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)
CBC in COPD
usually normal - r/o anemia
chronic bronchitis - polycythemia due to chronic hypoxia
leukocytosis may be present during acute exacerbations of COPD
Pulse Ox
if <92%,, assess further w/ ABG
ABG
usually mild-mod hypoxemia w/o hypercapnia
as disease progresses hypoxemia worsens and CO2 increases (respiratory acidosis)
When to obtain sputum culture
in-patient and unresponsive to initial abx tx
EKG findings in COPD
tachy
R atrial enlargement
R axis deviation and/or RVH
CXR findings
exclude other ddx
signs of air trapping (increased AP diameter, hyperinflaation, hyperlucency, flat diaphragms)
blebs or bullae (pathognomonic for emphysema)
perivascular or peribronchial markings in chronic bronchitis
Pathognomonic for emphysema
blebs or bullae
CXR findings for emphysema
hyperinflation (possibly w/ bullae)
flattening of diaphragms
enlargement of retrosternal air space
CXR findings suggestive of chronic bronchitis
cardiac enlargement
pulm. congestion
increased lung markings
chest CT
helpful, but not needed for dx
obtain if sxs suggest complication of COPD (pneumonia, pneumothorax, large bullae), alt. dx (PE) or if considering lung volume reduction surgery (HRCT)
Tx for group A
- SABA ORRRR
2. SABA + SAMA combo used PRN
Tx for group B
long-acting bronchodilator (LABA or LAMA)
Tx for group C
LAMA
Tx for group D
LABA + LAMA, or consider ICS + LABA
Effects of bronchodilators
bronchodilation
improved mucociliary clearance
diaphragmatic action
cardiact contractility
SABA drugs
albuterol - 2 puffs q 4-6 hrs
LABA drugs
salmeterol, formoterol
q12 h dosing
B2 agonists
bronchilation; no effect on sputum/secretions
SE of B2 agonists
palpitations, tachy, insomnia, tremors
SAMA drugs
ipratropium bromide (atrovent) Ipratropium plus albuterol (combivent)
2 puffs BID-QID
LAMA drugs
tiotripium bromide (spiriva) - q daily Umeclidinium (incruse ellipta) - q daily
anticholinergics
good bronchodilation;
reduces air trapping in lungs
less cardiac stim. effect
SE of anticholinergics
dry mouth, metallic taste, HA, cough
Combo meds for COPD
LAMA + LABA
bevespi aerosphere (BID) utibron neohaler (BID) Stiolto respimat (QD) Anoro Ellipta (QD)
Theophylline (methylxanthine)
used for refractory cases
toxicity is common
tachy, arrhythmias, seizures, HA, nasea
drug-drug interxns
Corticosteroids
alone or in combo w/ LABA
Advair, dulera, symbicort, breo ellipta
what do ICS do
reduce mucosal edema/inflammation by inhibiting prostaglandins –> dec secretions
increase responsiveness to beta-adrenergics
SE of ICS
oral candidiasis, bruising
Tx for AAT
Antiprotease (weekly-monthly injections)
costly and controversial
Lab values for AAT
<11 uM
Adjunct therapy for COPD
pulm. rehab (Stages B-D)
Oxygen (goal >90%)
lung volume reduction surgery?
Supplemental oxygen
prolongs survival
min. 12 hrs/day
indication for supplemental oxygen
chronic dyspnea at rest
PaO2 <55 or SaO2 <88%
Caution for supplemental O2
may reduce drive to breath and cause resp acidosis (maintain O2 sat 90-92%
Minimizing complications
flu vaccine
pneumo vaccine (PPV13, PCV23)
exercise
early recognition of infection
Acute exacerbation
increased dyspnea
increase in cough frequency/severity
sputum increases or becomes purulent
- contribute to high mortality
Trigger of acute exacerbations
respiratory illness (70%) pollution
viral most common: may lead to secondary bacterial pneumo (H. influenzae, S. pneumo M. catarrhalis, mycoplasma pneumo, pseudomonas)
outpatient management of acute exacerbation
increase dose of shortacting bronchodilator; add ipratropium if not taking it
oral steroids: 40mg/day x 5 days (reduces recovery time and hospital time)
abx (mod-severe)
hospitilization if severe
Abx for uncomplicated COPD acute exacerbation
Macrolide***
or cephalosporin, doxy, bactrim
Abx for complicated COPD acute exacerbation
fluoroquinolone (moxifloxacin, gemifloxacin, levofloxacin) ***
(or augmentin)
Indications for hospitilizations
severe s/sx severe COPD (FEV1<50) comorbidities new signs (cyanosis, edema, new arrhythmia) failure to respond to meds older insufficient home support
