CVPR Week 5: Obstructive Airway Disease Flashcards
(163 cards)
1
Q
Objectives
A
2
Q
Common obstructive lung diseases
5 listed
A
- Asthma
- Emphysema (COPD)
- Chronic bronchitis (COPD)
- Bronchiectasis
- Cystic fibrosis
3
Q
Asthma type of lung disease
A
Obstructive lung disease with reversible airflow obstruction
4
Q
Asthma types
A
different phenotypes
5
Q
Asthma inflammation
A
Inflammation is prominent
6
Q
Emphysema lung disease type
A
Obstructive “COPD” permanent enlargement/destruction of the respiratory bronchioles
7
Q
Chronic bronchitis lung disease type
A
“COPD” Sputum production 3 months/year for 2 years
8
Q
The less common obstructive lung diseases
2 listed
A
- Bronchiectasis
- Cystic fibrosis
9
Q
Bronchiectasis description
A
Enlarged airways and tortuous blood vessels (bronchial arteries) resulting from chronic infection
10
Q
Cystic fibrosis description
3 listed
A
- Hereditary disease
- multiple gene mutations
- bronchiectasis with chronic respiratory infections with a failure to thrive
11
Q
The most common obstructive lung diseases
3 listed
A
- Asthma
- Emphysema (COPD)
- Chronic Bronchitis (COPD)
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
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
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
15
Q
Types of bronchiectasis
3 listed
A
16
Q
What kind of bronchiectasis is this?
A
cylindrical bronchiectasis
17
Q
What kind of bronchiectasis is this?
A
cystic bronchiectasis
18
Q
What kind of bronchiectasis is this?
A
This is actually normal
19
Q
What kind of bronchiectasis is this?
A
Varicose bronchiectasis
20
Q
What is this?
A
bronchiectasis
21
Q
Obstructive ventilatory defect definition
A
essentially means that Forced Expiratory volume is decreased compared to the Forced vital capacity
22
Q
The earliest changes associated with airflow obstruction are in?
A
The small airways
23
Q
Changes on the flow-volume curve associated with airflow obstruction
A
24
Q
COPD classification by severity
A
25
COPD is classified as
FEV1/FVC = \< 0.7
26
Asthma Definition
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
27
Asthma diagnosis
3 listed
* 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
28
Asthma clinical features
5 listed
* Wheezing
* SOB
* Cough
* Chest tightness
* Variable Peak Expiratory Flow Rates (PEFR)
29
Asthma epidemiology
4 things listed
* 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
30
Asthma pathophysiology between phenotypes
* 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
31
Asthma phenotypes
5 listed
* Intermittent
* persistent
* exercise-associated
* aspirin-sensitive
* severe asthma
32
Asthma pathophysiology: Cells involved
6 listed
* T lymphocytes (Th2)
* Mast cells
* Eosinophils
* Macrophages
* Neutrophils
* Epithelial Cells
33
Asthma pathophysiology: T lymphocyte involvement
produce cytokines IL-4, IL-5, IL-13
34
Asthma pathophysiology: Mast cell involvement
* mediators of bronchoconstriction (histamine, cysteinyl-leukotrienes, prostaglandin D2)
35
Asthma pathophysiology: Eosinophil involvement
3 listed
* 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
36
Asthma pathophysiology: Macrophages involvement
2 listed
* most numerous cells in the airways
* can be activated by allergens to release inflammatory mediators and cytokines that amplify the inflammatory response
37
Asthma pathophysiology: Neutrophil involvement
* pathophysiological role remains uncertain
38
Asthma pathophysiology: Epithelial cell involvement
they produce more inflammatory mediators
39
Asthma pathophysiology diagram
40
Asthma pathophysiology diagram 2
41
Asthma pathophysiology diagram 3
42
Asthma pathophysiology main components of pathology
2 listed
* smooth muscle dysfunction
* airway inflammation
43
Asthma Smooth muscle dysfunction leads to?
4 listed
* Bronchoconstriction
* bronchial hyperreactivity
* hypertrophy/hyperplasia
* inflammatory mediator release
44
Asthma airway inflammation leads to?
45
Asthma smooth muscle dysfunction and airway inflammation leads to?
symptoms/exacerbations and disease progression
46
Asthma pathophysiology Acute response
4 listed
* Bronchoconstriction
* Edema
* Secretions
* Cough
47
Asthma pathophysiology: Chronic inflammation
3 listed
* Cell recruitment
* epithelial damage
* early structural changes
48
Asthma pathophysiology: Airway remodeling
3 listed
* cellular proliferation
* extracellular matrix increase
* structural changes
49
Epithelial damage in asthma
50
Intrinsic factors affecting disease expression of Asthma
* genetics of disease
* Duration of asthma
* severity of childhood asthma
* Gender
* Response to therapy
51
Extrinsic factors affecting disease expression of Asthma
9 listed
* Viral infections
* Allergen exposure
* \Airway irritants
* Exercise
* Compliance
* Season
* Time of day
* Occupational (10-15% of adult asthma)
* Western lifestyle i.e. obesity
52
Asthma comorbidities that worsen the asthma
4 listed
* GERD-association with asthma 15 - 40 % prevalence
* Sinusitis/Allergic Rhinitis
* Illicit drug use -- cocaine
* Non-compliance
53
Risk factors for death from asthma
* 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
54
Pharmacology in asthma goals of therapy
2 listed
Reducing impairment
Reducing risk
55
Reducing impairment in Asthma
4 listed
* Prevent chronic and troublesome symptoms
* maintain (near) normal pulmonary function
* Maintain normal activity levels
* Meet pts expectations for asthma care
56
Reducing risk in asthma
3 listed
* Prevent recurrent exacerbations
* Prevent progressive loss of lung function
* Avoid adverse medication side-effects
57
Medication types for asthma
7 listed
* short-acting β2 agonists
* long-acting β2 agonists
* Inhaled steroids
* Leukotriene modifiers
* Theophylline
* Oral steroids for exacerbations
* Omalizumab
58
Short-acting β2 agonists
2 listed
* Albuterol
* Levalbuterol
59
Long-acting β2 agonists
2 listed
* Salmeterol
* Formoterol
60
Inhaled steroids for asthma
4 listed
* Fluticasone
* budesonide
* Ciclesonide
* Mometasone
61
Leukotriene modifiers
3 listed
* Montelukast
* Zafilukast
* Zileutin
62
Theophylline for asthma
?
63
Oral steroids for asthma
for exacerbations
64
Omalizumab for asthma
Xolair injections every 2-4 weeks
65
Rescue medications for asthma
4 listed
* 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
66
Controller medication for asthma
5 listed
* inhaled steroids
* long-acting β2 agonists
* Cromolyn
* Leukotriene modifiers
* Theophylline
67
The rule of twos
5 listed
(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
Asthma medication to treat bronchoconstriction
* β2 agonists
* Theophylline
69
Asthma medication to treat the inflammation
3 listed
* inhaled steroids
* Leukotriene modifiers
* Cromolyn
70
Asthma use of inhaled corticosteroids
* 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
ICS effects in Asthma
72
ICS AKA
Inhaled corticosteroids
73
ICS and death from asthma
74
ICS route of administration
75
Severity and initiate treatment in patients
76
Daily medication in persistent asthma
77
Leukotriene modifiers
4 listed
* 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
Indicators of poor control for treatment of asthma
3 listed
* Nocturnal awakenings
* urgent care visits
* increased need for rescue medications
79
Before increasing medication for poor control of asthma consider
4 listed
* inhaler technique
* Compliance
* Environmental changes
* consider other diagnoses
80
Asthma exacerbations
6 listed
* Allergens
* Respiratory viral infections
* occupational agents
* Exercise stress
* Irritants
* Aspirin, sulfites
81
Therapy for exacerbations
4 listed
* 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
COPD description
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
COPD Epidemiology
84
COPD Death rates
85
COPD Pathogenesis
* cigarette smoking is the leading cause of COPD in western countries
* Burning of bio mass fuels is the leading cause world-wide
86
COPD Pathogenesis mechanisms
87
COPD Pathogenesis repair processes
88
COPD Pathogenesis and smoking cessation
89
Other phenomena of COPD disease progression
* increased oxidative stress
* Protease-antiprotease imbalance
90
COPD oxidative stress
3 listed
* 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
COPD Imbalance
4 listed
* 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
Overall mechanisms of cigarette-induced lung damage
93
COPD pathophysiology
* 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
Pink puffer phenotype
Emphysema
95
Emphysema is characterized by?
a loss of lung parenchyma with increased apoptosis of endothelial and epithelial alveolar cells
96
Blue bloater phenotype
smoking-induced COPD
97
Smoking-induced COPD is characterized by?
* 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
Risk factors for COPD
10 listed
99
COPD lung function decline
only 20-30% of patients who smoke develop COPD however they can develop the other risk factors
100
Lung function decline per year in COPD
101
What is the best way to treat and correct COPD
102
COPD: Lung function and death
103
COPD: Causes of death
* pulmonary
* cardiovascular
* cancer
104
COPD diagnosis
105
COPD reversibility
usually don't have any reversibility
106
COPD lung volumes
can show hyperinflation (increasing TLC) and air trapping (increasing RV)
107
COPD diffusing capacity
Reduced defusing capacity for CO:DLco
108
COPD Physical exam: Blue bloater
109
COPD Physical exam: pink puffer
110
COPD: Lab findings
4 listed
111
Chest X-ray of COPD: emphysema
* hyperinflation
* lateral flat diaphragm
* increase in retrosternal airspace
112
Treatment of COPD
113
Therapy for COPD
3 main
* Most important - Smoking cessation
* Oxygen therapy
* Drugs - help improve symptoms
114
How reducing environmental and smoking risk factors leads to lung deterioration rates in COPD
115
Short-acting β2 agonists
3 listed
* Albuterol
* Pirbuterol
* Levalbuterol
116
Long-acting β2 agonists
5 listed
* Salmeterol
* Formoterol
* Aformoterol
* Olodaterol
* Vilanterol
117
Short-acting antimuscarinics
* Ipratropium
118
Long-acting antimuscarinics
3 listed
* Tiotropium
* Aclidinium
* Umeclidinium
119
Inhaled corticosteroids agents
3 listed
* Budesonide
* Fluticasone
* Mometasone
120
phosphodiesterase inhibitors for COPD agents
2 listed
* Roflumilast
* Theophylline
121
Long-acting β2 agonists effects
5 listed
* Bronchodilation
* Improved lung emptying during tidal breathing and exertion
* reduced hyperinflation
* increased mucociliary transport
* Mucosal cytoprotection
122
Long-acting antimuscarinic agents onset
onset of action 30 minutes and peak 3 hours after dose
123
Long-acting antimuscarinic agents considerations with short-acting antimuscarinics
Stop short-acting ipratropium
124
Long-acting antimuscarinic agents effects for COPD
Have been shown to decrease exacerbation rate
125
Oxygen therapy for COPD
6 listed
* 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
Oral steroids for COPD considerations
* 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
ICS therapy for COPD
* 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
Side effects of ICS therapy for COPD
+ association with hip fractures
129
Stepwise approach for COPD Rx
130
Stepwise approach for COPD Rx GOLD guidelines
131
More GOLD guidelines
132
Pulmonary rehabilitation in COPD
6 listed
* 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
Other treatment modalities for COPD
6 listed
* Nutrition
* Flu vaccine
* Pneumovax
* Bullectomy
* Lung volume reduction surgery
* Lung transplant
134
Asthma vs COPD
Mast cells
Asthma: Increased and activated
COPD: normal
135
Asthma vs COPD
Dendritic cells
Asthma: Increased
COPD: Uncertain
136
Asthma vs COPD
Eosinophils
Asthma: Increased
COPD: Normal
137
Asthma vs COPD
Neutrophils
Asthma: Normal
COPD: Increased
138
Asthma vs COPD
Lymphocytes
Asthma: Th2
COPD: Th1, Tc1
139
Asthma vs COPD
Epithelium
Asthma: Often shed
COPD: Pseudostratified
140
Asthma vs COPD
Goblet cells
Asthma: Increased
COPD: Increased
141
Asthma vs COPD
Airway smooth muscle
Asthma: Increased
COPD: Minimal increase
142
Asthma vs COPD
Airway vessels
Asthma: Increased
COPD: Not increased
143
Asthma vs COPD Histopathology overview
* Mast Cells
* Dendritic cells
* Eosinophils
* Neutrophils
* Lymphocytes
* Epithelium
* Goblet cells
* Airway smooth muscle
* Airway vessels
144
Asthma age of onset
Usually \<40 years
145
COPD Age of onset
Usually \>40 years
146
Asthma smoking Hx
Not causal but worsens control
147
COPD smoking Hx
Usually \>10 pack-years
148
Asthma sputum production
Intermittent and variable
149
COPD Sputum production
Common
150
Allergies in Asthma
Common
151
Allergies in COPD
Infrequent
152
Asthma clinical symptoms
intermittent and variable
153
COPD Clinical symptoms
persistent and progressive
154
Asthma course of the disease
Stable (with exacerbations)
155
COPD Course of the disease
Progressive worsening (with exacerbations)
156
Asthma importance of nonrespiratory comorbid illnesses
usually not important
157
COPD importance of nonrespiratory comorbid illnesses
Often important
158
Asthma spirometry results
Often normalize over time
159
COPD spirometry results
May improve but do not normalize over time
160
Asthma vs COPD
* Age of onset
* Smoking Hx
* Sputum production
* Allergies
* Clinical symptoms
* Course of disease
* Importance of nonrespiratory comorbid illnesses
* Spirometry results
161
ACOS AKA
Asthma-COPD overlap syndrome
162
ACOS
163
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