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COPD

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Title: COPD


1
COPD
  • Michele Ritter, M.D.
  • Argy Teaching Resident, Feb. 2007

2
Definition
  • A disease state characterized by the presence of
    airflow obstruction due to chronic bronchitis or
    emphysema the airflow obstruction is generally
    progressive, may be accompanied by airflow
    hyperactivity, and may be viewed as partially
    reversible.
  • Includes emphysema and chronic bronchitis

3
Prevalence
  • COPD occurs in 4-6 of white males, and 1-3 of
    adult white females
  • The 4th most common cause of death in the United
    States
  • 14.2 million people in U.S. have COPD
  • Highest mortality rate is in white men, and the
    lowest is in hispanic women.

4
Types of COPD
  • Emphysema
  • Permanent and destructive enlargement of
    airspaces distal to the terminal bronchioles
    without obvious fibrosis and with loss of normal
    architecture
  • Always involves clinically significant airflow
    limitation.
  • pink puffer
  • Chronic Bronchitis
  • Presence of a cough productive of sputum not
    attributable to other causes on most days for at
    least 3 months over 2 consecutive years
  • May be present in the absence of airflow
    limitation.
  • blue bloater

5
COPD
6
Pathogenesis of COPD
  • Increased number of activated polymorphonuclear
    cells and macrophages produce elastases (such as
    human leukocyte elastase), resulting in lung
    destruction.
  • Increased oxidative stress caused by free
    radicals in cigarette smoke, the oxidants
    released by phagocytes, and polymorphonuclear
    leukocytes all may lead to apoptosis or necrosis
    of exposed cells

7
Pathogenesis of COPD (cont.)
  • Emphysema
  • 3 morphologic patterns
  • Centricacinar
  • focal destruction limited to the respiratory
    bronchioles and the central portions of acinus
  • associated with cigarette smoking
  • most severe in the upper lobes
  • Panacinar
  • involves the entire alveolus distal to the
    terminal bronchiole
  • develops in patients with homozygous
    alpha1-antitrypsin (AAT) deficiency
  • most severe in the lower lung zones
  • Distal acinar
  • Also called paraseptal
  • least common form
  • involves distal airway structures, alveolar
    ducts, and sacs
  • localized to fibrous septa or to the pleura and
    leads to formation of bullae (can result in
    pneumothorax)
  • Chronic Bronchitis
  • Mucus gland enlargement
  • Airway atrophy, focal squamous metaplasia,
    ciliary abnormalities, variable amounts of airway
    smooth muscle hyperplasia, inflammation, and
    bronchial wall thickening
  • Respiratory bronchioles display a mononuclear
    inflammatory process, lumen occlusion by mucous
    plugging, goblet cell metaplasia, smooth muscle
    hyperplasia, and distortion due to fibrosis
  • Airway walls to deform and narrow the airway
    lumen

8
Risk Factors
  • SMOKING!
  • 48 million smokers in the U.S.
  • 3000 new people take up smoking daily
  • Nearly all patients with symptomatic COPD are
    current or former smokers
  • 10-20 of smokers will develop symptomatic COPD.
  • In men who smoke one pack/day, the drop in FEV1
    per year was 9 mL more than in non-smokers
  • Occupational Exposures
  • Dusts, gases, fumes
  • Alpha1-antitrypsin deficiency
  • Alpha1-antitrypsin is an important protease
    inhibitor that usually presents elastases from
    causing lung destruction

9
Symptoms
  • Dyspnea
  • Cough (usually worse in morning, sputum
    production)
  • Wheezing
  • Cyanosis
  • Right heart failure
  • Weight loss, anorexia

10
Physical Exam
  • ?RR, ?HR, ?O2 saturation
  • Gen Barrel-chest, accessory muscle use
  • CV Quiet heart sounds
  • Resp Decreased breath sounds, wheezing, rhonchi,
    crackles

11
Labs
  • CBC ? Hgb/Hct
  • ABG ?pH, ?pCO2
  • Chemistry ?HCO3

12
Emphysema
13
Diagnosis of COPD
  • Look for secondary polycythemia
  • Hct gt52 in males, Hctgt47 in females
  • Measure alpha1-antitrypsin levels in all patients
    40 years or younger, or in those with family
    history.
  • Hyperinflation see on chest x-ray
  • Bullae seen on Chest x-ray or CT scan

14
Pulmonary Function Tests
15
Diagnosis of COPD Pulmonary Function Tests
  • ? Forced Expiratory Volume for 1 second (FEV1)
  • ?FEV1/FVC (Forced Vital Capacity) ratio
  • ? Total Lung Capacity (TLC)
  • ? Forced Residual Capacity (FRC)
  • ? Residual Volume (RV)
  • ? Vital Capacity (VC)

16
Pulmonary Function Tests
17
COPD Exacerbation
  • Typically manifest as increased sputum
    production, more purulent sputum and worsening of
    dyspnea.
  • Although infectious etiologies account for most
    exacerbations, exposure to allergens, pollutants
    or inhaled irritants may also play a role.
  • Bacterial infection is a factor in 70 to 75
    percent of exacerbations, with up to 60 percent
    caused by
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Antibiotic therapy has a small but important
    effect on clinical recovery and outcome.
  • Respiratory fluoroquinolone (Levofloxacin,
    Moxifloxacin)
  • Ceftriaxone azithromycin
  • Short courses of systemic corticosteroids may
    provide important benefits in patients with
    exacerbations of COPD.
  • Oxygen therapy to keep saturation Between 90-93
  • Non-invasive ventilation such as BiPAP can be
    helpful in avoiding intubation/mechanical
    ventilation.

18
Treatment of COPD
  • SMOKING CESSATION!
  • Short-acting bronchodilators
  • albuterol
  • Long-acting bronchodilator
  • salmeterol
  • Combination of anti-cholinergic and ?-agonist
    bronchodilator
  • Ipratropium albuterol (combivent)
  • Tiotropium (spiriva)
  • Methylxanthines (Theophylline)
  • Has anti-inflammatory affect, and improves
    respiratory muscle function, stimulates the
    respiratory center, and promotes bronchodilation
  • Adverse effects include anxiety, tremors,
    insomnia, nausea, cardiac arrhythmia, and
    seizures
  • Inhaled corticosteroids
  • Fluticasone (Flovent), budesonide (Pulmicort)
  • Combination of Inhaled corticosteroid and
    long-acting ?-agonist
  • Fluticasone salmeterol (Advair)
  • Oral Corticosteroids

19
Treatment of COPD (cont.)
  • Oxygen Therapy
  • Continous oxygen has been shown to cut mortality
    in half or decrease morbidity when compared with
    non-continous oxygen
  • Continuous (24 hours/day)
  • Resting Pa02 of 55 mm HG, or Resting oxygen
    saturation lt 88
  • Resting Pa02 of 56-59 mmHg or Oxygen Sat. lt89 in
    presence of dependent edema (suggestive of CHF),
    P pulmonale on ECG (P wave more than 3 mm in
    inferior leads) or cor pulmonale, or
    erythrocytosis (Hct gt 56)
  • Noncontinuous
  • During exercise when PaO2 is lt 55 mmHg or
    Oxygen sat. lt 88 with low level of exercise.
  • During sleep if Pa02 is lt 55 mmHg or Sa02 less
    than 88 with associated complications such as
    pulmonary hypertension, daytime somnolence,
    cardiac arrythmias.

20
Treatment of COPD (cont.)
  • Pulmonary Rehabilitation
  • Aimed at keeping patient conditioned with
    exercise, perception of dyspnea, quality of life
    and self-efficacy.
  • Surgery
  • Bullectomy
  • Resection of large bullae compressing normal lung
  • Lung volume reduction surgery
  • Pneumonectomy of nonuniform emphysematous lung
  • Double lung transplantation
  • Can be life-saving, but is costly, can be lack of
    donor availability and requires lifelong
    immunosuppression.

21
Treatment of COPD
22
Stages of COPD
23
Take Home Points
  • Smoking is the number one cause of COPD!
  • If smoking is stopped once COPD diagnosed, the
    progression of disease can slow down.
  • Treat COPD exacerbations with antibiotics and
    possibly with steroids.
  • Continuous oxygen is shown to decrease morbidity
    and mortality in COPD
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