Chronic+Obstructive+Airways+Disease+(COPD)

toc =Definition=


 * Characterized by airflow obstruction
 * > Due to chronic bronchitis or emphyema.
 * > Generally progressive
 * > May be accompanied by Pulmonary Hyperreactivity
 * > May be partially reversible


 * **Chronic Bronchitis**
 * > presence of productive cough > 3 mos in 2 successive years
 * > other causes of cough excluded


 * **Emphysema**
 * > Abnormal enlargement of terminal airspaces
 * > Destruction of alveolar walls
 * > Fibrosis absent

=Etiology=
 * Smoking
 * > 90% of attributable risk
 * > Prevalence 25% in smokers
 * > Passive smoke inhalation also implicated
 * Air Pollution
 * Occupational particulate exposure
 * Protease inhibitor deficiency
 * Family Hx of COPD

=Pathology=
 * Productive Cough consiting prymarily of glycosaminoglycans


 * Chronic irritation by pollutants alters biochemistry
 * > increase in submucosal glands


 * metaplastic changes
 * > Increase in goblet cells
 * > Reduction of serous acini
 * >> Reduction in lysozyme,lactoferrin,antiproteases
 * > Epithelial atrophy
 * >>Focal squamous metaplasia
 * > Loss of mucociliary activity
 * >> altered mucus properties
 * >> Ciliary damage


 * Increased susceptibility ot bacteria

Emphysmatic Pathophysiology:
 * Elastolytic enzymes
 * alpha-1 antitrypsin deficiency have early onset emphysema
 * > Different pattern of disease: homogenous distribution rather than following distribution of airways in COPD secondary to smoking


 * Inflammation in COPD**
 * Inflammation in bronchioles, parenchyma
 * Infiltration of macrophages, neutrophils
 * > macrophages 10x more numerous
 * > macrophages activated
 * > murine macrophage elastase MMP-12 knockouts are protected from smoke-related emphysema
 * develop fibrosis

=Symptoms=
 * Productive Cough
 * > Worse in AM
 * > Sputum mucoid
 * >> <60ml/day
 * >> purulent during exacerbation
 * Dyspnea
 * > Insideous onset
 * > worse with exertion
 * Wheezing

=Signs=
 * Early
 * > Prolonged Expiration
 * > Wheezing


 * Late
 * > Hyperinflation
 * >> Increased AP Diameter
 * >> Increased Diaphragmatic movement
 * > Decreased breath sounds
 * > Rhonchi or Rales

=Differential Diagnosis= Diagnosis is primarily by Pulmonary Function Testing (PFTs)
 * End Stage
 * > Accessory muscles used
 * > Pursed lips
 * > Braced by arms
 * > Cyanosis
 * > Cor pulmonale

Spirometry

 * decreased FEV1
 * > Poor FEV1 is a strong indicator of early mortality
 * decreased FEV1/FVC
 * concave appearance of Flow Volume Loop

Radiology

 * Imperfect (looking for big holes in sea of little holes)
 * most findings relate ot airway obstruction


 * Radiographic Findings:
 * > Overinflation
 * > Bullae
 * > Arterial insufficiency


 * Computed TOmography (CT) Findings:
 * > Better for emphysema
 * >> Better contrast resolution
 * >> better display of results
 * >>> Findings: unmarginated hypodsense area
 * >>> Pruning and distoriton of vessels

=Treatment=
 * Smoking cessation!
 * Bronchodilators
 * > B2 agonists
 * > Cholinergic Antagonists
 * > Corticosteroids
 * > Supplemental Oxygen
 * > Avoid infection
 * > Pulmonary rehab

COPD can be exacerbated by:
 * Environmental irritants
 * Gastro-Esophageal Reflux Disease (GERD)
 * viral or bacterial infections
 * Heart Failure, Arrhythmias, or Pulmonary Embolism

To treat exacerbated COPD:
 * eliminate underlyinc cause
 * > Reverse Airflow obstruction
 * >> B2 Agonist or Cholinergic Antagonist
 * > Treat Infection
 * >> //Haemophilus Influenzae,Streptococcus Pneumoniae,Moraxella catarrhalis,// Gram Negative Bacteria (GNBs)
 * > Mobilize secretions
 * > Monitor for hypoxemia