2 COPD Flashcards

1
Q

Highest prevalence of COPD is among…

A

65-74 year olds

Men and women affected almost equally

Morbidity increases with age and is greater in males

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2
Q

Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition:

A

Chronic obstructive pulmonary disease is a common, PREVENTABLE and TREATABLE disease that is characterized by persistent RESPIRATORY SYMPTOMS and AIRFLOW LIMITATION that is due to airway and/or alveolar abnormalities usually caused by SIGNIFICANT EXPOSURE TO NOXIOUS PARTICLES OR GASES.

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3
Q

What are the three clinical subtypes of COPD?

A

Chronic Bronchitis (predominant)

Emphysema (predominant)

Chronic Obstructive Asthma

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4
Q

Patients with Chronic Bronchitis are described as…

A

“Blue Bloaters” due to CYANOSIS and OVERWEIGHT body habitus

Hypoxemia and respiratory acidosis more common

Cor pulmonale from pulmonary HTN (b/c problems with both getting air in and out)

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5
Q

Patients with Emphysema are described as …

A

“Pink Puffers” because of pursed-lip breathing, skin color, and thin body habitus

Use a lot of accessory muscles to breath

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6
Q

Chronic bronchitis is defined as a chronic productive cough for ____________ with no other cause.

A

3 or more months during 2 consecutive years

Leads to structural changes:
• Mucous gland enlargement —> hyper secretion
• Bronchial squamous metastasis
• Loss of ciliary transport

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7
Q

In Chronic Bronchitis, inflammation of bronchial wall and infiltration of sub-mucosal layer is caused by ________

A

Neutrophils (vs eosinophils in asthma)

Chronic bacterial colonization and airway hyper-reactivity are thought to play an important role

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8
Q

Obstruction in chronic bronchitis is ….

A

Both inspiratory and expiratory

Hypoxemia and hypercapnia result form impeded ventilation

There is less parenchymal damage than emphysema

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9
Q

Pathologic enlargement of the air spaces distal to the terminal bronchioles due to destruction of the alveolar walls

A

Emphysema

Destructive process not clearly understood (may be too much elastase or too little antitrypsin activity)

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10
Q

Protease enzyme secreted by neutrophils and macrophages during inflammation

A

Neutrophil elastase - it destroys bacteria and host tissue (ie - elastin)

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11
Q

An inhibitor of neutrophil elastase

A

Alpha-1 Antitrypsin

When in deficiency there is breakdown of the lung structure by elastase

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12
Q

Describe what happens to the alveoli in emphysema

A

Reduced alveolar surface area available for gas exchange

Decreased elastic recoil

Loss of alveolar supporting structure = airway narrowing

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13
Q

Obstruction in emphysema is …

A

Mostly during exhalation

Not associated with significant hypoxemia until later in disease severity

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14
Q

Destruction of capillary beds in emphysema results in …

A

Reduced DLCO (diffusing capacity for carbon monoxide)

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15
Q

Chronic inflammation in asthma is primarily mediated by…

A

Eosinophils

Airway hyper-reactivity —> increased secretions, mucosal edema, constriction of bronchial smooth muscle —> airway obstruction

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16
Q

Is asthma reversible or irreversible?

A

Reversible!

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17
Q

Most common risk factor for COPD

A

Cigarette smoking - 80% of COPD patients, most have smoked at least 20 cigarettes a day for 20 or more years

Other risk factors:
• Environment/occupation
• Second hand smoke exposure
• Airway hyper-responsiveness (asthma)
• Genetic RF: alpha-1 antitrypsin deficiency (<1% of all cases)
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18
Q

How does cigarette smoking cause COPD?

A

Stimulates elastase enzymatic activity, causing degenerative changes in elastin and alveolar structures

Causes release of cytotoxic oxygen radicals from WBCs in lung tissue

Amount and duration contribute to disease severity

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19
Q

Examples of environmental exposures that can lead to COPD

A

Air pollution

Coal miners

Grain handlers

Metal molders

Workers exposed to dust

Cooking with biomass fuels (1/3 of the world)

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20
Q

A hereditary syndrome resulting in the early onset of emphysema (<1% of US cases)

A

Alpha-1 antitrypsin deficiency

Features of emphysema present at a younger age (≤45)

AAT is a protease inhibitor - inhibits elastase and several other proteolytic enzymes

The process of lung destruction is accelerated in smokers with AAT deficiency

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21
Q

Classic presentation of COPD

A

Dyspnea, chronic cough, and sputum production

Sx onset in 5th or 6gh decade of life

Most common early symptom is DYSPNEA ON EXERTION

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22
Q

Common comorbidities of COPD

A

CVD (HTN, CAD, stroke)

DM

Renal insufficiency

Osteoporosis

Psychiatric illness

Cognitive dysfunction

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23
Q

Gross physical exam findings in emphysema

A

Tripod positioning

Cyanosis

Tobacco staining of fingers (because the idiot is still smoking)

JVD, use of accessory muscles (neck and shoulder)

Pursed lip breathing

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24
Q

Why do patients with emphysema purse their lips?

A

In COPD, ordinary breathing allows early bronchial collapse on exhalation

Pursed-lip breathing achieves resistance to outflow at the lips, raising intrabronhial pressure, keeping the bronchi open. More air can thus be expelled.

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25
More specific physical exam findings in Emphysema
Lungs: Barrel chest (increased AP diameter) Prolonged expiration Increased resonance on percussion (b/c of air trapping) Decreased breath sounds (distant), wheezing, and crackles at base ``` Heart: S3 gallop (if cor pulmonale), RV lift ``` ABD: Hepatomegaly, pulm HTN if cor pulmonale Ext: Muscle wasting, peripheral edema
26
Altered structure (hypertrophy or dilation) and/or impaired function of the RIGHT ventricle that results from pulmonary HTN associated with diseases of the lung, vasculature, upper airway, or chest wall
Cor Pulmonale
27
Most common cause of cor pulmonale
COPD
28
Diagnostic study required for the diagnosis of COPD
Spirometry Will also do a CBC, BNP, cardiac enzymes, metabolic panel, AAT but spirometry is diagnostic Other tests: Pulse ox, ABG, EKG, sputum exam, CXR/HRCT
29
The amount of air forcefully exhaled during maximal forced expiration
Forced Vital Capacity (FVC) Normal is 80-120% Compared to Forced Expiratory Volume in 1 second (FEV1)
30
What is the FEV1/FVC ratio?
% of FVC expired in 1 sec Normal is 70-80%
31
How does spirometry diagnosis of COPD work?
First perform a pre and post-bronchodilator spirometry test (FEV1/FVC <0.7 is consistent with an obstructive pattern) Next review post-bronchodilator FEV1% predicted to determine GOLD grade I-IV
32
In addition to FEV1/FVC < 0.7 and a decreased FEV1, COPD patients will have:
Increased Total Lung Capacity (TLC) due to air trapping If severe emphysema, will also have decreased Diffusing Capacity of Carbon Monoxide (DLCO) because there’s not good air exchange occurring in capillary beds
33
What will you see on CBC in COPD patients?
Usually normal but useful to rule out anemia as cause of dyspnea Chronic bronchitis pt may have polycythemia secondary to chronic hypoxia Leukocytosis may be present during acute exacerbations of COPD
34
How to use Pulse Oximetry in COPD patients
If <92%, assess further with arterial blood gas Arterial Blood Gas really only done inpatient • Usually mild to moderate hypoxemia without hypercapnia (CO2 retention) • As disease progresses hypoxemia worsens and CO2 increases (respiratory acidosis)
35
When should you do a sputum culture on COPD patients?
When in-patient and unresponsive to initial abx treatment
36
Possible EKG findings in COPD
Tachycardia R atrial enlargement R axis deviation and/or RVH
37
Pathognomonic CXR findings for emphysema
Blebs (focal areas of blackness) or Bullae (larger blebs)
38
Why do we do a CXR in COPD?
Obtain to exclude other diagnoses and assess for comorbities See signs of air trapping - increased AP diameter, hyperinflation, hyperlucency, flat diaphragms Blebs or bullae Perivascular or peribronchial markings may be present in chronic bronchitis
39
CXR findings more suggestive of emphysema
Hyperinflation (possibly with bullae) Flattening of diaphragms Enlargement of retrosternal air space
40
CXR findings more suggestive of chronic bronchitis
Cardiac enlargement Pulmonary congestion Increased lung markings
41
Do we need to do a chest CT on COPD patients?
Helpful but not needed for routine Dx Obtain if SSx suggest a complication of COPD (PNA, pneumothorax, large bullae), alternate Dx (PE), or if considering lung volume reduction surgery (HRCT)
42
GOLD strategy for staging
Step 1 - Determine if obstructive pattern (FEV1/FVC ratio < 0.7) Step 2 - Determine severity (GOLD Grade 1-4, based on percent FEV1) Step 3 - Assess symptoms (use patient rating scale) Step 4 - Determine exacerbation risk (use frequency of exacerbations in past year)
43
What are the four GOLD grades?
GOLD 1 = Mild (FEV1 ≥ 80% predicted) GOLD 2 = Moderate (50% ≤FEV1, <80% predicted) GOLD 3 = Severe (30% ≤FEV1, <50% predicted) GOLD 4 = Very Severe (FEV1 <30% predicted)
44
How to use number of exacerbations to determine further risk of exacerbation
0-1 exacerbations in the past 12 months = Low risk 2 or more exacerbations OR 1 hospitalization for COPD = High risk
45
How do you prevent progression in COPD?
Stop smoking, you idiot!
46
How do you relieve symptoms in COPD?
Pharmacotherapy/pulm rehab/Oxygen Improve exercise tolerance Manage/prevent exacerbations Reduce mortality
47
3 min counseling for smoking cessation can increase quit rate by...
5-10%
48
Management of COPD for Group A patients (Gold 1-2, 0-1 exacerbations, mMRC 0-1)
Short-acting bronchodilator OR SABA + SAMA combo used PRN
49
Management of COPD for Group B patients (Gold 1-2, 0-1 exacerbations, mMRC 2+)
Long-acting bronchodilator (LAMA or LABA)
50
Management of COPD for Group C patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 0-1)
LAMA
51
Management of COPD for Group D patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 2+)
LABA + LAMA, consider ICS + LABA
52
Mainstay of treatment for COPD
Inhaled ß2-agonists and anticholinergics (short and long acting) Besides bronchodilation, may provide other effects such as ability to improve mucociliary clearance, diaphragmatic action, and cardiac contractility
53
Examples of short acting ß2 agonists (SABAs)
Albuterol (Ventolin, ProAir, Proventil) Usual dose = 2 puffs q4-6 hours (also available in neb form)
54
Examples of Long-acting ß2-agonists (LABA)
Salmeterol (Serevent) Formoterol (Foradil) q12h dosing - every day, not for rescues
55
Side effects of ß2 agonists
Palpitations Tachycardia Insomnia Tremors
56
Examples of anticholinergic bronchodilators
Short-acting: • Ipratropium bromide (Atrovent) - most common • Ipratropium plus albuterol (Combvent) • 2 puffs BID-QID, also in neb form Long-acting: • Tiotropium bromide (Spiriva) - once daily • Umeclidinium (Incruse Elliot’s) - once daily Good bronchodilation, reduces air trapping in lungs, less cardiac stimulation
57
Side effects of anticholinergics
Dry mouth Metallic taste HA Cough
58
Examples of LAMA+LABA combo meds
Used in category C/D disease Bevespi Aerosphere - BID Utibron Neohaler - BID Stiolto Respiratory - QD Anoro Ellipta - QD
59
Drug that was the standard bronchodilator for many years, but tendency now to avoid use except in refractory cases
Theophylline - a methylxanthine No long used commonly b/c lots of SE and drug interactions Debate over benefits: • Theophylline toxicity common problem • Can cause tachycardia, arrhythmias, seizures, HA, nausea • Potential for drug-drug interactions
60
Examples of corticosteroids
Advair, Dulera, Symbicort, Breo Ellipta (Inhaled form is available alone or in combo with LABA) Reduces mucosal edema/inflammation by inhibiting prostaglandins —> decreased secretions Increases responsiveness to beta-adrenergics
61
Side effects of corticosteroid use
Oral candidiasis (pt ed=rinse mouth after use) Bruising Increased risk of URI Kind of out of favor now b/c not as effective
62
Treatment for alpha1 antitrypsin deficiency
Antiprotease replacement therapy in the form of weekly or monthly injections Used in patients with serum alpha-1 antitrypsin levels <11uM) Treatment is costly and controversial
63
Examples of adjunct therapy for COPD patients
Pulmonary rehab (if GOLD stage B-D) - patient ed, exercise training, nutritional counseling and psychosocial support Oxygen - increases survival (but only if used ≥ 12 hours per day) • Goal: O2 saturation > 90% during rest, sleep, and exertion Lung volume reduction surgery —> improved lung recoil
64
Why do we use supplemental O2 in COPD patients?
Long-term continuous oxygen therapy prolongs survival (min 12 hours/day) Indicated if chronic dyspnea at rest PaO2 ≤ 55 mmHg or SaO2 ≤ 88% Caution - high flow O2 may reduce drive to breath and cause resp acidosis (maintain O2 sat 90-92%)
65
What do we do to minimize complications/exacerbations in COPD patients?
Educate ALL COPD patients about avoidance of risk factors Influenza vaccination Pneumococcal vaccination (PPV13 and PCV23) Regular exercise Early recognition of pulmonary infection (increased sputum production, fever, worsening dyspnea, fatigue, chest pain, hemoptysis)
66
How do we define an acute exacerbation of COPD?
Acute change in patient’s baseline dyspnea, cough, or sputum that is beyond normal variability, and sufficient to warrant a change in therapy Increased dyspnea Increase in cough frequency/severity Sputum increases or becomes purulent
67
Why do we care about acute exacerbations of COPD
Because they contribute to high mortality
68
70% of acute exacerbations are caused by...
Respiratory illnesses Pollution also common
69
Viral infections that most commonly lead to COPD exacerbations
Rhinovirus and influenza Viral most common, but may lead to secondary bacterial pneumonia
70
Most common bacterial pathogens causing pneumonia secondary to viral infections
H flu, Strep pneumo, Moraxella catarrhalis, Mycoplasma pneumo, and Pseudomonas (if hospitalized recently or recent abx use)
71
Outpatient management of an acute exacerbation includes...
Increased dose of short-acting bronchodilators (B2 agonist, add Ipratropium if not already taking) Oral steroids - 40 mg/day x 5 days (reduces recovery time and hospital time) Abx (for mod-severe exacerbations) Consider hospitalization if severe
72
Meds used in uncomplicated COPD exacerbation with no risk factors (Age <65, FEV1 > 50, <3 exacerbations/year, No cardiac disease)
Advanced macrolide (azithromycin, clarithromycin) OR Cephalosporins OR Doxy OR Bactrim
73
Meds used in complicated COPD exacerbations with 1 or more risk factors (age >65, FEV1<50, ≥3 exacerbations/year, cardiac disease)
Fluoroquinolone (levofloxacin) OR Augmentin If at risk for pseudomonas, use cipro and get sputum culture
74
Indications for hospitalization in COPD exacerbations
Severe SSx Severe underlying COPD (FEV1<50%) Onset of new physical signs (cyanosis, edema, new arrhythmia) Failure to respond to initial med mgmt Older age Insufficient home support