Asthma Oct13 M3 Flashcards

1
Q

asthma broad causes

A

genetic predisposition and environmental exposure

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2
Q

asthma 2 components and main one

A

main: airway inflammation, causes obstruction

some have bronchial hyperresponsiveness

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3
Q

affected of asthma worldwide

A

300M

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4
Q

3 consequences of the chronic inflammation in asthma

A
  • obstruction
  • leads to airways irritability (hyperresponsiveness)
  • injures the airways
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5
Q

asthma: first step to triggering

A

inhale something from environment, goes to epithelial lining of airways

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6
Q

what happens to pollutant in epith lining of airways and after

A

picked up by dendritic cell + presented to other inflammatory cells

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7
Q

what inflammatory cells the dendritic cell presents antigen to

A

lymphocytes, T lymphocytes in particular

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8
Q

what T lymphocytes do after antigen is presented

A

differentiate in diff types and cells

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9
Q

what TH2 cells do

A

T helper cell, liberate IL4,5,13 which stimulte other cells like B cells

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10
Q

what is special about the TH2 pathway

A

characteristic of allergic reaction

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11
Q

what B cells do once activated by ILs

A

produce IgE which stimulates mast cells, eosinophils, basophils

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12
Q

what mast cells, eosinophils, basophils do once stimulated by IgE

A

produe other ILs to keep pathway going

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13
Q

other proteins the stimulant can stimulate

A

IL33, IL35, TSLP (thymic stromal lymphopoeitin) which also stimulate inflamm response

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14
Q

Other response (than TH2) in asthma and what it does

A

TH17, produces IL17 to stimulate neutrophils

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15
Q

characteristic of neutrophils in the TH17 response

A

Are not reponsive to steroids

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16
Q

what inflamm mediators of asthma are steroid sensitive

A

all except Th17 and neutrophils

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17
Q

other component of asthma, what happens to SM

A

hypetrophy and hyperplasia of SM: excess bronchoconstriction

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18
Q

when suspect asthma

A

cough, wheeze (+ after excersie, + prolonged after infection, +at night, + when exposed to pollutant)

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19
Q

number 1 trigger for asthma

A

human rhinovirus (and other resp tract infections)

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20
Q

how is asthma diagnosed (4)

A

clinical, lung function, airway responsiveness, sputum to check inflamm status

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21
Q

lung function test done at home to test for asthma

A

blow in machine to get peak flow and check how it varies with time. more than 20% variability = asthma

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22
Q

something necessary when diagnosing asthma and why

A

spirometry. without it, wrong 30% of the time

23
Q

criteria for improvement of of FEV1 with bronchodilator to diagnose asthma

A

at least 12% increase and at least 200 ml increase in 30 minutes

24
Q

criteria for FEV1 improvement if asthma when given antiinflamm therapy over multiple days

A

20% and 250 mL improve in FEV1

25
methacholine test principle
give methacholine (cholinergic agonist) multiple times, double dose every time, check when FEV1 dropped by 20%
26
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
27
daytime symptoms frequency in controlled asthma
less than 4 per week
28
night time symptoms frequency in controlled asthma
0
29
physical activity level in controlled asthma
normal
30
exacerbations level in controlled asthma
mild, infrequent
31
absenteeism level accepted for control asthma
no absenteeism
32
SABA use frequency in controlled asthma
less than 4 per week
33
FEV1 or PEF in controlled asthma
more than 85% than best ever reached
34
diurnal variability in PEF (peak exp flow) in controlled asthma
less than 15%
35
2 types of SABAs and example
beta 2 agonist (salbutamol) | anticholinergics (ipratropium)
36
2 types of LABAs and example
beta 2 agonist (salmeterol) | anticholinergic (triotropium)
37
trick for recognizing bronchodilators
end in ol or ium
38
trick for recognizing ICS
end in ide and one
39
2 examples of ICS
fluticasone, budesonide
40
2 ICS-LABA combination therapies
- fluticasone, salmeterol | - budenoside, formoterol
41
oral medication in asthma (3rd level treatment) example
``` theophyllines leukotriene receptor antagonist oral CS macrolides Ig and cytokine antagonist ```
42
theophylline mechanism of action
phosphodiesterase inhibitor (PDE doesn't convert cAMP into AMP and cAMP can go inhibit MLCK
43
name of a leukotriene R inhibitor
montelukast
44
oral CS name
prednisone
45
macrolide def
antibiotic with antiinflamm activity
46
Ig and cytokine antagonists examples and mechanism
IgE, anti IL4, anti IL5, anti IL13 (soon anti IL33, anti TSLP)
47
2 goals (2 medications) in treating asthma
reliever and controller
48
how many steps in asthma treatment
5
49
step 1 asthma treatment
reliever: SABA
50
step 2 asthma treatment
reliever: SABA controller: low dose ICS
51
step 3 asthma treatment
reliever: SABA or low dose ICS and formoterol controller: low dose ICS + LABA (come together)
52
step 4 asthma treatment
reliever: SABA or low dose ICS and formoterol controller: high dose ICS + LABA
53
step 5 asthma treatment
reliever: SABA or low dose ICS and formoterol controller: add-on treatment (IgE, etc.)
54
profile of person with asthma difficult to treat
female gender, obesity, smoking