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CVPR > CVPR Week 5: Obstructive Airway Disease > Flashcards

CVPR Week 5: Obstructive Airway Disease Flashcards

1
Q

Objectives

A
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2
Q

Common obstructive lung diseases

5 listed

A
  • Asthma
  • Emphysema (COPD)
  • Chronic bronchitis (COPD)
  • Bronchiectasis
  • Cystic fibrosis
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3
Q

Asthma type of lung disease

A

Obstructive lung disease with reversible airflow obstruction

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4
Q

Asthma types

A

different phenotypes

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5
Q

Asthma inflammation

A

Inflammation is prominent

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6
Q

Emphysema lung disease type

A

Obstructive “COPD” permanent enlargement/destruction of the respiratory bronchioles

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7
Q

Chronic bronchitis lung disease type

A

“COPD” Sputum production 3 months/year for 2 years

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8
Q

The less common obstructive lung diseases

2 listed

A
  • Bronchiectasis
  • Cystic fibrosis
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9
Q

Bronchiectasis description

A

Enlarged airways and tortuous blood vessels (bronchial arteries) resulting from chronic infection

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10
Q

Cystic fibrosis description

3 listed

A
  • Hereditary disease
  • multiple gene mutations
  • bronchiectasis with chronic respiratory infections with a failure to thrive
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11
Q

The most common obstructive lung diseases

3 listed

A
  • Asthma
  • Emphysema (COPD)
  • Chronic Bronchitis (COPD)
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12
Q

Bronchiectasis clinical course

3 listed

A
  • Abnormal dilation of the bronchial tree
  • Causes scarring 7 obstructions & mucus accumulation distally
  • May eventually lead to right ventricular failure/respiratory failure
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13
Q

Congenital causes of Bronchiectasis

2 listed

A
  • When due to Kartagener’s presents as GI situs inversus and chronic sinusitis
  • Ciliary dyskinesia disorders
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14
Q

Acquired causes of Bronchiectasis

3 listed

A
  • often 2o to severe LRTI in childhood
  • Linked to pertussis & measles
  • Can occur post TB infection
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15
Q

Types of bronchiectasis

3 listed

A
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16
Q

What kind of bronchiectasis is this?

A

cylindrical bronchiectasis

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17
Q

What kind of bronchiectasis is this?

A

cystic bronchiectasis

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18
Q

What kind of bronchiectasis is this?

A

This is actually normal

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19
Q

What kind of bronchiectasis is this?

A

Varicose bronchiectasis

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20
Q

What is this?

A

bronchiectasis

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21
Q

Obstructive ventilatory defect definition

A

essentially means that Forced Expiratory volume is decreased compared to the Forced vital capacity

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22
Q

The earliest changes associated with airflow obstruction are in?

A

The small airways

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23
Q

Changes on the flow-volume curve associated with airflow obstruction

A
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24
Q

COPD classification by severity

A
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25
Q

COPD is classified as

A

FEV1/FVC = < 0.7

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26
Q

Asthma Definition

A

A common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction [fully/completely reversible], bronchial hyperresponsiveness, and underlying inflammation

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27
Q

Asthma diagnosis

3 listed

A
  • Diagnosis by history and to confirm, spirometry is used however may be normal if the asthma is under control at the time
  • However, a lack of bronchodilator response does not rule out asthma
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28
Q

Asthma clinical features

5 listed

A
  • Wheezing
  • SOB
  • Cough
  • Chest tightness
  • Variable Peak Expiratory Flow Rates (PEFR)
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29
Q

Asthma epidemiology

4 things listed

A
  • 40 million individuals died from asthma in 2015 a decrease of 26% from 1990
  • Asthma is the most common respiratory disease worldwide affecting 358 million in 2015
  • The U.S. Prevalence = 8.3%
  • The estimated annual cost of asthma in 2013 was 81.9 billion
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30
Q

Asthma pathophysiology between phenotypes

A
  • Distinct phenotypes of asthma exist however the pattern of airway inflammation does not vary significantly depending upon disease severity, persistence and duration
  • The cellular profile and the response of the structural cells in asthma are quite consistent
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31
Q

Asthma phenotypes

5 listed

A
  • Intermittent
  • persistent
  • exercise-associated
  • aspirin-sensitive
  • severe asthma
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32
Q

Asthma pathophysiology: Cells involved

6 listed

A
  • T lymphocytes (Th2)
  • Mast cells
  • Eosinophils
  • Macrophages
  • Neutrophils
  • Epithelial Cells
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33
Q

Asthma pathophysiology: T lymphocyte involvement

A

produce cytokines IL-4, IL-5, IL-13

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34
Q

Asthma pathophysiology: Mast cell involvement

A
  • mediators of bronchoconstriction (histamine, cysteinyl-leukotrienes, prostaglandin D2)

​

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35
Q

Asthma pathophysiology: Eosinophil involvement

3 listed

A
  • increased numbers of eosinophils exist in the airway of most but not all asthmatics
  • contain inflammatory enzymes, generate leukotrienes and express a wide variety of pro-inflammatory cytokines
  • may not be the only primary effector cell in asthma, it likely has a distinct role in different phases of the disease
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36
Q

Asthma pathophysiology: Macrophages involvement

2 listed

A
  • most numerous cells in the airways
  • can be activated by allergens to release inflammatory mediators and cytokines that amplify the inflammatory response
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37
Q

Asthma pathophysiology: Neutrophil involvement

A
  • pathophysiological role remains uncertain
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38
Q

Asthma pathophysiology: Epithelial cell involvement

A

they produce more inflammatory mediators

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39
Q

Asthma pathophysiology diagram

A
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40
Q

Asthma pathophysiology diagram 2

A
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41
Q

Asthma pathophysiology diagram 3

A
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42
Q

Asthma pathophysiology main components of pathology

2 listed

A
  • smooth muscle dysfunction
  • airway inflammation
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43
Q

Asthma Smooth muscle dysfunction leads to?

4 listed

A
  • Bronchoconstriction
  • bronchial hyperreactivity
  • hypertrophy/hyperplasia
  • inflammatory mediator release
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44
Q

Asthma airway inflammation leads to?

A
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45
Q

Asthma smooth muscle dysfunction and airway inflammation leads to?

A

symptoms/exacerbations and disease progression

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46
Q

Asthma pathophysiology Acute response

4 listed

A
  • Bronchoconstriction
  • Edema
  • Secretions
  • Cough
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47
Q

Asthma pathophysiology: Chronic inflammation

3 listed

A
  • Cell recruitment
  • epithelial damage
  • early structural changes
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48
Q

Asthma pathophysiology: Airway remodeling

3 listed

A
  • cellular proliferation
  • extracellular matrix increase
  • structural changes
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49
Q

Epithelial damage in asthma

A
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50
Q

Intrinsic factors affecting disease expression of Asthma

A
  • genetics of disease
  • Duration of asthma
  • severity of childhood asthma
  • Gender
  • Response to therapy
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51
Q

Extrinsic factors affecting disease expression of Asthma

9 listed

A
  • Viral infections
  • Allergen exposure
  • \Airway irritants
  • Exercise
  • Compliance
  • Season
  • Time of day
  • Occupational (10-15% of adult asthma)
  • Western lifestyle i.e. obesity
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52
Q

Asthma comorbidities that worsen the asthma

4 listed

A
  • GERD-association with asthma 15 - 40 % prevalence
  • Sinusitis/Allergic Rhinitis
  • Illicit drug use – cocaine
  • Non-compliance
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53
Q

Risk factors for death from asthma

A
  • prior severe exacerbations (such as intubation or ICU admission)
  • >= 2 hospital admits or >=3 ED visits past year
  • admit ED visit with the last month
  • Use of >2 canisters/month of β-agonist MDI
  • difficulty perceiving symptoms or severity
  • illicit drug use
  • low socioeconomic status or inner-city residence
  • lack of a written action plan
  • sensitivity to Alternaria
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54
Q

Pharmacology in asthma goals of therapy

2 listed

A

Reducing impairment

Reducing risk

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55
Q

Reducing impairment in Asthma

4 listed

A
  • Prevent chronic and troublesome symptoms
  • maintain (near) normal pulmonary function
  • Maintain normal activity levels
  • Meet pts expectations for asthma care
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56
Q

Reducing risk in asthma

3 listed

A
  • Prevent recurrent exacerbations
  • Prevent progressive loss of lung function
  • Avoid adverse medication side-effects
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57
Q

Medication types for asthma

7 listed

A
  • short-acting β2 agonists
  • long-acting β2 agonists
  • Inhaled steroids
  • Leukotriene modifiers
  • Theophylline
  • Oral steroids for exacerbations
  • Omalizumab
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58
Q

Short-acting β2 agonists

2 listed

A
  • Albuterol
  • Levalbuterol
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59
Q

Long-acting β2 agonists

2 listed

A
  • Salmeterol
  • Formoterol
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60
Q

Inhaled steroids for asthma

4 listed

A
  • Fluticasone
  • budesonide
  • Ciclesonide
  • Mometasone
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61
Q

Leukotriene modifiers

3 listed

A
  • Montelukast
  • Zafilukast
  • Zileutin
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62
Q

Theophylline for asthma

A

?

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63
Q

Oral steroids for asthma

A

for exacerbations

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64
Q

Omalizumab for asthma

A

Xolair injections every 2-4 weeks

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65
Q

Rescue medications for asthma

4 listed

A
  • β2 agonists: Albuterol
  • Used as needed with symptoms or flares or before exercise
  • opens the airway quickly
  • if you use this more than 2 times a week you may need a controller medicine
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66
Q

Controller medication for asthma

5 listed

A
  • inhaled steroids
  • long-acting β2 agonists
  • Cromolyn
  • Leukotriene modifiers
  • Theophylline
67
Q

The rule of twos

5 listed

A

(Who needs controller therapy)

  • Two β-agonist canisters/year
  • Two doses of β-agonists/week
  • Two nocturnal awakenings/month
  • Two unscheduled visits/year
  • Two prednisone bursts/year
68
Q

Asthma medication to treat bronchoconstriction

A
  • β2 agonists
  • Theophylline
69
Q

Asthma medication to treat the inflammation

3 listed

A
  • inhaled steroids
  • Leukotriene modifiers
  • Cromolyn
70
Q

Asthma use of inhaled corticosteroids

A
  • The mainstay of treatment for all asthmatics above mild intermittent disease (symptoms more than 2 times/week)
  • Blocks many of the inflammatory path, ways in asthma
  • Use with a spacer, rinse mouth after use
  • Increase or decrease dose in stepwise manner –may take 3 months for plateau
71
Q

ICS effects in Asthma

72
Q

ICS AKA

A

Inhaled corticosteroids

73
Q

ICS and death from asthma

74
Q

ICS route of administration

75
Q

Severity and initiate treatment in patients

76
Q

Daily medication in persistent asthma

77
Q

Leukotriene modifiers

4 listed

A
  • Anti-inflammatory, affecting cysteinyl leukotriene pathway
  • Effective allow decrease in ICs dosing
  • Decreases exercise induced bronchospasm by 30-50% compared to placebo
  • May be beneficial for true ASA allergic asthmatics
78
Q

Indicators of poor control for treatment of asthma

3 listed

A
  • Nocturnal awakenings
  • urgent care visits
  • increased need for rescue medications
79
Q

Before increasing medication for poor control of asthma consider

4 listed

A
  • inhaler technique
  • Compliance
  • Environmental changes
  • consider other diagnoses
80
Q

Asthma exacerbations

6 listed

A
  • Allergens
  • Respiratory viral infections
  • occupational agents
  • Exercise stress
  • Irritants
  • Aspirin, sulfites
81
Q

Therapy for exacerbations

4 listed

A
  • Steroid therapy
  • Early administration decreases total hospital admissions and relapses
  • Oral vs IV – equal efficacy
  • 125 mg solumedrol IV or 60 mg prednisone PO
82
Q

COPD description

A

A disease state characterized by airflow limitation that is not fully reversible… usually both progressive and associated with an abnormal inflammatory response of the lungs… and systemic manifestations

83
Q

COPD Epidemiology

84
Q

COPD Death rates

85
Q

COPD Pathogenesis

A
  • cigarette smoking is the leading cause of COPD in western countries
  • Burning of bio mass fuels is the leading cause world-wide
86
Q

COPD Pathogenesis mechanisms

87
Q

COPD Pathogenesis repair processes

88
Q

COPD Pathogenesis and smoking cessation

89
Q

Other phenomena of COPD disease progression

A
  • increased oxidative stress
  • Protease-antiprotease imbalance
90
Q

COPD oxidative stress

3 listed

A
  • Oxidative metabolism is over-activated in COPD
  • Bronchial inflammation involving phagocytes (neutrophils & macrophages) adds an internal production of oxidants
  • Anti-oxidants such as the glutathione system and the haemoxygenase (HO)-1 pathway insufficiently counteract oxidative stress
91
Q

COPD Imbalance

4 listed

A
  • proteases are produced by phagocytes within the airways
  • Activity is regulated by anti-proteases such as α1-antitrypsin, secretory leukoprotease inhibitor & tissue inhibitor of metalloproteinases (TIMPs)
  • Cigarette smoke inhibits the activity of antiproteases
  • α1-antitrypsin deficiency is a well-known cause of inherited COPD
92
Q

Overall mechanisms of cigarette-induced lung damage

93
Q

COPD pathophysiology

A
  • the permanent airflow limitation that defines COPD is linked to structural changes
  • Emphysema is characterized by a loss of lung parenchyma with increased apoptosis of endothelial and epithelial alveolar cells
  • pink puffer phenotype
94
Q

Pink puffer phenotype

95
Q

Emphysema is characterized by?

A

a loss of lung parenchyma with increased apoptosis of endothelial and epithelial alveolar cells

96
Q

Blue bloater phenotype

A

smoking-induced COPD

97
Q

Smoking-induced COPD is characterized by?

A
  • squamous cell metaplasia & goblet cell hyperplasia are hallmarks of smoking-induced COPD
  • in proximal and smaller airways the bronchial epithelium is also damaged
  • subepithelial changes also occur
    • basement membrane thickening
    • glands are enlarged & increased in #
    • smooth muscle mass is increased

This is the blue bloater phenotype

98
Q

Risk factors for COPD

10 listed

99
Q

COPD lung function decline

A

only 20-30% of patients who smoke develop COPD however they can develop the other risk factors

100
Q

Lung function decline per year in COPD

101
Q

What is the best way to treat and correct COPD

102
Q

COPD: Lung function and death

103
Q

COPD: Causes of death

A
  • pulmonary
  • cardiovascular
  • cancer
104
Q

COPD diagnosis

105
Q

COPD reversibility

A

usually don’t have any reversibility

106
Q

COPD lung volumes

A

can show hyperinflation (increasing TLC) and air trapping (increasing RV)

107
Q

COPD diffusing capacity

A

Reduced defusing capacity for CO:DLco

108
Q

COPD Physical exam: Blue bloater

109
Q

COPD Physical exam: pink puffer

110
Q

COPD: Lab findings

4 listed

111
Q

Chest X-ray of COPD: emphysema

A
  • hyperinflation
  • lateral flat diaphragm
  • increase in retrosternal airspace
112
Q

Treatment of COPD

113
Q

Therapy for COPD

3 main

A
  • Most important - Smoking cessation
  • Oxygen therapy
  • Drugs - help improve symptoms
114
Q

How reducing environmental and smoking risk factors leads to lung deterioration rates in COPD

115
Q

Short-acting β2 agonists

3 listed

A
  • Albuterol
  • Pirbuterol
  • Levalbuterol
116
Q

Long-acting β2 agonists

5 listed

A
  • Salmeterol
  • Formoterol
  • Aformoterol
  • Olodaterol
  • Vilanterol
117
Q

Short-acting antimuscarinics

A
  • Ipratropium
118
Q

Long-acting antimuscarinics

3 listed

A
  • Tiotropium
  • Aclidinium
  • Umeclidinium
119
Q

Inhaled corticosteroids agents

3 listed

A
  • Budesonide
  • Fluticasone
  • Mometasone
120
Q

phosphodiesterase inhibitors for COPD agents

2 listed

A
  • Roflumilast
  • Theophylline
121
Q

Long-acting β2 agonists effects

5 listed

A
  • Bronchodilation
  • Improved lung emptying during tidal breathing and exertion
  • reduced hyperinflation
  • increased mucociliary transport
  • Mucosal cytoprotection
122
Q

Long-acting antimuscarinic agents onset

A

onset of action 30 minutes and peak 3 hours after dose

123
Q

Long-acting antimuscarinic agents considerations with short-acting antimuscarinics

A

Stop short-acting ipratropium

124
Q

Long-acting antimuscarinic agents effects for COPD

A

Have been shown to decrease exacerbation rate

125
Q

Oxygen therapy for COPD

6 listed

A
  • Improves survival in COPD patients with chronic respiratory failure
  • Prevents the progression of pulmonary hypertension
  • relieves RV failure
  • Improves IQ scores and general alertness
  • Increases walking distance, overall endurance and general conditioning
  • Reverses polycythemia
126
Q

Oral steroids for COPD considerations

A
  • 10 - 20% of COPD patients have a significant response to oral steroids
  • old theory: 2-week steroid trial with documented improvement on PFTs to justify long term use of inhaled steroids
  • effective for acute exacerbation
  • Antibiotics decrease the relapse rate
127
Q

ICS therapy for COPD

A
  • Theoretical advantages for use in COPD however, clinical data was not as convincing
  • Effects on airway inflammation variable
  • No effect on preventing FEV1 decline
  • Possible decrease in the number of exacerbations
128
Q

Side effects of ICS therapy for COPD

A

+ association with hip fractures

129
Q

Stepwise approach for COPD Rx

130
Q

Stepwise approach for COPD Rx GOLD guidelines

131
Q

More GOLD guidelines

132
Q

Pulmonary rehabilitation in COPD

6 listed

A
  • All COPD patients can benefit from exercise training programs
  • Improves exercise tolerance
  • Improves symptoms of dyspnea and fatigue
  • Imporves quality of life measures
  • Reduces hospitalizations and days in the hospital
  • May improve survival
133
Q

Other treatment modalities for COPD

6 listed

A
  • Nutrition
  • Flu vaccine
  • Pneumovax
  • Bullectomy
  • Lung volume reduction surgery
  • Lung transplant
134
Q

Asthma vs COPD

Mast cells

A

Asthma: Increased and activated

COPD: normal

135
Q

Asthma vs COPD

Dendritic cells

A

Asthma: Increased

COPD: Uncertain

136
Q

Asthma vs COPD

Eosinophils

A

Asthma: Increased

COPD: Normal

137
Q

Asthma vs COPD

Neutrophils

A

Asthma: Normal

COPD: Increased

138
Q

Asthma vs COPD

Lymphocytes

A

Asthma: Th2

COPD: Th1, Tc1

139
Q

Asthma vs COPD

Epithelium

A

Asthma: Often shed

COPD: Pseudostratified

140
Q

Asthma vs COPD

Goblet cells

A

Asthma: Increased

COPD: Increased

141
Q

Asthma vs COPD

Airway smooth muscle

A

Asthma: Increased

COPD: Minimal increase

142
Q

Asthma vs COPD

Airway vessels

A

Asthma: Increased

COPD: Not increased

143
Q

Asthma vs COPD Histopathology overview

  • Mast Cells
  • Dendritic cells
  • Eosinophils
  • Neutrophils
  • Lymphocytes
  • Epithelium
  • Goblet cells
  • Airway smooth muscle
  • Airway vessels
144
Q

Asthma age of onset

A

Usually <40 years

145
Q

COPD Age of onset

A

Usually >40 years

146
Q

Asthma smoking Hx

A

Not causal but worsens control

147
Q

COPD smoking Hx

A

Usually >10 pack-years

148
Q

Asthma sputum production

A

Intermittent and variable

149
Q

COPD Sputum production

150
Q

Allergies in Asthma

151
Q

Allergies in COPD

A

Infrequent

152
Q

Asthma clinical symptoms

A

intermittent and variable

153
Q

COPD Clinical symptoms

A

persistent and progressive

154
Q

Asthma course of the disease

A

Stable (with exacerbations)

155
Q

COPD Course of the disease

A

Progressive worsening (with exacerbations)

156
Q

Asthma importance of nonrespiratory comorbid illnesses

A

usually not important

157
Q

COPD importance of nonrespiratory comorbid illnesses

A

Often important

158
Q

Asthma spirometry results

A

Often normalize over time

159
Q

COPD spirometry results

A

May improve but do not normalize over time

160
Q

Asthma vs COPD

  • Age of onset
  • Smoking Hx
  • Sputum production
  • Allergies
  • Clinical symptoms
  • Course of disease
  • Importance of nonrespiratory comorbid illnesses
  • Spirometry results
161
Q

ACOS AKA

A

Asthma-COPD overlap syndrome

162
Q

ACOS

163
Q

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CVPR (93 decks)

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