COPD Flashcards
COPD is characterized by…
What are the two classic types (although there is much overlap)
progressive airflow limitation and enhanced chronic inflammatory response
- small airway dz (blue bloaters-chron. bronchitis)
- parenchymal destruction (pink puffers-emphysema)
What happens in small airway disease? What is its nickname and what is predominant?
airway inflammation and airway remodeling
“BLUE BLOATER” chronic bronchitis predominant
What happens in parenchymal destruction? What is its nickname and what is predominant?
loss of alveolar attachments and decreased elastic recoil
“PINK PUFFER”, emphysema predominant
pink puffer description
Emphysema-predominant, adequate oxygenation for a longer time period
“Pink Puffer” b/c of pursed-lip breathing, pink skin and thin body habitus (air comes in easily but need to recruit accessory muscles to get it out)
blue bloater description
Chronic Bronchitis-predominant
hypoxemia and respiratory acidosis more common; cor pulmonale from pulm HTN
“Blue Bloaters” due to cyanosis and overweight body habitus
Chronic Bronchitis definition
chronic productive cough for 3 months during 2 consecutive years with no other casue
Structural changes in chronic bronchitis
- mucous gland hyperplasia->excess mucus and narrowing of bronchioles
- bronchial squamous metaplasia
- loss of ciliary tranport
What happens to the bronchial wall and what does that (primary mediator)?
inflammation of bronchial wall-infiltration of submucosal layer by NEUTROPHILS
What else is thought to play an important role in chronic bronchitis?
Chronic bacterial infection and hyper-reactivity are thought to play an important role
What kind of obstruction occurs in chronic bronchitis?
inspiratory and expiratory
What occurs due to impeded ventilation of chronic bronchitis?
How does parenchymal damage of chronic bronchitis compare to that of emphysema?
hypoxemia and hypercarbia
less parenchymal damage than emphysema
How is EMPHYSEMA characterized?
pathologic enlargement of the air spaces distal to the terminal bronchioles du to destruction of alveolar walls
What is the destructive process of emphysema?
not clearly understood (possibly too much elastase or too little antitrypsin activity)
3 structural changes in emphysema
- dramatic decline in alveolar surface area available for gas exchange
- decreased elastic recoil, which limits airflow
- loss of alveolar supporting structure
Emphysema: effect on capillary bed and the effect of this
emphysema destroys the capillary bed, resulting in reduced Co2 diffusing capacity
->hypercarbia (hypercapnia)
BUT NOT AS SIGNIFICANT HYPOXEMIA
When does airflow obstruction occur in emphysema?
airflow obstruction mostly during exhalation
What is asthma and what mediates it?
Asthma is a chronic inflammatory disorder of the airways-primarily EOSINOPHIL mediated
3 steps in asthma
airway hyper-reactivity->increased secretions, mucosal edema, constriction of bronchial smooth muscle->airway obstruction
[reversible]
Emphysema describe: age at sx onset, character of dyspnea, cough, sputum prod., sputum appear
Emphysema onset: usually after age 50 dyspnea: progressive, constant, severe cough: absent to mild sputum prod: absent to mild sputum appearance: clear, mucoid
Chronic bronchitis describe: age at sx onset, character of dyspnea, cough, sputum prod, sputum appearance
Chronic Bronchitis onset: usually late 30s-40s dyspnea: intermittent, mild to moderate cough: persistent, severe sputum production: persistent, severe sputum appearance: mucopurulent
When does COPD present?
5th or 6th decade
Cardinal sxs of COPD:
CARD SXS: dyspnea, chronic cough and sputum production
- cough usually occurs in the morning
- in early COPD dysp on sig exertion, but progresses to miminal exertion or rest
Exposure to what puts you at risk for COPD?
- tobacco smoke
- other inhaled irritants (occupational dusts, pollution)
DDx for COPD
Asthma, Bronchiectasis, CHF, Obliterative bronchiolitis, central airway stenosis, lung cancer, TB, coccidioidomycosis, cystic fibrosis (younger pts), acute bronchitis (80-90% viral)
Risk factors for COPD
- CIGARETTE SMOKING (#1 cause, 80% of COPD pts, most have at least 20 pack year hist)
- air pollution (indoor and outdoor)
- second hand smoke
- airway hyper-responsiveness
- Generic RF: alpha-1 antitrypsin deficiency
(<1% of all cases, causes premature emphysema)
How does cigarette smoking contribute to COPD?
- cig smoke stimulates elastase enzymatic activity, causing degenerative changes in elastin and alveolar structures
- causes release of cytotoxic oxygen radicals from WBCs in lung tissue
(amt. and duration of cig smoking contribute to dz severity)
What kind of environmental/occupational exposure will place the proletariat at risk for COPD?
coal miners, grain handlers, metal molders, workers exposed to dust, cooking with biomass fuels (1/3 of the world)
Name a hereditary syndrome that results in early onset of emphysema. What is the average age of appearance?
Alpha 1-antitripsin deficiency (<1% of US cases of emphysema)
onset: 53 y/o nonsmokers, 40 y/o smokers (process is accelerated in smokers w/AAT def)
What is Alpha 1-antitrypsin? What happens if it disappears?
AAT is a protease inhibitor which inhibits elastase and several other proteolytic enzymes
-if AAT is not present in adequate amt, elastase & other proteolytic enzymes destroy lung tissue
COPD physical exam HEENT
check oral cavity closely, look for tobacco staining
COPD physical exam neck
masses, JVD
COPD physical exam chest
“body habitus”-look for increased AP diameter (barrel chest), use of accessory muscles, rate, effort of breathing, central cyanosis
COPD physical exam lungs
decreased breath sounds, rhonchi, wheezes, crackles, prolonged exhalation (tends to be bilateral)
COPD physical exam percussion
hyper-resonant
COPD physical exam heart
possible gallop, RV life, PMI
COPD physical exam abdomen
possible hepatomegaly, tenderness
COPD physical exam exterior
cyanosis, clubbing, muscle wasting, tobacco stains on fingers, peripheral edema
Emphysema exam findings
increased AP diameter "distant" breath sounds hyper-resonant to percussion possible pursed-lip breathing using accessory muscles
COPD CBC results
usually normal, may show polycythemia (increased H/H) later in chron. bronchitis, due to hypoxemia
COPD ABG results
hypoxemia (not as significant in emphysema as chron bronch), hypercarbia (CO2 retention)
COPD EKG results
sinus tachycardia, peaked P waves, and right axis deviation, RVH
Should you do a sputum examination in COPD?
NOT usually recommended/helpful (can be colonized w/bacteria anyway)
-recommended if you’ve been treating a patient and they’re not getting better
3 CXR findings suggestive of emphysema
- hyperinflation (possibly with bullae)
- flattening of diaphragms
- enlargement of retrosternal air space
CXR findings suggestive of chronic bronchitis
- cardiac enlargement
- pulmonary congestion
- increased lung markings
CT for COPD? sens, spec?
CT, esp high resolution CT has much greater sensitivity and specificity than standard chest radiography for dx of COPD, but NOT necc. for ROUTINE work-up
name 3 pulmonary function tests (PFTs)
forced vital capacity (FVC)
forced expiratory volume in 1 second (FEV1)
FEV1/FVC
Define forced vital capacity (FVC). What would you see in COPD?
FVC: amount of air forcefully exhaled after a maximal inspiration (varies w/height & age)
-usually normal or slightly decreased in COPD vs. low in restrictive dz
Define FEV1? What is normal, what do you see in obstructive airway dz?
FEV1=forced expiratory volume in 1 sec
normal>80% of predicted
FEV1 DECREASES in obstructive airway dz
(reversible in asthma; increases w/bronchidilator)
FEV1/FVC: normal value, abnormal meanings
normal FEV1/FVC: 70-80%
decreased FEV1 w/normal FVC suggests obstructive airways dz
<70% post bronchodilator
GOLD guidelines severity of airflow limitation-1st step
patients must have FEV1/FVC<70% to be staged
GOLD Stage I COPD PVTs, sxs, and tx
mild COPD
FEV1/FVCor= 80% predicted
with or without sxs
Tx: short-acting bronchodilator
GOLD Stage 2 COPD PVTs, sxs and tx
moderate COPD
FEV1/FVC<80
DOE, w/ or w/out cough and sputum production
tx:
-short acting bronchodilator when needed
-regular tx w/one or more long-acting bronchodilators
-rehabilitation
