COPD Flashcards
COPD
Preventable and treatable disease characterized by airflow limitation and abnormal inflammatory response in response to noxious chemicals or gases.
Slow, progressive irreversible damage due to chronic bronchitis and/or emphysema
COPD Fax
3rd leading cause of death in US
14.2 mil have it
COPD Risk factors
Smoking is leading cause
Occupational risk
Alcohol, age, gender
COPD Patho
Site of obstruction is in the smaller conducting pathways.
Destruction of alveolar support
Loss of elastic recoil
Structural narrowing sue to inflammation
COPD lung volume changes
Residual volume and functional residual capacity are increased.
Total lung capacity often increased
Vital capacity is reduced
Reasons for decreased vital capacity
Air trapping
Decreased lung recoil
Incomplete lung clearance
COPD is mediated by CD__ Cells
CD8 T lymphocytes
Asthma is CD4
Definition of chronic bronchitis
Blue bloaters
Defined as persistent cough resulting in sputum production for more than 3 months in each of the past 2 years.
Pathologic findings of chronic bronchitis
Goblet cell hyperplasia
Excess mucous secretion
Fibrosis
Chronic bronchitis patients develop hypoxia and cyanosis earlier than emphysema pt’s. T or F
T
Class S/S of chronic bronchitis
Increasingly productive cough
Dyspnea and progressive exercise intolerance
Frequent pulmonary infxns
Weight gain
Emphysema
Pink puffers
Abnormal enlargement of the airspaces distal to the terminal bronchioles.
Destruction of the alveolar walls ad capillary beds.
Abnormal airspaces called bullae compress normal lung.
Loss of lung elasticity
Emphysema Causes
Smoking
Alpha-1 antitrypsin deficiency
Emphysema presentation
Long hx of progressive dyspnea Non-productive cough Initially able to over-ventilate and maintain normal blood gas levels Patients are usually cachectic Pursed lip breathing is helpful
Centrilobular Emphysema
Most common type
Characterized by focal destruction
Seen predominantly in male smokers
Most severe in upper lobes
Panlobular Emphysema
Involves entire alveolus distal to the temrinal bronchiole.
Most severe in lower lung zones
Generally in patients with AAT deficiency
Alpha-1 Antitrypsin Deficiency
Congenital
Should be considered in young patients who show signs of emphysema
Typically develop dyspnea around age 30-45 yo
Usually Scandinavian descent
What does AAT do?
Serves as protective screen that protects alveolar walls
Emphysema Labs
AAT levels
Chest x-ray
Chest CT
AAt deficiency tx
Treat with Prolastin
Weekly infusions of AAT protein
Physical signs of COPD
Barrel chest Accessory muscle use Peripheral cyanosis Clubbing Decreased breath sounds Hyper-resonance on percussion Low, flat diaphragm
COPD advanced disease findings
Intervals btw exacerbations becomes shorter Cyanosis SIgnificant hypoxia Polycythemia Pulmonary HTN R sided heart failure
COPD blood gas findings
Low pH
Hypercapnia
Renal compensation
Cor Pulmonale
Pulmonary HTN
R sided heart failure
Poor gas exchange
Constriction of blood vessels
COPD complications
Pneumonia (strep)
Pneumothorax
Secondary polycythemia
COPD Tx
Smoking cessation
Pulmonary rehab
Immunizations
Medications
COPD Medical tx
Log-acting Bronchodilators
Inhaled Steroids
Mucolytics
Associated with reduction of exacerbations
Should be considered for winter months
Long-term oxygen therapy
Only treatment shown to prolong survival.
Patients with O2 sat <90 should receive oxygen.
Lung Volume Reduction Surgery
Removal of diseased lung tissue letting the healthy tissue fxn better.
Not a cure, improved quality of life.
1st line Abx for COPD exacerbation
Septra
Amoxacillin
Doxycycline
Acute exacerbation Tx
Oxygen
Inhaled Bronchodilators
Glucocorticoids
Abx
D/C criteria for COPD exacerbation
Use of inhaled bronchodilators less frequently than every 4 hrs
Clinical and ABG stability for 12-24 hrs
Can eat, sleep and ambulate
Bronchiectasis
Requires infectious insult and impaired drainage.
Results in blockage and inflammation, mucosal edema, ulceration.
Permanent abnormal dilation and destruction of major bronchi and bronchiole walls
Bronchiectasis Etiologies
Often caused by recurrent inflammation and infxn.
May be present at birth
Defective host defenses
Cystic fibrosis is major cause.
Bronchiectasis Presentation
Symptoms may develop gradually. Chronic cough, foul smelling sputum Hemoptysis Weight loss Fatigue Clubbing, cyanosis, wheezing
Bronchiectasis Tx
Treat infxn (long-term abx) Mucolytics Removal of possible obstruction Physiotherapy Vaccination
