COPD & Asthma Patho Flashcards
1
Q
Most Common Obstructive Pulmonary Disease
A
- COPD
- Asthma
- Both decrease capacity for air to leave lungs
2
Q
COPD
A
- Leading cause of morbidity/mortality
- Common, preventable, treatable
- Persistent respiratory symptoms and airflow limitations
- Usually from exposure to noxious particles/gases
- Exacerbations and comorbidities contribute to severity
- Generally progressive and not same for everyone (especially if people don’t decrease exposure)
- Once developed, CANNOT be cured
3
Q
Contributing Factors
A
- Asthma
- Genes
- Infections
- Age & Gender
- Lung Growth & Development
- Particle exposure
- Socioeconomic status
4
Q
COPD Decreased Airflow Mechanisms
A
Inhales Noxious Particles ===> Chronic Inflammation ==/ Small Airway Disease & Parenchymal Destruction ==> Airflow Limitation
-Changes seen in airways, lung parenchyme, and pulmonary vasculature
5
Q
Small Airway Disease
A
- Airway inflammation
- Airway fibrosis
- Increased airway resistance
6
Q
Parenchymal Destruction
A
- Loss of aveolar attachments
- Decrease lung elastic recoil
7
Q
Cells & Mediators
A
- Inflammatory Cells
- Inflammatory Mediators
- Act complementary and redundant to each other causing widespread destruction
8
Q
COPD - Inflammatory Cells
A
- Neutrophils, Macrophages, CD8+, lymphocytes
- Release inflammatory mediators
- Interact with structural cells in airways and lung parenchyma
9
Q
COPD - Inflammatory Mediators
A
- TNF-alpha, interleukin 8, leukotriene By
- Attract inflammatory cells from circulation
- Amplify inflammation process
- Induce structural changes
10
Q
Oxidative Stress
A
- Amplifying mechanism
- Noxious gas/particles create reactive oxygen species
- These react with protein, lipids, and DNA causing cell injury
11
Q
Protease/Antiprotease Imbalance
A
- Amplifying mechanism
- Antiprotease prevents protease breakdown
- Protease breaks down connective tissue
- Increased protease occurs in COPD from inflammatory and epithelial cells
- Protease mediated destruction of elastin in connective tissue of lung parenchyma then occurs
12
Q
COPD - Pathological Change (3)
A
- Peripheral airways (bronchioles <2 mm)
- Lung parenchyma (bronchioles and alveoli)
- Pulmonary vasculature
13
Q
Peripheral Airways + COPD
A
- Cell Changes: increase in macrophages, CD8+, B lymphocytes, and fibroblasts
- Structural Changes: airway wall thickening, inflammatory exudate, airway narrowing
14
Q
Lung Parenchyma + COPD
A
- Cell Changes: Increase in macrophages, CD8+
- Structural Changes: alveolar wall destruction
15
Q
Pulmonary Vasculature + COPD
A
- Cell Changes: increase in macrophages, T lymphocytes
- Structural Changes: increase in smooth muscle causing pulmonary hypertension
16
Q
Physiological Abnormalities + COPD
A
- Develops with disease progression
- Airway limitations and air trapping
- Gas exchange abnormalities from parenchymal destruction
- Gas transfer worsens as disease progresses causing hypoxemia and hypercapnia
- Mucus hypersecretion - NOT in all patients, from increase in goblet cells, enlarged submucosal glands
- Pulmonary Hypertension
17
Q
Airway Limitations/Air Trapping + COPD
A
- Peripheral airway limitation
- Decreased inspiratory capacity
- Dyspnea & limitation of exercise capacity
- Decreased lung volumes
- Correlates with forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC)
18
Q
Pulmonary Function Tests
A
- Correlates with amount of inflammatory fibrosis
- Also correlates with exudate in small airways
19
Q
Pulmonary Hypertension + COPD
A
- Late COPD
- Vasoconstriction of small pulmonary arteries
- Progressive pulmonary hypertension can lead to right ventricular hypertrophy and eventually right-side heart failure
20
Q
COPD + Concomitant Chronic Disease
A
- Skeletal muscle wasting
- Osteoporosis
- Anemia
- CV Disease
- Diabetes
- Metabolic syndrome
21
Q
COPD Exacerbations
A
- Triggers - infections, environment, pollutants
- Increased inflammation
- Increased dyspnea, some hypoxemia
- Increased hyperinflation causing gas trapping
22
Q
COPD Indications
A
- *IF the following is present in 40+ y.o.**
- Dyspnea - progressive and persistent, worse with exercise
- Chronic cough - first symptoms, often discounted, may be intermittent and unproductive
- Chronic sputum production - any pattern
- Family history
- Expose to risk factors
23
Q
COPD Assessment
A
- Current level of symptoms - use validated questionnaire (CAT, mMRC)
- Severity of spirometric abnormality
- Exacerbation risk increased with worsening airflow limitation and history of previous exacerbations
- Presence of comorbidities - routinely looked for and treated
24
Q
Spirometry Abnormalities
A
- Diagnosis
- Decrease in pulmonary function tests with disease progression
- Decrease in FEV1
- Decrease in FEV1:FVC - Normal is >0.7, if bronchodilatory FEV1:FVC < 0.7 = COPD
25
Q
GOLD Levels
A
- COPD Assessment
- GOLD 1: Mild - FEV1 >= 80%
- GOLD2: Moderate - FEV1 is 50-79%
- GOLD3: Severe - FEV1 is 30-49%
- GOLD4: Very severe - FEV1< 30%
26
Q
COPD Grouping
A
- Group A - 0-1 moderate exacerbations with NO hospitalizations + mMRC 0-1 or CAT < 10
- Group B - 0-1 moderate exacerbations with NO hospitalizations + mMRC >= 2 or CAT >= 10
- Group C - >=2 moderate exacerbations or >=1 hospitalizations + mMRC 0-1 or CAT < 10
- Group D - >=2 moderate exacerbations or >=1 hospitalizations + mMRC >= 2 or CAT >= 10
27
Q
COPD Management Goals
A
- Prevent disease progression
- Relieve symptoms
- Improve exercise tolerance
- Improve health status
- Decrease exacerbations
- Decrease mortality
- Prevent/minimize SE from treatment
28
Q
Smoking Cessation
A
- KEY in treatment
- Most effective and cost-effective intervention to decrease COPD and stop progression
- Significantly slows disease
29
Q
Non-Pharm + COPD
A
- Physical activity - recommended for ALL with COPD
- Pulmonary rehab - Groups B-D
- Vaccinations - Flu, pneumonia, for ALL groups
30
Q
Pharm Treatment Effects + COPD
A
- Decrease symptoms
- Decrease exacerbations
- Improve health status
- Improve exercise tolerance
31
Q
Pharm Treatment + Group A
A
Bronchodilator
32
Q
Pharm Treatment + Group B
A
Long-acting Bronchodilator
33
Q
Pharm Treatment + Group C
A
Long-acting anticholinergic
34
Q
Pharm Treatment + Group D
A
-Long-acting anticholinergic +/- long-acting Beta-2 agonist
OR
-Long-acting Beta-2 agonist + Inhaled corticosteroid
35
Q
Oxygen Administration
A
- Increases survival when given long term
- With severe resting hypoxemia
- > 15 hours/day
36
Q
COPD Caused Death
A
- CV Disaese
- Lung Cancer
- Respiratory failure
37
Q
Asthma
A
- 7.7% of adults and 8.4% of children have disease
- ~3500 deaths/year
- Can occur at anytime BUT usually diagnosed at childhood
- Chronic inflammatory disorder
38
Q
Asthma + Host Factors
A
- Genes
- Obesity
- Gender
- Early growth characterisitics
39
Q
Asthma + Environmental Factors
A
- Allergens
- Occupational sensitizers
- Infections
- Socioeconmic inequalities
- Exposure to tobacco smoke
- Air pollution
- Diet
- Stress
40
Q
Asthma Pathophysiology
A
- Inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing
- Inflammation causes bronchial hyperresponsiveness (BHR)
- Airway obstruction - related to bronchospasm, edema, mucus hypersecretion
Cascade with many cells and mediators
41
Q
Asthma + Cells
A
- Lymphocytes - Th1 and Th2 cells
- Generation of IL-4, IL-5, IL-13 which mediates eosinophil inflammation and IgE production by B lymphocytes
- Mast cells - release bronchoconstrictors (cysteinyl, leukotrienes, histamines, PGD2)
- Eosinophil - increased number of airways of most with asthma
- Neutrophils - increased in airways and sputum of patients with severe asthma and in patients with asthma who smoke
42
Q
Asthma + Mediators
A
- Histamine - bronchoconstriction and inflammatory response
- Leukotrienes - bronchoconstriction, pro-inflammatory
- Cytokines - pro-inflammatory
- Chemokines, nitric oxide, PGD2
43
Q
Chronic Inflammation Consequences
A
- Airway Narrowing
- Mucus Production
- Bronchial Hyperresponsiveness
- Airway remodeling
- Increased NO
44
Q
Airway Narrowing
A
- Smooth muscle contraction
- Response to bronchoconstriction mediators
- Largely reversed by bronchodilators
- Airway edema from microvascular leakage in response to inflammatory mediators
45
Q
Mucus Production
A
- Produced by bronchial epithelial and goblet cells
- Bronchial glands - increased in size
- Goblet cells - increased in size and number
- Tends to be highly viscous
46
Q
Bronchial Hyperresponsiveness
A
- Exaggerated bronchoconstriction response to stimuli that isn’t dangerous for normal people
- Often used to diagnose asthma
- Inflammation - major factor to determine the degree of hyperresponsiveness
47
Q
Airway Remodeling
A
- May be irreversible
- Thickening of sub-epithelial reticular basement membrane
- Increased airway smooth muscle mass
- Mucus gland hyperplasia/hypersecretion
48
Q
Increase NO
A
- Produced by cell in respiratory tract
- Induced in response to pro-inflammatory cells
- Appears to amplify inflammation process
- May be useful to measure ongoing lower airway inflammation
49
Q
Asthma Clinical Manifestations
A
- Varies between patients
- Symptom free between attacks
- Attacks: dyspnea, chest tightness, coughing, wheezing
- Airway inflammation is a constant (even when asymptomatic)
- Air becomes trapped behind occluded and narrowed airways (hyperinflation)
- Increased energy needed to overcome tension and maintain ventilation (dyspnea, fatigue, coughing)
- Increase respiratory rate
- Increased expiration
- Wheezing
50
Q
Obesity + Asthma
A
- Increased prevalence of asthma
- Factors: mechanical changes, development of pro-inflammatory state, increased comorbidity prevalence
- Usually precedes asthma developmentally
51
Q
Exercise-Induced Bronchoconstrictor (EIB)
A
- 60-70% of people with asthma have this
- Increased ventilation leading to increased osmolality in airway lining fluid
- Mast cells triggered to release mediators resulting in bronchoconstriction
52
Q
Nocturnal Asthma
A
- Worse asthma in sleep
- Significant decrease in pulmonary function between bedtime and awakening
- Pathogenesis is unknown with diurnal patterns of endogenous cortisol secretion and circulating epinephrine
53
Q
Asthma Exacerbations
A
- Short-term worsening: trigger exposure
- Increased inflammation, airway edema, excessive accumulation of mucus, severe bronchospasm
- Result in profound airway narrowing
- Usually poorly responds to bronchodilation therapy
54
Q
Smoking + Asthma
A
- Neutrophil predominantly in inflammation
- Poorly responds to corticosteroids
55
Q
Drugs + Mechanisms
A
- Inflammation ==> Anti-inflammatory
- Bronchoconstriction ==> Beta-2 agonist
- Usually inhaled
56
Q
COPD Summary
A
- Cells: CD8+, T-lymph, neutrophils, macrophages
- Mediators: IL8, TNF-alpha
- Small bronchodilation response
- Poor response to steroids
57
Q
Asthma Summary
A
- Cells: CD4+, T-cells, eosinophils, mast cells
- Mediators: IL-4, IL-5, IL-13
- Large bronchodilator response
- Good response to steroids
