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820 > COPD & Asthma Patho > Flashcards

COPD & Asthma Patho Flashcards

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

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
  1. Airway Narrowing
  2. Mucus Production
  3. Bronchial Hyperresponsiveness
  4. Airway remodeling
  5. 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

820 (19 decks)

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