COPD Flashcards

1
Q

Define COPD

A

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

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2
Q

Main differnce between asthma and COPD

A

Asthma is rversible, COPD is progressive

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3
Q

Define 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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4
Q

Define chronic bronchitis:

A

Chronic cough for at least 3 months x 2 consecutive years

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5
Q

COPD Epidemiology is primarily…. It results in how many % of deaths?

A

Cigarette smoking: principal underlying cause of COPD and responsible for about 80% of deaths

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6
Q

What is unique about COPD’s prevelance?

A

3rd leading cause of death worldwide; only chronic illness with increasing mortality

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7
Q

Risk Factors of COPD

A

Exposure to Particles
Infections
Socio-economic status

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8
Q

What is the most significant risk factor of COPD?

A
  • SMOKING/EXPOSURE TO 2ND HAND SMOKE
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9
Q

What are some host factors of COPD?

A

1) Hereditary

1-antitrypsin deficiency predisposes susceptible people to emphysema

1-antitrypsin is a serum protein produced by the liver & normally found in the lungs.

It prevents neutrophil elastase from destroying lung tissue

Accounts for <5% of cases

2) AGE
3) Lung Growth and Development
4) Airway Hyperresposiveness (Hard to seperate and define cause and effect with asthma)

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10
Q

Pathophysiology of COPD Simple

A

Stimulus (e.g smoking) –> Inflammatory process –> narrowing of perfipheral pathways –> Decreased FEV1

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11
Q

What is noted in COPD patients in regards to pathopjhysiologuy?

A

A Protease-Antiprotease Imbalance is noted in the lungs of COPD patients. (Protease Mediated destruction of elastin is an important feature of emphysema)

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12
Q

In COPD, what may amplify the inflammatory response?

A

Oxidative stress may play an important role in amplifying the inflammatory process.

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13
Q

COPD has a specific pattern of what?

A

Specific pattern of inflammation: CD8+ (cytotoxic) lymphocytes and other Inflammatory cells & mediators induce structural changes in the lung parenchyma & Pulmonary vasculature

COPD –> Increase in residual volume –> GAS TRAPPING

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14
Q

In regards to COPD pathophysiology, these things occur:

A

Expiratory Flow Limiytation

Lung Hyperinflation

Gas Exchange Abnormality

Mucous Hypersecretionm

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15
Q

What is a hallmark of COPD? Why does it occur?

A

Expiratory Flow Limitation

Hallmark of COPD
Due to increased resistance from mucosal inflammation, airway remodelling, fibrosis & secretions

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16
Q

In COPD, the lungs will ______upon inhalation. Why does it occur? What is the result?

A

Lung hyperinflation

Obstruction of the small airways results in air-trapping which causes lung hyperinflation

Develops early in disease and causes exertional dypsnea

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17
Q

In regards to gas exchange, in COPD there is ______ Result?

A

Gas exchange abnormalities
Result in hypoxemia & hypercapnia
Gas transfer for O2 & CO2 worsens as disease progresses

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18
Q

In regards to mucouis, in COPD there is ______. This results in a _____

A

Mucous hypersecretion
Results in a chronic productive cough
Not necessarily associated with airflow limitation

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19
Q

What triggers an exacerbation? What occurs during a COPD exacerbation?

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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20
Q

With COPD, what other conditions may one have as a result later in life?

A

Significant Comorbid Illness
Pulmonary hypertension may develop late in course of COPD due to hypoxic vasoconstriction of small pulmonary arteries eventually leading to structural changes
Muscle wasting and cachexia, skeletal muscle dysfunction
Osteoporosis, depression and anemia, metabolic sydrome, cardiovascular, lung cancer

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21
Q

What are some comorbities associated with COPD?

A

Ischemic heart disease
Congestive heart failure
Arrhythmias
Pulmonary hypertension
Lung cancer
Osteoporosis and Fractures
Skeletal muscle dysfunction
Cachexia and Malnutrition
Glaucoma and Cataracts
Depression
Anxiety and Panic disorders
Metabolic disorders

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22
Q

Three cardinal sx of COPD?

A

Shortness of breath
Chronic cough
Phlegm

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23
Q

What other sx may be present?

A

Frequent lung infections
Reduced ability to go about daily activities
Barrel-shaped chest
Fatigue
Unexplained weight loss

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24
Q

End-stage COPD Sx?

A

Adopt positions that relieve dyspnea  relax diaphragm
Use of accessory respiratory muscles
Expiration through pursed lips
Cyanosis
Enlarged liver from right heart failure

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25
Q

How do patients with COPD initially present?

A

1) Extremely sedentary lifestyle and presents with general fatigue
—> Typically have avoided exertional dyspnea
—> Shifted expectations and limited their activity

2) Patient has complaints of dyspnea and chronic cough
–> Initially noted on exertion only
–> Progressively triggered by less exertion or at rest
–> Morning sputum production

3) Patient who presents with episodes of cough, sputum, wheezing, fatigue and dyspnea
–> May be initially diagnosed as asthma
–> Interval between episodes shortens

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26
Q

Asthma vs COPD: age of onset

A

Asthma - <40
COPD: <40

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27
Q

Asthma vs COPD: smoking History

A

Asthma: Not causal, but worsen control
COPD: Usually >10 pack years

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28
Q

Asthma vs COPD: Sputum Production

A

Asthma: Infrequent
COPD: Often

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29
Q

Asthma vs COPD: Allergies

A

Asthma: Often
COPD: Infrequent

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30
Q

Asthma vs COPD: Clinical Sx Length/ How long do the sx last?

A

A: Intermittent and variable
C: Persistet and progressive

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31
Q

Asthma vs COPD: Disease Course

A

A: Stable (withe xacerbations)
C: Progressive (with exacerbations)

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32
Q

Asthma vs COPD: Comorbid Illness

A

Important for both

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33
Q

Asthma vs COPD: Spirometry

A

A: often normalizes
C: May improve but never normalizes

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34
Q

Asthma vs COPD: Cause of Airway Inflammation

A

A: Eiosinophilic
C: Neutrophilic

35
Q

Asthma vs COPD: ICS response

A

A: Essential
C: Helpful in pt’s with moderate and frequent AECOPD

36
Q

Asthma vs COPD: Bronchodilators

A

A: PRN only
B: Regular tx

37
Q

Asthma vs COPD: Exercise training

A

A: Rarely used
C: Essential

38
Q

Asthma vs COPD: End of life discussions

A

A: Rare
C: Often essential

39
Q

A clinical diagnosis of COPD should be considered in any pt who has:

A

Dyspnea
Chronic Cough
Sputum Production
History of exposure to risk

40
Q

What is used to diagnose COPD? What is used to stage it?

A

Spirometry post-bronchodilator FEV1/FVC ratio <0.7 confirms diagnosis
FEV1 is used to stage

41
Q

Who should be screened for COPD?

A

Evidence does not currently support population screening with spirometry

-Screen patients who have risk factors:

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

–> if yes –> Spirometry

42
Q

MRC Scale

A

STUDY CHART

43
Q

What is the CAT Test?

A

Validated, short (8-item) and simple patient completed questionnaire

Reliable measure of the impact of COPD on a patient’s health status

44
Q

Suspect COPD in people who are:

A

Age > 40 years
Smokers or ex-smokers – quantify tobacco consumption
Progressive dyspnea, worse with exercise

45
Q

Spirometry is necessary for COPD ________. Values:

A

FEV1 / FVC < 70% after bronchodilator

46
Q

Staging of COPD CTS

A

STUDY CHART

47
Q

GOALS of TX 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

48
Q

What is the most effective intervention to reduce risk of COPD? Does it stop progression? What should one ask?

A

Smoking Cessation –> Just slows down the rate of progression (lung function will continue decreasoing if have COPD)
One should: The 5 A’s: Ask, Advise, Assess, Assist, Arrange

49
Q

In pt education, what should be taught?

A

Expectations of therapy must be discussed(cannot cure, but improve QOL – progressive life long tx – most likely will add on rather than take away)

Self management plans
prescriptions for oral steroids and antibiotics to fill when needed
advanced care directives

Inhaler technique – select best device for each individual patient

50
Q

What should be avoided in COPD? Why?

A

Sedatives/Narcotics: increased sensitivity to respiratory depression especially when sleeping

51
Q

All COPD pt’s should be encouraged to:

A

maintain an active lifestyle

52
Q

What vaccines should people with COPD get?

A

Annual Influenza vaccine
decreases serious illness / death by 50%

Pneumococcal vaccine
Recommended for all patients with COPD

Covid-19 Vacinne

53
Q

Who should get long-term oxygen tx? What is the goal?

A

SEVERE HYPOXEMIA

Does not change pulmonary function

Cornerstone of therapy

improves quality/ duration of life in select patients

Assess patient when stable
goal PaO2 > 60 mmHg

54
Q

Pharmacological tx is ________. The main stay of tx is…..

A

Empiric – individuals differ in response to treatment and side effects (start with something and go from there)

Bronchodilators are the mainstay in treatment and are prescribed regularly in COPD; larger doses may be used compared to treatment of asthma.

55
Q

Pharmacotx difference from asthma:

A

Compared to asthma:

Muscarinic antagonists have larger role
ICS have less of a role

If bronchodilator fails, confirm compliance and acceptable inhaler technique.

56
Q

SABA of Choice: Dose:

A

Slabutamol
Terbutaline

BOTH QID PRN

57
Q

SAMA of Choice Dose

A

Ipratropium QID PRN

58
Q

Can a combo be used? If so, what and dose? WHy?

A

Salbutamol + ipratropium –> QID PRN

Synergistic –> Better than used alone

59
Q

What is recommended in all stages of COPD?

A

PRN use of short acting bronchodilators is recommended in all stages of disease
Higher doses = more bronchodilation
May increase beyond recommended dose in severe disease

60
Q

SAMA LAMA MOA

A

Airway muscle tone is partially controlled by cholinergic innervation.

Inhaled anticholinergics competitively inhibit cholinergic receptors in bronchial smooth muscle. This block acetylcholine which reduces cGMP.

Acetylcholine leads to bronchoconstriction.

61
Q

SAMA vs SABA Comparison

A

Less effective than β2 agonists in asthma
Slower onset of action than SABA

62
Q

SAMA LAMA A/e

A

Dry mouth, cough, constipation, urinary retention, headache, metallic taste
Avoid eye contact – can precipitate glaucoma
Rinse mouth after inhalation to decrease dry mouth (less with SAMA)
Cardiovascular (stroke? iffy)

63
Q

LABA and LAMA Examples. DOSE:

A

Salmeterol BID
Formeterol BID
Indacterol OD
Oldaterol OD
Vilanterol (Only combo)

Tiotropium OD
Aclindium BID
Glycopyronnium OD
Umeclidium OD

64
Q

Compare LABA and LAMA

A

Both improve symptoms
LAMA (tiotropium) may be superior in decreasing exacerbations
LAMAs may be better tolerated (decreased withdrawal in RCTs)
Side effect profiles vary
LAMA: dry mouth, constipation
LABA: headache, dose dependent CV effects (racing heart

65
Q

ICS COPD

A

In contrast to asthma, inhaled corticosteroids should not be used as first-line medication.

ICS should not be used as monotherapy

ICS have evidence for reducing exacerbations, but inconsistent evidence for symptom improvement

Patients with a higher eosinophil count may respond better

Consider ICS side effects

66
Q

Which agent? What should one consider?

A

evidence, Availability, Onset, Side effects, Guidelines

67
Q

What LABAS work fast? WHich LAMA?

A

Formeterol, indacterol, oldaterol LABA

Glycopyrrinium – LAMA

Work within minutes

68
Q

Prophylatic azithromycin for who?

A

Recommended in patients who have normal QT interval on electrocardiograms(ECGs), no significant drug interactions with concomitant medications and no evidence of either indolent or active infection with atypical mycobacteria

Reduced exacerbation rates and improved QOL compared to placebo.
Azithromycin group had a higher rate of colonization with macrolide-resistant bacteria, and hearing deficits.

May also see dosed 3 x weekly

on 250mg OD x 1 year

69
Q

N-acetylcysteine MOA? Dosage form? Dose? USe?

A

A mucolytic agent with antioxidant properties

Mechanism of action of NAC inCOPDis not clearly understood
Optimal dose of NAC has not been determined

Injectable solution is administered orally

High-dose NAC, 600 mgorally twice daily, may be of benefit in reducing acute exacerbations in those who had 2 or more exacerbations in the previous2-yearperiod

chronic bronchitic phenotype at high risk of exacerbations

70
Q

Roflimast? MOA? Dose? USe? Spirometry? Rescue?

A

Phosphodiesterase IV inhibitor
Administered once daily (500 mcg tablet per day)

could be considered for addition to existing triple therapy (LAMA +ICS/LABA) for people withCOPDwho have had at least1 exacerbationin the past year.

Add-on to bronchodilator treatment

chronic bronchitic phenotype at high risk of exacerbations

Improves FEV1, decreases exacerbations
Not be used as a rescue medication

71
Q

Roflimast S/e?

A

diarrhea, weight loss, nausea, headache, sleep disturbances
Neuropsych effects – avoid in hx of depression with suicidal ideation

72
Q

Should theophylline be used in COPD?

A

NO - No longe rin guidelines

73
Q

Mild Excaerbation

A

worsening or new respiratory symptoms without a change in prescribed medications

74
Q

Moderate Exacerbation

A

prescribed antibiotic and/or oral corticosteroids

75
Q

Severe Exacerbation:

A

requiring a hospital admission or ED visit

76
Q

Low risk Exacerbation:

A

if they had 1 or less moderate exacerbation in the last year and did not require an ED visit or hospitalization

77
Q

High risk exacerbation

A

if they had at least 2 moderate or 1 severe exacerbation in the last year requiring a hospital admissions/ED visit.

78
Q

COPD Guidelines

A

STUDY CHART

79
Q

In the most severe cases, what is a tx of COPD?

A

Lung Volume Reduction Surgery

Lung Transplantation –> FEV1 <25% predicted and severe sx

80
Q

Stepping Up and Down in COPD:

A

Stepping up:
Usually treatment is progressive and additive
No absolute interval time at which evaluation should be performed after initiating change in therapy
–> consider 6 months after initiating long acting bronchodilator and 12 months after initiating ICS

STEPPING DOWN: QUESTIONABLE

If treatment benefits not realized, or side effects exceed benefits
In patients on ICS at low risk of morbidity and mortality, and exacerbation who have had a long period of stability

Close supervision and monitoring necessary
Taper steroids if considering stopping

81
Q

Definition of acute exacerbation:

A

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

82
Q

Consequences of AECOPD

A

Reduced health-related QOL
Accelerated decline in Lung function
Increased Mortality
Increased healthr esource ultilzation and costs

83
Q

Acute Exacerbation TX:

A

1) Bronchodilators
SAMA and SABA (salbutamol +/-ipratropium) become scheduled
Increase dose and frequency
long-acting inhalers can be continued but should not replace short-acting bronchodilators

2) Steroids (systemic)
Improve spirometry; decrease relapse rate. Restore lung function quicker
Dose:
typically 30-50 mg daily prednisone (or equivalent) x5-14 days

Antibiotics – should be given to:
Patients requiring mechanical ventilation
OR
Patients with at least 2/3 of the cardinal symptoms:
sputum purulence (change in phlegm color to yellow or green)
increased sputum volume
increased dypsnea

84
Q

ANTIBIOTIC CONSIDERATION:

A

Study Chart