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2. HDS Pulmonary > COPD > Flashcards

COPD Flashcards

1
Q

COPD

Definition

A

Disease state characterized by airflow obstruction that is not fully reversible.

Usually progressive and associated with an abnormal inflammatory response of the lungs.

Umbrella term for many different disease processes:

  • Chronic bronchitis
  • Emphysema
  • Asthma
    • ~ 15% of COPD patients have a reactive airways component ⇒ “asthma-COPD overlap syndrome”
  • Bronchiectasis
  • Cystic fibrosis
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2
Q

COPD

Epidemiology

A
  • Most common pulmonary disease ⇒ 32 million in the US
  • Leading cause of morbidity and mortality worldwide
  • 3rd leading cause of death in the US
    • ~ 20,000 deaths/yr
  • Greatest cause of missed days of work
  • 2nd highest cause of disability
  • 3:1 male to female ratio
    • Women morely likely to have COPD in countries with higher socioeconomic status
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3
Q

COPD

Etiology & Risk Factors

A
  • Tobacco smoke ⇒ leading cause of COPD
    • 15-20% of long-term smokers develop COPD
  • Exposure to secondhand smoke
  • Inhalation of smoke ⇒ from biomass fuel or ambient particle matter
  • Indoor air pollution ⇒ from heating and cooking with biomass in poorly ventilated dwellings
  • Outdoor air pollution
  • Alpha-1 Anti-trypsin deficiency
  • Occupational dusts and chemicals
  • Infections ⇒ especially severe childhood respiratory infections
  • Airway hyperresponsiveness
  • Gender
  • Age
  • Socioeconomic status
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4
Q

Smoking Effects

A

Smoke inhalation leads to:

  • ⊗ Ciliary mobility
  • ↑ Airway resistance by reflex bronchoconstriction
  • Altered MΦ function
  • Squamous metaplasia
  • Mucus gland hyperplasia
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5
Q

COPD

Pathogenesis

A

Not fully understood but multifactorial.

  • Hypersecretion of mucus
    • Likely a response to irritation
  • Impairment of lung clearance
  • Destruction of bronchial tissue
  • Alterations of lung defenses
  • Primary degenerative changes in collagen and elastic tissue of alveolar septa (emphysema)
  • Lung elastin damage by elastase
    • Normally present in lungs but also secreted by MΦ and PMNs
    • Countered by elastase inhibitors in serum (alpha-1-antitrypsin)
    • Imbalance or malfunction ⇒ excess elastase ⇒ destruction of elastin ⇒ loss of elastic recoil
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6
Q

COPD

Pathophysiology

A

Airflow obstruction results from:

  • Small airways disease
    • Airway inflammation
    • Mucus gland hyperplasia
    • Fibrosis, airway narrowing
    • Loss of airway tethering
  • Lung parenchymal destruction
    • Dilation/destruction of bronchioles
    • Enlargement and/or destruction of acinus
    • Decreased elastic recoil
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7
Q

Chronic Bronchitis

Definition

A

Clinically defined disease with increased mucous production and chronic or recurrent productive cough.

Cough:

Frequency ⇒ > 3 months per year

Duration ⇒ > 2 years

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8
Q

Emphysema

Definition

A

Morphologically defined disease with enlargement of air spaces due to destruction of alveolar septae.

⇒ Leads to loss of airway structural supoort resulting in functional obstruction to air flow

⇒ Different morphologic types

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9
Q

Chronic Bronchitis

vs

Emphysema

A
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10
Q

Chronic Bronchitis and Emphysema

Pathogenesis

A
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11
Q

Emphysema

Pathogenesis

A

Permanent and abnormal enlargement of terminal respiratory unit of acinus.

  • Described as “lung dry rot”
    • Alveolar distention
    • Destruction of alveolar septae
  • Tobacco use produces ROS that can inactivate antiproteases ⇒ “functional” α1AT deficiency
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12
Q

Emphysema

Types

A

Two main types:

  1. Centriacinar (aka Centrilobular - CLE)
  2. Panlobular (PLE)
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13
Q

Centriacinar

Emphysema

A

“Centrilobular Emphysema (CLE)”

  • Selective dilatation of respiratory bronchioles and alveolar ducts
  • Most common type
  • Usually smoking related
  • Most severe in upper lobes
  • See enlarged air spaces of varying sizes
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14
Q

Panlobular Emphysema

(PLE)

A
  • Dilatation of all components beyond the terminal bronchiole
  • Usually occurs in the lower lung
  • Severe forms in young people usually associated with α1AT deficiency
  • See enlarged airspaces of uniform size
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15
Q

CLE vs PLE

A
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16
Q

Bullous Disease

A

“Paraseptal Emphysema”

  • See > 1 cm dilatations of air spaces in the periphery of the lung adjacent to pleura
  • Occurs adjacent to scars with aging or from unknown factors
  • Does not qualify as true emphysema
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17
Q

Emphysema

Alveolar Changes

A
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18
Q

Emphysema

Expiration Changes

A
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19
Q

Chronic Bronchitis

Pathogenesis

A

May have no demonstrable pathology

or

May have any of the following:

  • Smoking related changes
    • Squamous metaplasia
    • Loss of cilia in bronchial epithelium
  • Hyperplastic bronchial mucus glands with chronic excessive mucus secretion
    • Measured using Reid index
  • Inflammatory infiltrates of bronchial wall
  • Globlet cell hyperplasia
  • Fibrosis and atrophy of bronchial walls
  • Smooth muscle hyperplasia
  • Bronchial hyperresponsiveness (50% of COPD)
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20
Q

Chronic Bronchitis

Smoking Effects

A

Occurs in cigarette smokers 10-12 years after starting.

Affects 10-15% of smokers.

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21
Q

Reid Index

A

Ratio of bronchial glands to the entire thickness of bronchial wall from epithelium to top of the cartilage.

Method for measuring degree of mucus gland hyperplasia.

22
Q

Chronic Bronchitis

Histology

A
23
Q

Chronic Bronchitis

Secondary Infections

A
  • Infections are common in the bronchi
  • Leads to further destruction of bronchial tissue
  • Haemophilus influenzae colonizes airway of smokers
    • Creates an immune reaction in airways
    • Isolated from sputum in 60% of stable chronic bronchitis pts
24
Q

COPD

Symptoms

A

Ranges in severity and may be applicable to all disease types.

  • Cough ± sputum production
  • Dyspnea ⇒ initially on exertion, later at rest
  • Wheezing
  • Decreased exercise tolerance
  • Weight loss and lack of appetite ⇒ late
  • Impaired mentation and fatigability ⇒ late and usually when cor pulmonale has occured
25
Q

COPD

Physical Exam

A
  • Slightly prolonged forced expiration
  • Decreased breath sounds at apices or bases
  • Scattered expiratory rhonchi and wheezes
  • Use of accessory muscles
  • Hyperresonance
  • ↑ AP diameter of chest
  • Low diaphragm
  • Inaudible heart sounds
  • Signs of cor pulmonale
    • Heart failure with JVD
    • Functional tricuspid insufficiency
    • Hepatojugular reflex
    • Hepatomegaly
26
Q

COPD

Radiographic Changes

A

Often normal but may show:

Emphysema ⇒ hyperinflation and/or loss of peripheral markings

Chronic bronchitis ⇒ increased bronchial markings

27
Q

Blue Bloater

A

Seen with chronic bronchitis

Stocky and obese

Markedly hypoxic and cyanotic

28
Q

Pink Puffer

A

Seen with emphysema:

Tachypnea

Prolonged expiration and pursed lip breathing

Hyperresonant chest

Diminished breath sounds

Cachexia

29
Q

Chronic Bronchitis vs Emphysema

Summary

A
30
Q

COPD

Diagnosis

A
  • Consider COPD if patient has symptoms of:
    • Dyspnea
    • Chronic cough or sputum production
    • Risk factors for the disease
  • Spirometry required for diagnosis
    • FEV1/FVC (FEV-1%) < 0.70 and FEV1 ≤ 80%
31
Q

COPD vs Asthma

Diagnosis

A
32
Q

COPD

Disease Staging

A

In patients with FEV-1%:

  • GOLD 1: Mild ⇒ FEV1 ≥ 80% predicted
  • GOLD 2: Moderate ⇒ FEV1 between 50-80% predicted
  • GOLD 3: Severe ⇒ FEV1 between 30-50% predicted
  • GOLD 4: Very severe ⇒ FEV1 ≤ 30% predicted
33
Q

COPD

Comorbidities

A

COPD patients are at increased risk for:

  • Cardiovascular disease
  • Respiratory infections
  • Osteoporsis
  • Anxiety and depression
  • Diabetes
  • Lung cancer
  • Bronchiectasis
34
Q

COPD Treatment

Preventative Measures

A
  • Smoking cessation ⇒ can greatly affect outcomes
  • Reduce indoor air pollution ⇒ use stove instead of open fire
  • Influenza and pneumococcal vaccination
    • Recommended for COPD patients
    • May reduce exacerbations or hospitalizations
  • Pulmonary rehabilitation
    • Reduces hospitalizations and mortality in recent COPD exacerbations
  • Physical activity
    • Possibly as effective as smoking cessation
    • Physical inactivity is likely very detrimental
35
Q

COPD Treatment

Maintenance Pharmacotherapy

Effectiveness

A
  • Improves quality of life
  • Improves COPD symptoms
  • Reduces exacerbations
  • Improves exercise tolerance
  • Does not improve lung function decline long-term
36
Q

Bronchodilators

Overview

A
  • Reduces exacerbations and hospitalizations
  • Improves symptoms and health status
  • Combining different classes may improve efficacy
  • Inhaled are best and safest
  • Long-acting more convenient and effective
37
Q

Bronchodilator

Classes

A
  • β-agonists
    • SABA ⇒ short-acting
      • Albuterol
    • LABA ⇒ long-acting
      • Salmeterol
      • Formoterol
  • Anti-cholinergics (muscarinic antagonists)
    • SAMA ⇒ short-acting
      • Ipratropium
    • LAMA ⇒ long-acting
      • Tiotropium ⇒ appears superior to LABA in recurrent exacerbations
38
Q

Inhaled Corticosteroids

A
  • Does not appear to slow decline in lung function
  • May decrease frequency of exacerbations if FEV1 > 60%
  • Often used in combo with LABA or LAMA
  • Long term use may increase risk for PNA
  • Withdrawal from treatment may lead to exacerbations
39
Q

Combination Therapy

A

ICS + LABA

or

ICS + LABA + Anticholinergic (tiotropium)

  • Appears to provide even more benefit
  • ↓ Exacerbations in moderate-severe COPD
  • Caution in pts with cardiac disease
    • Can exacerbate arrhythmias
40
Q

Roflumilast

A
  • Phosphodiesterase-4 inhibitor
  • Used in pts with severe and very severe COPD
  • Reduces COPD exacerbations treated with oral steroids
41
Q

Theophylline

A
  • Phosphodiesterase inhibitor
  • Oral or IV only
  • Less effective and less tolerated than bronchodilators
  • Low dose theophylline reduces exacerbations
    • Does not improve post-bronchodilator lung function
  • Poor risk/benefit ratio
  • Drug interactions, toxicity
    • Risk of osteoporosis and DM
  • Use only in select cases
42
Q

Oral Steroids

A

Chronic systemic oral steroids not recommended.

Unfavorable risk-to-benefit ratio.

Only used in very severe cases.

43
Q

Surgical Interventions

A
  • Lung volume reduction surgery (LVRS)
    • More effective than medical therapy for pts with upper-lobe emphysema and low exercise capacity
    • High costs
    • For very select pts
  • Lung transplantation ⇒ very severe COPD
    • Can improve quality of life and functional capacity
  • Bullectomy ⇒ for giant bullae
    • Can improve dyspnea
44
Q

COPD Treatment

Summary

A
  • Long-acting preferred over short-acting
  • ICS + LABA/LAMA recommended for pts at high risk for exacerbations
  • Steroid monotherapy (inhaled/oral) not recommended
  • Roflumilast may be useful to reduce exacerbations
    • Patients with FEV1 < 50%, chronic bronchitis, or frequent exacerbations
  • Pulmonary rehab and physical activity encouraged
45
Q

COPD Exacerbations

A
  • Acute episodes of worsening SOB ± dyspnea, cough, and change in sputum (volume, purulence)
  • Often triggered by infections
    • Viral
    • Bacterial
      1. Strep pneumoniae
      2. Haemophilus influenzae
      3. Moraxella catarrhalis
46
Q

COPD Exacerbation

Treatment

A
  • Mild cases
    • Often can be treated at home with rest and inhalers
  • Moderate cases
    • Oral prednisone 40mg x 5 days
    • Possible abx
    • Inhaled bronchodilators
  • Severe cases
    • Hospitalization
    • IV steroids
    • Abx
    • Inhaled bronchodilators
    • Supportive measures ⇒ O2, NIPPV, intubation
47
Q

Alpha-1-antitrypsin Deficiency (AATD)

Overview

A
  • Deficiency of anti-protease alpha-1-antitrypsin
    • Allows lung enzymes (elastases) to break down lung proteins
    • Creates inflammation ⇒ emphysema
  • Accounts for 1% of all COPD cases
  • Autosomal co-dominant transmission
    • PI*MM ⇒ normal
    • PI*ZZ ⇒ homozygous for z allele
    • PI*M or null alleles ⇒ varying risks of COPD
48
Q

Alpha-1-Antitrypsin Deficiency

Clinical Presentation

A

Suspect and test for AATD in patients with:

  • COPD in a never smoker
  • COPD development at < 50 y/o
  • Strong Fhx of COPD
  • COPD with lung basilar predominance on CXR
  • COPD with associated unexplained liver disease
49
Q

Alpha-1-Antitrypsin Deficiency

Diagnosis

A

Serum Alpha-1-Antitrypsin level

Genetic testing

50
Q

Alpha-1-Antitrypsin Deficiency

Treatment

A

Same as regular COPD + replacement therapy

• Intermittent IV infusions of α1AT appears to slow rate of decline in lung function in pts with airflow obstruction

2. HDS Pulmonary (28 decks)

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