COPD

Question 1

What are the asthma mediators?

Answer 1

IL-4/5 and leukotrienes

Question 2

What are the COPD mediators?

Answer 2

TNF, IL-8, LTB4

Question 3

What does the main defining pathology of asthma involve?

Answer 3

Bronchoconstriction in association with mucous plug. Therefore the administration of steroids decreases inflammation and bronchodilators help with reducing reversible airway obstruction (Dilation of airways, agonists stimulating beta-2-adrenergic receptors)

Question 4

Can bronchodilators and corticosteroids be used to treat irreversible airway obstruction?

Answer 4

No

Question 5

Inflammatory cells for asthma vs COPD

Answer 5

Asthma - eosinophils, mast cells and Th2

COPD - neutrophils, macrophages, Tc1 lymphocytes

Question 6

Explain the pathology of asthma

Answer 6

Mucous plug forms due to hypertrophic mechanisms concerned with hyper-responsiveness, smooth muscle cell hypertrophy, and hyperplasia of goblet and epithelial cells. Submucosal glands are embedded within the smooth muscle, contraction stimulates mucous secretion. Airway is further obstructed due to airway constriction (folds), by contractile ring of smooth muscles.

Question 7

Explain the pathophsyiology behind COPD

Answer 7

Distinctively occurs due to the absence of epithelial folding, bronchoconstriction isn’t prevalent; the predominant mechanisms include chronic inflammation and mucous hypersecretion (hypertrophy of goblet cells and submucosal glands)

Airways obstruction within distal airways > Causes hyperinflation due to air trapping this is associated with hyperresonance and an increased RV.

Inflammation of bronchi contributes to mucous hypersecretion (more susceptible infection)

Question 8

What are the symptoms of COPD?

Answer 8

Sensation of breathlessness, considering the thoracic cavity is restricted

Question 9

Emphysema

Answer 9

Destruction of lung tissue, alveolar degeneration associated with proteases degrading lung tissue (present on CT scan). Homogenous colour = normal.

COPD involved with mineral lung tissue, normal alveolar dysfunction and impaired GE.

Peri-bronchial inflammation and fibrosis causing the bronchiole lumen to decrease. Epithelial cells are exposed to cigarette smoke, therefore producing TGF-Beta → Fibroblast activation.

Macrophages MCP-I recruits more macrophages (autocrine/paracrine communication); increased pro-inflammatory macrophages produce neutrophil chemotactic factors (CXCL8 and LTB4) → Neutrophils secrete proteases (Neutrophil elastase and matrix metalloproteases) to cause alveolar destruction and degeneration of alveolar attachments → reduced elasticity and capacity to hold bronchioles open.

Activation of cytotoxic CD8 lymphocyte cells.

Question 10

Background COPD - Chronic bronchitis

Answer 10

Obstructive disorder associated with chronic inflammation of the bronchioles in addition to mucous hypersecretion reducing the diameter of the lumen; subsequently causes an obstructive disorder since the airflow is reduced (FEV1).

COPD - rate of decline is faster, smoker is more susceptible. Smoking stoppage will distort the trajectory of decline, patients who don’t reach max peak lung function will be predisposed and susceptible to decline.

Question 11

Treatments for COPD

Answer 11

Protease inhibitors and anti-oxidants; coupled with smoking cessation.

Bronchodilator and anti-inflammatory glucocorticosteroids relatively ineffective.