COPD Flashcards
What is the mechanism behind hyperventilation? (i.e. when does it occur and what’s the underlying physiology)
Occurs in respiratory acidosis, when the chemoreceptors in the ventral surface of medulla pick up the decrease in pH in CSF.
Hyperventilation is triggered to remove the acidic CO2 from the system. (only temporary respiratory compensation not very effective)
Name the different histological layers of bronchial airway, and briefly their functions.
Mucosa: pseudostratified ciliated columnar with goblet cells to release mucous to trap bacteria and cilia to propel and remove them.
LP: contain elastic recoil and contains blood vessels
Muscularis: smooth muscle
Submucosa: contains collagen and cartilage, allowing bronchial gland secretions to lubricate and humidify the air
Adventitia: contains lymph vessels, nerves, and blood vessels, providing immune support and blood supply.
What are the two underlying pathologies in COPD?
Emphysema and chronic bronchitis.
What is emphysema?
Normally the alveoli or distal to terminal bronchioles are lined by elastic bands to increase lung compliance and lung elasticity. But in emphysema there is increased protease activity by: 1. Increased protease production via WCC, 2. decrease inhibition of anti-proteases by oxidative damage.
Consequently there is loss of alveoli elastic recoil and lung compliance, and there is collapse of the airways leading to gas trapping.
What is chronic bronchitis and what can cause it?
It is characterised by chronic cough and chronic hyper-secretion and fibrosis of the small airways. It leads to airtrapping, reduced lung volume and results in V/Q mismatch.
What is acute exacerbation of COPD?
There is an acute infection superimposed on underlying chronic bronchitis. This is defined as chronic cough for 3 months over 2 consecutive years.
It can be caused by strep pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Uncommon agents include chlamydia p, mycoplasma p, staph, enterobacterium, Klebsiella
Explain the pathogenesis of cor pulmonale from COPD.
In a normal response to poorly-ventilated areas of the lung, to compensate there is increased BF to the areas with better ventilation. There is vasoconstriction of the poorly-ventilated areas. This increases pulmonary vascular resistance, leading to pulmonary hypertension. This leads to right heart working harder to pump against pulmonary HTN, and leads to RHF (cor pulmonale).
