COPD Flashcards
cause obstruction of the airways, usually through a combo of bronchoconstriction and inflammation.
ie. asthma, bronchitis (chronic or acute) and emphysema
COPD; chronic obstructive pulmonary disease
COPD is used to describe a specific progressive disorder that slowly alters the structures of the respiratory system over time, irreversibly affecting lung function.
-periodic exacerbations, respiratory infection, with increased symptoms of dyspnea and sputum (mucus or mucopurulent matter expectorated from the lungs) production.
-airways and lung parenchyma do not return to normal.
-present progressive destructive changes
-Not Curable, but managed. Usually includes both chronic bronchitis and emphysema.
-narrowing of sm. bronchioles
Leads to impaired gas exchange.
Chronic obstructive pulmonary disease
repeated exposure to repiratory irritants that begin to damage the structures with in the lungs.
-damage to small and large airways cause increase mucous production.
Causing arrest in cilia action.
-excessive amounts of fluid accumulate with the lung mucosal cells, causing edema.
-resulting in airflow limitation.
-air trapping
-hyperinflation, leading to Bronchitis; (inflammation of the mucous membranes of the bronchial tubes)
Pathophysiology and Etiology
inflammation of the mucous membranes of the bronchial tubes
Bronchitis
disorder of excessive bronchial mucous secretions; productive cough. -lasts 3 or more months -cigarette smoking leading contibutor -Inhaled irritants; vasodilation, congestion, and edema of the bronchial mucosa `Goblet cells increase by size and # `mucous glands enlarge `thick mucous produced `impaired ability to clear
persistant airway edema, excessive mucous production, and impaired airway clearance.
Chronic bronchitis
Lilly; Cont. inflammation and low grade infection of the bronchi
destruction of the walls of the alveoli, with resulting enlargement of abnormal air spaces.
- inflammatory cells, surface area for alveolar-capillary diffusion is reduced, affecting air exchange.
- Elastic recoil is lost, reducing Vol. air
- cigarette smoking strong indicator
with loss of interstitial membranes and airway support tissue, resulting in Airway collapse and loss of alveolar surface area for gas exchange.
Emphysema
Lilly; cond. in which the air spaces enlarge as a result of the destruction of the alveolar walls
Not smoking, smoking cessation.
decrease exposure to 2nd hand smoke
occupational irritants, air pollutants
Prevention
Smoking #1
Occupational exposure to irritants
asthma suffers
9/11 victims
Risk Factors with COPD
forced expiratory volume in 1 second; is the amount of air that can be exhaled in 1 sec as measured by a spirometer
-reading and symptom manifestation
determinants in COPD severity
FEV1
Absent; minor
chronic could sputum production
no SOB
Early stages
chronic productive cough
dyspnea
excerise intolerance
“smokers cough”
Symptoms; finally seeking help from physician
cough copious, thick, tenacious sputum, cyanosis evidence of right sided heart failure; ie. distended neck veins, edema, liver enlargement and an enlarged heart. -Low Rhonchi; possibly wheezing;
Manifestations of Chronic Bronchitits
Insidious onset Dyspnea; 1st symptom (initially only with exerction) progresses to even at rest. Cough minimal or absent Airtrapping; hyperinflation increases anterposterior chest; barrel chest thin, tachypneic tripod position, (sitting, leaning forward) -pursed-lip breathing;
Emphysema
prolongs the expiratory phase; promotes more alveolar emptying
-exhaling through a narrow opening between lips
pursed-lip breathing
prolonged impairment of gas exchange is a result of COPD eventually results in
Cardiac dysfunction
chest pain
hypertension
heart having to work harder to provide oxygen through the bloodstream
Cardiac dysfunction
makes breathing difficult to eat.
Tachycardia
- PT
- Nutrionists
- pharmacists
- family members
- counselors
Collaborate with
PFT; pulmonary function testing
-extent and progression of COPD
Ventilation; Perfusion scanning. VQ mismatch, extent to which lung tissue is ventilated but not perfused (dead space) or not adequately ventilated.
Radiosotope injected or inhaled to illustrate areas of shunting and absent capillaries
Serum a1-antitrypsin levels 1% deficency with fam hx 80-260 mg/dL
ABG;s evaluate gas exchange
pulse Oximetry; O2 sat %
Exhaled CO2; evaluate alveolar ventilation; 35-45 mmHG
CBC’s with WBC diff. shows increase in WBC’s, shows RBC’s and Hct (chronic hypoxia)
Chest Xray; sm patches indicatie of the hyperinflated alveolar sacs filled with secretions; common in emphysema.
flattened diaphragm; barrel chest in chronic bronchitis; and possible infection.
**lung transplant; no other treatment avail.
-Pharm therapy
Diagnostic Tests
used for severe and progressive hypoxemia. O2 therapy improves exercise tolerance, mental functioning and quality of life with advanced COPD.
O2 therapy
