COPD - Headley Flashcards
Definition of COPD 1) reversibility 2) in response to what 3) what contributes to severity
1) airflow limitation that is not fully reversible 2) limitation is progressive and associated with an abnormal chronic inflammatory response of the lungs to noxious particles or gases 3) exacerbations and comorbidities contribute to overall severity
COPD - what is indicative of airflow limitation? (part of clinical assessment)
reduced FEV1
COPD - what defines the reversibility (or lack of)?
reversibility less than 15%, or fixed
COPD - what cells are part of the immune response?
macrophages, neutrophils, CD8+ T cells
COPD - what happens during the inflammatory response? (what changes take place in the lung)
remodelling or airways, destruction of parenchyma
COPD - what are some noxious particles/gases that contribute to cause?
cigarette smoke, coal dust, pollution, biomass fuels
COPD - what constitutes the remodelling of airways
inflammation, fibrosis, luminal plugs (due to gobelt cell hyperplasia) and increased resistance
COPD - what constitutes the parenchymal destruction
loss of alveolar attchements, decrease of elastic recoil (increase compliance)
what pattern have we seen for COPD death rates for females in the past 20 years
they have doubled
what population has the lowest death rates from COPD? race and sex
black female
Compare COPD to the 6 leading causes of death in the US as far as death rates
only COPD death rates have been increasing since 1970
what is the primary risk factor for COPD
smoking
how many people total in the US smoke?
47.2 million
what percentage of males in the US smoke
28%
what percentage of women in the US smoke
23%
how many smokers are there worldwide?
1.1 billion
how many smokers does the WHO estimate by 2025 worldwide?
1.6 billion
what percentage of predicted FEV1 is associated with exertional dyspnea?
FEV1 = 40% - 60% predicted
what percentage of FEV1 is associated with disability?
30%
what cutoff of FEV1 (actual value) yields a 5 year mortality rate of 50%
less than 1 L
Compare the slope of the FEV1 decline of a smoker to a non smoker
the smoker will have a steeper decline in FEV1 than the non smoker (decreases faster)
What happens to the FEV1 decline curve of a smoker who quits?
the curve becomes less steep, and follows that of the non smoker - but FEV1 NEVER INCREASES!
In addition to inhaled pollutants, what are 4 other risk factors for COPD
1 - nutrition 2 - infections 3 - socio-economic status 4 - aging
for smokers, what pack year history is the cutoff for risk of COPD
20 pack year history. anything less, will rarely see COPD
for COPD, what are the presenting symptoms and at what age?
productive cough or acute chest illness seen in fifth decade of life (40s)
when does dyspnea on exertion present for COPD
sixth (50s) or seventh (60s) decade
what test is required for dx of COPD? what are the test results?
spirometry - post bronchodilator FEV1/FVC less than 0.7 confirms presence of persistent airflow limitation, COPD
what other disease course can progress into an irreversible airflow obstruction, indistinguishable from COPD?
long history of asthma
what is the end all be all definition of chronic bronchitis? (will be on exam)
productive cough, sputum, for 3-moths in 2 consecutive years
what is the number one thing to look for on clinical exam for airflow limitation in COPD
wheezing
what is the number 2 thing to look for on clinical exam for airflow limitation in COPD
prolongation of forced expiratory time
what are 2 observations (inspection) of patient that indicate hyperinflation in COPD
1 - barrel chest 2 - pursed lip breathing
what do you look for on CXR as a sign of hyperinflation in COPD
low diaphragm position
what would you auscultate as a result of hyperinflation in COPD
distant heart and breath sounds
what 3 features or impairments of mechanics of breathing are seen in COPD
1 - chest/abdominal wall paradoxical movements
2 - use of accessory muscles
3 - in-drawing of lower intercostal spaces
on clinical exam, what are signs of hypoxemia to look for in COPD
cyanosis or bluish color of mucosal membranes - lips and fingernails
auscultation of heart in COPD - what abnormalities might be heard
signs of cor pulmonale - split of S2, murmurs of P or T valve areas
cor pulmonale associated with COPD - what are other signs that can be seen
JVD, liver enlargement, or peripheral edema
what is the utility of doing a PFT with bronchodilator i.e. bronchodilator reversibility
1 - exclude asthma 2 - determine prognosis
for a bronchodilator reversiblity PFT (spirometry, albuterol, another spiromtery) what measures would indicated reversibility
and improvement of FEV1 greater than 200 cc and more than 15% improvement from baseline
what changes do we expect in static lung volumes in advanced COPD?
TLC, RV, RV/TLC are all increased
What happens to DLCO in COPD?
it is reduced in pt w/ predominant emphysema - this is because emphysema is a disease of the alveoli, thus impeding gas diffusion
How do we assess the risk of exacerbations of COPD? (this is on test)
use the history of exacerbations and spirometry - two or more exacerbations w/in the last year or an FEV1 less than 50% predicted value are indicators of high risk
define an exacerbation of COPD
an acute event characterized by a worsening of the pt’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication
what is the indication for performing an A1AT deficiency screening?
when COPD develops in patients of Caucasian descent under 45 years or with a strong family history of COPD
1) what are the characteristics of blue bloaters?
2) physical exam, O2 status
3) auscultate lungs
4) PVD exam
5) auscultate heart sounds
1) COPD w/ chronic respiratory failure and heart failure
2) cyanosis at rest or mild exertion
3) crackles at lung bases
4) edema of ankles
5) loud 2nd heart sound in pulmonary area (difficult to hear in COPD)
1) what are characteristics of pink puffers? O2 status?
2) breath sounds
3) type of breathing (inspection)
4) body habitus
5) characteristic breathing mechanism, body position
1) little or no hypoxia at rest
2) breathlessness and wheezing is severe on mild exertion
3) expiratory pursed lip breathing (auto-PEEP)
4) thin, underweight
5) tendency to lean forward over a support to assist breathing
are the majority of pts blue bloaters or pink puffers?
the majority of pts have a mixed pattern
what is the classification of pink puffer with regard to respiratory failure?
type A (I) - mild hypoxemia but not hypercapnic (maintain gas exchange)
what is the classification of blue bloaters with regard to respiratory failure?
type B (II) - they are hypoxemic and hypercapnic
which, of pink puffer and blue bloater, is emphysema predominant? chronic bronchitis predominant?
pink puffer - emphysema blue bloater - chronic bronchitis
compare the predominance of CHF in pink puffers vs blue bloaters
pink puffers - rarely CHF
blue bloaters - CHF, edema
what is the body habitus of blue bloaters?
obese
when you see someone with an O2 tank catch on fire in Gold Strike, were they a pink puffer or blue bloater?
blue bloaters carry around O2 tanks because they’re hypoxic as fuck
long term, what does chronic hypoxemia cause in blue bloaters?
polycytehmia (elevated Hct), pulmonary HTN, and cor pulmonale
when do pink puffers develop severe hypoxemia and hypercapnia?
when they are near death
what are the breathing characteristics of pink puffers? and why is this impt?
dyspnea, tachypnea, and high minute ventilation (RR x TV) pts inc their MV enough to blow off excessive CO2 and maintain pCO2 in normal range - at the cost of a high WOB
why are pink puffers thin?
high WOB, high energy expenditure just trying to breathe
what is the (brief) pathophysiology behind cigarette smoking causing COPD
the cigarette smoke causes lung inflammation which overwhelms anti-oxidants and anti-proteinases. The imbalance favoring oxidative stress and proteinases leads to alveolar damage and COPD pathology
for asthmatic airway inflammation - what are the typical inflammatory mediators? (potential test question)
CD4+ T cells and eosinophils
for COPD airway inflammation, what are the typical inflammatory mediators? (potential test question)
CD8+ T cells, CD68+ macrophages, neutrophils (need to know the 68+ macs)
what percentage of patients have a mixed pattern of chronic bronchitis plus emphysema?
90%
why does hypoxemia and hypercapnia develop in COPD? (this is must know)
they develop due to ventilation-perfusion mismatching
MUST KNOW - characterize smoking emphysema and A1AT emphysema with regards to lobular pattern and location in lungs
smoking - centrolobular, upper lobes (smoke rises)
A1AT - panlobular, lower lobes
what are bullae? how do they form?
bullae are emphysematous spaces greater than 1 cm in diameter they form b/c emphysema results in a significant loss of alveolar attachments
what is the significance of loss of alveolar attachments in emphysema?
loss of radial traction on airways, such that they collapse on expiration (dynamic airway collapse) - this is the obstruction, leads to air trapping, and thus hyperinflation
In addition to hyperinflated lungs and a flat diaphragm, what is another key finding in CXR of COPD
tear drop shaped heart
what does a flow-volume loop reveal in chronic bronchitis
airflow obstruction during expiration and inspiration
What changes do we see in the lung volumes of pure chronic bronchitis? lung compliance? elastic recoil? DLCO?
all normal - bronchitis is a disease of the airways, not the alveoli
what does the flow-volume loop reveal in pure emphysema
airflow obstruction during expiration but not inspiration
what happens to the RV, TLC and VC in pure emphysema?
RV and TLC increase while VC actually decreases
what is a characteristic finding in COPD on the expiratory arm of the flow-volume loop?
scooping - tells you there is airflow obstruction
recall the spirometry requirements for making a diagnosis of COPD
1) reduce FEV1 % predicted post bronchodilator
2) reduced forced expiratory ratio (FEV1/FVC) less than 70% (0.7)
in addition to spirometry, what 2 other entities must be present for dx of COPD
symptoms of cough, sputum, maybe dyspnea
exposure to risk factos (smoke, coal miner, etc)
what is the most common cause of an exacerbation of COPD? what 6 bugs?
bacterial infection of the tracheobronchial tree (infectious bronchitis) 1) S. pneumoniae 2) H. influenza 3) Pseudomonas aeruginosa 4) Moraxella catarralis 5) Mycoplasma 6) Chlamydia
what are the 3 main treatment options for COPD
1) O2 (target sat of 88-92%)
2) Bronchodilators
3) systemic corticosteroids
what 3 cardinal symptoms indicate the use of antibiotics for the tx of COPD
1) increased dyspnea 2) increased sputum volume 3) increased sputum purulence
management of stable COPD includes 7 things 1) smoking 2) vaccination 3) vaccination 4) an inhaled gas 5) an inhaled therapy (not B agonist) 6) something general 7) another generality
1) smoking cessation adn avoidance of noxious agents
2) influenza vacc
3) pneumococcal vacc
4) long term O2 therapy in selected pts
5) inhaled glucocorticoid therapy in pts w/ moderate to severe COPD
6) pulm rehabilitation
7) nutritional therapy
Management of stable COPD - long term O2 therapy is the most impt drug in hypoxic pts - what does it improve? (5)
1) survival
2) exercise
3) sleep
4) QOL
5) cognitive performance
management of stable COPD - what does long term O2 therapy reduce/prevent (2)
1) pulmonary HTN
2) polycythemia
management of stable COPD - long term O2 therapy - what is your target PaO2 and SaO2
PaO2 - 60
SaO2 - 90
management of stable COPD - long term O2 therapy - how many hours must it be worn per day to be effective
15-24 hours per day
management of stable COPD - long term O2 therapy - what are the indications? 1) PaO2 2) SaO2 3) PaO2 + what symptoms 4) overall goal
1) PaO2 less than 55
2) SAO2 less than 88%
3) PaO2 = 56-59 w/ either p-pulmonale of EKG, pedal edema, or polycythemia
4) goal - maintain sats above 90% during rest, sleep, and with exertion
there are 3 mechanisms that cause worsening hypercapnia (inc in PaCO2) if you give a chronic COPD pt supp 100% O2. what is the first - relates to pulm hypoxic vasoconstriction
the pt currently has hypoxic vasoconstriction to make sure blood only goes to well ventilated areas of lung. If you give 100% O2 - will get rid of hypoxic vasoconstriction, but there are still poorly ventilated portions of lung, and now there is blood flow there, with no gas exchange. Thus they cannot blow off as much CO2, so CO2 will go up
there are 3 mechanisms that cause worsening hypercapnia (inc in PaCO2) if you give a chronic COPD pt supp 100% O2. what is the second? relates to neurologic process
Mild*** depression of central chemoreceptor drive of respiration in response to inc O2 –> but they will not quit breathing all together
there are 3 mechanisms that cause worsening hypercapnia (inc in PaCO2) if you give a chronic COPD pt supp 100% O2. what is third? - think about Haldane effect
3) Haldane effect - O2 binds to Hb more readily than CO2 - in a hypoxic patient with elevated CO2, both O2 and CO2 will bind to Hb - give them 100% supp O2, it will knock the CO2 off and the CO2 will then dissolve in the blood - will be measured as a pCO2
Muthiah exam question - what happens to FEV1 decline curve when you quit smoking? does it increase?
it DOES NOT increase; it will decline at a less steep rate, thus can cut losses
Muthiah exam question - what effect does exercise and pulmonary rehabilitation have on exercise tolerance and FEV1
they will improve exercise tolerance, but will not increase the FEV1
Muthiah exam question - compare the reversibility of FEV1 in asthma vs COPD
asthma - FEV1 fully reversible
COPD - FEV1 partially reversible
Muthiah exam question - what are the differences in lobular pattern and location in the lung for smoking epmhysema vs A1AT emphysema?
smoking - centrolobular, upper lobes
A1AT - panlobular, lower lobes
