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PHAR253 > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

respiratory disorder largely caused by smoking that is characterized by:
-progressive, partially reversible airway obstruction
-lung hyperinflation
-systemic manifestations
-increasing frequency and severity of exacerbations

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2
Q

What is emphysema?

A

abnormal enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis

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3
Q

What is chronic bronchitis?

A

chronic cough for at least 3 months x 2 consecutive years

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4
Q

Provide a brief overview of the epidemiology of COPD.

A

772,200 (4%) Canadians >35yrs with COPD
cigaretter smoking is the principle underlying cause of COPD
-responsible for 80% of deaths
3rd leading cause of death worldwide

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5
Q

What are the non-host risk factors for COPD?

A

exposure to particles
-cigarette smoking/exposure to 2nd hand smoke
-occupational dusts, organic and inorganic
-outdoor air pollution
-indoor air pollution
infections
-frequent childhood respiratory problems/prior TB or HIV
socio-economic factors

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6
Q

What is the most significant risk factor for COPD

A

cigarette smoking/exposure to 2nd hand smoke

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7
Q

What are the host risk factors for COPD?

A

genetics: 1-antitrypsin deficiency
age (because of particle exposure?)
lung growth and development
airway hyper-responsiveness
-asthma=increased risk?

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8
Q

What is 1-antitrypsin?

A

serum protein produced by the liver and normally found in lungs
prevents neutrophil elastase from destroying lung tissue

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9
Q

What is the pathophysiology of COPD?

A

stimulus (smoking)–>inflammatory process–>narrowing of peripheral airways–> reduced FEV1
-oxidative stress may play an important role in amplifying the inflammatory process
-a protease-antiprotease imbalance is noted in the lungs of COPD patients (protease mediated destruction of elastin)
-increased CD8 and other inflammatory mediators induce structural changes

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10
Q

Describe expiratory flow limitation as part of the pathophysiology of COPD.

A

hallmark of COPD
due to increased resistance from mucosal inflammation, airway remodeling, fibrosis & secretions

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11
Q

Describe lung hyperinflation as part of the pathophysiology of COPD.

A

obstruction of the small airways results in air-trapping which causes lung hyperinflation
develops early in disease and causes exertional dyspnea

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12
Q

Describe gas exchange abnormalities as part of the pathophysiology of COPD.

A

results in hypoxemia & hypercapnia
gas transfer for O2 & CO2 worsens as disease progresses

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13
Q

Describe mucous hypersecretion as part of the pathophysiology of COPD.

A

results in chronic productive cough
not necessarily associated with airflow limitation

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14
Q

Describe exacerbations as part of the pathophysiology of COPD.

A

triggered by infection, environmental pollutants or unknown
during exacerbations there is increased hyperinflation and gas trapping with decreased expiratory flow

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15
Q

Describe significant comorbid illness as part of the pathophysiology of COPD.

A

pulmonary HTN may develop late in course of COPD due to hypoxic vasoconstriction of small pulmonary arteries
muscle wasting and cachexia, skeletal muscle dysfunction
osteoporosis, depression, anemia, metabolic syndrome, CV, lung disease

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16
Q

What are the three cardinal symptoms of COPD?

A

phlegm
chronic cough
shortness of breath

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17
Q

Aside from the cardinal symptoms, what are some other symptoms of COPD?

A

barrel-shaped chest
fatigue
frequent lung infections
unexplained weight loss
reduced ability for daily activities

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18
Q

What are the end-stage symptoms of COPD?

A

adopt positions that relieve dyspnea
use of accessory respiratory muscles
expiration through pursed lips
cyanosis
enlarged liver from right heart failure

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19
Q

How do patients initially present with COPD?

A

sedentary lifestyle and general fatigue
-avoiding exertional dyspnea
-shifted expectations and limited their activities
complains of dyspnea and chronic cough
-initially noted on exertion only
-progressively triggered by less exertion
-morning sputum production
episodes of cough, sputum, wheezing, fatigue, and dyspnea
-intervals between episodes shortens

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20
Q

Differentiate asthma and COPD using the following parameters:
-age on onset
-smoking history
-sputum production
-allergies
-clinical symptoms
-disease course
-importance of co-morbid illness
-spirometry
-airway inflammation
-response to ICS
-role of bronchodilators
-role of exercise training
-end of life discussions

A

age on onset
-COPD: usually >40 yrs
-asthma: usually <40 yrs
smoking history
-COPD: usually >10 pack-years
-asthma: not causal, but worsens control
sputum production
-COPD: often
-asthma: infrequent
allergies:
-COPD: infrequent
-asthma: often
clinical symptoms
-COPD: persistent and progressive
-asthma: intermittent and variable
disease course
-COPD: progressive worsening
-asthma: stable
importance of co-morbid illness
-COPD: often important
-asthma: often important
spirometry
-COPD: may improve but never normalizes
-asthma: often normalizes
airway inflammation
-COPD: neutrophilic
-asthma: eosinophilic
response to ICS
-COPD: helpful in mod-severe dx and freq AECOPD
-asthma: essential for optimal control
role of bronchodilators
-COPD: regular therapy usually necessary
-asthma: prn only
role of exercise training
-COPD: essential therapy
-asthma: rarely formally used
end of life discussions
-COPD: often essential
-asthma: rarely necessary

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21
Q

When should we consider a clinical diagnosis for a patient?

A

any patient who has:
-dyspnea
-chronic cough
-sputum production
-history of exposure to risk

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22
Q

What is required to make a diagnosis of COPD?

A

spirometry
spirometry post-bronchodilator FEV1/FVC ratio <0.7 confirms diagnosis

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23
Q

True or false: evidence supports population screening with spirometry for COPD

A

false

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24
Q

Which patients should be screened for COPD?

A

smokers/ex-smokers >40yrs who have:
-persistent cough or sputum production
-frequent respiratory tract infections
-progressive activity-related SOB
-evening wheeze

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25
Q

What are some good questions to ask when screening someone for COPD?

A

do you cough regularly
do you cough up phlegm regularly?
do even simple chores make you short of breath?
do you wheeze when you exert yourself or at night?
do you get frequent colds that persist longer than those of other people?
IF YES–>SPIROMETRY

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26
Q

What are the steps in the clinical evaluation of COPD?

A
  1. pulmonary function testing
    -must determine degree of reversibility
    -FEV1 <80% and FEV1/FVC ratio <0.7
  2. assessment of risk factors
    -quantification of tobacco consumption
    -record environmental exposures
  3. assessment of severity of breathlessness using the MRC dyspnea scale or CAT test
  4. assessment of frequency and severity of exacerbations
  5. assessment of symptoms that could point to complications
  6. assessment of the symptoms that suggest comorbidities
  7. assessment of medications
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27
Q

Describe the mMRC dyspnea scale.

A

grade 0:
-breathless with strenuous exercise
grade 1: mild
-SOB when hurrying on level or walking uphill
stage 2: moderate
-walks slower than people of same age on level or stops for breath while walking at own pace on same level
stage 3: moderate
-stops for breath after walking 100m or after few mins on same level
stage 4: severe
-too breathless to leave house, or dressing

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28
Q

What is the CAT test?

A

validated, short and simple patient completed questionnaire
reliable measure of the impact of COPD on a patients health status
score ranging from 0-40:
-0-10=low impact
-10-20=medium impact
-21-30=high impact
->30=very high impact

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29
Q

What is the spirometry that can diagnose someone with COPD?

A

post bronchodilator FEV1 <80% predicted
FEV1/FVC ratio < 70%

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30
Q

What are the corresponding spirometry values for the stages of COPD?

A

mild:
-FEV1 >80% predicted
-FEV1/FVC ratio <0.7
moderate:
-FEV1 50-79% predicted
-FEV1/FVC ratio <0.7
severe:
-FEV1 30-49% predicted
-FEV1/FVC ratio <0.7
very severe:
-FEV1 <30% predicted
-FEV1/FVC <0.7

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31
Q

How is FEV1 used in assessing COPD?

A

used to stage/assess severity

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32
Q

What are the goals of treatment for COPD?

A

prevent disease progression
prevent and treat exacerbations
alleviate breathlessness and other respiratory symptoms
improve exercise tolerance and daily activity
prevent and treat complications of the disease
improve health status
reduce mortality

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33
Q

What are the 8 possible treatments of COPD?

A

smoking cessation
eliminate occupation/environmental exposures
comprehensive patient/family education
avoid sedatives/narcotics in severe disease
rehabilitation programs
vaccines
long-term oxygen therapy
pharmacologic therapy

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34
Q

What is the single most effective intervention to reduce the risk of COPD and the only intervention that has been shown to slow its progression?

A

smoking cessation

35
Q

What are the five A’s of smoking cessation?

A

ask
advise
assess
assist
arrange

36
Q

What are the important aspects of comprehensive patient/family education for COPD?

A

expectations of therapy must be discussed
self management plans
-Rxs for oral steroids and antibiotics to fill prn
-advanced care directives
inhaler technique
-select best device for each patient

37
Q

Why should sedatives/narcotics be avoided in severe disease?

A

increased sensitivity to respiratory depression especially when sleeping

38
Q

What are some examples of pulmonary rehabilitation programs?

A

respiratory, physical and occupational therapy
exercise conditioning
nutritional counseling
psychosocial support
vocational rehabilitation

39
Q

True or false: COPD patients should not carry out an active lifestyle

A

false
all COPD patients should be encouraged to maintain an active lifestyle

40
Q

What are the benefits of pulmonary rehabilitation?

A

reduced dyspnea
increased exercise endurance
improved quality of life
reduced leg discomfort
decreased fatigue
reduced resource utilization related to AECOPD
trend toward reduced mortality

41
Q

Which vaccinations are recommended for COPD patients?

A

influenza
pneumococcal
COVID

42
Q

Describe oxygen therapy for COPD.

A

does not change pulmonary function
cornerstone of therapy
-improves quality/duration of life in selected patients
assess patient when stable
goal PaO2 > 60mmHg

43
Q

What is the mainstay of treatment for COPD?

A

bronchodilators
-larger doses may be used compared to treatment in asthma

44
Q

What is the role of muscarinic antagonists and ICS for COPD compared to asthma?

A

muscarinic antagonists have larger role
ICS have less of a role

45
Q

What should you investigate if a bronchodilator has failed for a COPD patient?

A

technique and compliance

46
Q

What is an example of a SAMA? What is its dosing frequency?

A

ipratropium
-QID prn

47
Q

What is the use of short acting bronchodilators in all stages of COPD treatment?

A

prn use
-higher doses=more bronchodilation
-may increase beyond recommended dose in severe disease

48
Q

What is the MOA of SAMAs and LAMAs?

A

competitively inhibit cholinergic receptors in bronchial smooth muscle
-blocks ACh which reduces cGMP
-airway muscle tone is partially controlled by cholinergic innervation

49
Q

Compare SAMAs to SABAs in terms of efficacy and onset.

A

SAMAs are less effective than B2 agonists in asthma
slower onset of action than SABA

50
Q

What are the adverse effects of SAMAs and LAMAs?

A

dry mouth (rinse mouth after)
cough
constipation
urinary retention
headache
avoid eye contact (can precipitate glaucoma)

51
Q

What are examples of LAMAs?

A

tiotropium
glycopyrronium
aclidinium
umeclidinium

52
Q

Compare LABAs and LAMAs.

A

both improve symptoms
LAMA may be superior in decreasing exacerbations
LAMA may be better tolerated
side effects profile vary:
-LAMA: dry mouth, constipation
-LABA: headache, dose dependent CV effects
cost is similar

53
Q

True or false: just like asthma, ICS are used 1st line in COPD

A

false

54
Q

Why are ICS not used first line in COPD?

A

evidence for reducing exacerbations but inconsistent evidence for symptom improvement
consider ICS AEs (increased risk of pneumonia)

55
Q

Which COPD patients might respond better to ICS?

A

those with higher eosinophil count

56
Q

What is the dosage regimen of prophylactic azithromycin in COPD?

A

250mg OD x 1yr
-lower exacerbation rates and improved QOL
-higher rate of macrolide-resistant bacteria and hearing deficits
-may also see dosed 3x weekly

57
Q

Which patients would be eligible for prophylactic azithromycin?

A

normal QT interval
no significant DIs
no evidence of indolent or active infection with atypical mycobacteria

58
Q

What is the role of N-acetylcysteine in COPD?

A

600mg po BID may be of benefit in reducing acute exacerbations in those who had 2 or more exacerbations in the previous 2 yrs
-optimal dose has not been determined
-mucolytic agent with antioxidant properties

59
Q

Which phenotype of COPD is at higher risk of exacerbations from NAC?

A

chronic bronchitis

60
Q

What is the MOA of roflumilast?

A

phosphodiesterase inhibitor

61
Q

What is the role of roflumilast in COPD? What is its dose?

A

add-on to bronchodilator treatment
could be considered for addition to existing triple therapy (LAMA/LABA/ICS) for ppl with COPD who have had at least 1 exacerbation in the past year
not to be used as rescue medication
dose: 500mcg po OD

62
Q

What are the side effects of roflumilast?

A

diarrhea, weight loss, nausea, headache, sleep disturbances
neuropsych effects (avoid in hx of depression with suicidal ideation)
less tolerated than inhaled meds

63
Q

True or false: theophylline is still in the COPD guidelines

A

false

64
Q

Differentiate between the different severities of AECOPD.

A

mild exacerbation:
-worsening or new respiratory symptoms without a change in medications
moderate exacerbation:
-prescribed antibiotic and/or po corticosteroid
severe exacerbation:
-requiring a hospital admission or ED visit

65
Q

Differentiate between low-risk of exacerbation and high-risk of exacerbation.

A

low-risk:
-1 or less moderate exacerbations in the last year and did not require ED or hospital
high-risk:
-at least 2 moderate or 1 severe exacerbation in last yea requiring ED or hospital

66
Q

What is the treatment algorithm for COPD?

A

mild: CAT <10, mMRC 1, FEV1>80%
-LAMA or LABA
moderate and severe: CAT >10, mMRC >2, FEV1<80
-low AECOPD risk: LAMA/LABA*, LAMA/LABA/ICS
-high AECOPD risk: LAMA/LABA/ICS**, LAMA/LABA/ICS +prophylactic macrolide/PDE4i/mucolytic agents
all have short-acting bronchodilator prn

67
Q

What are two possible surgeries that can be considered for a COPD patient?

A

lung volume reduction surgery
lung transplantation
-5 year survival rate is ~60%

68
Q

Describe stepping up treatment of COPD.

A

usually treatment is progressive and additive
no absolute interval at which evaluation should be performed after initiating change in therapy, consider 6months after initialing long acting bronchodilator and 12 months after
initiating ICS

69
Q

Describe stepping down treatment in COPD.

A

questionnable…may be considered
-if benefits not realized or AE>benefits
-patients on ICS at low risk of morbidity/mortality and long period of stability
close supervision and monitoring necessary

70
Q

What is the definition of an acute COPD exacerbation?

A

sustained worsening of dyspnea, cough or sputum production leading to an increase in the use of maintenance medications and/or supplementation medications

71
Q

What is the most frequent cause of medical visits, hospitalizations and death among COPD patients?

A

acute exacerbations

72
Q

What are the consequences of AECOPD?

A

reduced health-related quality of life
increased mortality
increased health resource utilization and costs
accelerated decline in lung function

73
Q

What is the treatment of AECOPD?

A

bronchodilators (salbutamol+/-ipratropium)
-SAMA and SABA become scheduled
-increase dose and frequency
-long acting inhalers can be continued but should not replace short acting dilators
systemic steroids
-improve spirometry; decrease relapse rate
-restore lung function quicker
consider antibiotics
-should be given to patients requiring mechanical ventilation
-patients with at least 2/3 cardinal symptoms

74
Q

What is the typical dose of systemic steroids for AECOPD?

A

30-50mg daily prednisone (or equiv) x 5-14d

75
Q

What percentage of AECOPD are thought to be infectious in nature?

A

50%
-many are viral and remainder are due to bacterial infection

76
Q

What is the antibiotic choice for AECOPD for patients without risk factors?

A

amoxicillin
doxycycline
cotrimoxazole
5-7 days

77
Q

What is the antibiotic choice for AECOPD for patients with risk factors?

A

amoxiclav (5-10d)
cefuroxime (5-10d)
levofloxacin (3-5d)

78
Q

Who should be hospitalized for AECOPD?

A

severe symptoms
acute respiratory failure
physical symptoms (cyanosis, edema)
failure to respond to initial management
presence of serious comorbidities
insufficient home support

79
Q

What is the discharge criteria following AECOPD?

A

B2 agonist required no more than q4h
patient able to walk across room
patient able to eat and sleep without dyspnea
clinically stable for 12-24h
arterial blood gases stable for 12-24h
patient understands correct use of meds
follow-up and home care arrangements complete
health care team is confident

80
Q

Which LAMA is dosed BID?

A

aclidinium
the other three are dosed OD

81
Q

Which LAMAs accumulate in renal impairment?

A

tiotropium
glycopyrronium

82
Q

What is the onset of LAMAs?

A

within minutes
LABAs also work within minutes

83
Q

What are the factors that should have us suspect COPD in a patient?

A

age > 40
smoker or ex smoker
progressive dyspnea, worse with exercise

84
Q

Can there be overlap between asthma and COPD?

A

growing recognition that patients may have concurrent symptoms
no consensus on definition

PHAR253 (16 decks)

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