Chronic bronchitis

Published on 02/04/2015 by admin

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Last modified 02/04/2015

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100 Chronic bronchitis

Instruction

Examine this patient’s chest.

Salient features

History

• Productive cough

• Increasing dyspnoea

• Weight loss

• History of smoking

• History of α1-antitrypsin deficiency.

Examination

• Begin with examination of the sputum pot.

Observe the patient:

• From the end of the bed: for obvious breathlessness, pursed lip breathing and symmetrical chest movements—and count respiratory rate.

• Look for nail changes such as tar staining.

• Feel the palms for warmth and the pulse for rapid bounding pulse (signs of carbon dioxide retention).

• Look at the lips and tongue for central cyanosis.

Examine the neck:

• Comment on the active contractions of the accessory muscles of respiration such as sternocleidomastoids, scaleni and trapezii.

• Palpate for tracheal deviation and measure the distance between the cricoid cartilage and suprasternal notch (less than three fingers’ breadth in emphysema).

• Comment on the raised JVP.

Examine the chest:

• Comment on barrel-shaped chest

• Inspiratory retraction of the lower ribs (Hoover’s sign)

• Use of accessory muscles of respiration.

• Palpate for:

• apex beat
• chest expansion
• vocal fremitus.

• Percuss looking for:

• hyper-resonance and obliteration of cardiac and liver dullness.

• Auscultate for:

• breath sounds (diminished breath sounds)
• vocal resonance
• forced expiratory time (FET): the end-point is detected by auscultating over the trachea in the suprasternal notch; normal individuals can empty their chest from full inspiration in ≤4 s and prolongation to >6 s indicates airflow obstruction.
• loud pulmonary second heart sound.

Examine the abdomen:

• Palpable liver to look for hepatic displacement (comment on upper border of liver by percussion).

Finally:

Tell the examiner that this patient is at increased risk for cardiovascular disease, osteoporosis, lung cancer and depression.

Remember: Airflow obstruction as measured by spirometry is defined as a ratio of the postbronchodilator forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) of <0.70.

Diagnosis

This patient has features of COPD (lesion) caused by cigarette smoking (aetiology) and is very cyanosed at rest (functional status).

Questions

What do you understand by the term chronic bronchitis?

Chronic bronchitis is cough with mucoid expectoration for at least 3 months in a year for 2 successive years.

What is the definition of emphysema?

Emphysema is the abnormal permanent enlargement of the airway distal to the terminal respiratory bronchioles with destruction of their walls. Clinical, radiological and lung function tests give an imprecise picture in an individual case but a combination of all these features gives a reasonable picture.

What do you understand by the term chronic obstructive pulmonary disease?

COPD is a condition characterized by airflow limitation that is not fully reversible and is usually progressive and associated with an abnormal inflammatory response. The term COPD encompasses chronic obstructive bronchitis (with obstruction of small airways) and emphysema (with destruction of lung parenchyma, loss of lung elasticity and closure of small airways). Most patients also have mucus plugging (N Engl J Med 2000;343:269).

Advanced-level questions

What is the mechanism reduction in expiratory capacity in chronic obstructive pulmonary disease?

Dynamic hyperinflation is considered to be an important factor in the reduction of exercise capacity and the development of dyspnoea.

COPD is caused by a variable mixture of three processes including loss of alveolar attachments, inflammatory obstruction of the airway and luminal obstruction with mucus. Alveolar attachments ensure a radial tethering effect, which is important for keeping small airways patent in the normal lung. At smaller lung volumes, airways narrow because of decreased lung elasticity and weaker tethering effects. As a result, maximal expiratory airflow decreases as the lung empties and ceases at 25 to 35% of total lung capacity. The remaining air (or residual volume) may account for as much as 60 to 70% of predicted total lung capacity. Patients with COPD must breathe at larger lung volumes to optimize expiratory airflow, but this requires greater respiratory work because the lungs and chest wall become stiffer at larger volumes. These effects are worse with exercise. A normal lung meets the increased ventilatory demands of exercise by increasing both tidal volume and respiratory rate, with little change in the final end-expiratory lung volume. Whereas in COPD the respiratory rate does increase in response to exercise, but with insufficient expiratory time, breaths become increasingly shallow and end-expiratory lung volume progressively enlarges, a phenomenon called dynamic hyperinflation (N Engl J Med 2010;362:1407–16).

What is the role of inflammatory mechanisms in chronic obstructive pulmonary disease?

In COPD, reactive oxygen species (ROS), pathogen associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs) activate families of pattern recognition receptors (PRRs) that include the toll-like receptors (TLRs). This understanding has led to the hypothesis that COPD is also a disease of innate immunity. COPD is characterized by abnormal response to injury, with altered barrier function of the respiratory tract, an acute phase reaction and excessive activation of macrophages, neutrophils and fibroblasts in the lung. Macrophages and epithelial cells in airways are activated by cigarette smoke and other irritants (in developing countries, the inhalation of smoke from biomass fuels is an important cause of COPD, particularly among women who cook in poorly ventilated homes) and these release neutrophil chemotactic factors including interleukin-8 and leukotriene B4. Neutrophils and macrophages then release proteases that break down connective tissue in the lung parenchyma, resulting in emphysema, and also stimulate hypersecretion of bronchial mucus. The chronic inflammatory process in COPD differs markedly from that seen in bronchial asthma, with different inflammatory cells, mediators, inflammatory effects and responses to treatment.

What is the role of proteolysis in chronic obstructive pulmonary disease?

In COPD, the protease-antiprotease balance is tipped in favour of proteolysis because of either an increase in proteases (including neutrophil elastase, proteinase 3, cathepsins, matrix metalloproteases 1, 2, 9 and 12) or a deficiency of antiproteases (including α1-antitrypsin, elafin, secretory leukoprotease inhibitor and tissue inhibitors of matrix metalloproteases).

What is the main cause of death and disability in chronic obstructive pulmonary disease?

Mortality and disability from COPD is related to an accelerated decline in lung function over time, with a loss of >50–60 ml/year in the forced expiratory volume in 1 s (FEV1), compared with a normal loss of 20–30 ml/year. The progressive reduction in FEV1

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