COPD Flashcards

1
Q

COPD

A
chronic obstructive pulmonary disease
>limitation of airflow through lungs
*preventable and treatable
*not fully reversible
>progressive
>pulmonary inflammatory response to noxious particles or gases
>eventually systemic symptoms develop
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2
Q

COPD II

A
chronic bronchitis
*upper airway problem
emphysema
*lower alveolar destruction
These conditions co-exist
*goal: maintain oxygenation and tissue perfusion
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3
Q

Incidence and prevalence of COPD:

A

> 12.1 million americans have COPD >18ys old
4th leading cause mortality in U.S. more common in men
women with COPD on rise
highest incidence in white amercians
more than 50% die within 10 years of diagnosis
predicted to become 3rd leading cause of death worldwide by 2020
primary cause-cigarette smoking

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4
Q

Pathophysiology of COPD:

A

> primary disease process is chronic inflammation
*airways, pulmonary blood vessels, lung parenchyma
inhalation of noxious particles (how disease starts): releases inflammatory cells, increased mucus production, damage and repeated healing, and remodeling and fibrosis

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5
Q

Most common characteristics of COPD:

A

inability to expire air (hyper airflow of the lungs), airway obstruction leads to progressive air trapping, and residual air+loss of elastic recoil = hyperinflation (barrel chest)*

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6
Q

other common characteristics of COPD:

A

> gas exchange abnormalities
*alveolar destruction (blebs and bullae), hypoxemia, hypercapnia
mucus hypersecretion and cilia dysfunction
loss of elastic recoil
pulmonary vascular changes
*pulmonary hypertension
*cor pulmonale

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7
Q

Cor pulmonale:

A

enlargement of the right side of the heart

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8
Q

Pathophysiology: Vascular changes

A

> pulmonary vascular changes
*blood vessels thicken
*surface area for diffusion of O2 decreases
*hypoxemia at rest=late stage
*may need supplemental O2 earlier with exercise
Cor pulmonale - right sided hypertrophy of pulmonary artery>leads to right sided heart failure

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9
Q

COPD: Chronic bronchitis

A

> presence of chronic productive cough for 3 or more months in each of 2 successive years when other causes of chronic cough are excluded
bronchi and bronchioles affected
irritants cause:
*inflammation, congestion, bronchospasm, mucosal edema
smaller airways affected first

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10
Q

Chronic bronchitis: Pathophysiology

A

> inflammation and scarring of bronchiole lining
*decreased airflow, excessive mucous accumulation, cough develops, and ciliary function decreases
bacteria multiply causing infection

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11
Q

COPD: Emphysema

A

> abnormal permanent enlargement of the air space distal to the terminal bronchioles (alveoli)
10 % of pts with COPD have pure emphysema
*most have mix of chromic bronchitis and emphysema
COPD vs Asthma
High level of proteases
alveoli destroyed: bullae formed
*loss of elastic recoil
*alveoli overstretching
*bronchioles collapse
loss of lung elasticity with lung hyperinflation
results: increased work of breathing, decreased area for gas exchange, air trapping in lungs

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12
Q

Risk factors: COPD

A

cigarette smoking, occupational risks, air pollution, infection, genetics, and aging

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13
Q

Cigarette smoking:

A
>smoking causes destruction of alveolar walls
*smoke causes hyperplasia of cells
*increased mucus production
*reduces airway diameter
>smoke reduces ciliary action
>smoke releases proteases in lungs:
*breaks down elastin in found in alveoli
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14
Q

COPD: Cigarette smoking

A

> clinically significant airway obstruction develops in about 15% of smokers
passive smoking also contributes to respiratory problems (SHS)

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15
Q

COPD: occupation and environment:

A

> COPD can develop with intense or prolonged exposure to:

  • environmental tobacco smoke
  • occupational dusts, vapors, irritants, or fumes
  • high levels of air pollution
  • fumes from indoor heating or cooking with fossil fuel
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16
Q

COPD: infection

A

> risk factor for and symptom of COPD
recurring infections impair normal defense mechanisms
cycle of chronic inflammation
repeated infections worsen pathologic destruction of lung tissue
haemophilus influenza, streptococcus pneumonia**

17
Q

Genetic risk:

A

> alpha 1 antitrypsin deficiency (AAT)
*genetic factor identified for COPD
*serum protein produced by liver
AAT protects lungs from inhaled organisms/pollutants
*inhibits lysis of lung tissue by proteolytic enzymes (proteases)
smoking worsens disease process
symptoms by age 40, minimal tobacco use, family hx
treatment is AAT adm IV

18
Q

Aging lung changes:

A
>aging changes similar to emphysema
>gradual loss of elastic recoil
>lungs become rounded and smaller
>loss of alveolar supporting structures
>decreased number of functional alveoli
>thoracic cage changes from osteoporosis and calcification of costal cartilage
>decreased chest compliance and elastic recoil increases work of breathing
>decreased ability to clear secretions
19
Q

Clinical manifestations of COPD:

A

> symptoms develop slowly
20 pack year smoking history
diagnosis is considered with:
cough, sputum production, dyspnea, and exposure to risk factors
chronic intermittent cough is earliest symptom

progressive dyspnea usually prompts medical attention
*occurs with exertion in early stages and present at rest with advanced disease

20
Q

Late stage clinical manifestations of COPD:

A

> Alveoli over distended
* increasing amounts of air trapped
flattened diaphragm
abdominal breathing no longer effective
breathes with intercostal and accessory muscles
not efficient breathing
PE: wheezing, chest tightness, prolonged expiratory phase, decreased breath sounds, accessory muscles, pursed lip breathing, tri-pod position, hypoxemia, hypercapnia, cyanosis, and polycythemia

21
Q

Weight and muscle mass:

A

> chronic fatigue
anorexia and weight loss in advanced COPD
underweight with adequate caloric intake
takes all their energy to BREATHE

22
Q

Chronic bronchitis “blue bloater”:

A
>right heart failure
> obese*
>cough with sputum
> accessory muscle use
> coarse rhonchi/wheezing*
23
Q

Emphysema “pink puffer”:

A
> thin, barrel chest*
> little or no cough or sputum
> pursed lip breathing
> accessory muscle use
> tripod position
> decreased lung sounds or wheezing*
24
Q

Complications of COPD:

A

> Cor pulmonale
exacerbations of COPD
acute respiratory failure
depression/anxiety

25
Q

COPD exacerbations:

A

> exacerbations are natural coarse of disease
characterized by change in patients baseline: dyspnea, cough, and sputum
acute onset
increased frequency
associated with poorer outcomes
primary cause: bacterial or vial infections, air pollution
careful assessment
changes in plan of care
teaching

26
Q

Acute respiratory failure:

A

Caused by:
> exacerbations if COPD
> Cor Pulmonale
> discontinuing bronchodilator or corticosteroid medications
> overuse of sedatives, benzodiazepines, and opioids
> surgery/pain of chest/abdomen

27
Q

Depression/anxiety:

A
> depression
> anxiety complications
> teach about disease
> provide emotional support
> anti-depressant/ anti anxiolytics
> mental health consult
28
Q

Diagnostic studies:

A
> pulmonary function test
> CXR
> ABGS/sputum/CBC/AAT/genealogy
> EKG/ echo
> SPO2
29
Q

Pulmonary function testing:

A

> lung volume test:
* residual volume (air in lung after expiration)
* functional residual capacity ( increased amount of air left after expiration)
flow volume tests:
* FVC ( forced volume capacity)
* FEV1: (forced expired volume in the first second of expiration)**how to rank severity of disease
* FEV1:FVC- ratio
diffusion tests

30
Q

ABGs:

A
> low PaO2
> ^ PaCO2
> low pH
> ^ bicarbonate level
* typical findings in late stages of COPD
31
Q

Collaborative care:

A
Primary goal of care:
> prevent progression
> relieve symptoms
> prevent/treat complications
> prevent/treat exacerbations
> promote patient participation
> improve quality of life
> decrease mortality risk
> evaluate exposure to irritants (control or avoid)
> flu/pneumo vx
> treat ASAP 
> smoking cessation (most effective intervention)*
32
Q

Stages of COPD:

A

> stage I: mild
stage II: moderate
stage III: severe
stage IV: very severe