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Pulmonology > Asthma > Flashcards

Asthma Flashcards

1
Q

When are inhaled or systemic used for asthma control?

A

Inhaled is for chronic control while systemic is for acute or life threatening attacks

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2
Q

Can you step down on Asthma treatment?

A

Yes, if they have controlled symptoms for a long time

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3
Q

Why does exercise worsen COPD?

A

Due to the resistance in the airways from mucous, increasing respiratory rate diminishes tidal volume, lowering alveolar ventilation and inspiratory capacity

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4
Q

What childhood illness can predispose Asthma?

A

RSV, though there are several others

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5
Q

What are the two types of factors that influence Asthma?

A

Host factors and environmental factors

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6
Q

What is Group D COPD?

A

High risk with more symptoms

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7
Q

What do Eosinophils release and how does it lead to airway remodeling?

A

Subendothelial fibrosis (basement membrane thickening), hypertrophy of smooth muscles, and goblet cell hyperplasia

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8
Q

How are acute asthma exacerbations treated?

A

Albuterol for bronchodilation + systemic glucocorticosteroids like prednisone (NOT INHALED)

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9
Q

What is a Th2 phenotype?

A

Factors that predispose allergic diseases like asthma, such as widespread use of antibiotics and western lifestyle

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10
Q

Is the pulmonary component of COPD fully treatable?

A

No, it is not fully reversible and therefore the patient never has normal function

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11
Q

What is Mild Persistent asthma?

A

Symptoms more than 2 days per week but not daily, but still having normal lung function

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12
Q

What do IL 4 IL 5 and IL 13 activate in Asthma?

A

Mast Cell and Eosinophils

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13
Q

How does exercise alter breathing?

A

Respiratory rate goes up while end expiratory volume/FRC goes down

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14
Q

What attracts Neutrophils, and which disease?

A

IL-8 and LTB4, released by Macrophages in COPD

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15
Q

What triggers a COPD exacerbation?

A

Infections with a virus or bacteria, which causes an inflammatory response and worsening of the disease

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16
Q

What is the role of Alpha1AntiTrypsin and why does it predispose smoking damage?

A

A1AT normally inhibits neutrophil elastase, but A1AT deficient people who are exposed to smoke cannot inhibit the elastase leading to damage

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17
Q

How is COPD diagnosed?

A

FEV1/FVC ratios on spirometry

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18
Q

What is a COPD exacerbation?

A

A change in the patient’s baseline state

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19
Q

How do bronchodilators help treat COPD, and why is it not enough?

A

Bronchodilators help fix the increased resistance due to mucous in the large airways, but FEV1/FVC1 can never be fixed because the emphysema in the alveoli are not addressed

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20
Q

Is there a preventative strategy for COPD?

A

Nope

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21
Q

What cell type is predominant in COPD?

A

Neutrophils

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22
Q

Where is IgE measured?

A

IgE is measured in the blood

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23
Q

How does Asthma appear on spirometry?

A

Concave upward appearance that lines up with obstructive physiology

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24
Q

Is COPD progressive?

A

Yes, usually progressive and associated with abnormal inflammatory response to noxious particles

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25
Q

What should be done when given an inhaled bronchodilators?

A

Counsel the patient that they need to increase their activity level

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26
Q

What are the Pi genotypes?

A 
Normal = PiMM
Carrier = PiZ*
Deficient = PIZZ
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27
Q

What is a Th1 phenotype?

A

Factors that induce protective immunity, such as presence of older siblings, early exposure to day care, TB

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28
Q

Why is Asthma poorly controlled in the population?

A

People fail to correctly identify intermittent vs persistent asthma

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29
Q

How is COPD diagnosed?

A

COPD is diagnosed with a FEV1/FVC ratio < 0.7

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30
Q

What are host factors that effect Asthma development?

A

Host factors = atopy, airway hyperresponsiveness, gender, and obesity

Environmental factors = indoor/outdoor allergens, occupational sensitizers, dust, pollution/smoke

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31
Q

Is Asthma more common in children or adults?

A

Childrens

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32
Q

What is the risk domain for Asthma?

A

The frequency of asthma exacerbations

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33
Q

What is the key effector cell in Asthma?

A

Eosinophils

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34
Q

What is the main treatment for COPD vs asthma?

A

Bronchodilators for COPD, Inhaled Corticosteroids for Asthma

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35
Q

How does COPD cause hypoxemia?

A

V/Q mismatch

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36
Q

When should a bronchodilator be given alone in Asthma?

A

NEVER

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37
Q

Does COPD thicken the basement membrane?

A

No, only Asthma does

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38
Q

How does COPD cause destruction of the alveolar spaces?

A

Loss of elastic fibers in the alveoli lead to loss of elastic recoil

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39
Q

What is peribronchiolar fibrosis?

A

Small airway changes in COPD, where the terminal bronchioles are fibrotic and less compliant

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40
Q

What are the goals of Asthma management?

A

Maintain control of symptoms and prevent exacerbations

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41
Q

What does airway remodeling refer to in Asthma?

A

Changes in the airways due to constant Eosinophil mediated inflammation in the airways, including goblet cell hyperplasia, basement membrane thickening, and smooth muscle hypertrophy

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42
Q

What treatment should be prescribed to someone who has intermittent Asthma symptoms with nocturnal symptoms or exacerbations?

A

Albuterol is the first line treatment, while ICS can be prescribed if someone has more than two attacks per year or nocturnal symptoms or exacerbations

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43
Q

What is the chemoattractant for Eosinophils?

A

IL 5

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44
Q

What does the presence of CD8 cells in COPD suggest?

A

An antigenic process in people that are more susceptible to develop COPD

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45
Q

What are symptoms of Asthma?

A

Episodes of wheezing, cough at night, cough after exposure to allergens

46
Q

What Interleukin cytokines are responsible for IgE synthesis?

A

IL-13, IL-4, IL-5

47
Q

What is the common adjunct to asthma medication?

A

Leukotriene antagonists like Montelukast, which are added as a second line

48
Q

How does COPD alter breathing?

A

Higher FRC and RV, since they breath at higher volumes

49
Q

How does Methacholine Bronchoprovocation work?

A

Methacholine causes a decrease in FEV1/FVC, and people who drop with low doses of Methacholine are diagnosed with Airway Hyperresponsiveness (not necessarily Asthma)

50
Q

Why do people with COPD not report symptoms?

A

They avoid strenuous activity, and therefore don’t feel dyspnea

51
Q

What is the main emergency asthma medication?

A

Albuterol

52
Q

What happens after Eosinophils are recruited to the lungs?

A

Eosinophils release more cytokines and Leukotrienes

53
Q

What is the goal in the treatment of Asthma?

A

Remove the variability in lung function

54
Q

What type of mAb can help treat Asthma?

A

Anti-IgE, but never as a first line

55
Q

What cytokines are released by T cells to induce B cells to produce IgE?

A

IL 13 and IL 4

56
Q

What is kept the same between intermittent and persistent asthma?

A

Both have normal lung function

57
Q

What does dynamic hyperinflation refer to in COPD?

A

Idea that IC drops due to high lung volumes in COPD, leading to breathlessness

58
Q

What is COPD?

A

A preventable and treatable disease with extrapulmonary effects

59
Q

What does the impairment domain for Asthma refer to?

A

How impaired their lung function is by FEV1/FVC and by symptoms (less than 2 times per month) and albuterol use (less than 2 times per week)

60
Q

How is the severity of COPD classified?

A

Use the mMRC or CAT scale to assess symptoms and severity

61
Q

How are macrophages made dysfunctional in COPD?

A

Macrophages exposed to cigarette smoke lose phagocytic capability and begin releasing IL-8 and LTB4 to attract Neutrophils

62
Q

Which patients with COPD have worse outcomes and why?

A

Patients with COPD who have frequent exacerbations have faster lung function decline and higher mortality

63
Q

Does the Asthma control test decide if someone should be on a controlled medicine?

A

No, only symptom frequency; it helps us assess how well we’re controlling the asthma and how to adjust therapy

64
Q

When is screening for A1AT deficiency indicated?

A

In all patients in COPD

65
Q

What should persistent asthma be treated with?

A

Inhaled corticosteroids

66
Q

What is the diagnostic test for Asthma?

A

There isn’t one; it’s based on clinical history

67
Q

What is the cellular makeup of COPD?

A

The alveolar macrophage, which releases chemotactic factors that attract neutrophils/monocytes/CD8 Cells to the airway

68
Q

What does emphysema do to the outward flow ratio?

A

Loss of elastic recoil pressure due to loss of elastic fibers as well as increased resistance due to peribronchiolar fibrosis + large airways clogged with mucous = lower FEV1/FVC1 = obstructive lung physiology

69
Q

What should be done if a patient has COPD exacerbations?

A

Add an Inhaled Corticosteroid Steroids

70
Q

How is COPD best questioned?

A

Ask people about their activity to account for reduced exercise tolerance and behaviors that avoid exercise

71
Q

When are LABAs used to treat Asthma?

A

Only as a second line for Asthma

72
Q

How does COPD show up on CXR?

A

Overinflation of the lung, with flattened diaphragm and more space in front of the heart on a side view

73
Q

Are people Th1 or Th2?

A

A mix of both, set by environmental drivers

74
Q

How do exacerbations worsen COPD?

A

Inflammation

75
Q

What can trigger an asthma exacerbation?

A

Allergen, respiratory infections (RSV), weather changes, exercise, air pollution, and food

76
Q

What characterizes Asthma?

A

Variable, intermittent, and episodic bouts of obstructive lung physiology

77
Q

How is COPD mismanaged in women?

A

Frequently misdiagnosed as Asthma, more often than men

78
Q

What guides the asthma diagnosis, symptoms and exacerbations or lung function?

A

Symptoms and exacerbations more than 2/time unit, regardless of lung function

79
Q

What does IgE do in Asthma?

A

Bind an antigen and trigger Histamine release by Mast Cells

80
Q

When is Asthma more common by sex?

A

More common in boys in childhood, more common in women in adulthood

81
Q

What is the difference between intermittent and persistent asthma?

A

Having symptoms more than twice per week (persistent), regardless of asthma

82
Q

Does COPD thicken smooth muscle?

A

No, only Asthma does

83
Q

What does Exacerbation treatment entail?

A

Oxygen, inhaled bronchodilators, systemic corticosteroids, antibiotics

84
Q

What do neutrophils do that damage the lung?

A

After being recruited by Macrophages, Neutrophils release elastase, cathepsins, and MMPs which cause alveolar wall destruction and mucus hypersecretion

85
Q

What genetic factor predisposes COPD?

A

Alpha 1 Antitripsin deficiency, specifically PiZZ genotype

86
Q

What is small airway disease in COPD?

A

Chronic Bronchitis

87
Q

How is COPD severity assessed?

A

Frequency of symptoms assessed by CAT as well as exacerbations per year

88
Q

What is the main line therapy for Asthma?

A

Inhaled corticosteroids

89
Q

How are spirometry tests used to diagnose Asthma?

A

Since Asthma is episodic, take multiple spirometry measurements and look for high variability; can also give someone a peak flow device for home measurements

90
Q

What type of inflammatory T cell response characterizes allergic inflammation?

A

Asthma and other allergic inflammation is characterized by a Th2 response

91
Q

Why does COPD have a flatter volume-time curve?

A

Lower elastic recoil lowers the slope, and people exhale longer to clear the lungs of air

92
Q

What in a clinical history would point to Asthma?

A

Allergies, spirometry (can be hard to measure since Asthma is episodic and can be normal), improvement with bronchodilator, methacholine bronchoprovocation (not diagnosing asthma, but hyperreactive asthma)

93
Q

How should asthma exacerbations be described to patients?

A

As a “flare up”, not an exacerbation, episode, or attack

94
Q

What populations are most commonly effected by Asthma?

A

Black children, low-income populations, and children living in inner cities

95
Q

What is the early Asthma response?

A

Histamine and cytokine release by mast cells in the airways

96
Q

What should be done if a patient has Asthma exacerbations?

A

Add a bronchodilator

97
Q

What drives COPD?

A

Exposures to cigarette smoke, air pollution, and occupational dusts

98
Q

Why is it difficult to control Asthma by tracking risk?

A

People who have exacerbations several times a year may go to different places to get steroids, and so people don’t track it well enough to adjust therapy

99
Q

What is the late Asthma response?

A

Ongoing airway inflammation and destruction that predisposes damages

100
Q

How does inflammation mediate COPD?

A

Small airway disease and parenchymal destruction

101
Q

What is the cutoff for persistent asthma in the risk domain?

A

More than two exacerbations per year, regardless of impairment domain status

102
Q

How do inhaled corticosteroids affect lung function in asthma over time?

A

Over time, the lung function normalizes with persistent ICS use, but most people don’t use it long enough

103
Q

Who is at special risk for asthma exacerbations?

A

People who have been hospitalized, treated with oral corticosteroids, poor adherence, or has a near fatal asthma attack

104
Q

What is the mechanism of hypoxia in Asthma?

A

V/Q mismatch

105
Q

Does COPD quality of life correlate with FEV1 or exercise capacity?

A

No

106
Q

What changes in the large airways does COPD cause?

A

Inflammation and overproduction of mucous

107
Q

What is the treatment for persistent asthma?

A

ICS

108
Q

Where is the AAT gene encoded?

A

A single gene on chromosome 14, Pi

109
Q

What does it mean when worsening asthma should be managed as a continuum?

A

Self management can control asthma symptoms like increasing inhaler use

110
Q

What does atopy induce?

A

Allergic rhinitis, asthma, hay fever eczema

111
Q

What is atopy?

A

The bodies predisposition to develop IgE in response to exposure to environmental allergens, which can be measured in the blood

Pulmonology (22 decks)

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