2. HDS Pulmonary > COPD > Flashcards

COPD Flashcards

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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

Study These Flashcards
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

23
Q

Chronic Bronchitis

Secondary Infections

Study These Flashcards
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

Study These Flashcards
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
COPD Physical Exam
* 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
COPD Radiographic Changes
Often normal but may show: **Emphysema** ⇒ hyperinflation and/or loss of peripheral markings **Chronic bronchitis** ⇒ increased bronchial markings
27
Blue Bloater
_Seen with chronic bronchitis_ ## Footnote **Stocky and obese** **Markedly hypoxic and cyanotic**
28
Pink Puffer
_Seen with emphysema:_ ## Footnote **Tachypnea** **Prolonged expiration and pursed lip breathing** **Hyperresonant chest** **Diminished breath sounds** **Cachexia**
29
Chronic Bronchitis vs Emphysema Summary
30
COPD Diagnosis
* 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
COPD vs Asthma Diagnosis
32
COPD Disease Staging
_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
COPD Comorbidities
_COPD patients are at increased risk for:_ * Cardiovascular disease * Respiratory infections * Osteoporsis * Anxiety and depression * Diabetes * Lung cancer * Bronchiectasis
34
COPD Treatment Preventative Measures
* ***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
COPD Treatment ## Footnote **Maintenance Pharmacotherapy** **Effectiveness**
* Improves quality of life * Improves COPD symptoms * Reduces exacerbations * Improves exercise tolerance * **Does not improve lung function decline long-term**
36
Bronchodilators Overview
* **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
Bronchodilator Classes
* **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
Inhaled Corticosteroids
* **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
Combination Therapy
**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
Roflumilast
* **Phosphodiesterase-4 inhibitor** * Used in pts with severe and very severe COPD * Reduces COPD exacerbations treated with oral steroids
41
**Theophylline**
* **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
Oral Steroids
**Chronic systemic oral steroids not recommended.** Unfavorable risk-to-benefit ratio. Only used in very severe cases.
43
Surgical Interventions
* **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
COPD Treatment Summary
* 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
COPD Exacerbations
* **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
COPD Exacerbation Treatment
* **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
Alpha-1-antitrypsin Deficiency (AATD) Overview
* **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
Alpha-1-Antitrypsin Deficiency Clinical Presentation
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
Alpha-1-Antitrypsin Deficiency Diagnosis
Serum Alpha-1-Antitrypsin level Genetic testing
50
Alpha-1-Antitrypsin Deficiency Treatment
**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
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