Chronic obstructive pulmonary disorder (COPD)

Contents

Chronic obstructive pulmonary disorder

• Etio- pathogenesis

• Symptoms

Objectives

At the end of this PDF Notes, student will be able to

• Define COPD

• Explain the pathophysiology of COPD

• Describe the symptoms of COPD

Chronic Obstructive Pulmonary Disease
(COPD)

“A chronic slowly progressing disorder characterized by air flow obstruction leading to reduced pulmonary inspiratory & expiratory capacity”

• Disease may co-exist with asthma

Two major forms of COPD

• Chronic bronchitis

• Emphysema

Chronic bronchitis

• Characterized by excessive mucus production by the tracheo-bronchial followed by edema & bronchial inflammation leading to airway obstruction

• It is associated with cigarette smoking & air pollution

Pathogenesis of chronic bronchitis

Two pathological processes underlining the development of chronic bronchitis include

1. Hypersecretory disorder

• Characterized by expectoration with increased susceptibility to respiratory infections

• Normally, cilia & mucus in the bronchi protect against inhaled irritants which are trapped and expectorated

• Persistent irritation causes proliferation of mucus secreting glands & goblet cells in the bronchial epithelium leading to hypersecretion of thick & viscous mucus

• Accumulation of mucus inturn causes inflammation and recurrent viral & bacterial infections

2. Chronic inflammation & edema causes thickening of bronchio & alveolar walls

• Alveoli gets distorted, affects blood vessels closely associated with them, leading to vasoconstriction and pulmonary hypertension

• Reduction of gas exchange across alveolar epithelium – hypoxemia

• Sustained pulmonary hypertension – increased right ventricular pressure within heart, right ventricular hypertrophy and failure

• Pulmonary edema results followed by activation of renin angiotensin, aldosterone system, salt & water retention – reduction in renal blood flow

Emphysema

• Condition of permanent destructive enlargement of respiratory bronchioles, alveolar ducts & alveolar sac

• Adjacent alveoli becomes indistinguishable from one another

2 main consequence of emphysema

• Loss of available gas space & impaired gas exchange

• Loss of elastic recoil in the small airways leading them to collapse during expiration

Pathogenesis of emphysema

Arise as a consequence of 2 critical imbalances

Protease – antiprotease imbalance
Oxidant – antioxidant imbalance

Protease – anti protease theory

• Emphysema results from gradual progressive loss of elastic tissue in lungs due to an imbalance between proteolytic enzymes & protective factors

• Macrophages & neutrophills releases lysosomal enzymes (elastase) – capable of destroying connective tissue in the lungs

• Normal condition – protective mechanism called α₁ – anti trypsin or α₁ – protease inhibitor inhibits proteolytic enzyme and prevent damage

• α₁ – anti trypsin is present in serum, tissue fluids & macrophages

• Deficiency of α₁ – anti trypsin causes destruction of elastic tissue leading to emphysema

Oxidant – antioxidant imbalance

• Normally lungs contains anti oxidants like SOD, glutathione - reduces oxidative damage

• Tobacco smoke, activated neutrophills – increases oxygen free radicals – depletes antioxidant mechanism – tissue damage

• Inactivation of antiproteases, functional deficiency without enzyme deficiency

Symptoms of COPD

• Chronic cough ( after 20 or > cigarettes/day)

• Dyspnea (during physical activity and rest)

• Frequent respiratory infections

• Production of purulent sputum

• Bluish discoloration of lips and nail beds

• Morning headaches

• Wheezing

• Weight loss

• Pulmonary hypertension

• Peripheral oedema

• Hemoptysis

Summary

• COPD is the most prevalent manifestation of obstructive lung disease, mainly comprises chronic bronchitis and emphysema

• Reduction of overall personal exposure to tobacco smoke, occupational dusts, chemicals and pollutants is an important goal to prevent the onset and progression of COPD

• Risk factors for COPD include host factors (a, -antitrypsin deficiency and airway hyperresponsiveness) and exposures (tobacco smoke, occupational dusts and chemicals, indoor and outdoor pollutants, infections) and socio-economic status