12. Epidemiology, sign, symptoms, etiology, phenotypes and diagnosis of COPD

Question 1

Epidemiology of COPD

Answer 1

• Current prevalence between male and female are reaching parity [3:2 ratio] but before it was heavily skewed towards male [due to smoking]
• Pevalence is about 6%

Question 2

Etiology of COPD

Answer 2

• Tobacco smoking and second hand exposure to tobacco smoke is the biggest risk factor to COPD
• Exposure to air pollution or fine dusts
• Alpha 1 antitrypsin deficiency [decreases ability to control PMN activity in alveoli, leading to increased destruction; addition to smoking this solidifies COPD at young age]
• Primary ciliary dyskinesia [Kartagner syndrome]
• Chronic asthma and recurrent pulmonary infections, TB can also lead to alveoli and airway destruction

Divided overall into Endogenous and Exogenous factors

Question 3

Phenotypes of COPD

Answer 3

COPD mainfests and is diagnosed as
- Chronic Bronchitis
- Emphysema

The 2 often can coexist and can also manifest with chronic asthma too

Emphysema has 2 subtypes, Panacinar/Panlobular [associated with AATD, destruction of entire acinus and usually affects lower lobe] and Centrilobular [most common type, classsicaly in smokers, destruction of central portion of the acinus, sparing distal alveoli]

Question 4

Chronic Bronchitis pathogenesis

Answer 4

Chronic productive cough [sputum volume is high] that lasts > 3 months for 2 consecutive years. It is diagnosed based on clinical features in addition to spirometry and chest imaging to rule out other causes of symptoms [emphysema, bronchitis, pneumonia]

Considered obstructive pulmonary disease because of excessive mucus production and inflammation that blocks major airway branches leading to air trapping

Chronic inflammation, hypertrophy of goblet cells leading to increased mucus production, hyperplasia of smooth muscle cells of small airways and vasculature leading to PAH

Question 5

Emphysema pathogenesis

Answer 5

Excessive destruction of alveoli and enlargement of distal terminal bronchioles leading to air trapping and increased air quantity in lungs

Imbalance between proteases in alveoli and inhibition or proteases

Increase in protease activity increases in tobacco smoking due to overactive alveolar macrophages and PMN neutrophils

Decreased inhibition of protease activity occurs in alpha-1 antitrypsin deficiency which is a genetic disease

Question 6

Signs and Symptoms of COPD

Answer 6

• Chronic productive cough
• Dyspnea and Tachypnea, Tachycardia
• Extended expiration phase
• Increased work for breathing
• Puffed lips [to help increase outflow due to enlarged airways]
• Usage of accessory muscles for breathing
• Cyanosis and hypoxemia [CO2 being the dominant gas in enlarged airways]
• Congested neck veins [complication of PAH]
• Barrel chest
• Peripheral edema
• Weight loss and cachexia [due to added effort to prevent lung collapse and breathing over years]

Bolded conditions are more severe manifestations of COPD

Any patient presenting with dyspnea should undergo ABCDE management and quick ddx for serious, immediate life threatening condition

Question 7

Diagnostic approach and results

Answer 7

• Chest X ray [Pulmonary hyperinflation, flattened diaphragm, horizontal ribs and widened intercoastal spaces, long and narrow heart shadow]
• Spirometry [Decreased FEV1/FVC < 70% after bronchodilator inhalation; decreased FEV1]
• Full body plethysmography [Increased Total Lung capacity, FRV, RV]
• Single Breath diffusing capacity [decreased DLco]
• Assessment for respiratory failure [pulse oxymeter, ABG]
• CT chest [to ddx of emphysema subtypes in addition to patient history]
• AATD test