Asthma Flashcards

1
Q

3 main characteristics of asthma

A

airway inflammation, reversible airflow obstruction, airway hyperresponsiveness

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2
Q

describe allergic asthma pathogenesis (main cytokines, cells involved)

A

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

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3
Q

how is non-allergic eosinophilic asthma different from allergic?

A

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

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4
Q

describe pathogenesis of apsirin exacerbated respiratory disease (AERD)

A

inhibition of COX enzyme shunts eicosanoids towards LOX pathway, increased leukotriene production and bronchoconstriction

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5
Q

list some Th2 high asthma types

A

AERD, allergic asthma, late-onset eosinophilic

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6
Q

list some Th2 low asthma types

A

obesity associated, smoking/PMN, very late onset (esp women)

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7
Q

pathogenesis of neutrophilic asthma

A

driven by Th17, recruitment of PMNs

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8
Q

contrast eosinophilic and neutrophilic asthma

A

eos: mild,moderate, or severe
- Th2 or innate lymphoid
- steroid responsive

PMNs: severe asthma, Th17 cells, steroid resistant

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9
Q

effects of eos and PMNs in airway wall

A

release cytokines, eicosanoids, peroxidases, ROS

amplifies inflammation, promotes hyperresponsiveness, promotes airway remodeling

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10
Q

3 characteristics of airway remodeling in asthma

A

basement membrane thickening, smooth muscle hyperplasia, mucous metaplasia (lots of large goblet cells)

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11
Q

why target IL-5 w/ drugs?

A

active in both allergic and non allergic eosinophilic asthma

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12
Q

flow volume curve w/ asthma

A

lower peak flow, scooped out descent

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13
Q

volume time curve w/ asthma

A

much lower FEV1, more linear and lower slope curve

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14
Q

DLCO in asthma

A

usually normal or even elevated- maybe from hyperinflation

this is in contrast to emphysema, ILD, PAH which has reduced DLCO

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15
Q

4 main asthma Sx

A

cough, wheeze, chest tightness, dyspnea

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16
Q

physical exam findings

A

lower airway: wheeze, prolonged expiration

upper airway: enlarged turbinates, pale/inflamed mucosa

accessory muscle use, intercostal retractions, decreased breath sounds

eczema

17
Q

Dx tests for asthma (3 categories)

A

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

18
Q

signs of asthma in induced sputum

A

charcot leyden crystals, curschmann spirals

eosinophils, creola bodies

19
Q

primary rescue med

A

albuterol sulfate

20
Q

benefit of spacer

A

improves drug delivery to lungs

21
Q

3 main controller meds

A

inhaled corticosteroids, ICS+long acting beta agonists (LABA), leukotriene modifier (montelukast)

22
Q

3 controller meds for more severe disease

A

long acting anti muscarinics (tiotropium), theophylline (PDE4 inhibitor), monoclonal antibodies (omalizumab, benralizumab, mepolizumab)

23
Q

what is dynamic hyperinflation

A

gas is trapped in alveoli from obstructed expiration, increases with each inhale

occurs with rapid RR (exercise, high RR setting on ventilator)

24
Q

describe auto peep

A

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

25
Q

consequences of auto peep

A

can cause cardiogenic shock, increased intrathoracic pressure increases RV afterload, decreases RV output and LV preload- overall CO and MAP decline