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Flashcards in COPD & Asthma Patho Deck (57):
1

Most Common Obstructive Pulmonary Disease

-COPD
-Asthma
-Both decrease capacity for air to leave lungs

2

COPD

-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

Contributing Factors

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

4

COPD Decreased Airflow Mechanisms

Inhales Noxious Particles ===> Chronic Inflammation ==/ Small Airway Disease & Parenchymal Destruction ==> Airflow Limitation

-Changes seen in airways, lung parenchyme, and pulmonary vasculature

5

Small Airway Disease

-Airway inflammation
-Airway fibrosis
-Increased airway resistance

6

Parenchymal Destruction

-Loss of aveolar attachments
-Decrease lung elastic recoil

7

Cells & Mediators

-Inflammatory Cells
-Inflammatory Mediators
-Act complementary and redundant to each other causing widespread destruction

8

COPD - Inflammatory Cells

-Neutrophils, Macrophages, CD8+, lymphocytes
-Release inflammatory mediators
-Interact with structural cells in airways and lung parenchyma

9

COPD - Inflammatory Mediators

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

10

Oxidative Stress

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

11

Protease/Antiprotease Imbalance

-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

COPD - Pathological Change (3)

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

13

Peripheral Airways + COPD

-Cell Changes: increase in macrophages, CD8+, B lymphocytes, and fibroblasts
-Structural Changes: airway wall thickening, inflammatory exudate, airway narrowing

14

Lung Parenchyma + COPD

-Cell Changes: Increase in macrophages, CD8+
-Structural Changes: alveolar wall destruction

15

Pulmonary Vasculature + COPD

-Cell Changes: increase in macrophages, T lymphocytes
-Structural Changes: increase in smooth muscle causing pulmonary hypertension

16

Physiological Abnormalities + COPD

-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

Airway Limitations/Air Trapping + COPD

-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

Pulmonary Function Tests

-Correlates with amount of inflammatory fibrosis
-Also correlates with exudate in small airways

19

Pulmonary Hypertension + COPD

-Late COPD
-Vasoconstriction of small pulmonary arteries
-Progressive pulmonary hypertension can lead to right ventricular hypertrophy and eventually right-side heart failure

20

COPD + Concomitant Chronic Disease

-Skeletal muscle wasting
-Osteoporosis
-Anemia
-CV Disease
-Diabetes
-Metabolic syndrome

21

COPD Exacerbations

-Triggers - infections, environment, pollutants
-Increased inflammation
-Increased dyspnea, some hypoxemia
-Increased hyperinflation causing gas trapping

22

COPD Indications

**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

COPD Assessment

-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

Spirometry Abnormalities

-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