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PH-RS15

Bronchiectasis and other changes of the bronchial lumen

How infection, inflammation and failed mucus clearance feed each other until bronchi are permanently widened, why cystic fibrosis and ciliary defects start the cycle, and what narrowing or blocking a bronchus does to the lung beyond.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe the normal bronchial wall and how mucociliary clearance keeps the lower airways clean.
  • Explain how impaired clearance, bacterial infection and neutrophilic inflammation form a self-sustaining cycle that destroys the bronchial wall.
  • Relate the main causes, including CFTR variants in cystic fibrosis and primary ciliary dyskinesia, to how and where bronchiectasis develops.
  • Predict the effect of a partial, complete or long-standing block of a bronchus on the lung beyond it.
  • Recognise the cylindrical, varicose and cystic forms, the signet-ring sign and the key tests, and explain how each main treatment acts on the cycle.

What it is

Bronchiectasis is permanent, abnormal widening of bronchi whose walls have lost their muscle, elastic tissue and cartilage, caused by a self-sustaining cycle of infection and inflammation in airways that cannot clear their mucus. It is the shared end point of many causes. The lumen of a bronchus can also be narrowed (stenosis) or blocked, from inside, from its wall or by pressure from outside; a lasting block is one route into bronchiectasis.

3 types to tell apart
Focal and diffuse
Focal bronchiectasis affects one area, usually after a severe pneumonia or behind a blocked bronchus; diffuse bronchiectasis involves many lobes and usually has a systemic cause, such as cystic fibrosis, ciliary dyskinesia or immune deficiency.
Cystic fibrosis and non-cystic fibrosis bronchiectasis
Often described separately, because cystic fibrosis (CF) has its own cause, organisms and treatments, including medicines that act on the faulty CFTR protein.
Traction bronchiectasis
Airways pulled open by scarred lung around them in pulmonary fibrosis. It is a sign of the fibrosis, not a primary disease of the airways.

US spelling: fibres → fibers.

Normal function

The bronchial wall and the mucus escalator

A bronchus is a tube with a layered wall. Its lining is a with scattered ; beneath it lie a loose lamina propria rich in elastic fibres, a spiral of , a submucosa with and plates of that hold the lumen open. Each bronchus runs beside a branch of the pulmonary artery of about the same width, and both taper as they divide towards the edge of the lung.

Mucus from goblet cells and glands floats on a thin, watery periciliary layer. The cilia beat in that layer and push the mucus blanket, with trapped dust and microbes, up towards the throat: the mucociliary escalator. Coughing clears what the cilia cannot.

Salt transport sets the depth of the watery layer. Lining cells secrete chloride and bicarbonate through the CFTR channel and absorb sodium through epithelial sodium channels (ENaC), and water follows the salt. Antibodies (mostly IgA), antimicrobial proteins and macrophages deal with what is trapped, so very few bacteria live in healthy lower airways.

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