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Pulm > Lecture 5: COPD > Flashcards

Lecture 5: COPD Flashcards

1
Q

What are the two pathophysiologic categories of COPD?

A
  1. Chronic bronchitis
  2. Emphysema
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2
Q

What symptoms are characteristic of COPD?

A
  • Dyspnea
  • Cough
  • Sputum production
  • Airflow obstruction
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3
Q

How common is COPD?

A
  • > 10 million in the US
  • > 120k deaths annually
  • 4th leading cause of death

High burden due to high resource utilization

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4
Q

What are the key physiologic markers of COPD?

A
  • Airflow obstruction
  • Extensive airway destruction
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5
Q

What disease is characterized primarily by alveolar destruction in COPD?

A

Emphysema

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6
Q

What disease is characterized by increased sputum production and obstruction of more central airways in COPD?

A

Chronic bronchitis

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7
Q

What is a blue bloater usually describing?

A

Obese male that is constantly coughing.

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8
Q

What does a classic emphysema patient look like?

A
  • Barrel chest
  • Older and thinner
  • Hyperinflated diaphragm with flattened diaphragms.
  • Quiet chest
  • Severe dyspnea
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9
Q

What is the clinical diagnosis criteria for chronic bronchitis?

A
  • Daily productive cough > 3+ months
  • Must be in at least 2 consecutive years
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10
Q

What is the diagnostic criteria for emphysema?

A

Permanent enlargement and destruction of airspaces distal to terminal bronchioles.

Does not require a CXR, but CXR will be noticeably abnormal.

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11
Q

How does mild COPD often present on PE?

A
  • Usually normal
  • Maybe prolonged expiration or faint-end expiratory wheeze with forced expiration.
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12
Q

How does moderate/severe COPD typically present on PE?

A
  • Lung hyperinflation (via percussion)
  • Decreased breath sounds, wheezes (bilateral)
  • Crackles at lung bases (bilateral)
  • Distant heart sounds
  • Increased AP diameter (closer to 1:1)
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13
Q

How do end-stage COPD patients typically present?

A
  • Tripodding + calloused elbows
  • Accessory muscle use
  • Pursed lips
  • Hoover’s sign (lower intercostal space retraction during inspiration)
  • Cyanosis
  • Nail clubbing (rare)
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14
Q

What are the abnormal PE findings most characteristic of chronic bronchitis?

A
  • Coarse rhonchi/wheezing
  • Hepatomegaly
  • Increased JVP
  • Peripheral edema

Suggestive of R-sided HF

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15
Q

What are the abnormal PE findings most characteristic of emphysema?

A
  • Expiration with pursed lips
  • Hyperresonant percussion
  • Wheezing, rales
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16
Q

Who gets screened for COPD?

A
  • 1 of the 3 cardinal symptoms.
  • OR
  • Gradual decline in activities with risk factors for COPD.
  • CAPTURE questionnaire. (2-4 = clinically significant)

Cardinal symptoms:
Dyspnea
Sputum volume
Sputum production

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17
Q

What does COPD look like on spirometry in regards to BD administration?

A

COPD is defined by irreversible or partially reversible but limited airflow.

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18
Q

What labs/diagnostics are recommended in a patient with COPD?

A
  • Pulse ox every visit
  • CBC, BMP (or CMP), TSH, BNP/NT-proBNP, serum alpha-1-antitrypsin
  • CXR (not required to diagnose COPD)
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19
Q

What PFT findings suggest obstructive disease?

A
  • FVC > 80%
  • FEV1/FVC < 0.7
  • OR
  • FVC < 80% with TLC > 80%

AKA they either breath out very slowly or they cant breath out a lot in general even though their lung capacity is fine overall.

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20
Q

When should DLco be considered in PFT testing?

A
  • Severe FEV1
  • Resting O2 <= 92%
  • Exertional hypoxemia < 90% on 6MWT
  • Severe dyspnea (mMRC >= 2)

Mainly to assess severity of emphysema.

Lower DLco decreases in proportion to severity of disease

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21
Q

What are ABGs specifically used for?

A
  1. Determining pH levels
  2. Determining metabolic vs respiratory acidosis/alkalosis
  3. Determining compensation for above
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22
Q

In COPD, what generally becomes elevated in ABGs the worse the COPD?

A

pCO2 should increase.

Worsening pO2.

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23
Q

What does negative base excess suggest on ABG? Positive?

A
  • Negative = metabolic acidosis
  • Positive = metabolic alkalosis
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24
Q

When is a CXR indicated for COPD workup?

A
  • Dyspnea/cough etiology unknown
  • R/o complicating process during acute exacerbations
  • Comorbidity evaluation
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25
Q

What is characteristic of emphysema on CXR?

A
  • Hyperinflation
  • Flattened diaphragm
  • Increased retrosternal air space
  • Long, narrow heart shadow
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26
Q

How is COPD staged?

A

Global initiative for COPD (GOLD)

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27
Q

What is GOLD severity determined by and how many stages are there?

A
  • Gold 1: Mild with FEV1 >= 80%
  • Gold 2: Moderate with FEV1 50-80%
  • Gold 3: Severe with FEV1 30-50%
  • Gold 4: Very severe with FEV1 < 30%

Requires spirometry

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28
Q

What are the two ways to assess symptoms for COPD staging?

A
  • mMRC: severity of breathlessness (0-4)
  • CAT: assess multitude of symptoms present (0-40)
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29
Q

What are the GOLD ABE Assessment protocol steps?

A
  1. Spirometrically confirmed COPD
  2. GOLD assessment of obstruction
  3. Exacerbation history per year
  4. Assessment of symptoms/risk of exacerbations

Example: CAT of 22 with 1 moderate exacerbation without hospitalization is B.

30
Q

Stage this patient

FEV1 60%, ➔ 1 exacerbation ➔ No hospitalizations ➔ mMRC 2

31
Q

Stage this patient

FEV1 45%, ➔ 3 exacerbation ➔ No hospitalizations ➔ CAT 13

32
Q

What are the primary goals of managing COPD?

A
  • Improving symptoms
  • Decreased number of exacerbations
  • Improve quality of life and functioning
33
Q

What pharmacological support is available for smoking cessation?

A
  • NRT
  • Bupropion (caution in eating disorders/seizure disorder)
  • Varenicline (Chantix)
34
Q

What is the role of oxygen in COPD management?

A
  • Good in patients with severe, chronic, resting arterial hypoxemia.
  • Careful with potential oxygen trapping in acute exacerbations.
35
Q

In what classes of COPD is pulmonary rehabilitation indicated for?

A

Class B and E.

36
Q

What does pulmonary rehab consist of?

A
  • Exercise training
  • Promotion of healthy behaviors
  • Psychological support
37
Q

What are the SABAs and their SEs?

A
  • Albuterol and Levalbuterol.
  • Tachycardia, tremor, cardiac arrhythmias

Rescue inhaler

38
Q

What is the SAMA and its SEs?

A
  • Ipratropium bromide
  • Dry mouth/eyes, metallic taste, and prostatic symptoms.
39
Q

What are the LABAs and their frequency of use?

A
  • Arformeterol (NEB only, QD/BID)
  • Salmeterol (BID)
  • Formeterol (BID)
40
Q

What are the LAMAs and their frequency of use?

A
  • Tiotropium (Spiriva, QD)
  • Umeclinidium (Incruse ellipta, QD)
  • Revefenacin (Yupelri Neb, QD)
  • Aclinidium (Tudroza Pressair, BID)
  • Glycopyrrolate (Seebri Neohaler, BID)
41
Q

What is the pharmacologic recommendation for Group A COPD? B? E?

A
  • A: single BD
  • B: LABA + LAMA
  • E: LABA + LAMA (can add ICS if eosinophil > 300)
42
Q

For followup of dyspnea, what should be the first step if the current medication regimen is not working?

A

Switch to a different inhaler combo.

43
Q

What eosinophil count contraindicates ICS use in COPD?

A

Once it goes < 100, d/c ICS and use roflumilast or azithromycin.

44
Q

When is ICS removal indicated in COPD?

A
  • Pneumonia
  • Inappropriately added
  • Lack of response
  • Can attempt trial descalation if tolerating well.
45
Q

What is roflumilast’s MOA and drug class?

A

PDE-4 inhibitor to reduce inflammation and pulmonary remodeling.

Reduces exacerbations in severe COPD.

46
Q

Who is roflumilast contraindicated in?

A
  • Psychiatric patients
47
Q

What is theophylline’s drug class and MOA?

A
  • Drug class: non-specific phosphodiesterase inhibitor
  • MOA: relaxes smooth muscle, which increases diaphragm contraction force.

Indicated in refractory COPD

48
Q

What is the main concern regarding theophylline use?

A

Toxicity and hepatic impairment.

49
Q

How often is COPD management/follow up?

A
  • 1-3 months after initiating therapy.
  • 3-6 months once stabilized
  • Annual spirometry at minimum.
50
Q

What is the concern with untreated COPD exacerbation?

A

Development of PNA

51
Q

What historical findings characterize a COPD exacerbation?

A
  • Worsening of symptoms over hours-days
  • More rapid course of symptoms and increased respiratory compromise.
  • Increased mucus production
  • Hemoptysis
52
Q

What PE findings might suggest acute COPD exacerbation?

A
  • Wheezing and tachypnea
  • Respiratory compromise
  • Abnormal breathing
  • Decreased mental status
53
Q

What aspects of acute COPD exacerbation require changes in patient management?

A
  • Severe symptoms
  • Acute respiratory failure
  • new PE findings (cyanosis, peripheral edema)
  • Failure to respond to standard therapy
  • Serious comorbidities (arrhythmias, CHF)
  • Insufficient home support
54
Q

What are the treatment options for acute COPD exacerbation management?

A
  • Adjust BD therapy
  • Spaces/nebs
  • Oral glucocorticoid (5 days max)
  • ABX for increased cough, sputum, or purulence.
  • Non-invasive mechanical ventilation (BiPAP)

ABX treatment depends on exposure history.

55
Q

What is the target spO2 level for acute COPD exacerbation patients admitted?

A

88-92% to prevent O2 trapping.

Do not over oxygenate if spO2 is fine.

56
Q

What would prompt ICU admission for acute COPD exacerbation?

A
  • Severe dyspnea unresponsive to initial treatment.
  • Mental status changes
  • Worsening hypoxemia w/ respiratory acidosis unresponsive to therapy.
  • Invasive ventilation
  • Hemodynamic instability.
57
Q

What is the purpose of alpha-1 antitrypsin?

A

Protects the lungs from neutrophil (elastase) damage

Made in the liver, migrates via blood.

58
Q

What are the two pathophysiologic processes of ATT1 deficiency?

A
  • Loss of elastin in alveolar wall and early onset emphysema
  • Accumulation of ATT in liver, leading to liver damage.
59
Q

How does ATT1 deficiency present?

A
  • Symptoms of chronic liver disease
  • Young age with emphysema symptoms
  • Panniculitis: inflammation of SubQ tissue, resulting in hot and painful nodules on the thigh or butt
60
Q

What workup is recommended for suspect ATT1 deficiency?

A
  • Low serum ATT1
  • PFT
  • CXR
61
Q

How is ATT1 managed?

A
  • Same as COPD + possible infusion of donor ATT.
  • Smoking cessation
62
Q

What is bronchiectasis?

A
  • Irreversible focal or diffuse dilation and destruction of the bronchial walls
  • Multifactorial etiology, generally inflammation of the airways.
63
Q

How does bronchiectasis present typically?

A
  • Chronic, daily productive cough
  • Copious, foul-smelling, thick, purulent sputum.
  • Rales/rhonchi/wheezing on PE.
  • Increased sputum volume/production in acute exacerbations
64
Q

What are tram tracks and what are they associated with?

A
  • Dilated airways.
  • Often associated with bronchiectasis.
65
Q

What is a hallmark description of a CT chest for bronchiectasis?

A

Honeycomb/ballooned presence.

66
Q

What are the most common risk factors associated with OSA?

A
  • Age
  • Male
  • Obesity
  • Smoking
  • COPD
67
Q

What is the pathophysiology of OSA?

A
  • Recurrent and functional collapse of pharyngeal airflow in sleep.
  • Reduced airflow = fragmented sleep and gas exchange disturbances.
68
Q

What is the workup for OSA?

A
  • Sleep apnea questionnaires (Berlin or STOP-BANG)
  • In-lab polysomnography (FIRST LINE)
  • Home sleep apnea test
  • Overnight oximetry
69
Q

What is the diagnostic criteria for OSA?

A
  • 5+ obstructive respiratory events per hour of sleep + somnolence/snoring/gasping/HTN/CAD/CVA
  • 15+ obstructive respiratory events per hour of sleep.

Either criteria

70
Q

What are the primary treatments for OSA?

A
  • Weight loss
  • CPAP or APAP (mainstay)
  • Oral appliances
  • Upper airway surgery
  • Hypoglossal nerve stimulationo

Pulm (12 decks)

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