Asthma/COPD Patho Flashcards

1
Q

COPD

A

Preventable, common, Treatable
Persistent Respiratory symptoms and airflow limitation
Caused by exposure to noxious particles or gases
Exacerbation and Cormobidities contribute to severity.
ONCE DEVELOPED, CANNOT BE CURED

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2
Q

Factors that Influence COPD

A

Particle exposure, Genes, asthma, lung growth/development, age/gender, infections, Socioeconomic status.

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3
Q

Inflammatory Cells

A

Neutrophils, Macrophages, CD8 lymphocytes

Release inflammatory mediators and interact with the structural cells in airways and lung parenchyma.

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4
Q

Inflammatory Mediatiors

A

TNF alpha, Interleukin 8 and leukotriene B4

Attract inflammatory cells from circulation, amplify inflammatory process, induce structural changes

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5
Q

Protease break down

A

Increase proteases in COPD Patients from inflammatory and epithelial cells.

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6
Q

Protease Destruction of elastin

A

Major connective tissue in lung parenchyma

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7
Q

Peripherial Airway Limitation

A

Reduces inspiratory capacity. Dyspena/ limitation of exercise capacity and reduction in lung volumes. Correlated with forced expiratory volume.

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8
Q

Physiologial abnormalities/ symptoms of COPD

A

Gas exchange abnormalities

Possible low oxygen in blood (hypoxemia) and increased CO2 in blood (Hypercapnia)

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9
Q

Mucus Hypersecretion

A

Increased goblet cells and enlarged submucosal glands

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10
Q

Pulmonary Hypertension

A

Vasoconstriction of small pulmonary arteries

may lead to right ventricular hypertrophy and then to right side cardiac failure.

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11
Q

concomitant chronic diseases of COPD

A
Skeletal muscle wasting
Osteoporosis
Anemia
CVD
Diabetes
Metabolic syndrome
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12
Q

Exacerbations of COPD

A

Triggers (Infections and enviornmental pollutants)
Increased Inflammation
Dyspnea, Hypoxemia
Increased hyperinflation and gas trapping

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13
Q

Goals of COPD management

A
Prevent disease progression
§ Relieve symptoms
§ Improve exercise tolerance
§ Improve health status
§ Reduce exacerbations
§ Reduce mortality
§ Prevent or minimize side effects from
treatment
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14
Q

Treatment of COPD Pharm and NONpharm

A

Helps to get exercise
Pulmonary Rehab which includes groups B-D
Vaccines

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15
Q

Group A COPD

A

Bronchodilator

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16
Q

Group B COPD

A

Long acting Bronchodilator

17
Q

Group C COPD

A

Long acting anticholinergic

18
Q

Group D COPD

A

Long acting anticholinergic +/- Long acting Beta 2 agonist
Or
Long acting Beta 2 agonist+/- inhaled corticosteroid

19
Q

Does long term oxygen been shown to help?

A

Yes with pts with severe resting hypoxemia greater than 15 hours per day

20
Q

Death By COPD

A

CVD, Lung cancer, and respiratory failure

21
Q

Asthma definition

A

Chronic inflammatory Disorder that involves interactions between host and environment

22
Q

Host factors for asthma

A

Genes, Obesity, gender, and early growth characteristics

23
Q

Enviornmental Exposures to Asthma

A
Allergens
• Occupational sensitizers
• Infections
• Socioeconomic
inequalities
• Exposure to tobacco
smoke
• Air pollution
• Diet
• Stress
24
Q

Asthma Pathophysiology

A

Inflammation causes recurrent episodes of wheezing, SOB, Breathlessness, chest tightness and coughing.
Inflammation causes Bronchial Hyperresponsivenes and can lead to airway obstruction.

25
Mast Cells Asthma
Release bronchoconstrictor mediatiors | Cysteinyl leukotrienes histamine, PGD2
26
Eosinophils Asthma
Increased numbers of the cells in airways of most people with asthma. Possible marker
27
Neutrophils Asthma
Increased numbers of cells in airways and sputum with severe asthma and pts with asthma that smoke
28
Airway narrowing Asthma
Smooth Muscle Contraction Response to Bronchoconstrictor mediators. reversed by bronchodilators Airway edema Micro vascular leakage in response to inflammatory mediators.
29
Bronchial Hyperresponsiveness
Exaggerated Bronchoconstriction response to stimuli that is innocuous to a healthy person. Used to diagnose asthma Inflammation is a major factor in determining the degree of airway hyperresponsiveness
30
Airway remodeling
Possibly an irreversible process. Thickening of sub-epithelial reticular BM Increase in airway smooth muscle mass mucus gland hyperplasia and hypersecretion.
31
Nitric Oxide
Produced in the respiratory tract Induced in pro inflammatory cells amplifies inflammatory process Useful measurement of ongoing lower airway inflammation