Asthma Oct13 M3 Flashcards
asthma broad causes
genetic predisposition and environmental exposure
asthma 2 components and main one
main: airway inflammation, causes obstruction
some have bronchial hyperresponsiveness
affected of asthma worldwide
300M
3 consequences of the chronic inflammation in asthma
- obstruction
- leads to airways irritability (hyperresponsiveness)
- injures the airways
asthma: first step to triggering
inhale something from environment, goes to epithelial lining of airways
what happens to pollutant in epith lining of airways and after
picked up by dendritic cell + presented to other inflammatory cells
what inflammatory cells the dendritic cell presents antigen to
lymphocytes, T lymphocytes in particular
what T lymphocytes do after antigen is presented
differentiate in diff types and cells
what TH2 cells do
T helper cell, liberate IL4,5,13 which stimulte other cells like B cells
what is special about the TH2 pathway
characteristic of allergic reaction
what B cells do once activated by ILs
produce IgE which stimulates mast cells, eosinophils, basophils
what mast cells, eosinophils, basophils do once stimulated by IgE
produe other ILs to keep pathway going
other proteins the stimulant can stimulate
IL33, IL35, TSLP (thymic stromal lymphopoeitin) which also stimulate inflamm response
Other response (than TH2) in asthma and what it does
TH17, produces IL17 to stimulate neutrophils
characteristic of neutrophils in the TH17 response
Are not reponsive to steroids
what inflamm mediators of asthma are steroid sensitive
all except Th17 and neutrophils
other component of asthma, what happens to SM
hypetrophy and hyperplasia of SM: excess bronchoconstriction
when suspect asthma
cough, wheeze (+ after excersie, + prolonged after infection, +at night, + when exposed to pollutant)
number 1 trigger for asthma
human rhinovirus (and other resp tract infections)
how is asthma diagnosed (4)
clinical, lung function, airway responsiveness, sputum to check inflamm status
lung function test done at home to test for asthma
blow in machine to get peak flow and check how it varies with time. more than 20% variability = asthma
something necessary when diagnosing asthma and why
spirometry. without it, wrong 30% of the time
criteria for improvement of of FEV1 with bronchodilator to diagnose asthma
at least 12% increase and at least 200 ml increase in 30 minutes
criteria for FEV1 improvement if asthma when given antiinflamm therapy over multiple days
20% and 250 mL improve in FEV1
methacholine test principle
give methacholine (cholinergic agonist) multiple times, double dose every time, check when FEV1 dropped by 20%
metacholine test classification of asthma
drop 20%
- at less 4 mg per ml: severe
- between 4 and 16 mg per ml: moderate
- more than 16 mg per ml: no AHR
daytime symptoms frequency in controlled asthma
less than 4 per week
night time symptoms frequency in controlled asthma
0
physical activity level in controlled asthma
normal
exacerbations level in controlled asthma
mild, infrequent
absenteeism level accepted for control asthma
no absenteeism
SABA use frequency in controlled asthma
less than 4 per week
FEV1 or PEF in controlled asthma
more than 85% than best ever reached
diurnal variability in PEF (peak exp flow) in controlled asthma
less than 15%
2 types of SABAs and example
beta 2 agonist (salbutamol)
anticholinergics (ipratropium)
2 types of LABAs and example
beta 2 agonist (salmeterol)
anticholinergic (triotropium)
trick for recognizing bronchodilators
end in ol or ium
trick for recognizing ICS
end in ide and one
2 examples of ICS
fluticasone, budesonide
2 ICS-LABA combination therapies
- fluticasone, salmeterol
- budenoside, formoterol
oral medication in asthma (3rd level treatment) example
theophyllines leukotriene receptor antagonist oral CS macrolides Ig and cytokine antagonist
theophylline mechanism of action
phosphodiesterase inhibitor (PDE doesn’t convert cAMP into AMP and cAMP can go inhibit MLCK
name of a leukotriene R inhibitor
montelukast
oral CS name
prednisone
macrolide def
antibiotic with antiinflamm activity
Ig and cytokine antagonists examples and mechanism
IgE, anti IL4, anti IL5, anti IL13 (soon anti IL33, anti TSLP)
2 goals (2 medications) in treating asthma
reliever and controller
how many steps in asthma treatment
5
step 1 asthma treatment
reliever: SABA
step 2 asthma treatment
reliever: SABA
controller: low dose ICS
step 3 asthma treatment
reliever: SABA or low dose ICS and formoterol
controller: low dose ICS + LABA (come together)
step 4 asthma treatment
reliever: SABA or low dose ICS and formoterol
controller: high dose ICS + LABA
step 5 asthma treatment
reliever: SABA or low dose ICS and formoterol
controller: add-on treatment (IgE, etc.)
profile of person with asthma difficult to treat
female gender, obesity, smoking
