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Chronic Obstructive Pulmonary Disease

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Chronic Obstructive Pulmonary Disease

COPD Pathogenesis

Background

COPD is defined as a disease state with airflow limitation that is not fully reversible.

COPD include: emphysema; destruction and enlargement of alveoli, chronic bronchitis; a clinical condition with chronic cough and phlegm, small airway disease; narrowing of the small bronchioles.

Diseases without chronic obstruction are not included within the COPD. Ex:Chronic bronchitis without chronic airway obstruction is not included.

 

Epidemiology And Etiology

COPD is caused by long term exposure with toxic substances and gases. Smoking is the cause for over 90% in developed countries. However, only 10-20% of heavy smokers develop COPD.

 

Pathophysiology

The most consistent pathological finding in COPD is increased number of mucus secreting goblet cells in the bronchil mucosa, especially in the larger bronchi. In more severe cases the bronchi are inflamed and filled with pus.

Goblet Cells Increased

Microscopically there is acute and chronic inflammatory infiltration in the walls of bronchi and bronchioles. Lymphoid follicles may develop in severe cases. In contrast to asthma, the lymphocytic infiltrate is predominantly CD8+. The epithelium become ulcerated and squamous epithelium replaces the columnar cells. Scarring and thickening of the walls after the inflammation cause narrowing of the small airways.

 

The initial inflammation is considered as improvement of airway function, if smoking is stopped early. In later stages inflammation continuous even if smoking is stopped.

In later stages of the airways disease leads to progressive squamous cell metaplasia, and fibrosis of the bronchial walls. These consecutive changes are the physiological development of airflow limitation. If the airway narrowing is combined with emphysema the resulting airflow limitation is even more severe.

Read About Emphysema

Emphysema leads to air trapping inside the lungs and airflow limitation. Expiration capacity decreases while TLC increases due to the loss of lung elastic recoil.

V/Q mismatch, caused by premature closure of airways in expiration and mucus plugging inside small airways, leads to a fall in PaOand increased work of respiration.

Many patients have low normal PaCO2 value due to increased ventilation in response to their hypoxia. Patients who fail to maintain their respiratory effort have increased PaCO2. Rise in CO2 stimulates the respiration in short term but these patients become insensitive to CO2 in long term and they depend on hypoxaemia to drive their ventilation. Attempts to abolish hypoxaemia by administering oxygen can make the situation much worse by decreasing respiratory drive in these patients who depend on hypoxia to drive their ventilation.

 

In summary, three mechanisms have been suggested for this limitation of airflow in small airways (<2 mm in diameter).

  • Loss of elasticity and alveolar attachments of airways due to emphysema. This reduces the elastic recoil and the airways collapse during expiration.
  • Inflammation and scarring cause the small airways to narrow.
  • Mucus secretion, which blocks the airways.

Each of these narrows the small airways and causes air trapping leading to hyperinflation of the lungs, V/Q mismatch, increased work of breathing and breathlessness.

 

Symptoms
  • productive cough with white or clear sputum
  • wheeze
  • breathlessness

usually following many years of a smoker’s cough. In these patients colds seem to be chest settled and often infective exacerbations occur with purulent sputum. Symptoms worsen by cold, foggy weather and atmospheric pollution.

Other systemic effects;

  • hypertension
  • osteoporosis
  • muscle mass loss
  • weight loss
  • weakness

 

Signs

In mild COPD there may be no signs or only quiet wheezes. In severe disease, the patient is tachypnoeic, with prolonged expiration.

Intercostal indrawing on inspiration and pursing the lips on expiration may be seen. Chest expansion is poor, the lungs are hyperinflated, and there is loss of the normal cardiac and liver dullness.

Patients who remain responsive to CO2 are usually breathless and rarely cyanosed. Heart failure and oedema are not often except as terminal events.

Patients who are not responsive to CO2 are often cyanosed and oedematous but not particularly breathless.

Those with hypercapnia may have peripheral vasodilatation, a bounding pulse, and when the PaCO2 is above about 10 kPa, a coarse flapping tremor of the outstretched hands. Severe hypercapnia leads to confusion and progressive drowsiness.

 

Diagnosis

Diagnosis usually based on a history of breathlessness and sputum production in a chronic smoker. In the absence of a history of smoking asthma is more likely explanation unless there is a family history suggesting α1-antitrypsin deficiency.

 

Investigations
  • Lung Function Test shows if there is an airflow limitations. In many patients the airflow limitation is partly reversible. It can be difficult to distinguish between COPD and asthma.
  • Chest X-ray is often normal, even when the disease is advanced.
  • High-resolution CT scans are useful, particularly when the plain chest X-ray is normal.
  • Blood gases are often normal at rest, but patients desaturate on exercise. In more advanced cases there is resting hypoxaemia and there may also be hypercapnia.
  • α1-Antitrypsin levels and genotype are worth measuring in premature disease or lifelong non-smokers.

 

Lung Function Test

 

Management

COPD management

 

 

References


Kumar and Clark’s Clinical Medicine; 812

Harrison’s Principles of Internal Medicine

Wikipedia

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The art of medicine consists in amusing the patient while nature cures the disease.

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