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Asthma Flashcards

1
Q

what is the atopic triad

A

asthma, allergic rhinitis, atopic dermatitis (eczema)

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2
Q

describe the allergic asthma phenotype in terms of treatment

A

usually responds well to ICS

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3
Q

describe the non-allergic asthma phenotype in terms of treatment

A

usually less response to ICS

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4
Q

when does allergic asthma usually present

A

childhood, associated with PMH or FH of allergic disease such as eczema, allergic rhinitis, or food and drug allergy

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5
Q

when does non-allergic asthma usually present

A

adults, occupational asthma, asthma with obesity

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6
Q

what does the biodiversity hypothesis suggest

A

exposure to microbe-rich environments protects against allergic and autoimmune diseases

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7
Q

TH1 is what type of immunity

A

cell-mediated protective immunity (no allergies)

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8
Q

TH2 is what type of immunity

A

antibody mediated immunity (allergies, asthma)

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9
Q

who is likely to differentiate to TH1 immunity

A

older siblings, early daycare exposure, rural, childhood infections, microbial exposure

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10
Q

who is likely to differentiate to TH2 immunity

A

only child, widespread use of antibiotics, urban environment

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11
Q

describe TH1/TH2 shift

A

at birth, predominant TH2. As exposure to bacterial/viral infections occur, shifts towards TH1. If TH1 doesn’t mature, TH2 predominates which favors allergy, allergic rhinitis, and eczema

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12
Q

T2 inflammation/eosinophilic/allergic asthma is present when

A

at an early age

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13
Q

T2 asthma is associated with

A

atopy, allergy, elevated IgE, eosinophilia, elevated FeNO

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14
Q

non-TH2/non-eosinophilic asthma is present

A

later in life

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15
Q

describe some protective factors for developing asthma

A

being the younger sibling, natural birth, breastfeeding, higher socioeconomic status, healthy diet, low pollution rates, exercise, microbial exposures, farm living

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16
Q

describe some risk factors for developing asthma

A

asthma family history, c-section, formula feeding, sheep/hay farming, urban living, respiratory viral infections, lower socioeconomic status, obesity, use of antibiotics

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17
Q

what medications can be asthma triggers

A

ASA/NSAIDs, non selective beta blockers

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18
Q

which beta blockers are asthma triggers

A

propranolol and carvedilol

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19
Q

what is samter’s triad

A

asthma, nasal polyps, aspirin/NSAID sensitivity

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20
Q

how does aspirin/NSAID exacerbated respiratory disease occur

A

the arachidonic pathway changes: NSAIDs block COX so PGE2 not available to keep 5 lipoxygenase in check= more leukotrienes (bronchospasm, increase permeability, mucus)

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21
Q

3 major characteristics of asthma

A

chronic airway inflammation, variable degree of airflow obstruction and narrowing, bronchial hyperresponsiveness

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22
Q

FEV1/FVC ratio of ___ demonstrates obstruction

A

<70%

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23
Q

what will demonstrate airway reversibility after beta2 agonist inhalation

A

FEV1 increases by more than 12% and 200 mL

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24
Q

what does airway reversibility demonstrate

A

asthma

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25
Q

what does a peak flow meter measure

A

peak expiratory flow rate (PEFR): the fastest speed a person can blow air out of lungs after taking as big of a breath as possible

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26
Q

what type of inhale for MDIs and soft mist inhalers

A

slow and deep

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27
Q

what type of inhale for DPI

A

deep and forceful

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28
Q

ICS place in therapy for asthma

A

primary maintenance therapy, best outcomes

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29
Q

corticosteroids mechanism

A

glucocorticoid receptor agonist in the lungs to provide anti-inflammatory, immunosuppressive, and antiproliferative effects to mitigate responses to various stimuli

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30
Q

ICS onset of action

A

variable, up to 2-4 weeks for max effect

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31
Q

ICS side effects

A

oral candidiasis, URTI, sinusitis, hoarseness, cough, pneumonia

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32
Q

which class may slow bone growth in children

A

ICS

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33
Q

systemic corticosteroids place in therapy

A

reserved for poorly controlled, in the setting of an acute exacerbation not relieved by rescue agents

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34
Q

OCS drug interactions

A

CYP3A

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35
Q

OCS side effects

A

HTN, fluid retention, hyperglycemia, GI upset, insomnia, infection, adrenal axis suppression, glaucoma, pulmonary TB

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36
Q

OCS cautions

A

immunosuppressed, HTN, DM

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37
Q

OCS counseling

A

take with food

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38
Q

name the ICS agents

A

fluticasone, budesonide, mometasone, beclomethasone

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39
Q

name the OCS agents

A

prednisone, dexamethasone, methylprednisolone

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40
Q

name the SABAs

A

albuterol, levoalbuterol

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41
Q

SABA place in therapy

A

drug of choice for acute asthma exacerbations, most effective for relieving acute bronchospasm

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42
Q

SABA mechanism

A

selective B2 adrenergic agonist: binds to B2 receptors in the lungs, resulting in bronchial smooth muscle relaxation, increase cAMP

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43
Q

SABA onset

A

1-2 minutes neb, 2-5 minutes MDI/DPI

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44
Q

SABA duration

A

3-4 hours neb, <6 hours MDI

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45
Q

SABA side effects

A

tremor, tachycardia (less with levo), chest pain, hypokalemia, hypomagnesemia, hyperglycemia

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46
Q

SABA risk?

A

regular use= poor asthma control. RISK WITH SABA ONLY THERAPY

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47
Q

regular or overuse of SABA causes

A

beta receptor downregulation, lack of response, increased use

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48
Q

counseling: if giving albuterol with ICS in a separate inhaler

A

albuterol FIRST, then ICS

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49
Q

LABA agents

A

formoterol, olodaterol, salmeterol, vilanterol

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50
Q

LABA place in therapy

A

chronic therapy for asthma IN COMBINATION with ICS. monotherapy for mild COPD, combo with LAMA for persistent COPD

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51
Q

LABA onset

A

1-2 minutes formoterol olodaterol. >10 minutes salmaterol vilanterol

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52
Q

LABA duration

A

> 12-24 hours

53
Q

black box warning LABA

A

never monotherapy for asthma!!!!!!!! LABA monotherapy is for COPD only.

54
Q

important point for LABA

A

do not take two different LABAs. use same combination for reliever and maintenance.

55
Q

SAMA agent

A

ipratropium

56
Q

SAMA place in therapy

A

mainly COPD and acute asthma exacerbations (emergency)

57
Q

SAMA mechanism

A

competitive inhibitor of cholinergic (muscarinic) receptors in the bronchial smooth muscle leading to bronchodilation

58
Q

SAMA onset

A

15-30 minutes

59
Q

SAMA duration

60
Q

SAMA side effects

A

headache, flushing, blurred vision, tachycardia, palpitations

61
Q

LAMA agents

A

aclidinium, glycopyrrolate, tiotropium, umeclidinium

62
Q

LAMA place in therapy

A

mainly for COPD. tiotropium for sever asthma >12 after ICS/LABA`

63
Q

tiotropium duration

A

> 24 hours

64
Q

LAMA side effects

A

headache, blurred vision, flushed skin, tachycardia, palpitations, acute urinary retention, cough

65
Q

general cons of biologics

A

increased infection risk, high cost, need to avoid live vaccines

66
Q

biologics place in therapy

A

not first line or monotherapy. decrease exacerbations. add on to standard therapy for severe asthma step 4-5 in patients with T2 phenotype. may decrease OCS dose

67
Q

LTRA agents

A

montelukast, zafirlukast

68
Q

5-lipoxygenase inhibitor

69
Q

LTRA mechanism

A

interfere with pathway that allows mast cells and eosinophils to release leukotriene mediators. reduce symptoms associated with allergic component of asthma: swelling and smooth muscle contraction

70
Q

LTRA onset

71
Q

LTRA duration

A

up to 24 hours

72
Q

LTRA side effects

A

URI, fever, headache, pharyngitis, cough.

73
Q

FDA boxed warning for montelukast

A

neuropsychiatric effects

74
Q

risk with zafirlukast

A

hepatotoxicity

75
Q

methylxanthine agents

A

theophylline, theophylline ER

76
Q

theophylline place in therapy

77
Q

theophylline mechanism

A

inducing smooth muscle relaxation to result in bronchodilation

78
Q

theophylline side effects

A

caffeine-like effects at therapeutic levels: n/v, headache, insomnia. toxic level effects: persistent vomiting, arrhythmias, seizures

79
Q

theophylline monitoring

A

narrow therapeutic window requiring blood monitoring. normal level <20 mcg/mL

80
Q

chromone agent

A

cromolyn sodium

81
Q

cromolyn place in therapy

A

adjunct; EIB or add on for allergic asthma

82
Q

cromolyn mechanism

A

mast cell stabilizer: inhibits release of histamines and leukotrienes from mast cells during allergic response

83
Q

anti-IgE mAb

A

omalizumab

84
Q

omalizumab mech

A

inhibits binding of IgE to mast cells and basophils: thus decreases mediators of allergic response

85
Q

omalizumab side effects

A

anaphylaxis, urticaria, thrombocytopenia, malignancy, CV

86
Q

omalizumab monitoring

A

weight, IgE levels, platelets

87
Q

IL-5 antagonists

A

mepolizumab, relizumab, benralizumab

88
Q

IL-5 antagonist mechanism

A

inhibit IL-5 signaling, reducing the production and survival of eosinophils

89
Q

IL-5 antagonist side effects

A

hypersensitivity, headache, fatigue, herpes zoster (mepolizumab), malignancy

90
Q

IgG4 antibody

91
Q

IgG4 antibody mechanism

A

inhibits IL-4 and IL-13 signaling/ inflammatory response by binding to IL-4Ra subunit

92
Q

IgG4 antibody side effects

A

favorable tolerability: injection site reaction, oropharyngeal pain, eosinophilia

93
Q

thymic stromal lymphopoietin blocker

A

tezepelumab

94
Q

tezepelumab side effects

A

pharyngitis, arthralgia, back pain

95
Q

what are some medication-related asthma risks

A

high SABA use >1 canister per month, not prescribed ICS, poor adherence, incorrect inhaler technique

96
Q

what are some comorbidities than increase risk of asthma symptom

A

obesity, chronic rhinosinusitis, GERD, food allergy, pregnancy and hormonal changes

97
Q

asthma control test score?

A

> 19/25 is well controlled. 19 or less is not controlled.

98
Q

mild asthma by GINA definition

A

symptoms <4-5 days per week

99
Q

moderate asthma by GINA definition

A

symptoms most days or waking with asthma >1 time per week

100
Q

severe asthma by GINA definition

A

daily symptoms or waking with asthma >1 time per week AND low lung function

101
Q

what are options for reliever treatment asthma

A

SABA, low dose ICS-formoterol. (alt: SAMA for acute exacerbation)

102
Q

what are options for controller or maintenance asthma treatment

A

ICS, LABA, LAMA, LTRA, biologics

103
Q

treatment for mild or moderate acute asthma exacerbation

A

albuterol 4-10 puffs q20min for 1 hour, continue hourly x1-3. Likely take oral corticosteroids at home.

104
Q

treatment for severe acute asthma exacerbation

A

albuterol + ipratropium MDI or neb q20min or continuously for 1 hour, then q1-4h prn. + oral corticosteroids. adjunct (magnesium, ketamine, heliox) helpful.

105
Q

treatment for life threatening acute asthma exacerbation

A

IV corticosteroids

106
Q

treatment for green zone

A

take long term control agent only. uses reliever before exercise, avoid triggers.

107
Q

treatment for yellow zone

A

increase usual reliever, contact clinician, OCS burst

108
Q

role of TH2 in pathophysiology of asthma

A

releases IL-4 and IL-5

109
Q

role of IL-4 in pathophysiology of asthma

A

differentiation of CD4 to plasma cells: producing IgE antibodies

110
Q

role of IL-5 in pathophysiology of asthma

A

proliferation, activation, and survival of eosinophils

111
Q

role of IgE in pathophysiology of asthma

A

bind to and activate mast cells

112
Q

role of leukotrienes in pathophysiology of asthma

A

bronchoconstriction

113
Q

role of TSLP in pathophysiology of asthma

A

inflammatory mediator in response to allergens

114
Q

role of dendritic cells in pathophysiology of asthma

A

stimulate TH2

115
Q

role of mast cells in pathophysiology of asthma

A

release histamine and leukotrienes

116
Q

mediators of early phase allergen reaction?

A

histamine, prostaglandins, leukotrienes

117
Q

mediators of late phase allergen reaction?

A

eosinophils, neutrophils, macrophages, T lymphocytes, prostaglandins, leukotrienes, thromboxones, PAF

118
Q

what does airway remodeling include

A

fibrosis, epithelial cell injury, mucus hypersecretion, smooth muscle hypertrophy, angiogenesis

119
Q

bronchoprovocation testing

A

patient is given methacholine, positive test is fall in FEV1 by 20%

120
Q

exercise challenge test

A

positive if FEV1 falls 10% for adults or 12% for children

121
Q

baseline eosinophil count of ____ is a predictor for T2 asthma

122
Q

which DPIs could be mistaken for a MDI

A

respiclick, redihaler, digihaler

123
Q

how to load the dose for ellipta

A

sliding cover down

124
Q

how to load the dose for diskus and inhub

A

sliding lever

125
Q

how to load the dose for respiclick, digihaler, redihaler

A

opening the cap

126
Q

how to load the dose for twisthaler

A

twist counterclockwise

127
Q

how to load the dose for flexhaler

A

twist as far as it goes in any direction, then back in the other direction until it clicks

128
Q

how to load the dose for pressair

A

press the button, control window will turn green. it will then turn red if you inhaled correctly

129
Q

how to load the dose for handihaler

A

SINGLE USE: you have to put a capsule in and puncture it. don’t swallow the capsule idiot

Pulmonology (2 decks)

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