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Respiratory Final > Asthma > Flashcards

Asthma Flashcards

1
Q

3 cardinal features of asthma

A
  • airway inflammation
  • reversible airflow obstruction
  • airway hyper responsiveness
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2
Q

why are lungs hyper inflated in asthma

A
  • mucus is obstructing the airway lumen and air cannot get out.
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3
Q

T2 high asthma phenotypes secrete

A
  • IL-4,5,13
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4
Q

aspirin exacerbated respiratory disease characterized by

A
  • asthma
  • recurrent sinus with nasal polyps
  • sensitivity to aspirin and other NSAIDS
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5
Q

pathology of allergic asthma

A
  • dendritic cells infiltrate airway and sample antigens in airway lumen
  • dendritic cells migrate to regional lymph nodes and present to T cells.
  • T cells differentiate into Th2 and produce IL-4, 5, 13
  • IL-4 cause B lymphocytes to switch to IgE
  • IgE antibodies bind to mast cells
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6
Q

how are mast cells activated in allergic asthma

A
  • 2 IgE antibodies on mast cell bind antigen
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7
Q

result of mast cell activation in allergic asthma

A
  • rapid synthesis of arachadonic acid metabolites (prostaglandins and leukotrienes)
  • synthesis of pro-inflammatory cytokines
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8
Q

result of pro-inflammatory mediators in allergic asthma

A
  • airway smooth muscle - bronchoconstriction
  • blood vessels - vasodilation and increased permeability
  • epithelial cells - mucous cell metaplasia (mucous cells where they shouldn’t be)
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9
Q

how do eosinophils get involved in asthma

A
  • IL-5 and eotaxin produced by Th2 lymphocytes and mast cells release eosinophils from bone marrow
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10
Q

result of eosinophils in allergic asthma

A
  • pro-inflammatory effects
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11
Q

what is a transcription factors in TH2 cells that is critical for production of TH2 cytokines IL-4,5,13

A
  • GATA-13
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12
Q

what is late-onset eosinophilic asthma associated with

what is it not associated with

A
  • associated with eosinophils

- not associated with allergy

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13
Q

non-allergic, late-onset eosinophilic asthma mediator

what do they react to

A
  • ILC2

- TSLP, IL-25, IL-33

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14
Q

result of stimulation of ILC2 in non-allergic, late-onset eosinophilic asthma

A
  • secretes IL-5 and IL-13
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15
Q

why is non-allergic, late-onset eosinophilic asthma referred to as non-allergic?

A
  • does not make IL-4 for IgE class switching

- and no mast cells involved

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16
Q

how does aspirin exacerbated respiratory disease work?

A
  • blocks cyclooxyrgenase

- shunts everything down leukotriene path (LTC4)

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17
Q

result of LTC4

A
  • vasodilate
  • increased capillary permeability
  • mucous cell metaplasia and mucous production
  • bronchoconstriction
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18
Q

Th17 cells involved in which asthma

airways domination is by

A
  • neutrophilic asthma

- neutrophils

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19
Q

Th-17 secretes which cytokines (and their role

A
  • IL-17 (recruit neutrophils)

- IL-21 (stimulates NK cells, B cells and Th17 cells)

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20
Q

between eosinophils and neutrophils, which is steroid responsive?

A
  • eosinophils
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21
Q

3 remodeling changes in asthmatic airways

A
  • basement membrane thickening from fibrosis
  • smooth muscle hyperplasia
  • mucous cell metaplasia
22
Q

MOA of albuterol

A
  • activates beta 2 adrenergic receptors on airway smooth muscle
  • increases intracellular cAMP
  • relaxes airway smooth muscle
23
Q

airflow obstruction in asthma results from narrowing of airway lumen and intraluminal obstruction by

A
  • mucus
24
Q

flow-volume curve in asthma

A
  • low peak expiratory flow

- scooped out appearance during expiration

25
Q

FEV1 in asthma

A
  • reduced FEV1
26
Q

FVC is mild/moderate asthma

why

A
  • generally normal

- most air will eventually be exhaled

27
Q

FEV1/FVC ratio in mild/moderate asthma

A
  • reduced
28
Q

FEV1 versus FVC in severe asthma

impact on ratio

A
  • FEV1 falls much greater than FVC

- so ratio is still low

29
Q

DLCO in asthmatics

A
  • normal or elevated
30
Q

DLCO in COPD

A
  • reduced
31
Q

how do we see airway hyper responsiveness in asthmatics

A
  • airways constrict even further after exposure to stimuli that do not affect caliber of airways in normal individuals
32
Q

what is a good test to diagnose asthma in patients suspected of having asthma whose baseline spirometry is normal

A
  • methacholine test
33
Q

asthma symptoms

A
  • cough
  • chest tightness
  • wheeze
  • dyspnea
34
Q

wheezing is indicative of what airway obstruction

A
  • lower airway obstruction
35
Q

upper airway obstruction is indicative of what sound

A
  • stridor
36
Q

wheezing in heard on inspiration/expiration?

A
  • expiration usually
37
Q

stridor is heard on inspiration/expiration?

A
  • both
38
Q

skin symptoms of asthma

A
  • eczema
39
Q

upper airway symptoms of asthma

A
  • enlarged nasal turbinates

- pale or inflamed nasal mucosa

40
Q

symptoms of asthma during severe exacerbations

A
  • accessory muscle use
  • intercostal retractions
  • decreased breath sounds
41
Q

what is the clinical indication of a significant response in FEV1 post bronchodilator

A
  • > 12% improvement
42
Q

how does the methacholine test work

A
  • inhale methacholine and watch for drop in FEV1
43
Q

what is PC20

A
  • provocative concentration that causes FEV1 to fall by 20%
44
Q

what is a gas also high in asthmatics

A
  • exhaled nitric oxide
45
Q

what would you look for in sputum of asthma

A
  • eosinophils
  • Carcot-Leyden crystals
  • Curschmann’s spirals
  • Creola bodies
46
Q

what is the rescue medication for asthma treatment

side effect

what do you give if side effect is present

A
  • albuterol sulfate
  • tachycardia
  • levalbuterol
47
Q

MOA of nebulizer ipatropium

A
  • anti-cholinergic
  • blocks M3 receptors on airway smooth muscle
  • blocks contraction
48
Q

asthma patients are started on

A
  • inhaled corticosteroids
49
Q

if inhaled corticosteroid medications are insufficient, what do we give patients

A
  • inhaled corticosteroids + long acting beta agonists
50
Q

patients with severe airway obstructions who are mechanically ventilated with a high respiratory rate get what

what will come next

A
  • breath stacking
  • dynamic hyperinflation
  • auto peep
51
Q

how auto peep causes cardiogenic shock

A
  • increased intrathoracic pressure from auto-peep
  • increased RV afterload
  • decreased RV preload
  • decreased RV cardiac output
  • decreased LA and LV filling
  • cardiac shock
52
Q

treatment for cardiogenic shock and auto peep in patients with obstructive airway disease

A
  • remove from ventilator

- start vent at lower respiratory rate giving patient more time to exhale

Respiratory Final (20 decks)

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