COPD Flashcards
highest COPD prevalence
65-74 YO
morbidity greater in males
Pathphys behind COPD
inflammation –> small airway disease (inflammation/remodeling) & parenchymal destruction (loss of alveolar attachments/decrease in elastic recoil) –> airflow limitation
chronic bronchitis
mucous blocks airways;
inflammation and swelling further narrows airway
Emphysema
damage to alveoli prevent air exchange;
air becomes trapped
Blue bloater
Chronic bronchitis
cyanosis and overweight
hypoxemia and respiratory acidosis more common; cor pulmonale from pulm HTN (trouble getting air in AND out)
Pink puffer
emphysema
pursed-lip breathing
skin color and thin body
accessory mm. use (makes them thin)
gets air in but can’t get it out
COPD subtypes
chronic bronchitis
emphysema
chronic obstructive asthma
What is considered chronic bronchitis?
chronic PRODUCTIVE cough for 3+ months during 2 consecutive yrs w/ no other cause
Structural change for chronic bronchitis
mucous gland enlargement –> hyper secretion
bronchial squamous metaplasia
loss of ciliary transport
inflammation of bronchial wall and infiltration of sub-mucosal layer by NEUTROPHILS
obstruction is INSPIRATORY and EXPIRATORY
hypoxemia & hypercapnia
less parenchymal damage than emphysema
Emphysema changes
entrapment of air in spaces distal to terminal bronchioles due to destruction of alveolar walls
decreased elastic recoil
loss of alveolar supporting structure = airway narrowing
not clearly understood:
- may be too much elastase
- may be too little antitrypsin activity
obstruction is EXPIRATORY
not associated w/ significant hypoexmia until later in disease (destruction of capilarry bed, resulting in reduced DLCO)
neutrophil elastase
protease enzyme secreted by . neutrophils and macrophages during inflammations; destroys bacteria and host tissue
alpha-1 antitrypsin
inhibitor of neutrophil elastase; deficiency leads to breakdown of lung structure by elastase
Asthma
chronic inflammatory disorder of airways - EOSINOPHIL MEDIATED
airway hyper-reactivity –> increased secretions, mucosal edema, constriction of bronchial smooth mm. –> airway obstruction
REVERSIBLE
Risk factors for COPD
SMOKING! enviornmental/occupation second hand smoke hyper-responsiveness (asthma) genetic RF: alpha-1-antitrypsin deficiency (premature emphysema)
Cig smoking
stimulates elastase
causes cytotoxic oxygen radicals from WBC’s in lung tissue
How to dx alpha-1-antitrypsin deficiency
emphysema <45 YO
process accelerated in smokers w/ AAT deficiency
Clinical presentation of COPD
dyspnea (DOE earliest sx), chronic cough, sputum production
PE findings for COPD
tripod positioning cyanosis tobacco staining of fingers JVD, use of accessory mm. pursed lip breathing Lung: barrel chest, prolonged expiration, increased resonance on percussion, decreased breath sounds, wheezing, crackles at bases Heart: S3 gallop, RV lift ABD: hepatomegaly Ext: muscle wasting, peripheral edema
pursed lip breathing
ordinary breathing allows early bronchial collapse on exhalation; pursed lip breathing achieves resistance to outflow, raising intrabronchial pressure, keep bronchi open; thus more air can be expelled
Heart in COPD
S3, RV lift
Cor pulmonale
altered strucutre (hypertrophy or dilation) and/or imparied funciton of RV that results from pulmonary HTN associated w/ COPD
Labs/dx for COPD
spirometry CBC, BNP, cardiac enzymes, metabolic panel, AAT pulse ox ABG EKG Sputum exam CXR/HRCT
FVC (forced vital capacity)
amt of air forcefully exhaled during max forced expiration (N: 80-120%)
FEV1 (forced expiratory volume in 1 sec)
normal: 80-120%
FEV1/FVC ratio
% of FVC expired in 1 sec (N: 70-80%; or greater that LLN 5th percentile)
Dx of COPD
- pre and post bronchodilator (FEV1/FVC <0.7 is obstructive pattern)
- review post-bronchodilator FEV1% predicted - determine GOLD grade
PFT in COPD
FEV1/FVC < 0.7
decreased FEV1
increased TLC (vital capacity + RV)
Decreased DLCO (if severe emphysema)