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chronic obstructive pulmonary disease

Written by Wong Sze Yuin

Last Reviewed: April 2019

Review Due: April 2020

 

DEFINITION

‘a chronic, obstructive disease of the airways characterized by progressive airflow limitation that interferes with normal breathing and is not fully reversible’

'chronic bronchitis is defined clinically as production of sputum on most days for at least three consecutive months in at least two years'

'emphysema is defined histologically as abnormal, permanent enlargement of air spaces distal to the terminal bronchiole with alveolar wall destruction' 

AETIOLOGY

Tobacco smoking

Air pollution

Occupational exposure to dust, fumes and chemicals

Alpha-1 antitrypsin deficiency

 

SIGNS AND SYMPTOMS

Consider COPD in patients over 35 presenting with these characteristic symptoms:

Chronic cough

Regular sputum production (white or clear)

Exertional breathlessness

Wheeze

Frequent winter ‘bronchitis’

In patient's with mild COPD, there may be few or little signs on examination. More signs, including some of those below, may be present in severe disease.

Inspection:

Use of accessory muscles

Coarse flapping tremor/asterixis

Barrel chest

Palpation:

Reduced chest expansion

Percussion:

Hyperresonance

Auscultation:

Reduced air entry

Wheeze

 

PATHOPHYSIOLOGY

The hallmark of COPD is chronic inflammation that affects central and peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature. Changes are progressive and usually irreversible.
 

There is narrowing and remodelling of airways, increased number of goblet cells, enlargement of mucus-secreting glands of the central airways and subsequent vascular bed changes leading to pulmonary hypertension.

 

Host response to inhaled stimuli generates the inflammatory reaction responsible for the changes in the airways, alveoli, and pulmonary blood vessels. Activated macrophages, neutrophils, and leukocytes are the core cells in this process.
 

In emphysema, the final outcome of the inflammatory responses is elastin breakdown and subsequent loss of alveolar integrity. 
 

In chronic bronchitis, these inflammatory changes lead to ciliary dysfunction and increased goblet cell size and number, causing excessive mucus secretion.

 

Investigations

Spirometry

FEV1:FVC <0.7 (Obstructive)​

No/little reversibility with bronchodilator

FBC

Raised Haematocrit (Secondary Polycythaemia)

CXR

May show hyperinflation, flattened diaphragm, large central pulmonary arteries, bullae and decreased peripheral vascular markings

Alpha 1 Antitrypsin Level

If suspicion of deficiency, for example in those with a positive family history, non-smokers or young patients

 

TREATMENT

non-pharmacological

Smoking cessation advice

One-off pneumococcal vaccination

Annual influenza vaccination

Pulmonary rehabilitation

pharmacological

SABA: Short Acting Beta2 Agonists (e.g. Salbutamol)

LABA: Long Acting Beta2 Agonists (e.g. Salmeterol)

LAMA: Long Acting Muscarinic Antagonists (e.g. Tiotropium)

LCCI: LABA + Inhaled Corticosteroid

 
 

EPIDEMIOLOGY

An estimated 1.2 million people are affected by COPD in the UK. There are 115,000 new diagnoses a year.

REFERENCES