Obstructive (4)- Gomez Flashcards
Obstructive (airway) diseases
Limit rate of flow
FEV1/FVC reduced (less than 0.7)
Due to resistance at any level (airway restriction &/or lost of elastic recoil)
Emphysema (= COPD), chronic bronchitis, bronchiectasis, asthma
Restrictive diseases
Limit total lung capacity (TLC) and residual volume (RV)
Near normal flow rates (FEV1 may be mildly reduced due to decreased TLC but FEV1/FVC is near normal ≈70%)
Chest wall disorders, obesity, ARDS, interstitial fibrosis, pneumoconioses
EmphysemaClassification
Centriacinar/centrilobular (>95%) - SMOKING, upper lobes
Panacinar/panlobular (2-5%)
Alpha-1 antitrypsin def., smoking; lower lobes
Distal acinar/paraseptal
Subpleural and adjacent to septae
Irregular/paracicatrical
Emphysema pathophysiology
: proteolytic digestion of alveolar walls
Neutrophil-secreted elastase is 1o villain (inhibited by alpha-1-AT)
People with genetic alpha-1 antitrypsin deficiency –> develop emphysema early in life
- about 1% of emphysema patients, made much worse with smoking
Tobacco also destroys alpha-1 antitrypsin AND creates free radicals (ROS)
EmphysEmA: Elastase, Alpha-1 Antitrypsin
Emphysema clinical and treatments
Barrel chest
Low FEV1, high TLC & RV
Low FEV1 due to bronchiole collapse and fibrosis, and ?loss of elastic recoil?
Forward leaning and pursed lips in attempt to squeeze air out
Gas exchange may be adequate → pink puffer
Formation of bullae (Bullous emphysema) & pneumothorax
stop smoking- stop progression
treatment- bronchodilators (really only helps with airway disease or concomitant chronic bronchitis), steroids, bullectomy, transplant
Other Conditions With Increased Air
Compensatory hyperinflation
Occurs because of loss of adjacent tissue (no wall destruction) [more room for the lung to expand]
Obstructive overinflation
Overexpansion by trapped air
Ball valve obstruction by object [often pennies]
Collaterals feeding around obstruction, life-threatening
Alveolar pores of Kohn
Bronchiloloalveolar canals of Lambert
Congenital lobar overinflation from lack of bronchial cartilage
Interstitial emphysema
Any air in interstitium (subcutaneous tissue, mediastinum, lung, etc.) [often from trauma. NO digestion of the alveoli]
Chronic Bronchitis
Clinically defined as
3 months of productive cough/year for 2 consecutive years
Hypersecretion of mucus, markedly increased goblet cells, superimposed infections because of mucus obstruction
Hypertrophy of bronchial submucosal glands
increased “Reid Index”, normal less than or equal to 0.4
Bronchiolitis obliterans in small airways
Gas exchange impaired with cyanosis → blue bloaters
(have hypercapnia and hypoxemia)
dyspnea on exertion and cor pulmonale common
“Reid” Index
Thickness of glands/Thickness of wall*
Asthma
episodic partially reversible bronchoconstriction
Recurrent wheezing/breathlessness/chest tightness and cough
Most often night, early morning
Can evolve into acute severe asthma (status asthmaticus) and death
Incidence increasing
Atopic Asthma
Type I Hypersensitivity
Atopy: genetic tendency to develop IgE antibodies to inhaled allergens
Begins in childhood
Stimulation of subepithelial vagal receptors
Parasympathetic stimulation provokes bronchoconstriction
Can do skin allergen testing for confirmation
RAST (radioallergosorbent test) testing
- Often get positivity for huge number of allergens
- High false positive rates have been reported
Asthma Other Types besides atopic
Nonatopic Asthma
- Associated with pulmonary infections (mainly viral) and air pollutants
- No allergic indicators (i.e. eosinophils, IgE)
- Thought that infection lowers threshold for vagal responses leading to bronchospasm
Drug-Induced Asthma
Uncommon form of disease
Can also cause urticaria
** Aspirin classic cause
- Thought to inhibit cyclooxygenase pathway of arachidonic acid
- Does not inhibit lipoxygenase route, favoring leukotriene production
- Leukotrienes favor *** bronchoconstriction
- Can also cause Type I allergic type reaction
Exercise-induced Asthma
Occupational Asthma
Asthma morphology
Overinflated lungs
Airway remodeling:
Epithelial injury
Subbasement membrane fibrosis
Eosinophils in inflammatory bronchial wall infiltrates
Hypertrophy/hyperplasia of submucosal glands and goblet cell metaplasia (Over production of thick mucus)
Hypertrophy/hyperplasia of smooth muscle
Increased vascularity
shed epithelium
curschmann spirals, can see with asthma and other diseases that lead to shed epithelium
Bronchiectasis
Permanent dilation of bronchi & bronchioles
Caused by tissue destruction secondary to infection
–> Foul smelling (+/- bloody) sputum
can –> cor pulmonale
May develop brain abscesses and amyloidosis
pulmonary sequestration (giant spaces)
* Associated with Genetic disorders (cystic fibrosis, primary ciliary dyskinesia*), Obstruction, and many infections. *
