Obstructive Lung Disease Flashcards
Extrinsic Asthma
Initiated by Type 1 hypersensitivity reaction induced by exposure to an outside agent
I.e. Allergic asthma, occupational asthma
Intrinsic Asthma
Initiated by non-immune mechanisms, i.e. inhaled irritants, exercise, etc.
Inflammatory cells present in asthma
Mast cells - activated by allergen via IgE receptors; release histamine
Eosinophils - release proteins that damage epithelial cells
Macrophages - activated by allergens to release cytokines
Neutrophils - present in airways and sputum
Structural changes in airways - asthma
Increased smooth muscle proliferation
Blood vessel proliferation
Mucus hyper-secretion
Final common pathway is airway narrowing
Asthma LFTs
Decreased FEV1/FVC - reversible or improved with a beta-adrenergic agonist, defined as improvement of > 12% or an absolute increase of > 200 mL
TLC, RV, FRC increased due to air-trapping
Methacholine challenge
Patient performs serial spirometry after inhaling progressively larger concentrations of bronchoconstrictor, stimulating airway obstruction
Asthmatics require less methacholine to reduce FEV1 by 20% (lower PC20)
Asthma treatments to reduce airway tone
Beta agonists - short acting (albuterol) vs. long acting
Anti-cholinergics (Ipratropium) - reduce vasoconstriction
Leukotriene inhibitors - reduce vasoconstriction
Phosphodiesterase inhibitors - increase intracellular cAMP
Asthma treatments to reduce inflammation
Corticosteroids - reduce # of inflammatory cells, decrease airway edema
Mast cell stabilizers
Anti-IgE therapy
Definition of COPD
Irreversible airflow limitation (FEV1/FVC < 0.70)
Includes elements of chronic bronchitis and emphysema
GOLD I
Mild COPD, defined as FEV1/FVC < 0.70
AND
FEV1 < 80% predicted
GOLD II
Moderate COPD, defined as FEV1/FVC < 0.70
AND
FEV1 50-70% predicted
GOLD III
Severe COPD, defined as FEV1/FEV < 0.70
AND
FEV1 30-50% predicted
Gold IV
Very severe COPD, defined as FEV1/FEV < 0.70
AND
FEV1 < 30% Predicted
Chronic Bronchitis - Definition
Productive cough present for 3 months/year over a 2-year period without another identified medical cause
Histologic changes in chronic bronchitis
Hypertrophy of submucosal glands
Increased number of goblet cells
Increase in size and number of smooth muscle cells
Squamous metaplasia
Final common pathway is narrowing of the airway lumen and obstruction by mucus with increased airflow resistance
Emphysema - Definition
Abnormal, permanent enlargement of alveoli with destruction of alveolar septa; leads to increased lung compliance with loss of elastic recoil
Centriacinar Emphysema
Scarring and dilation of the respiratory bronchioles and adjacent alveoli, resulting in the development of pathologically enlarged air spaces
Most often associated with smoking
Panacinar Emphysema
Scarring and dilation of the entire respiratory bronchiole + alveolar unit
More commonly seen in alpha-1-anti-trypsin deficiency
PFTs in COPD
Decreased FEV1/FVC (< 0.70)
Increased RV/FRC/TLC due to hyperinflation
Reduced DLCO due to destruction of the air-blood barrier (emphysema only)
Bronchiectasis
Abnormal dilation of the proximal, medium-sized bronchi due to destruction of the muscular and elastic components of their walls; requires infectious/inflammatory insult + impaired drainage leading to sustained tissue damage
Dilated airways are collapsible, resulting in obstruction
Cystic Fibrosis - Genetics & Clinical Characteristics
Autosomal recessive mutation in the CFTR gene, resulting in dysfunctional chloride secretion across epithelial surfaces
Major clinical complications: recurrent sinus and pulmonary infections with resultant bronchiectasis and airway obstruction; pancreatic insufficiency and pancreatitis, male infertility
Ivacaftor
Targeted genetic therapy for CF aptients with G551D mutation in the CFTR gene (4% of CF patients); restores function of the mutant CF protein