COPD

Question 1

Define COPD

Answer 1

1) Airflow limitation that is not fully reversible.
2) It encompasses both emphysema and chronic bronchitis. 3) The airflow limitation is usually progressive and is
4) associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

Question 2

Define emphysema

Answer 2

outcome of the inflammatory responses is elastin breakdown and subsequent loss of alveolar integrity–> so you get pathological enlargement of distal air spaces.

Question 3

Define chronic bronchitis

Answer 3

Productive cough occurring on most days in 3 consecutive months over 2 consecutive years.

Question 4

How does smoking contribute to pathophys of COPD?

Answer 4

Presence of smoke particles in the lungs leads to:

1) inflammatory response with
2) increased macrophage and neutrophil infiltration into the lungs.
3) These immune cells release cytokines, chemokines and elastases which
4) Damages the lung parenchyma over time.

Question 5

Where is a1-antitrypsin made?

Answer 5

In the liver

Question 6

What is a1AT deficiency?

Answer 6

Alpha-1 antitrypsin is a serine protease inhibitor (SERPIN) secreted by the liver into the blood which inhibits the enzyme neutrophil elastase from damaging the lung tissue.

Deficiency of this alpha-1 antitrypsin leads to unopposed elasteolysis (destruction of the elastin fibers in alveolar walls) and development of early emphysema.

Question 7

What is a1-AT?

Answer 7

A serine protease inhibitor (SERPIN)

Question 8

What are the 4 key pathophys components to emphysema?

Answer 8

1) Parenchymal destruction
2) V/Q matched defect
3) Mild hypoxia
4) Cachexia

Question 9

Pathophys of parenchymal destruction in emphysema

Answer 9

Recurrent damage to the alveoli eventually leads to septal destruction along with the capillary bed also.

Question 10

Pathophys of matched VQ defect in emphysema

Answer 10

Since both the terminal bronchioles and alveoli along with the capillary bed have been destroyed, a matched defect exists between the ventilation and perfusion; areas of low ventilation also have poor perfusion.
Non cyanotic (“pink”): Matched V:Q defect; no hypoxemia.

Question 11

Pathophys of mild hypoxoa in emphysema

Answer 11

Despite the “matched” V/Q defect, overtime hyperventilation develops and cardiac output (CO) drops which leads to areas of poor blood flow in relatively well oxygenated areas. Due to this poor CO, the rest of the body suffers from tissue hypoxia

Question 12

Pathophys of cachexia in emphysema

Answer 12

At the pulmonary level, the low CO leads to pulmonary cachexia; which induces weight loss and muscle wasting. This gives these patients the characteristic “pink-puffer” appearance.

Question 13

Will breath sounds be increased or decreased in emphysema? Why?

Answer 13

Hyperinflation of alveoli and destruction of alveolar architecture causes decreased airway resistance.

Question 14

Pathogenesis of chronic bronchitis

Answer 14

Fibrosis and smooth muscle hypertrophy + excess mucus build-up reducing the airway lumen.
Major site of increased airway resistance is the small airways

Question 15

What are the 4 key pathophys components to chronic bronchitis?

Answer 15

1) Small airway inflammation
2) V/Q mismatch
3) Severe hypoxia and hypercarbia
4) Pulmonary hypertension and cor pulmonale

Question 16

Pathophys of small airway inflammation in chronic bronchitis

Answer 16

inflammation in the smaller bronchioles and mucus secretions further narrow the airway lumen.
Despite this, the parenchyma are relatively less damaged

Question 17

Pathophys of VQ mismatch in chronic bronchitis

Answer 17

The physiologic response leads to a drop in ventilation and compensation with the rise in CO. Increased perfusion in the areas of poor ventilation takes place eventually causing hypoxia and secondary polycythemia.

Question 18

Pathophys of severe hypoxia and hypercarbia in chronic bronchitis

Answer 18

Chronic V/Q mismatch leads to decreased oxygenation/deoxygenation of the blood resulting in hypoxemia and increased CO2 retention (respiratory acidosis ensues).

Question 19

Pathophys of pulmonary HTN and cor pulmonale in chronic bronchitis

Answer 19

Chronic hypercapnia and respiratory acidosis lead to arterial vasoconstriction in the lungs. With the retrograde pressure build-up, the right ventricular pressures continue to rise and eventually causing RV failure. Otherwise, known as cor pulmonale.

Question 20

Define polycythaemia

Answer 20

abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers. It may be a primary disease of unknown cause, or a secondary condition linked to respiratory or circulatory disorder or cancer.

Question 21

Signs and symptoms of chronic bronchitis

Answer 21

1) copious sputum production
2) Chronic cough
3) cyanotic
4) wheeze on auscultation
5) Ronchi

Question 22

Do you hear a wheeze on auscultation of chronic bronchitis? Why

Answer 22

Due to airway obstruction.

Question 23

What is a ronchi?

Answer 23

A gurgling sound that may be heard due to mucus hypersecretion in the airways.

Question 24

Why are pts with chronic bronch blue?

Answer 24

The mismatched V/Q defect leads to inadequate oxygenation of the blood; most prominent in the lips and the nail beds.