GeriQBank · Paper IV

Changes in the airways in emphysema and asthma

Moderate YieldAsked ×17-mark noteNeeds clinical review

Topic: Respiratory Medicine
Chapter: Infectious Diseases & Respiratory Medicine
Years asked: Not recorded in the source
Frequency: Set 1× in Paper IV (2009–2025)

As set in the university paper

Describe the changes seen in the airways in emphysema and asthma.
Paper IV · Respiratory Medicine · asked ×1 · 7-mark note · see in paper list

Answer framework

Emphysema — definition; protease–antiprotease cause; loss of recoil and air trapping; centriacinar, panacinar and paraseptal types
Asthma — Th2 inflammation and variable obstruction; airway remodelling; fixed obstruction
Key contrasts — where, how, and the nature of airflow limitation
Older people — ageing lung; asthma mortality; inflammaging

An exam answer plan drawn from the detailed answer below. Use it to attempt the question first.

Detailed answer

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Attempt it firstOutline your answer as a 7-mark note before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer

Short revision answer

Emphysema is permanent enlargement of airspaces beyond the terminal bronchioles with wall destruction and no obvious fibrosis. Smoke-driven inflammation releases proteases (neutrophil elastase, MMP-12, cathepsins) that destroy elastin, while oxidants inactivate antiproteases such as alpha-1 antitrypsin (inherited deficiency predisposes, especially in smokers).
Lost elastic fibres remove recoil and the alveolar attachments that hold small airways open, so they collapse on expiration and trap air.
Types: centriacinar (commonest; smoking and dust; around proximal respiratory bronchioles; upper lobes), panacinar (uniform; lower lobes; alpha-1 antitrypsin deficiency) and paraseptal (acinar edges under the pleura); centriacinar and panacinar can coexist.
Asthma: chronic, often eosinophilic Th2 inflammation (IL-4, IL-13) causes variable airflow limitation through bronchoconstriction, oedema, mucus and hyper-responsiveness.
Remodelling of large and small airways: goblet cell hyperplasia and mucus, damaged epithelium with apoptosis, thickened reticular basement membrane (subepithelial fibrosis), more smooth muscle, angiogenesis, matrix deposition thickening the wall, and weaker cartilage — explaining the fixed obstruction some patients develop.
Contrasts: emphysema destroys the airspaces (protease imbalance, lost recoil, permanent limitation); asthma thickens and narrows the airway wall (inflammatory remodelling, variable limitation that can become fixed).
In old age: ageing alone dilates alveoli and ducts without true emphysema, lowers recoil and stiffens the chest wall (costochondral calcification, kyphosis); lung function falls faster in asthma, asthma death risk is more than five times higher and hasn't fallen, and "inflammaging" may sustain remodelling.

Condensed by GeriClinics from the detailed answer below, with no new facts added.

A. Emphysema

Definition: permanent enlargement of the airspaces beyond the terminal bronchioles, with destruction of their walls and without obvious fibrosis. It affects mainly the alveoli, and the small airways indirectly.

Cause: cigarette smoke and other irritants set up an inflammation rich in proteases (neutrophil elastase, MMP-12, cathepsins) that break down elastin, while oxidants inactivate protective antiproteases such as alpha-1 antitrypsin. Inherited alpha-1 antitrypsin deficiency predisposes to emphysema, especially in smokers.

Loss of elastic fibres removes the lung's elastic recoil and the alveolar attachments that tether small airways open, so small airways collapse on breathing out and air is trapped.

Centriacinar (centrilobular) emphysema: the commonest type, linked to smoking and dust. It enlarges the airspaces around the proximal respiratory bronchioles, sparing the distal alveoli, and mainly affects the upper lobes.

Panacinar (panlobular) emphysema: uniform enlargement from the respiratory bronchiole to the alveoli, mainly in the lower lobes; alpha-1 antitrypsin deficiency is a major cause.

Paraseptal (distal acinar) emphysema: enlarged airspaces at the edges of the acini, under the pleura.

Centriacinar and panacinar types can coexist, for example upper-lobe centriacinar with lower-lobe panacinar emphysema.

B. Asthma

Chronic airway inflammation, often eosinophilic and driven by Th2 cytokines such as IL-4 and IL-13, causes variable airflow limitation through bronchoconstriction, airway oedema, mucus secretion and airway hyper-responsiveness.

Airway remodelling, the structural change of chronic asthma, affects both large and small airways:

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Goblet cell hyperplasia and metaplasia, with excess mucus

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Damaged epithelium, with epithelial cell apoptosis

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Thickened reticular basement membrane from subepithelial collagen deposition (subepithelial fibrosis)

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Increased airway smooth muscle mass

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New blood vessel formation (angiogenesis)

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Extracellular matrix deposited in the lamina propria and submucosa, thickening the wall

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Reduced integrity of the airway cartilage

10.

Remodelling can explain the persistent, fixed airflow obstruction that develops in some people with asthma.

C. The key contrasts

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Where: emphysema destroys the air spaces beyond the terminal bronchioles; asthma thickens and narrows the airway wall itself.

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How: emphysema follows a protease–antiprotease imbalance that destroys elastin; asthma follows inflammation that remodels the wall.

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Airflow limitation: in emphysema it comes from lost recoil and collapsing small airways and is permanent; in asthma it is variable, but can become fixed with remodelling.

D. Older people

11.

Ageing alone dilates alveoli and alveolar ducts without true emphysema or fibrosis, reduces elastic recoil, and stiffens the chest wall (costochondral calcification, spinal degeneration, kyphosis).

12.

Lung function falls faster in people with asthma, and the risk of death from asthma is more than five times higher in older people, whose asthma mortality has not fallen.

13.

Persistent low-grade inflammation with ageing ("inflammaging") may help sustain airway remodelling in older people with asthma.

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References

Takahashi M, Fukuoka J, Nitta N, et al. Imaging of pulmonary emphysema: a pictorial review. Int J Chron Obstruct Pulmon Dis. 2008;3(2):193–204. — Definition and centriacinar, panacinar and paraseptal types. Open access (CC BY-NC)
Bentaher A, Glehen O, Degobert G. Pulmonary Emphysema: Current Understanding of Disease Pathogenesis and Therapeutic Approaches. Biomedicines. 2025;13(9):2120. — Protease–antiprotease imbalance and elastin loss. Open access (CC BY 4.0)
Hough KP, Curtiss ML, Blain TJ, et al. Airway Remodeling in Asthma. Front Med (Lausanne). 2020;7:191. — Structural changes in asthma; ageing and the lung. Open access (CC BY 4.0)

Written in GeriClinics' own words from the sources above, and checked against them. Not yet clinically reviewed.

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