COPD (wk 8) Flashcards

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6
Q

Describe the burden of disease of COPD

A

-~6% of Americans; mortality slowly decreasing
-0.1% die secondary COPD
-Higher rates in Native American and Alaska Native populations
-Globally ~10%

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7
Q

What are the risk factors for COPD?

A

1) Smoking is by far the single biggest risk factor, vaping, e-cigarette, Cannabis
2) Age > 45
3) Genetic: Alpha-1 antitrypsin deficiency (AATD)
4) Environmental pollutants
5) RTI: childhood infections, MTB, HIV
6) Childhood asthma: COPD-Asthma overlap
7) Native American & Alaska Native populations
-Socioeconomic and high smoking rates

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8
Q

Is screening asymptomatic pts for COPD recommended? Explain

A

Treatment of COPD is directed at symptom control, not curative, so screening asymptomatic patients is not recommended
-Advise smokers to quit or cut back
-Do not screen patient
-Evaluate symptomatic patients

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9
Q

Who should be evaluated for COPD?

A

1) Dyspnea that is:
-Progressive over time
-Worse with exercise
-Persistent
2) Recurrent Wheeze
3) Chronic cough: may be intermittent & may be non-productive
4) Recurrent lower RTI
5) History of risk factors
-Tobacco smokers, environmental smoke, occupational (dusts, vapors, gases, etc.)
-Host factors: genetics, developmental, PMHx (childhood asthma, RTI, LBW, Preemie)

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10
Q

Describe the presentation of COPD using OLDCARTS

A

1) Onset: slowly progressive, older adults
2) Duration: persistent, non-reversible
3) Timing: chronic with exacerbations – often associated with RTI
4) Location: pulmonary system
5) Character: progressive dyspnea (DOE or at rest) and productive cough
6) Aggravating: activity, smoking, respiratory tract infections
Alleviating: rest, reduced or quit smoking
7) Risk factors: smoking history (increased PYH increased risk), Alpha-1 AT (especially younger age), older adult with smoking history
8) Associated Symptoms: frequent RTI, cachexia or obesity, cyanosis, dependent edema

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11
Q

COPD PE:
1) What will VS be like?
2) What about general PE?
3) What might you see on an abd. exam?

A

1) May be normal or increased HR and RR & dyspneic at rest
2) Normal to frequent productive cough, pink to cyanotic, cachectic to obese, comfortable at rest or anxious and dyspneic
3) Paradoxical breathing

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12
Q

COPD PE:
1) What will breath sounds be like?
2) What would a chest exam be like?
3) What may the lower extremities show?
4) What about the skin?

A

1) Decreased to wheezing, crackles (“junky”).
2) May demonstrate normal to barrel chest, hyperresonance on percussion, accessory muscles, pursed lip breathing.
3) May demonstrate dependent pitting edema (usually bilat.)
4) May be pink to cyanotic

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13
Q

1) How do bronchitis predominant (blue bloaters) typically present?
2) What will you see on exam?
3) What drives their breathing?
4) What is important to remember regarding these pts?

A

1) As obese, chronic productive cough +/- wheezing, relatively comfortable at rest, significant DOE
2) EXAM: Obese, crackles and wheezing on chest auscultation (junky sounding), cyanotic, peripheral edema
CO2 retainers/O2 driven….. Retained CO2 resets chemoreceptors, chronic respiratory acidosis leads to dusky (blue) skin color
May become apneic with supplemental oxygen!! as their respiratory drive is O2 driven

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14
Q

1) How do emphysema predominant (pink puffers) typically present?
2) What will you see on exam?
3) What drives their breathing?
4) What is important to remember regarding these pts?

A

1) Present with significant SOB at rest = anxious, pursed lipped breathing, 2–3-word sentences, cachectic appearing, minimal coughing
Exam: labored breathing - tachypnea, accessory muscles, barrel chested, pink skin (increased rate and depth of breathing – minute ventilation), diminished BS on auscultation (referred upper airway sounds)
CO2 responsive/driven
Very responsive to CO2 retention, CO2 chemoreceptors drives hyperventilation resulting in increased minute ventilation resulting in pink skin, responds to supplemental oxygen as their respiratory drive is CO2 driven

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15
Q

What are some intrathoracic DDXs for chronic cough?

“won’t ask us this”

A

1) COPD – slowly progressive, h/o tobacco use or other risk factors, spirometry
2) Asthma – episodic, worse @ night, AR, begins in kids, spirometry
3) Lung cancer – h/o smoking, constitutional symptoms, hemoptysis
4) MTB – any age, endemic region, CXR findings, culture,
Bronchiectasis – large volume purulent sputum, associated with bacterial RTI, HRCT shows bronchial dilation
5) Left heart failure – CXR enlarged heart, pulmonary edema, spirometry demonstrates restriction vs. obstruction
6) Interstitial lung disease – restrictive pattern on spirometry, HRCT
7) Cystic fibrosis – children, sweat chloride test, genetics
Idiopathic cough

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16
Q

What are some extrathoracic DDXs for chronic cough?

“won’t ask us this”

A

Chronic allergic rhinitis
Postnasal drip (PND)
Upper airway cough syndrome
GER
Medications (ACEi, amiodarone)

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17
Q

1) Obstruction in middle aged or older adults is indicated by what FEV1/FVC ratio?
2) What does FEV1% predicted demonstrate with SABAs?

A

1) <0.7 or 70%
2) DOES NOT demonstrate improvement as in asthma

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18
Q

1) When would you need to get

A

1) CXR or high-resolution chest CT to exclude lung masses
2) ECG in patients with ? Cor pulmonale or CHF
Pulse oximetry at rest, exertion, and during sleep to evaluate need for home oxygen (Medicare requirement)
Alpha-1 Antitrypsin deficiency screening – COPD Dx in Caucasian < 45 y/o or FHx of COPD

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19
Q

1) Is a COPD exam diagnostic?
2) What might a CXR show?

A

1) EXAM: Rarely diagnostic
2) Often normal
-Lungs: Hyperinflation, Widened AP diameter, Flattened diaphragm
-Narrow heart
-Bullae

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20
Q

Who should you give a Alpha-1 Antitrypsin Deficiency test to?

A

-GOLD recommends testing all patients Dx with COPD (but not always done)
-Particularly, young patients Dx with COPD should be tested for A1AT def

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21
Q

List the 4 GOLD categories for severity of airflow obstruction based on FEV1

A

1) GOLD 1: Mild, FEV1 >/= 80% predicted
2) GOLD 2: Moderate, 50% </= FEV1 <80% predicted
3) GOLD 3: Severe, 30% </= FEV1 <50% predicted
4) GOLD 4: Very severe, FEV1 <30% predicted

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22
Q

What are the 2 validated clinical tools to evaluate Sx?

A

MMRC (modified medical research counsel) dyspnea scale
OR
CAT (COPD assessment test)

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23
Q

1) What does the Modified Medical Research Council (mMRC) Dyspnea Scale measure? Why is this useful?
2) How does it grade this?

A

1) Measure breathlessness
Key symptom in many
Patients with COPD

Symptoms grade:

Low = 0-1
High = 2+

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24
Q

1) What does the CAT assessment measure?
2) How is it scored?

A

1) Multidimensional symptoms scale
2) Low < 10; High = 10+

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25
Q

What are the Tx goals of COPD?

A

1) Reduce symptoms
Relieve symptoms
Improve exercise tolerance
Improve health status
2) Reduce risk
Prevent/slow disease progression
Prevent/treat exacerbations
Reduce mortality

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26
Q

What 7 things should be included in an initial COPD assessment?

A

1) FEV1 – GOLD 1-4
2) Symptoms – CAT or mMRC
3) Exacerbation history
4) Smoking status – smoking cessation intervention in all patients (EBM grade A)
5) Blood eosinophil count
6) Alpha-1 AT
7) Comorbidities

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27
Q

What should you include in COPD initial management?

A

1) Smoking cessation
2) Vaccination
3) Active lifestyle and exercise
4) Initial Rx
5) Patient self management education
-Risk factors
-Inhaler technique
-Breathlessness
-Written action plan
6) Manage comorbidities

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28
Q

List the 5 As of smoking cessation

A

Ask
Advise to stop or cut back on smoking
Assess willingness to quit or cut back
Assist with FDA approved smoking cessation Rx
Arrange follow up

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29
Q

1) What is a risk factor for lung cancer and COPD?
2) What increases risk of lung cancer above this?

A

1) Smoking
2) COPD

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30
Q

Smoking + COPD = ______x risk of lung cancer over smokers w/o COPD

A

4.5x

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31
Q

What vaccinations are recommended?

A

1) Yearly influenza
2) Covid-19
3) Pneumonia – PCV 20 or 21
4) RSV age 60+
5) Tdap
6) Zoster vaccine 50+

32
Q

GOLD guidlines:
1) How to Tx group A?
2) Group B?
3) Group C?

A

1) Any bronchodilator
2) LABA + LAMA
3) LABA + LAMA (may add ICS if blood eos >/=300)

33
Q

What do you do if a pt has both asthma and COPD?

A

Tx the predominant Sx.
1) If wheezing is the worst Sx, treat them like an asthma pt.
2) If coughing, sputum production, and SOB that’s persistent and progressive is the main Sx, treat as COPD

34
Q

What are you treating in COPD? (i.e. what’s the main goal?)

A

Symptoms and risk

35
Q

1) When are dry powder inhalers appropriate?
2) When are metered-dose inhalers and soft mist inhalers appropriate?

A

1) Only if the pt can make a forceful and deep inhalation
2) When pt can perform a slow and deep inhalation. Give them a spacer device if needed for metered inhalers.

36
Q

What is the COPD management cycle?

A

1) Review: Sx (dyspnea), exacerbations
2) Assess: Inhaler techinque & adherence + non-pharm Txs
3) Adjust: Escalate, switch inhaler device or molecules, de-escalate

37
Q

pulmonary rehabilitation:
1) What is it?
2) Who is it appropriate for?
3)

A

Multidisciplined structured program in exercise training, education, nutritional counseling and behavior/mental health support
Appropriate for patient groups B & E
Cochrane review: improved dyspnea, fatigue, emotional well bearing, & sense of control over disease
Functional benefits: increase of 6-minute walk test ~ 44 meters
Improved QOL and exercise capacity maintained for 12 months

38
Q

1) What does regular use of ICSs do to COPD pts? When might ICSs be used in this population?
2) Are oral corticosteroids appropriate for COPD pts?

A

1) Increases risk of pneumonia, especially in severe COPD ICS added if patient also has features of asthma
2) Long term use has significant side effects without any evidence of benefits

39
Q

41

A

In patients with chronic bronchitis, severe COPD, and h/o exacerbations:
Roflumilast (Daliresp) – PDE-4i
Improves lung function and reduces severe exacerbations
Decreases pulmonary inflammation via inhibiting breakdown of intracellular cyclic adenosine monophosphate (c-AMP)

40
Q

41

A

NOTE: PDE-5i - inhibits breakdown of intracellular c-GMP which relaxes smooth muscle in vessels and leads to increased blood flow in penis and lungs

41
Q

Are prophylactic antibiotics appropriate for COPD? Explain

A

1) Daily long-term macrolides (azithromycin or clarithromycin) for 6-12 months:
Decrease exacerbations over 1 year
NNT 8 to prevent 1 exacerbation over 50 weeks
Resistance is a concern
2) Use of tetracycline and fluroquinolones show no benefit and increase harm

42
Q

What group of drugs is recommended as add on (adjunct therapy) after optimizing inhaler therapy if needed? Give an example

A

Phosphodiesterase-4 inhibitors (PDE-4i)
-like Roflumilast (Daliresp)

43
Q

1) Do mucolytics help?
2) Are antitussives recommended?

A

1) Regular use decease exacerbations in select patients
Who benefits … difficult to characterize
2) Not recommended long term as they have no evidence of benefit

44
Q

43

A

Methylxanthines (Theophylline)
MOA – acts as non-selective PDE-4i or bronchodilator
Not generally recommended due to:
Low therapeutic ratio
Low toxicity threshold
Significant interaction with other medications

45
Q

Biologics

A

Moderate to severe COPD and h/o exacerbations, chronic bronchitis, and higher blood eosinophile counts
Dupilumab reduces exacerbations, improves lung function and QOL

46
Q

1) What is not recommended for COPD?
2) What doesn’t have good evidence?

A

1) Statins are not recommended for COPD
Leukotriene modifies have not been studied adequately in COPD

47
Q

45

A

Long term oxygen therapy recommended in COPD patients with severe resting hypoxia
PaO2 - 55 mmHg or less or SpO2 of 88% or less, measured after breathing room air 30 minutes
Used at least 15 hours/day
Target SpO2 is 88-92%
Decreases mortality

48
Q

45

A

If tissue hypoxia is noted (HCT 55% or greater, Cor pulmonale, or secondary pulmonary hypertension), then COPD patients benefit even if PaO2 > 55 mmHg or SpO2 > 88%
Does not improve outcomes or QOL in exertional hypoxia
Nocturnal oxygen therapy does not appear to improve outcomes in patients w/ isolated nocturnal hypoxia such as sleep apnea

49
Q

46

A

Group 1
SaO2 </= 88% at rest, awake, room air
Rx for nocturnal O2 use – sleep SaO2 </= 88% when SaO2 awake is >/= 89% or Decrease of SaO2 > 5% associated with symptoms reasonably attributed to hypoxemia (mental confusion, insomnia, nocturnal restlessness.
Exercise Rx for O2 use – during exercise SaO2 </= 88% when awake resting room air SaO2 is >/= 89% and evidence that oxygen during exercise improves hypoxemia
Group 2
SaO2 =89% + dependent edema suggestive of CHF or P pulmonale on ECG (P wave > 3mm) or HCT > 56%

50
Q

47

A

Lung volume reduction
Expensive, associated with high mortality
Candidates – severe upper lobe emphysema and low exercise capacity
Increased survival rates vs. Rx only after 12 months
Lung transplant
Severe COPD
Increases health status and lung capacity without affecting survival
Bronchoscopy interventions to decrease end expiratory volume
Increase exercise tolerance, health status, and lung function @ 6-12 months
Refer pulmonologist prior to surgery

51
Q

not on exam
What are some factors that improve prognosis?

A

BMI - 21 or less
FEV1 % predicted
6 min walk test
mMRC dyspnea scale

52
Q

COPD comorbidities:
1) What is common?
2) What condition shares smoking tobacco as a major risk factor with COPD?

A

1) CVD
2) Lung cancer

53
Q

List some COPD comorbidities besides CVD and lung cancer

A

Osteoporosis
Depression/anxiety
Sleep disturbances
GERD – increased risk of exacerbation

54
Q
A

Annual LDCT for screening ages 50-80 and 20 PYH smoking, currently smoking or have quit less than 15 years. Stop when quit > 15 years, or reach 85 y/o

55
Q

Exacerbation of COPD (ecopd): What is it characterized by?

A

Characterized by acute changes in the cardinal symptoms of COPD:
1) Increased severity and frequency of cough
2) Increased sputum production – volume and/or changes in color
3) Increased dyspnea

56
Q

List 3 conditions that often cause ECOPD

A

Respiratory treat infection (RTI), PE, HFR

57
Q

Copd exacerbationscontributors/triggers:
1) What are the more frequent triggers?
2) What are the less frequent?

A

1) RTI
Pulmonary emboli – Well’s Score clinical probability (DVT, Fx, cancer, surgery, etc.)
D-dimer, CTA
Hear failure (HF) – CXR, BNP, Echo

58
Q

When it comes to RTI causes of COPD, how common is each of the most popular ones?

A

H. Influenza 13-50%
M. catarrhalis 9-21%
S. pneumoniae 7-26%
Pseudomonas aeruginosa 1-13%

59
Q

52

A

Thorough clinical assessment
Look for symptoms & signs of CAP, HF, PE
Assess:
Symptoms: severity of dyspnea, cough
Signs: tachypnea, tachycardia, sputum volume/color, respiratory distress with accessory muscle use.
Pulse ox, labs, CRP, ABG
Appropriate environment of care
Establish trigger

60
Q

Describe the HPI of ECOPD using OLDCARTS

A

Onset, Duration, Timing: symptoms – cough, sputum, dyspnea - acutely increased over baseline
Location: respiratory tract
Character: productive cough, large sputum volume, +/-change in color, may be blood tinged
Aggravating: recent RTI
Alleviating: n/a
Associated symptoms: etiology specific (CAP, HF, PE)

61
Q

ECOPD
1) When should you observe?
2) What would the VS be?
3) What do you need to rule out?

A

1) Observation: acute respiratory distress, productive cough
VS: tachypnea, tachycardia, Fever?, hypoxia/cyanotic
3) r/o URI, sinusitis, AOM w. good HEENT exam

62
Q

Respiratory ECOPD

A

Respiratory: mild to severe respiratory signs
In general, would expect to hear diffuse wheezing or other adventitious sounds
Mild: RR < 22, HR < 95, resting SaO2 <92% RA, CRP < 10 mg/L (if obtained)
Moderate: 3/5 of the following
RR 24+, HR 95+, resting pulse ox < 92% RA, ABG (if obtained) may show hypoxia (PaO2 < 60 mmHg) &/or hypercapnia (PaCO2 > 45 mmHg) but no acidosis
Severe: dyspnea, RR, HR, SaO2 same as moderate; ABG shows onset/worsening hypercapnia (PaO2 > 45 mmHg) and acidosis (Ph < 7.35)

63
Q

~ 80% or ECOPD can be treated as outpatient, sometimes after initial treatment in clinic or ER
Mild to moderate ECOPD

64
Q

What are some potential indications for ECOPD admission?

A

Severe exacerbation
Acute respiratory failure
Failure to respond to therapy
Presence of serious comorbidities – HF, new arrhythmias, etc.
Insufficient home support

65
Q

What are the goals of ECOPD Tx?

A

1) Reverse airflow limitation with short acting bronchodilators and systemic glucocorticoids
2) Treat infection as this is most common etiology
3) Exclude DDX – PE, HF, etc.
4) Ensure appropriate oxygenation
5) Avert intubation and mechanical ventilation

66
Q

How do you manage severe, but not life threatening, ECOPD?

A

1) Administer supplemental oxygenation
2) Bronchodilators
3) Consider OCS
4) Consider antibiotics when RTI suspected
5) Consider non-invasive mechanical ventilation – CPAP, BiPAP
6) Monitor fluid balance
7) Consider SQ heparin (Lovenox)
8) ID and manage comorbid conditions

67
Q

What bronchodilators do you need to use for ECOPD?

A

SABA +/- SAMA initial therapy
Inhaler or nebulizer
Once stable consider using LAMA + LABA

68
Q

ECOPOral corticosteroids (OCS)

A

Systemic glucocorticoids (PO nearly equivalent to IV) – improve lung function, oxygenation, and shorten recovery
Prednisone 40-60 mg (or equivalent) QD x 5 days

Monitor for side effects: hyperglycemia, fluid retention, hypertension

69
Q
A

Empiric antibiotics - check Sanford ID guide for recommendations
Commonly used: macrolides (azithromycin, clarithromycin), 2nd/3rd generation cephalosporin (cefuroxime, cefpodoxime, cefdinir), Augmentin, or respiratory fluoroquinolone (levofloxacin or moxifloxacin)

70
Q

ECOPD

A

Reassess in 2-3 days
If improved, continue Rx for 3-5 more days (~ 7 days)
If not improved, evaluate Rx plan (bronchodilators, steroids, Gram stain/culture, comorbid conditions (PE, HF, Pneumothorax, pneumonia, etc.)

71
Q

What do you need to screen ECOPD pts for?

A

Influenza, covid-19 and treat with appropriate specific antiviral therapy in addition to above therapy

72
Q

Non-pharmacological ECOPD Txs:
1) Which is better, titrated O2 or high flow O2?

A

Titrated oxygenation decreases mortality when compared to high flow oxygen
Non-invasive mechanical ventilation 1st mode of ventilation used in COPD with acute respiratory failure (CPAP, BiPAP)
Improves gas exchange, reduces work of breathing and need for intubation, decreases hospitalization duration and improves survival

73
Q
A

Chest physiotherapy no benefit
Resistance training improves dyspnea and QOL
Early pulmonary rehab in hospitalized patients improves dyspnea

74
Q

Sum up ECOPD Tx

A

Assess, initiate treatment, determine cause, reassess and disposition (environment of care)
Short acting bronchodilators
Systemic corticosteroids for ~ 5 days
Antibiotics when indicated for 5-7 days
Supplemental oxygen PRN
Consider non-invasive mechanical ventilation as 1st mode early Acute respiratory failure

75
Q

How do you Tx mild, moderate, and severe ECOPD pharmacologically? (grading is arbitrary)

A

Mild – SABA +/- SAMA only
Moderate – SABA +/- SAMA and OCS +/- antibiotics
Severe – requires admission or ER visit, may be associate with respiratory failure

76
Q

Asthma COPD overlap syndrome (ACOS):
1) Is this term still used?
2) What indicates the presence of COPD?
3) What indicates both COPD and asthma?

A

This term is not longer encouraged in the GOLD 2023 update
If patient has significant airflow limitations based on post bronchodilator FEV1/FVC ratio = COPD
If also has significant reversibility, patient may have both COPD and Asthma
Treat based on predominant diagnosis