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Pulmonology > COPD - Headley > Flashcards

COPD - Headley Flashcards

1
Q

Definition of COPD 1) reversibility 2) in response to what 3) what contributes to severity

A

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

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2
Q

COPD - what is indicative of airflow limitation? (part of clinical assessment)

A

reduced FEV1

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3
Q

COPD - what defines the reversibility (or lack of)?

A

reversibility less than 15%, or fixed

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4
Q

COPD - what cells are part of the immune response?

A

macrophages, neutrophils, CD8+ T cells

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5
Q

COPD - what happens during the inflammatory response? (what changes take place in the lung)

A

remodelling or airways, destruction of parenchyma

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6
Q

COPD - what are some noxious particles/gases that contribute to cause?

A

cigarette smoke, coal dust, pollution, biomass fuels

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7
Q

COPD - what constitutes the remodelling of airways

A

inflammation, fibrosis, luminal plugs (due to gobelt cell hyperplasia) and increased resistance

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8
Q

COPD - what constitutes the parenchymal destruction

A

loss of alveolar attchements, decrease of elastic recoil (increase compliance)

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9
Q

what pattern have we seen for COPD death rates for females in the past 20 years

A

they have doubled

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10
Q

what population has the lowest death rates from COPD? race and sex

A

black female

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11
Q

Compare COPD to the 6 leading causes of death in the US as far as death rates

A

only COPD death rates have been increasing since 1970

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12
Q

what is the primary risk factor for COPD

A

smoking

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13
Q

how many people total in the US smoke?

A

47.2 million

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14
Q

what percentage of males in the US smoke

A

28%

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15
Q

what percentage of women in the US smoke

A

23%

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16
Q

how many smokers are there worldwide?

A

1.1 billion

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17
Q

how many smokers does the WHO estimate by 2025 worldwide?

A

1.6 billion

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18
Q

what percentage of predicted FEV1 is associated with exertional dyspnea?

A

FEV1 = 40% - 60% predicted

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19
Q

what percentage of FEV1 is associated with disability?

A

30%

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20
Q

what cutoff of FEV1 (actual value) yields a 5 year mortality rate of 50%

A

less than 1 L

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21
Q

Compare the slope of the FEV1 decline of a smoker to a non smoker

A

the smoker will have a steeper decline in FEV1 than the non smoker (decreases faster)

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22
Q

What happens to the FEV1 decline curve of a smoker who quits?

A

the curve becomes less steep, and follows that of the non smoker - but FEV1 NEVER INCREASES!

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23
Q

In addition to inhaled pollutants, what are 4 other risk factors for COPD

A

1 - nutrition 2 - infections 3 - socio-economic status 4 - aging

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24
Q

for smokers, what pack year history is the cutoff for risk of COPD

A

20 pack year history. anything less, will rarely see COPD

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25
Q

for COPD, what are the presenting symptoms and at what age?

A

productive cough or acute chest illness seen in fifth decade of life (40s)

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26
Q

when does dyspnea on exertion present for COPD

A

sixth (50s) or seventh (60s) decade

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27
Q

what test is required for dx of COPD? what are the test results?

A

spirometry - post bronchodilator FEV1/FVC less than 0.7 confirms presence of persistent airflow limitation, COPD

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28
Q

what other disease course can progress into an irreversible airflow obstruction, indistinguishable from COPD?

A

long history of asthma

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29
Q

what is the end all be all definition of chronic bronchitis? (will be on exam)

A

productive cough, sputum, for 3-moths in 2 consecutive years

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30
Q

what is the number one thing to look for on clinical exam for airflow limitation in COPD

A

wheezing

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31
Q

what is the number 2 thing to look for on clinical exam for airflow limitation in COPD

A

prolongation of forced expiratory time

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32
Q

what are 2 observations (inspection) of patient that indicate hyperinflation in COPD

A

1 - barrel chest 2 - pursed lip breathing

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33
Q

what do you look for on CXR as a sign of hyperinflation in COPD

A

low diaphragm position

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34
Q

what would you auscultate as a result of hyperinflation in COPD

A

distant heart and breath sounds

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35
Q

what 3 features or impairments of mechanics of breathing are seen in COPD

A

1 - chest/abdominal wall paradoxical movements

2 - use of accessory muscles

3 - in-drawing of lower intercostal spaces

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36
Q

on clinical exam, what are signs of hypoxemia to look for in COPD

A

cyanosis or bluish color of mucosal membranes - lips and fingernails

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37
Q

auscultation of heart in COPD - what abnormalities might be heard

A

signs of cor pulmonale - split of S2, murmurs of P or T valve areas

38
Q

cor pulmonale associated with COPD - what are other signs that can be seen

A

JVD, liver enlargement, or peripheral edema

39
Q

what is the utility of doing a PFT with bronchodilator i.e. bronchodilator reversibility

A

1 - exclude asthma 2 - determine prognosis

40
Q

for a bronchodilator reversiblity PFT (spirometry, albuterol, another spiromtery) what measures would indicated reversibility

A

and improvement of FEV1 greater than 200 cc and more than 15% improvement from baseline

41
Q

what changes do we expect in static lung volumes in advanced COPD?

A

TLC, RV, RV/TLC are all increased

42
Q

What happens to DLCO in COPD?

A

it is reduced in pt w/ predominant emphysema - this is because emphysema is a disease of the alveoli, thus impeding gas diffusion

43
Q

How do we assess the risk of exacerbations of COPD? (this is on test)

A

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

44
Q

define an exacerbation of COPD

A

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

45
Q

what is the indication for performing an A1AT deficiency screening?

A

when COPD develops in patients of Caucasian descent under 45 years or with a strong family history of COPD

46
Q

1) what are the characteristics of blue bloaters?
2) physical exam, O2 status
3) auscultate lungs
4) PVD exam
5) auscultate heart sounds

A

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)

47
Q

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

A

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

48
Q

are the majority of pts blue bloaters or pink puffers?

A

the majority of pts have a mixed pattern

49
Q

what is the classification of pink puffer with regard to respiratory failure?

A

type A (I) - mild hypoxemia but not hypercapnic (maintain gas exchange)

50
Q

what is the classification of blue bloaters with regard to respiratory failure?

A

type B (II) - they are hypoxemic and hypercapnic

51
Q

which, of pink puffer and blue bloater, is emphysema predominant? chronic bronchitis predominant?

A

pink puffer - emphysema blue bloater - chronic bronchitis

52
Q

compare the predominance of CHF in pink puffers vs blue bloaters

A

pink puffers - rarely CHF

blue bloaters - CHF, edema

53
Q

what is the body habitus of blue bloaters?

A

obese

54
Q

when you see someone with an O2 tank catch on fire in Gold Strike, were they a pink puffer or blue bloater?

A

blue bloaters carry around O2 tanks because they’re hypoxic as fuck

55
Q

long term, what does chronic hypoxemia cause in blue bloaters?

A

polycytehmia (elevated Hct), pulmonary HTN, and cor pulmonale

56
Q

when do pink puffers develop severe hypoxemia and hypercapnia?

A

when they are near death

57
Q

what are the breathing characteristics of pink puffers? and why is this impt?

A

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

58
Q

why are pink puffers thin?

A

high WOB, high energy expenditure just trying to breathe

59
Q

what is the (brief) pathophysiology behind cigarette smoking causing COPD

A

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

60
Q

for asthmatic airway inflammation - what are the typical inflammatory mediators? (potential test question)

A

CD4+ T cells and eosinophils

61
Q

for COPD airway inflammation, what are the typical inflammatory mediators? (potential test question)

A

CD8+ T cells, CD68+ macrophages, neutrophils (need to know the 68+ macs)

62
Q

what percentage of patients have a mixed pattern of chronic bronchitis plus emphysema?

A

90%

63
Q

why does hypoxemia and hypercapnia develop in COPD? (this is must know)

A

they develop due to ventilation-perfusion mismatching

64
Q

MUST KNOW - characterize smoking emphysema and A1AT emphysema with regards to lobular pattern and location in lungs

A

smoking - centrolobular, upper lobes (smoke rises)

A1AT - panlobular, lower lobes

65
Q

what are bullae? how do they form?

A

bullae are emphysematous spaces greater than 1 cm in diameter they form b/c emphysema results in a significant loss of alveolar attachments

66
Q

what is the significance of loss of alveolar attachments in emphysema?

A

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

67
Q

In addition to hyperinflated lungs and a flat diaphragm, what is another key finding in CXR of COPD

A

tear drop shaped heart

68
Q

what does a flow-volume loop reveal in chronic bronchitis

A

airflow obstruction during expiration and inspiration

69
Q

What changes do we see in the lung volumes of pure chronic bronchitis? lung compliance? elastic recoil? DLCO?

A

all normal - bronchitis is a disease of the airways, not the alveoli

70
Q

what does the flow-volume loop reveal in pure emphysema

A

airflow obstruction during expiration but not inspiration

71
Q

what happens to the RV, TLC and VC in pure emphysema?

A

RV and TLC increase while VC actually decreases

72
Q

what is a characteristic finding in COPD on the expiratory arm of the flow-volume loop?

A

scooping - tells you there is airflow obstruction

73
Q

recall the spirometry requirements for making a diagnosis of COPD

A

1) reduce FEV1 % predicted post bronchodilator
2) reduced forced expiratory ratio (FEV1/FVC) less than 70% (0.7)

74
Q

in addition to spirometry, what 2 other entities must be present for dx of COPD

A

symptoms of cough, sputum, maybe dyspnea

exposure to risk factos (smoke, coal miner, etc)

75
Q

what is the most common cause of an exacerbation of COPD? what 6 bugs?

A

bacterial infection of the tracheobronchial tree (infectious bronchitis) 1) S. pneumoniae 2) H. influenza 3) Pseudomonas aeruginosa 4) Moraxella catarralis 5) Mycoplasma 6) Chlamydia

76
Q

what are the 3 main treatment options for COPD

A

1) O2 (target sat of 88-92%)
2) Bronchodilators
3) systemic corticosteroids

77
Q

what 3 cardinal symptoms indicate the use of antibiotics for the tx of COPD

A

1) increased dyspnea 2) increased sputum volume 3) increased sputum purulence

78
Q

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

A

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

79
Q

Management of stable COPD - long term O2 therapy is the most impt drug in hypoxic pts - what does it improve? (5)

A

1) survival
2) exercise
3) sleep
4) QOL
5) cognitive performance

80
Q

management of stable COPD - what does long term O2 therapy reduce/prevent (2)

A

1) pulmonary HTN
2) polycythemia

81
Q

management of stable COPD - long term O2 therapy - what is your target PaO2 and SaO2

A

PaO2 - 60

SaO2 - 90

82
Q

management of stable COPD - long term O2 therapy - how many hours must it be worn per day to be effective

A

15-24 hours per day

83
Q

management of stable COPD - long term O2 therapy - what are the indications? 1) PaO2 2) SaO2 3) PaO2 + what symptoms 4) overall goal

A

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

84
Q

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

A

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

85
Q

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

A

Mild*** depression of central chemoreceptor drive of respiration in response to inc O2 –> but they will not quit breathing all together

86
Q

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

A

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

87
Q

Muthiah exam question - what happens to FEV1 decline curve when you quit smoking? does it increase?

A

it DOES NOT increase; it will decline at a less steep rate, thus can cut losses

88
Q

Muthiah exam question - what effect does exercise and pulmonary rehabilitation have on exercise tolerance and FEV1

A

they will improve exercise tolerance, but will not increase the FEV1

89
Q

Muthiah exam question - compare the reversibility of FEV1 in asthma vs COPD

A

asthma - FEV1 fully reversible

COPD - FEV1 partially reversible

90
Q

Muthiah exam question - what are the differences in lobular pattern and location in the lung for smoking epmhysema vs A1AT emphysema?

A

smoking - centrolobular, upper lobes

A1AT - panlobular, lower lobes

Pulmonology (31 decks)

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