Chronic obstructive pulmonary disorder (COPD) - B. Pharma 2nd Semester Pathophysiology notes pdf

Chronic obstructive pulmonary disorder (COPD)


Chronic obstructive pulmonary disorder

       Etio- pathogenesis



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

“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


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


       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

  1. Protease – antiprotease imbalance
  2. 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


       Weight loss

       Pulmonary hypertension

       Peripheral oedema



       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

Post a Comment