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Bloc B - Respiration > Asthma Oct13 M3 > Flashcards

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
Q

methacholine test principle

A

give methacholine (cholinergic agonist) multiple times, double dose every time, check when FEV1 dropped by 20%

26
Q

metacholine test classification of asthma

A

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
Q

daytime symptoms frequency in controlled asthma

A

less than 4 per week

28
Q

night time symptoms frequency in controlled asthma

A

0

29
Q

physical activity level in controlled asthma

A

normal

30
Q

exacerbations level in controlled asthma

A

mild, infrequent

31
Q

absenteeism level accepted for control asthma

A

no absenteeism

32
Q

SABA use frequency in controlled asthma

A

less than 4 per week

33
Q

FEV1 or PEF in controlled asthma

A

more than 85% than best ever reached

34
Q

diurnal variability in PEF (peak exp flow) in controlled asthma

A

less than 15%

35
Q

2 types of SABAs and example

A

beta 2 agonist (salbutamol)

anticholinergics (ipratropium)

36
Q

2 types of LABAs and example

A

beta 2 agonist (salmeterol)

anticholinergic (triotropium)

37
Q

trick for recognizing bronchodilators

A

end in ol or ium

38
Q

trick for recognizing ICS

A

end in ide and one

39
Q

2 examples of ICS

A

fluticasone, budesonide

40
Q

2 ICS-LABA combination therapies

A
  • fluticasone, salmeterol

- budenoside, formoterol

41
Q

oral medication in asthma (3rd level treatment) example

A 
theophyllines
leukotriene receptor antagonist
oral CS
macrolides
Ig and cytokine antagonist
42
Q

theophylline mechanism of action

A

phosphodiesterase inhibitor (PDE doesn’t convert cAMP into AMP and cAMP can go inhibit MLCK

43
Q

name of a leukotriene R inhibitor

A

montelukast

44
Q

oral CS name

A

prednisone

45
Q

macrolide def

A

antibiotic with antiinflamm activity

46
Q

Ig and cytokine antagonists examples and mechanism

A

IgE, anti IL4, anti IL5, anti IL13 (soon anti IL33, anti TSLP)

47
Q

2 goals (2 medications) in treating asthma

A

reliever and controller

48
Q

how many steps in asthma treatment

A

5

49
Q

step 1 asthma treatment

A

reliever: SABA

50
Q

step 2 asthma treatment

A

reliever: SABA
controller: low dose ICS

51
Q

step 3 asthma treatment

A

reliever: SABA or low dose ICS and formoterol
controller: low dose ICS + LABA (come together)

52
Q

step 4 asthma treatment

A

reliever: SABA or low dose ICS and formoterol
controller: high dose ICS + LABA

53
Q

step 5 asthma treatment

A

reliever: SABA or low dose ICS and formoterol
controller: add-on treatment (IgE, etc.)

54
Q

profile of person with asthma difficult to treat

A

female gender, obesity, smoking

Bloc B - Respiration (36 decks)

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