COPD Flashcards

1
Q

Chronic rsp sx caused by airway abnormalities (bronchitis) and/or alveoli abnormalities (emphysema) that cause persistent, progressive airflow obstruction

A

COPD

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2
Q

2 pathophysiologic categories of COPD

A

Chronic bronchitis
Emphysema

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3
Q

COPD typically occurs in the setting of ___ ___ that emit noxious particles/gases

A

combustible products
cigs, environment

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4
Q

____ + ____ are key physiologic markers of COPD

A

airflow obstruction
extensive airway destruction

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5
Q

Small airways are narrowed by a number of factors:

A

Immune cells, molecules, mucus, fibrotic tissue

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6
Q

The pattern of pathologic change depends on the features of the individual’s underlying disease: (3)

A

Chronic bronchitis, emphysema, alpha-1 antitrypsin deficiency

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7
Q

3 MC sx of COPD

A

coughing
dyspnea
sputum production

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8
Q

associated sx of COPD

A
  • Weight gain
  • Weight loss - has worse prognosis
  • Activity limitation
  • Wheezing +/- chest tightness
  • Syncope
  • Anxiety / depressive symptoms
  • Increased respiratory rate
  • Signs of heavy smoking - Yellowing of fingers / nails
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9
Q

risk factors of COPD

A
  • Family history
  • Smoking history - Consider age at initiation, average amount smoked per day since initiation, cessation date if applicable
  • Environmental history - Secondhand smoke exposure, air pollution, occupational exposure
  • History of childhood pulmonary infections, HIV, or TB
  • Asthma
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10
Q

PE findings of mild COPD

A

often normal
may pick up on prolonged expiration, faint end-expiratory wheeze with forced expiration

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11
Q

PE findings of mod/severe COPD

A

Lung hyperinflation → ↑ resonance with percussion
Decreased breath sounds, wheezes
Crackles at lung bases
Distant heart sounds
Increased AP diameter

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12
Q

PE findings of end-stage/chronic rsp failure

A
  1. Tripod posturing
    - calloused forearms, swollen bursae on extensor surface of forearms
  2. Use of accessory muscles for breathing
  3. Expiring through pursed lips
  4. Hoover’s sign → lower intercostal interspace retraction during inspiration
  5. Cyanosis
  6. Rarely nail clubbing
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13
Q

presentation of chronic bronchitis vs emphysema

A
  1. Chronic Bronchitis
    - Obese, stocky
    - Productive cough >3 months for 2 consecutive years
    - Coarse rhonchi / wheezing
    - Hepatomegaly
    - Increased JVP
    - Peripheral edema
    - complications: Cor pulmonale
  2. emphysema
    - Thin, barrel chest
    - Scant cough & sputum
    - Expiration with pursed lips
    - Hyperresonant percussion
    - Wheezing, rales
    - Complications: Pneumothorax
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14
Q

ddx for COPD

A

Anemia
Heart failure
Asthma
Interstitial lung disease
Alpha-1 antitrypsin deficiency
Bronchiectasis¹
Tuberculosis
Obliterative bronchiolitis
Diffuse panbronchiolitis

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15
Q

when to screen for COPD? what critieria?
what is the score signifying COPD?

A

at least 1 of the 3 cardinal sx OR
gradual decline in activity with risk factors for COPD
CAPTURE Questionnaire
score 2-4 = COPD

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16
Q

Performed before and after bronchodilator administration

A

spirometry

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17
Q

how is COPD diagnosed thru spirometry

A
  • irreversible or partially reversible airflow limitation after bronchodilator administration
  • Evidence of obstruction: FVC > 80% with FEV₁/FVC < 0.7
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18
Q

additional testing/work-up for COPD

A

Pulse ox every visit
Labs - CBC, BMP, TSH, BNP/NT-proBNP, serum alpha-1 antitrypsin
CXR

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19
Q

Measures amount and speed of air inhaled and exhaled

A

PFT

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20
Q

Forced Expiratory Volume in 1 second

A

FEV1

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21
Q

Similar to spirometry but includes analysis of intrathoracic volume

A

Plethysmography

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22
Q

when should you use Diffusing Capacity of Lungs

A
  • In presence of moderate / severe airflow limitations (FEV₁ ≤50% predicted)
  • Resting O2 ≤92%
  • Exertional hypoxemia (<90%)
  • Severe dyspnea (mMRC ≥2)
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23
Q

is DLCO necessary for routine assessment for COPD?

A

naurr

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24
Q

Great assessment for the severity of emphysema

A

DLCO

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25
Q

as DLCO decreases, what does that say about severity of disease

A

more severe

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26
Q

indications for Arterial Blood Gas

A

Low FEV₁ (< 40% predicted)
Low O₂ saturation on pulse ox (< 92%)
Depressed LOC
Assessment of hypercapnia in “CO₂ retainers” who are given supplemental oxygen (risk of hypercapnic respiratory failure)
Signs of right heart failure

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27
Q

ABG of mild COPD

A

normal pCO2

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28
Q

ABG of mod/severe COPD

A

worsening pO₂ and elevated pCO₂

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29
Q

what components does an ABG measure?

A
  1. pO₂ - oxygen pressure in arterial blood
  2. pCO₂ - amount of CO2 in arterial blood
  3. pH - acidity or alkalinity of arterial blood
  4. SaO₂ - oxygen saturation
  5. HCO₃ - bicarb
  6. Base excess - amount of acid or base required to restore a liter of blood to its normal pH at a PaCO2 of 40 mmHg
    - Base excess increases in metabolic alkalosis and decreases (or becomes more negative) in metabolic acidosis
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30
Q

T/F: Imaging is required for diagnosing COPD

A

F

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31
Q

which imaging choice has a greater sensitivity in detecting disease

A

CT > CXR

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32
Q

indications for imaging in COPD

A
  1. Dyspnea/cough etiology is unclear
  2. R/o complicating process during acute exacerbations
    - Pneumonia, pneumothorax, HF
  3. Evaluate for comorbidities
    - Lung CA, bronchiectasis, pleural disease, ILD, heart failure
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33
Q

CXR of chronic bronchitis vs emphysema

A
  1. Chronic Bronchitis - likely normal unless complications or comorbidities are present
  2. Emphysema
    - Hyperinflation
    - Flattened diaphragm
    - Increased retrosternal air space
    - Long, narrow heart shadow
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34
Q

3 stagings for COPD

A
  1. GOLD
  2. mMRC
  3. CAT
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35
Q

COPD staging is based on what 3 factors

A

Staging is multidimensional:
1. Airflow limitations
2. Symptom severity
3. Exacerbations

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36
Q

GOLD Staging for COPD

A

mild - FEV1 > 80%
mod - 50-80%
severe - 30-50%
very severe - <30%

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37
Q

which staging assess severity of breathlessness

A

Modified Medical Research Council Dyspnea Scale (mMRC)

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38
Q

which staging assesses multitude of sx present

A

COPD Assessment Test (CAT)

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39
Q

> 2 moderate exacerbations or >1 leading to hospitalization lands them at what stage?

A

E

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40
Q

0-1 moderate exacerbations (not leading to hospital) lands them at what stage

A

A or B
A = mMRC 0-1, CAT <10
B = mMRC >2, CAT >10

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41
Q

goals of COPD therapy

A

Improve sx
Decreased number of exacerbations
Improve patient functioning and quality of life

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42
Q

COPD therapy goals must be achieved with both __ and __

A

pharm + nonpharm management

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43
Q

nonpharm management for COPD

A
  1. SMOKING CESSATION
    - Ask every patient at every visit!
    - Pharm: NRT, Bupropion, Varenicline
  2. Behavioral counseling
  3. Vaccinations
    - Influenza, COVID-19, PCV-20 OR PCV-13 followed by PCV-23, Tdap , Zoster in pts >50
  4. wt loss & nutrition
    - BMI, vit. D
  5. Regular, progressive exercise
  6. Oxygen therapy
  7. pulm rehab
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44
Q

indications for oxygen therapy

A

pO2 ≤ 55 mmHg on ABG
O2 sat ≤ 88%
pO2 55-60 + RHF or erythrocytosis

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45
Q

pulm rehab is indicated in what COPD class

A

B and E

46
Q

components of pulm rehab

A
  1. Exercise training
  2. Promotion of healthy behaviors
    - Smoking cessation, regular exercise, healthy nutrition, proper medication use, adherence to prescribed medications, and disease self-management
  3. Psychological support
    - Providing coping strategies for chronic illness
47
Q

what med is Used for immediate relief of dyspnea

A

short-acting bronchodilator

48
Q

3 categories of meds for COPD pharm management

A
  1. short-acting bronchodilator
  2. long-acting bronchodilator
  3. inhaled corticosteroids
49
Q

SE of SABA

A

Tachycardia
Tremor
Cardiac arrhythmia

50
Q

SABA meds

A

Levalbuterol
albuterol

51
Q

SE of SAMA

A

Dry mouth / eyes, metallic taste, prostatic symptoms

52
Q

Ipratropium Bromide

A

SAMA

53
Q

med of SABA + SAMA

A

Albuterol + Ipratropium

54
Q

SE of LABA

A

Tachycardia
Tremor
Headache

55
Q

LABA meds

A

Arformeterol (both QD and BID)
Salmeterol
Formeterol

56
Q

SE of LAMA

A

Dry mouth, constipation, urinary retention

57
Q

Tiotropium

A

LAMA

58
Q

Umeclidinium

A

LAMA

59
Q

Revefenacin

A

LAMA

60
Q

Aclidinium

A

LAMA

61
Q

Glycopyrrolate

A

LAMA

62
Q

Meds of LABA+LAMA

A

Olodaterol /Tiotropium
Vilanterol/Umeclidinium
Formoterol/Glycopyrrolate
Formoterol/Aclidinium

63
Q

LABA + ICS meds

A

Salmeterol/Fluticasone propionate
Vilanterol/Fluticasone furoate
Formoterol/Budesonide

64
Q

LABA+LAMA+ICS meds

A

Fluticasone furoate/Umeclidinium/ Vilanterol
Beclometasone/Formoterol/ Glycopyrronium
Budesonide/Formoterol/ Glycopyrrolate

65
Q

initial meds for COPD

A

E = LABA + LAMA (+ ICS if blood eos >300)
A = a bronchodilator
B = LABA + LAMA

66
Q

how do you change management for dyspnea

A

choose another LABA or LAMA
may need LABA + LAMA
switch inhaler devices or molecules, implement/escalte nonpharm management, investigate other causes

67
Q

how do you change management for exacerbations

A

choose another LABA or LAMA
blood eos <300 = LABA+LAMA
>300 = LABA+LAMA+ICS
add rodflumilast - FEV1 <50% + chronic bronchitis
add azithromycin - for former smokers

68
Q

when to add an ICS

A
  1. strongly favors
    - hx of hospitalization for exacerbations
    - >2 moderate exacerbations/yr
    - hx asthma
  2. favor
    - 1 moderate exaceration/yr
    - blood eos 100 - <300
  3. against use
    - repeated pneumonia events
    - blood eos <100
    - hx mycobacterial infection
69
Q

indications for ICS removal

A
  1. pneumonia
  2. inappropriate indications
  3. lack of response
  4. trial de-escalation
70
Q

MOA of Roflumilast

A

suppresses cytokine release and inhibits pulmonary neutrophil infiltration → reduces inflammation, pulmonary remodeling and mucociliary malfunction

71
Q

class of Roflumilast

A

phosphodiesterase-4 (PDE-4) inhibitor

72
Q

indications for Roflumilast

A

reduce exacerbations in severe COPD

73
Q

SE of roflumilast

A
  1. Psychiatric reaction → anxiety, depression, insomnia
    - Avoid if possible in pts with mental health history
  2. N/V/D, weight loss, and dyspepsia
74
Q

class of theophylline

A

non-specific phosphodiesterase inhibitor

75
Q

MOA of theophylline

A

relaxes smooth muscle → suppresses airway response to noxious stimuli → increased diaphragm contraction force

76
Q

indication for Theophylline

A

refractory COPD

77
Q

SE of Theophylline

A

Anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and seizures
TOXICITY CAN OCCUR

78
Q

caution with Theophylline

A

avoid with liver impairment

79
Q

f/u for COPD

A

1-3 months initially
3-6 months once stable
spirometry annually/PRN

80
Q

risk factors for acute COPD exacerbations

A

Advanced age
Chronic productive cough
Duration of COPD
History of prior antibiotic therapy
COPD-related hospitalization within past year
Comorbid conditions (CAD, CHF, DM)
Respiratory infections (trigger ~70% of exacerbations)

81
Q

presentation of COPD exacerbation

A

similar to regular but happening over hrs-days +
rsp compromise
decreased mental status
wheezing and tachypnea

82
Q

for COPD exacerbations you must ask about: (4)

A

Time course of the symptom
Baseline level of symptoms
Severity of respiratory compromise
Sputum characteristics

83
Q

most COPD exacerbations (80%) are managed where?

A

outpatient

84
Q

when to consider inpatient management

A
  • Severe sx → sudden worsening of resting dyspnea, high respiratory rate, decreased O2 sat, confusion, drowsiness
  • Acute respiratory failure
  • Onset of new PE findings (cyanosis, peripheral edema)
  • Failure to respond to initial medical management
  • Presence of serious comorbidities (CHF, arrhythmias)
  • Insufficient home support*
85
Q

acute COPD exacerbation outpatient management

A
  1. Adjust bronchodilator therapy
  2. Consider spacers / nebulizer therapy
  3. Consider oral glucocorticoid therapy - prednisone
  4. Abx for increased cough, sputum production, and purulence
    - azithromycin, clarithromycin
    - cefuroxime, cefdinir
    - Amoxicillin-clavulanate
    - levofloxacin, moxifloxacin
  5. maybe non-invasive mech vent
86
Q

COPD exacerbation inpatient management

A
  1. Supplemental O2 (target → 88-92%)
  2. Reverse obstruction → SABA +/- SAMA q4h; systemic corticosteroids
  3. IV abx → Levaquin, Ceftriaxone, or Piperacillin-Tazobactam
  4. Initiate pulmonary rehab
87
Q

when to consider inpatient management ICU admission

A

Not responding to initial emergency therapy
Mental status changes
worsening hypoxemia (pO2 <5.3 kPa or 40 mmHg) +/- severe or worsening respiratory acidosis (pH<7.25) despite O2 and NIV
Invasive mechanical ventilation needed
Hemodynamically unstable

88
Q

hospital DC and f/u timeline

A

1-4 wks
then
12-16 wks

89
Q

an enzyme naturally produced by the liver and migrates to the lungs via the blood
protects the lungs from neutrophil (elastase) damage

A

Alpha-1 Antitrypsin

90
Q

ATT deficiency occurs when there is a ___ preventing its release from the liver

A

genetic defect of ATT

91
Q

2 pathophysiologic processes for ATT deficiency

A

ATT deficiency in the lungs leads to loss of elastin in the alveolar wall and early onset emphysema
An accumulation of ATT in the liver leads to destruction of hepatocytes and liver disease

92
Q

presentation of ATT def

A

Same as emphysema in COPD at much younger age
Symptoms of chronic hepatitis, cirrhosis, or hepatocellular carcinoma
Symptoms of panniculitis → inflammation of subcutaneous tissue

93
Q

consider diagnostic testing for ATT def with these factors:

A

In patients <45
Non-smokers or minimal smoking (<10-15 years)
FH of emphysema and/or liver disease
Adult onset asthma that does not respond to bronchodilators
Panniculitis or unexplained liver disease

94
Q

work up for ATT def

A
  1. Low serum alpha-1 antitrypsin levels
    - Genetic testing needed to confirm phenotype
  2. PFT, CXR should be assessed
95
Q

management for ATT def

A

Refer to provider specializing in disease
Aggressive lifestyle modifications
Pharmacotherapy, O2 therapy, vaccinations as indicated in COPD
Prompt management of acute respiratory infections
Pulmonary rehab

96
Q

An irreversible focal or diffuse dilation and destruction of the bronchial walls

A

Bronchiectasis

97
Q

pathophys of Bronchiectasis

A

multifactorial
1. Infectious insult in addition to impaired draining/obstruction and impaired host defense
- Often results from recurrent inflammation or infection of the airways
2. Leads to inflammation, mucosal edema, cratering, ulceration, and neovascularization of airway

98
Q

presentation of Bronchiectasis

A
  1. Chronic daily productive cough
    - Copious, foul-smelling, thick, purulent sputum is characteristic
  2. Rales/rhonchi/wheezing on exam
  3. Acute exacerbations
    - Increased sputum volume and purulence
99
Q

imaging for Bronchiectasis

A

CXR to r/o pneumonia
Not always sensitive but “tram tracks”
CT - Ballooned or “honeycomb”

100
Q

work-up for bronchiectasis

A

Sputum cx → directs abx in infectious exacerbations
Bronchoscopy → assess for underlying mass or FB in focal disease

101
Q

tx for bronchiectasis

A
  1. Non-pharm management as in COPD
  2. Empiric antibiotics for acute exacerbations
    - Amoxicillin, Amoxicillin-clavulanate, Doxycycline, TMP-SMX
    - Consider long-term abx for pts with ≥ 3 exacerbations/yr
  3. Bronchial hygiene
    - Mucolytic therapy, bronchodilators, chest physiotherapy
  4. Surgical resection → indicated in poorly controlled focal disease
  5. Lung transplant (definitive) → indicated when FEV₁ <30% predicted
102
Q

Most common sleep-related breathing disorder

A

OSA

103
Q

OSA is MC in who?

A

More common males, Asians and young African Americans
Increased prevalence in U.S. due to obesity

104
Q

risk factors for OSA

A

Increasing age, male, obesity, smoking, craniofacial or upper airway abnormalities
Comorbid conditions such as pregnancy, ESRD, CHF, COPD, hx of stroke (CVA)

105
Q

pathophys of OSA

A

Recurrent, functional collapse of pharyngeal airway during sleep → reduced airflow → intermittent disturbances in gas exchange and fragmented sleep

106
Q

presentation of OSA

A

Signs of disturbed sleep
Daytime somnolence secondary to disturbed sleep
Obstructive apneas, hypopneas, or respiratory-related arousals

107
Q

work up for OSA

A
  • Sleep Apnea Questionnaire - Berlin Questionnaire, STOP-BANG
  • Polysomnography - first-line
  • Home sleep apnea testing
  • Overnight oximetry
108
Q

OSA criteria

A
  1. ≥5 obstructive respiratory events (apneas, hypopneas, or respiratory-related arousals) per hour of sleep plus one or more of the following:
    - Sleepiness, non-restorative sleep, fatigue, insomnia
    - Waking with breath-holding, gasping, or choking
    - Habitual snoring or breathing interruptions
    - HTN, mood disorder, cognitive dysfunction, CAD, CVA
  2. ≥15 or more predominantly obstructive respiratory events per hour of sleep, regardless of associated symptoms or comorbidities
109
Q

complications with OSA

A

Excessive daytime sleepiness, inattention, fatigue
Drowsy driving and associated MVA
Cardiovascular morbidity (HTN, pulmonary HTN, CAD, arrhythmias, CHF, CVA)
Metabolic syndrome and DM2
Nonalcoholic fatty liver disease (NASH)
Perioperative complications
Increased all-cause mortality (2-3x’s general population)

110
Q

goals of OSA therapy

A

Reduce or eliminate apneas, hypopneas, and/or oxygen desaturations during sleep
Improve sleep quality and daytime function

111
Q

management for OSA

A
  • Wt loss is paramount
  • Continuous positive airway pressure (CPAP) or Automatic positive airway pressure (APAP) - mainstay of therapy
  • Oral appliances
  • Upper airway surgery (UPPP², tonsillectomy, adenoidectomy)
  • Hypoglossal nerve stimulation³