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COPD & Asthma Patho Flashcards

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1
Q

Most Common Obstructive Pulmonary Disease

A
  • COPD
  • Asthma
  • Both decrease capacity for air to leave lungs
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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
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3
Q

Contributing Factors

A
  • Asthma
  • Genes
  • Infections
  • Age & Gender
  • Lung Growth & Development
  • Particle exposure
  • Socioeconomic status
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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

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5
Q

Small Airway Disease

A
  • Airway inflammation
  • Airway fibrosis
  • Increased airway resistance
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6
Q

Parenchymal Destruction

A
  • Loss of aveolar attachments

- Decrease lung elastic recoil

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7
Q

Cells & Mediators

A
  • Inflammatory Cells
  • Inflammatory Mediators
  • Act complementary and redundant to each other causing widespread destruction
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8
Q

COPD - Inflammatory Cells

A
  • Neutrophils, Macrophages, CD8+, lymphocytes
  • Release inflammatory mediators
  • Interact with structural cells in airways and lung parenchyma
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9
Q

COPD - Inflammatory Mediators

A
  • TNF-alpha, interleukin 8, leukotriene By
  • Attract inflammatory cells from circulation
  • Amplify inflammation process
  • Induce structural changes
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10
Q

Oxidative Stress

A
  • Amplifying mechanism
  • Noxious gas/particles create reactive oxygen species
  • These react with protein, lipids, and DNA causing cell injury
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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
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12
Q

COPD - Pathological Change (3)

A
  1. Peripheral airways (bronchioles <2 mm)
  2. Lung parenchyma (bronchioles and alveoli)
  3. Pulmonary vasculature
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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
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14
Q

Lung Parenchyma + COPD

A
  • Cell Changes: Increase in macrophages, CD8+

- Structural Changes: alveolar wall destruction

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15
Q

Pulmonary Vasculature + COPD

A
  • Cell Changes: increase in macrophages, T lymphocytes

- Structural Changes: increase in smooth muscle causing pulmonary hypertension

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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
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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)
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18
Q

Pulmonary Function Tests

A
  • Correlates with amount of inflammatory fibrosis

- Also correlates with exudate in small airways

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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
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20
Q

COPD + Concomitant Chronic Disease

A
  • Skeletal muscle wasting
  • Osteoporosis
  • Anemia
  • CV Disease
  • Diabetes
  • Metabolic syndrome
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21
Q

COPD Exacerbations

A
  • Triggers - infections, environment, pollutants
  • Increased inflammation
  • Increased dyspnea, some hypoxemia
  • Increased hyperinflation causing gas trapping
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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
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23
Q

COPD Assessment

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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

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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
GOLD Levels
- 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
COPD Grouping
- 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
COPD Management Goals
- Prevent disease progression - Relieve symptoms - Improve exercise tolerance - Improve health status - Decrease exacerbations - Decrease mortality - Prevent/minimize SE from treatment
28
Smoking Cessation
- KEY in treatment - Most effective and cost-effective intervention to decrease COPD and stop progression - Significantly slows disease
29
Non-Pharm + COPD
- Physical activity - recommended for ALL with COPD - Pulmonary rehab - Groups B-D - Vaccinations - Flu, pneumonia, for ALL groups
30
Pharm Treatment Effects + COPD
- Decrease symptoms - Decrease exacerbations - Improve health status - Improve exercise tolerance
31
Pharm Treatment + Group A
Bronchodilator
32
Pharm Treatment + Group B
Long-acting Bronchodilator
33
Pharm Treatment + Group C
Long-acting anticholinergic
34
Pharm Treatment + Group D
-Long-acting anticholinergic +/- long-acting Beta-2 agonist OR -Long-acting Beta-2 agonist + Inhaled corticosteroid
35
Oxygen Administration
- Increases survival when given long term - With severe resting hypoxemia - >15 hours/day
36
COPD Caused Death
- CV Disaese - Lung Cancer - Respiratory failure
37
Asthma
- 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
Asthma + Host Factors
- Genes - Obesity - Gender - Early growth characterisitics
39
Asthma + Environmental Factors
- Allergens - Occupational sensitizers - Infections - Socioeconmic inequalities - Exposure to tobacco smoke - Air pollution - Diet - Stress
40
Asthma Pathophysiology
- 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
Asthma + Cells
- 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
Asthma + Mediators
- Histamine - bronchoconstriction and inflammatory response - Leukotrienes - bronchoconstriction, pro-inflammatory - Cytokines - pro-inflammatory - Chemokines, nitric oxide, PGD2
43
Chronic Inflammation Consequences
1. Airway Narrowing 2. Mucus Production 3. Bronchial Hyperresponsiveness 4. Airway remodeling 5. Increased NO
44
Airway Narrowing
- Smooth muscle contraction - Response to bronchoconstriction mediators - Largely reversed by bronchodilators - Airway edema from microvascular leakage in response to inflammatory mediators
45
Mucus Production
- 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
Bronchial Hyperresponsiveness
- 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
Airway Remodeling
- May be irreversible - Thickening of sub-epithelial reticular basement membrane - Increased airway smooth muscle mass - Mucus gland hyperplasia/hypersecretion
48
Increase NO
- 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
Asthma Clinical Manifestations
- 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
Obesity + Asthma
- Increased prevalence of asthma - Factors: mechanical changes, development of pro-inflammatory state, increased comorbidity prevalence - Usually precedes asthma developmentally
51
Exercise-Induced Bronchoconstrictor (EIB)
- 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
Nocturnal Asthma
- 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
Asthma Exacerbations
- 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
Smoking + Asthma
- Neutrophil predominantly in inflammation | - Poorly responds to corticosteroids
55
Drugs + Mechanisms
- Inflammation ==> Anti-inflammatory - Bronchoconstriction ==> Beta-2 agonist - Usually inhaled
56
COPD Summary
- Cells: CD8+, T-lymph, neutrophils, macrophages - Mediators: IL8, TNF-alpha - Small bronchodilation response - Poor response to steroids
57
Asthma Summary
- Cells: CD4+, T-cells, eosinophils, mast cells - Mediators: IL-4, IL-5, IL-13 - Large bronchodilator response - Good response to steroids
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