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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
What should be done when given an inhaled bronchodilators?
Counsel the patient that they need to increase their activity level
26
What are the Pi genotypes?
``` Normal = PiMM Carrier = PiZ* Deficient = PIZZ ```
27
What is a Th1 phenotype?
Factors that induce protective immunity, such as presence of older siblings, early exposure to day care, TB
28
Why is Asthma poorly controlled in the population?
People fail to correctly identify intermittent vs persistent asthma
29
How is COPD diagnosed?
COPD is diagnosed with a FEV1/FVC ratio < 0.7
30
What are host factors that effect Asthma development?
Host factors = atopy, airway hyperresponsiveness, gender, and obesity Environmental factors = indoor/outdoor allergens, occupational sensitizers, dust, pollution/smoke
31
Is Asthma more common in children or adults?
Childrens
32
What is the risk domain for Asthma?
The frequency of asthma exacerbations
33
What is the key effector cell in Asthma?
Eosinophils
34
What is the main treatment for COPD vs asthma?
Bronchodilators for COPD, Inhaled Corticosteroids for Asthma
35
How does COPD cause hypoxemia?
V/Q mismatch
36
When should a bronchodilator be given alone in Asthma?
NEVER
37
Does COPD thicken the basement membrane?
No, only Asthma does
38
How does COPD cause destruction of the alveolar spaces?
Loss of elastic fibers in the alveoli lead to loss of elastic recoil
39
What is peribronchiolar fibrosis?
Small airway changes in COPD, where the terminal bronchioles are fibrotic and less compliant
40
What are the goals of Asthma management?
Maintain control of symptoms and prevent exacerbations
41
What does airway remodeling refer to in Asthma?
Changes in the airways due to constant Eosinophil mediated inflammation in the airways, including goblet cell hyperplasia, basement membrane thickening, and smooth muscle hypertrophy
42
What treatment should be prescribed to someone who has intermittent Asthma symptoms with nocturnal symptoms or exacerbations?
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
43
What is the chemoattractant for Eosinophils?
IL 5
44
What does the presence of CD8 cells in COPD suggest?
An antigenic process in people that are more susceptible to develop COPD
45
What are symptoms of Asthma?
Episodes of wheezing, cough at night, cough after exposure to allergens
46
What Interleukin cytokines are responsible for IgE synthesis?
IL-13, IL-4, IL-5
47
What is the common adjunct to asthma medication?
Leukotriene antagonists like Montelukast, which are added as a second line
48
How does COPD alter breathing?
Higher FRC and RV, since they breath at higher volumes
49
How does Methacholine Bronchoprovocation work?
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
Why do people with COPD not report symptoms?
They avoid strenuous activity, and therefore don't feel dyspnea
51
What is the main emergency asthma medication?
Albuterol
52
What happens after Eosinophils are recruited to the lungs?
Eosinophils release more cytokines and Leukotrienes
53
What is the goal in the treatment of Asthma?
Remove the variability in lung function
54
What type of mAb can help treat Asthma?
Anti-IgE, but never as a first line
55
What cytokines are released by T cells to induce B cells to produce IgE?
IL 13 and IL 4
56
What is kept the same between intermittent and persistent asthma?
Both have normal lung function
57
What does dynamic hyperinflation refer to in COPD?
Idea that IC drops due to high lung volumes in COPD, leading to breathlessness
58
What is COPD?
A preventable and treatable disease with extrapulmonary effects
59
What does the impairment domain for Asthma refer to?
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
How is the severity of COPD classified?
Use the mMRC or CAT scale to assess symptoms and severity
61
How are macrophages made dysfunctional in COPD?
Macrophages exposed to cigarette smoke lose phagocytic capability and begin releasing IL-8 and LTB4 to attract Neutrophils
62
Which patients with COPD have worse outcomes and why?
Patients with COPD who have frequent exacerbations have faster lung function decline and higher mortality
63
Does the Asthma control test decide if someone should be on a controlled medicine?
No, only symptom frequency; it helps us assess how well we're controlling the asthma and how to adjust therapy
64
When is screening for A1AT deficiency indicated?
In all patients in COPD
65
What should persistent asthma be treated with?
Inhaled corticosteroids
66
What is the diagnostic test for Asthma?
There isn't one; it's based on clinical history
67
What is the cellular makeup of COPD?
The alveolar macrophage, which releases chemotactic factors that attract neutrophils/monocytes/CD8 Cells to the airway
68
What does emphysema do to the outward flow ratio?
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
What should be done if a patient has COPD exacerbations?
Add an Inhaled Corticosteroid Steroids
70
How is COPD best questioned?
Ask people about their activity to account for reduced exercise tolerance and behaviors that avoid exercise
71
When are LABAs used to treat Asthma?
Only as a second line for Asthma
72
How does COPD show up on CXR?
Overinflation of the lung, with flattened diaphragm and more space in front of the heart on a side view
73
Are people Th1 or Th2?
A mix of both, set by environmental drivers
74
How do exacerbations worsen COPD?
Inflammation
75
What can trigger an asthma exacerbation?
Allergen, respiratory infections (RSV), weather changes, exercise, air pollution, and food
76
What characterizes Asthma?
Variable, intermittent, and episodic bouts of obstructive lung physiology
77
How is COPD mismanaged in women?
Frequently misdiagnosed as Asthma, more often than men
78
What guides the asthma diagnosis, symptoms and exacerbations or lung function?
Symptoms and exacerbations more than 2/time unit, regardless of lung function
79
What does IgE do in Asthma?
Bind an antigen and trigger Histamine release by Mast Cells
80
When is Asthma more common by sex?
More common in boys in childhood, more common in women in adulthood
81
What is the difference between intermittent and persistent asthma?
Having symptoms more than twice per week (persistent), regardless of asthma
82
Does COPD thicken smooth muscle?
No, only Asthma does
83
What does Exacerbation treatment entail?
Oxygen, inhaled bronchodilators, systemic corticosteroids, antibiotics
84
What do neutrophils do that damage the lung?
After being recruited by Macrophages, Neutrophils release elastase, cathepsins, and MMPs which cause alveolar wall destruction and mucus hypersecretion
85
What genetic factor predisposes COPD?
Alpha 1 Antitripsin deficiency, specifically PiZZ genotype
86
What is small airway disease in COPD?
Chronic Bronchitis
87
How is COPD severity assessed?
Frequency of symptoms assessed by CAT as well as exacerbations per year
88
What is the main line therapy for Asthma?
Inhaled corticosteroids
89
How are spirometry tests used to diagnose Asthma?
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
What type of inflammatory T cell response characterizes allergic inflammation?
Asthma and other allergic inflammation is characterized by a Th2 response
91
Why does COPD have a flatter volume-time curve?
Lower elastic recoil lowers the slope, and people exhale longer to clear the lungs of air
92
What in a clinical history would point to Asthma?
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
How should asthma exacerbations be described to patients?
As a "flare up", not an exacerbation, episode, or attack
94
What populations are most commonly effected by Asthma?
Black children, low-income populations, and children living in inner cities
95
What is the early Asthma response?
Histamine and cytokine release by mast cells in the airways
96
What should be done if a patient has Asthma exacerbations?
Add a bronchodilator
97
What drives COPD?
Exposures to cigarette smoke, air pollution, and occupational dusts
98
Why is it difficult to control Asthma by tracking risk?
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
What is the late Asthma response?
Ongoing airway inflammation and destruction that predisposes damages
100
How does inflammation mediate COPD?
Small airway disease and parenchymal destruction
101
What is the cutoff for persistent asthma in the risk domain?
More than two exacerbations per year, regardless of impairment domain status
102
How do inhaled corticosteroids affect lung function in asthma over time?
Over time, the lung function normalizes with persistent ICS use, but most people don't use it long enough
103
Who is at special risk for asthma exacerbations?
People who have been hospitalized, treated with oral corticosteroids, poor adherence, or has a near fatal asthma attack
104
What is the mechanism of hypoxia in Asthma?
V/Q mismatch
105
Does COPD quality of life correlate with FEV1 or exercise capacity?
No
106
What changes in the large airways does COPD cause?
Inflammation and overproduction of mucous
107
What is the treatment for persistent asthma?
ICS
108
Where is the AAT gene encoded?
A single gene on chromosome 14, Pi
109
What does it mean when worsening asthma should be managed as a continuum?
Self management can control asthma symptoms like increasing inhaler use
110
What does atopy induce?
Allergic rhinitis, asthma, hay fever eczema
111
What is atopy?
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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