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obstructive lung diseases
physiological explanation
unifying symptom
unifying sign
diseases due to airway obstructions that worsen with expiration, as lung emptying becomes slowed
symptom = dyspnea
sign = wheezing
bronchial asthma
chronic inflammatory disorder of bronchial mucosa, causing hypersensitivity and airway constriction
hypersensitivity # that bronchial asthma corresponds to
Type 1 hypersensitivity - allergy response
2 phases of bronchial asthma response
early / acute phase
late phase
early/acute phase: bronchial asthma
type 1 hypersensitivity repsonse: allergen exposure in bronchial mucosa activates B cells to produce IgE → IgE complexes with mast cells → mast cells degranulate and release chemicals (histamine, leukotrines, prostaglandins) causing vasodilation, increasing capillary permeability.
mucosal edema, mucosal secretion, and bronchial smooth muscle contraction also occurs
late phase: bronchial asthma
4-8 hours after early response and may be more severe
inflammatory chemicals are released: chemokines in early response attract neutrophils, eosinophils, lymphocytes to area → bronchospasm, edema, mucous secretion
cell damage, mucous accumulation to ciliated epithelial cells. mucous accumulates more and can lead to irreversible long-term airway damage
obstructed airway makes expirations difficult and air becomes trapped in alveoli → blood perfusion over alveoli decreases, causing capillary collapse → hypoxemia occurs
hypoxemia stimulates respiratory centre → hyperventilation → CO2 diffuses out of blood → hypocapnia → respiratory alkalosis
describe what continues to occur in late stage bronchial asthma after hypoxemia worsens, hypocapnia occurs, and respiratory alkalosis occurs
airway obstruction increases air trapping, hyperexpanding lungs and thorax, and decreasing tidal volume. CO2 levels begin rising and hypercapnia occurs, leading to respiratory acidosis → now a life-threatening situation requiring mechanical ventilation!
mainstays of bronchial asthma treatment
avoiding allergens
inhaling bronchodilators, anti-inflammatories
acute attack = adrenaline
COPD
chronic obstructive pulmonary disease characterized by airway obstruction causing difficult exhalations
examples of COPD diseases
emphysema
chronic bronchitis
chronic bronchitis
hypersecretion of mucous and chronic cough for at least 3/12 months of year, for at least 2 consecutive years
most common cause of chronic bronchitis
smoking
physiological development of chronic bronchitis
chronic irritant inspiration → airway inflammation → edema, thick mucous
continued inflammation increases size, number of mucous glands, goblet cells in airway epithelium
inflammation harms ciliated epithelial cells, so mucous is not cleared
airways narrow from thickened bronchial wall, making expiration difficult
obstruction leads to hypoxemia
airways collapse early in expiration, causing air trapping → decreased tidal volume, hypoventilation, and hypercapnia
are pathologic changes in chronic bronchitis reversible?
no
treatment of chronic bronchitis
ceasing smoking
bronchodilators
chest physical therapy
antibiotics (infection)
steroids
oxygen therapy
emphysema