3 cardinal features of asthma
why are lungs hyper inflated in asthma
T2 high asthma phenotypes secrete
aspirin exacerbated respiratory disease characterized by
pathology of allergic asthma
how are mast cells activated in allergic asthma
result of mast cell activation in allergic asthma
result of pro-inflammatory mediators in allergic asthma
how do eosinophils get involved in asthma
result of eosinophils in allergic asthma
what is a transcription factors in TH2 cells that is critical for production of TH2 cytokines IL-4,5,13
what is late-onset eosinophilic asthma associated with
what is it not associated with
- not associated with allergy
non-allergic, late-onset eosinophilic asthma mediator
what do they react to
- TSLP, IL-25, IL-33
result of stimulation of ILC2 in non-allergic, late-onset eosinophilic asthma
why is non-allergic, late-onset eosinophilic asthma referred to as non-allergic?
- and no mast cells involved
how does aspirin exacerbated respiratory disease work?
- shunts everything down leukotriene path (LTC4)
result of LTC4
Th17 cells involved in which asthma
airways domination is by
- neutrophils
Th-17 secretes which cytokines (and their role
- IL-21 (stimulates NK cells, B cells and Th17 cells)
between eosinophils and neutrophils, which is steroid responsive?
3 remodeling changes in asthmatic airways
MOA of albuterol
airflow obstruction in asthma results from narrowing of airway lumen and intraluminal obstruction by
flow-volume curve in asthma
- scooped out appearance during expiration