epithelium with mucus-secreting goblet cells: mucus traps particles and cilia sweep it upwards (the mucociliary escalator).

Width matters greatly for flow: in a simple tube, halving the radius raises resistance about sixteen-fold. In health most resistance lies in medium-sized bronchi, because the many small airways lie side by side; when thousands narrow together, as in asthma, resistance rises steeply.

Point to it on the model