COPD Flashcards

1
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease
* Lung condition characterized by chronic pulmonary symptoms (cough, dyspnea,
sputum) and evidence of airflow limitation
* WHO Defenition: Heterogeneous lung condition characterized by chronic
respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to
abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli
(emphysema) that cause persistent, often progressive, airflow obstruction”
* COPD patients often report they are “hungry” for air
* Usually progressive and not fully reversible

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2
Q

Prevalence of COPD

A

Prevalence: Around 6% of US adults
* Prevalence increases with age, and mostly occurs in patients ≥ 40 years old

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3
Q

Mortality of COPD

A

Mortality: Generally in the top 5 leading
causes of death in the US annually

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4
Q

COPD Clinical Risk Factors:

A
  • Envornmental Exposures (smoking, pullution, etc.)
  • Persistent Asthma, airway hyperresponsiveness, allergies, or atopy
    *Infections (Childhood pneumonia, Tuberculosis, HIV)
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5
Q

Molecular (genetic) Risk Factors of COPD:

A

Gene polymorphisms
* Alpha 1-antitrypsin (AAT) deficiency
* Connective tissue disorders

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6
Q

Clinically significant COPD develops in ___% of smokers

A

15

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7
Q

How Cigarette smoking leads to COPD:

A
  • smoking Interferes with ciliary motility, damages epithelium
  • Inhibits alveolar leukocytes from clearing bacteria
  • Induces macrophages to release neutrophil chemotactic factors
  • Causing tissue destruction
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8
Q

Non-reversible (persistent) airflow limitation

A

Defined as the reduced ability to
exhale efficiently, with a postbronchodilator FEV1/FVC < 0.7

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9
Q

Non-reversible (persistent) airflow limitation in the airways

A

: Small airway narrowing or obstruction
- Usually caused by Chronic Bronchitis and/or Chronic Obstructive Asthma

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10
Q

Non-reversible (persistent) airflow limitation in the alveoli

A

enlargement of the airspaces
accompanied by destruction of the airspace walls
- Usually caused by Emphysema

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11
Q

COPD pathology of the airways

A

Various factors lead to chronic inflammation, increased numbers of goblet cells, mucus gland hyperplasia, fibrosis, narrowing/reduction in the number of small airways, and airway collapse (more prominent in chronic bronchitis)

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12
Q

COPD pathology of the lung parenchyma

A

Permanent dilation or destruction of the alveolar ducts, alveolar sacs, and alveoli (more prominent in emphysema)

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13
Q

Emphysema

A

Defined as specific structural changes associated with COPD
* Permanent enlargement of air spaces
* Destruction of alveolar walls
* Lacks obvious fibrosis

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14
Q

Emphysema: “pink puffer”

A
  • Less surface area for gas exchange
  • Collapse of alveoli during
    expiration
  • Body compensates through
    hyperventilation
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15
Q

Emphysema classifications

A

Centriacinar (centrilobular)
● Localized to the proximal respiratory bronchioles
● Focal destruction, predominantly upper lung zones
Panacinar (panlobular)
● Destroys the entire alveolus uniformly
● Predominantly lower half of lungs
Paraseptal (distal)
● Localized around the septae of the pleura, adjacent to foci of fibrosis
● Airflow often preserved but can lead to spontaneous pneumothorax

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16
Q

Emphysema radiologic findings

A
  • Flattening of the diaphragm
  • ↑ retrosternal air space (Usually >2.5cm)
  • Long, narrow heart shadow
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17
Q

Alpha-1 Antitrypsin

A
  • A protein produced in the liver which
    acts in the lungs and liver
  • Protects the lungs from damage
    caused by neutrophil elastase, an
    enzyme that disrupts connective tissue
    and causes inflammation
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18
Q

Alpha-1 antitrypsin Deficiency (AATD)

A
  • Autosomal co-dominant genetic disease
  • Severe disease is rare (<100,000 in the US)
  • Present in 2% to 3% of patients with COPD
  • Increases risk of developing emphysema
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19
Q

Alpha-1 Antitrypsin Deficiency (AATD) symptoms

A
  • Mild disease may have no symptoms and go undiagnosed
  • Shortness of breath, wheezing, chronic
    cough, increased sputum production
  • Decreased exercise capacity
  • Frequent respiratory infections
  • Symptoms of chronic hepatitis/cirrhosis (like jaundice)
  • Unique features of AATD emphysema are younger onset and basilar-predominant pattern of emphysema
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20
Q

Alpha-1 Antitrypsin Deficiency (AATD) testing

A
  • Testing for AATD should be performed on all adults with persistent
    airflow obstruction on spirometry, especially if:
  • Emphysema in a young individual (eg, age ≤45 years)
  • Emphysema in a nonsmoker or minimal smoker
  • Emphysema characterized by predominant basilar changes
  • History of unexplained chronic liver disease
  • Various methods exist, but most common is testing serum AAT
    levels and targeted genotyping for the most common variants
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21
Q

Chronic Bronchitis

A

“Blue bloaters”
* Defined by a chronic bronchial
inflammation, leading to a
productive cough over a defined
period. It can be preceded or
followed by development of
airflow limitation
* Chronic Bronchitis is considered
COPD only when permanent
airflow obstruction occurs

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22
Q

Chronic Bronchitis

A
  • Chronic inflammation of the bronchi and
    bronchioles
  • Results in excessive secretions, and
    mucus buildup.
  • Tissues swell and bronchial tubes may
    narrow or close off
  • Fibrosis of bronchial wall can occur
23
Q

Histological features of chronic bronchitis

A
  • Lymphocytic infiltration
  • Enlargement of mucin secreting glands
  • Bronchial epithelium may exhibit squamous dysplasia/metaplasia
24
Q

The difference between asthma and COPD is:

A

Most patients with asthma
have reversible airflow
obstruction. If the obstruction
is completely reversible, it is
not considered COPD

25
Q

COPD Signs and Symptoms

A

3 cardinal
* Dyspnea
* Chronic cough
* Sputum production

others
* Wheezing
* Chest tightness

26
Q

Typical Onset/Presentations of COPD:

A
  1. Patients with very sedentary lifestyles, but few complaints:
  2. Patients presenting with dyspnea and chronic cough:
  3. Patients who present with episodes of increased cough, purulent sputum,
    wheezing, fatigue, and dyspnea that occur intermittently, with or without
    fever:
27
Q

Systemic manifestations of COPD

A
  • Obesity
  • Depression or anxiety
  • Osteoporosis
  • Advanced Disease:
  • Weight loss
  • Anemia
  • Pulmonary hypertension
  • Cor pulmonale
28
Q

Limitated expiratory flow + Preserved inspiratory flow =

A

It takes longer to exhale than it does to inhale

29
Q

Exam for COPD:

A

● Limitated expiratory flow + Preserved inspiratory flow
= It takes longer to exhale than it does to inhale
● Hyperinflation of the lungs (eg, increased resonance to percussion)
● Decreased breath sounds, wheezes, crackles at the lung bases
● Distant heart sounds

30
Q

Exam - End-stage findings of COPD:

A

● Accessory respiratory muscle use
● Depressed diaphragm with limited movement.
● Positions that relieve dyspnea, like leaning forward and weight supported on the palms or elbows (tripod position)
● Expiration through pursed lips
● Cyanosis
● Elevated jugular venous pressure
● Peripheral edema

31
Q

Emphysema exam findings:

A

● Tachypnea
● Hyperresonance with percussion
● Diffusely diminished breath sounds
● Patients are often thin
● Increased anteroposterior diameter
of the chest (“barrel chest”)

32
Q

Chronic Bronchitis exam findings

A
  • Hypercapnia
  • Hypoxemia
  • Cyanosis
33
Q

COPD Lab Testing

A
  • Lab testing is not diagnostic
  • Check BNP for heart failure
  • Serum chemistries
  • Elevated serum bicarbonate may indicate chronic hypercapnia
  • Testing for alpha-1 antitrypsin (AAT) deficiency
    Exercise Capacity: can help evaluate risk of mortality
  • Six-minute walking distance, evaluating for desaturation
34
Q

COPD Imaging

A
  • Imaging is not needed to diagnosis of COPD, but is helpful for other reasons
  • Chest X-Ray:
  • CT-Scan: More sensitive and specific
35
Q

COPD pulmonary function testing

A

SPIROMETRY
* Essential for the diagnostic evaluation of patients with suspected COPD.
* Performed pre and post bronchodilator administration (like albuterol) to
determine if airflow limitation is reversible.
* Irreversible airflow limitation is a defining physiologic feature of COPD.
* FEV1/FVC is the ratio of forced expiratory volume in 1 second over forced
vital capacity. Less than 70% of predicted defines COPD

36
Q

Additional Pulmonary Function Testing in COPD:

A

Lung Volume testing -
* Done using body plethysmography.
* Used to determine whether the reducted FVC is due to air trapping,
hyperinflation, or some other restrictive condition.
Diffusing capacity for carbon monoxide (DLCO):
* Helps clarify the degree of emphysema in smokers with airflow limitation

37
Q

What will an ABG show in mild to moderate COPD?

A

mild to moderate hypoxemia without hypercapnia

38
Q

What will an ABG show in severe COPD?

A

hypoxemia worsens and hypercapnia may develop

39
Q

Management goal in COPD

A

*The goal of COPD management
*Prevent the recurrence of exacerbations

40
Q

A comprehensive disease management strategy for COPD is associated with _____

A

a lower hospitalization rate and fewer ER visits

41
Q

A comprehensive disease management strategy for COPD includes the following:

A
  • Patient education session
  • Self-treatment plan for exacerbations
  • Monthly follow-up call from a case manager
42
Q

COPD management program (4 components)

A

*Assess and monitor disease
*Reduce risk factors
*Manage stable COPD
*Manage exacerbations

43
Q

Reduce risk factors of COPD

A

*Vaccines
*Smoking cessation

44
Q

Pharmacologic treatment for COPD

A

*Bronchodilators - Central to symptom management
*Inhaled glucocorticosteroids (ICS)
*If used, an ICS should be combined with a long-acting beta 2-agonist
* Oral glucocorticosteroids
Long-term treatment not recommended
Beneficial during exacerbations
* Phosphodiesterase-4 inhibitors (roflumilast)
* AAT augmentation therapy
* Antibiotics: Generally, long-term treatment not recommended in stable COPD.
* Mucoactive agents (N-acetylcysteine)
* Antitussives (benzonatate)
* Regular use contraindicated in stable COPD, no conclusive evidence of benefit

45
Q

Long-term administration of
oxygen for > ___ hours per day
increases survival

A

15

46
Q

Beneficial impact of oxygen therapy in COPD

A
  • Pulmonary hemodynamics
  • Hematologic characteristics
  • Exercise capacity
  • Lung mechanics
  • Mental state
47
Q

Exercise training for COPD

A
  • Patients of all stages benefit from exercise
    training programs
    *Improves dyspnea and fatigue
  • Minimum length of an effective program is 6 weeks
  • Benefits wane after program ends
48
Q

COPD patients are the largest single category of ____

A

lung transplant patients

49
Q

Pulmonary rehabilitation

A
  • Decreases airflow limitation
  • Prevents secondary complications
  • Alleviates respiratory symptoms
  • Reduces hospitalization in patients with recent exacerbations
  • Reduces anxiety/depression and improves exercise tolerance
  • Team approach
  • Emphasizes the following
50
Q

COPD Exacerbations

A

*Exacerbations are characterized by a change in the patient’s
baseline dyspnea, cough, and/or sputum that is beyond normal
day-to-day variations
*Most common causes
*Infection
*Air pollution
* 30% unidentified

51
Q

T/F COPD Exacerbations often occur in clusters

A

T - Increased risk of another attack in the 8 weeks following the initial
episode

52
Q

BODE: What is it?

A
  • Body mass index, airflow Obstruction, Dyspnea and Exercise capacity
  • BODE index may be a better predictor of the number and severity of
    exacerbations in COPD than FEV1
53
Q

COPD Exacerbations treatment

A
  • Oxygen therapy
  • Inhaled bronchodilators
  • Corticosteroids
  • Hospitalization
  • Initiate LABA before discharge
    *Antibiotics if bacterial infection is suspected
54
Q

Long-term monitoring of COPD

A

*Patients with severe or unstable disease should be seen
monthly
*When their condition is stable, patients may be seen biannually
*Check theophylline level with each dose adjustment, when
interacting medications are added, and routinely every 6-12
months