Asthma Flashcards
3 main characteristics of asthma
airway inflammation, reversible airflow obstruction, airway hyperresponsiveness
describe allergic asthma pathogenesis (main cytokines, cells involved)
Th2 cells activated by allergens/dendritic cells, release IL-4, IL-5, IL-13, IL-4 stimulates B cells to produce IgE which prompts mast cell degranulation (LTs, histamine, PGs, cytokines): mucus, vasodilation, bronchoconstriction
IL-5 stimulates eosinophils
how is non-allergic eosinophilic asthma different from allergic?
driven mainly by innate lymphoid cells rather than Th2, lack antigen receptors and dont produce IL-4/stimulate IgE and mast cells
still produce IL-5 and eosinophil activation
describe pathogenesis of apsirin exacerbated respiratory disease (AERD)
inhibition of COX enzyme shunts eicosanoids towards LOX pathway, increased leukotriene production and bronchoconstriction
list some Th2 high asthma types
AERD, allergic asthma, late-onset eosinophilic
list some Th2 low asthma types
obesity associated, smoking/PMN, very late onset (esp women)
pathogenesis of neutrophilic asthma
driven by Th17, recruitment of PMNs
contrast eosinophilic and neutrophilic asthma
eos: mild,moderate, or severe
- Th2 or innate lymphoid
- steroid responsive
PMNs: severe asthma, Th17 cells, steroid resistant
effects of eos and PMNs in airway wall
release cytokines, eicosanoids, peroxidases, ROS
amplifies inflammation, promotes hyperresponsiveness, promotes airway remodeling
3 characteristics of airway remodeling in asthma
basement membrane thickening, smooth muscle hyperplasia, mucous metaplasia (lots of large goblet cells)
why target IL-5 w/ drugs?
active in both allergic and non allergic eosinophilic asthma
flow volume curve w/ asthma
lower peak flow, scooped out descent
volume time curve w/ asthma
much lower FEV1, more linear and lower slope curve
DLCO in asthma
usually normal or even elevated- maybe from hyperinflation
this is in contrast to emphysema, ILD, PAH which has reduced DLCO
4 main asthma Sx
cough, wheeze, chest tightness, dyspnea
physical exam findings
lower airway: wheeze, prolonged expiration
upper airway: enlarged turbinates, pale/inflamed mucosa
accessory muscle use, intercostal retractions, decreased breath sounds
eczema
Dx tests for asthma (3 categories)
reversible obstruction: spirometry pre/post bronchodilation, peak flow variability (normally not variable)
hyperresponsiveness: methacholine challenge test
inflammation: exhaled NO (elevation indicates excess inflamed epithelial cells), induced sputum
signs of asthma in induced sputum
charcot leyden crystals, curschmann spirals
eosinophils, creola bodies
primary rescue med
albuterol sulfate
benefit of spacer
improves drug delivery to lungs
3 main controller meds
inhaled corticosteroids, ICS+long acting beta agonists (LABA), leukotriene modifier (montelukast)
3 controller meds for more severe disease
long acting anti muscarinics (tiotropium), theophylline (PDE4 inhibitor), monoclonal antibodies (omalizumab, benralizumab, mepolizumab)
what is dynamic hyperinflation
gas is trapped in alveoli from obstructed expiration, increases with each inhale
occurs with rapid RR (exercise, high RR setting on ventilator)
describe auto peep
increased positive end expiratory pressure- incomplete expiration of prior breath causes pressure in lungs to be higher than atm
can be from ventilation that leads to dynamic hyperinflation
increases intra-thoracic pressure
consequences of auto peep
can cause cardiogenic shock, increased intrathoracic pressure increases RV afterload, decreases RV output and LV preload- overall CO and MAP decline
