Chronic Obstructive Pulmonary Disease (COPD) Flashcards

1
Q

In what groups is COPD more common?

A

women - slightly
smokers
lower socioeconomic status
rural settings

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2
Q

What percentage of COPD cases are NOT associated with smoking?

A

25%

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3
Q

How much money do Americans spend on COPD? 2010? 2020?

A

$32 billion in 2010

estimated $49 billion in 2020

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4
Q

Chronic Obstructive Pulmonary Disease

A

persistent respiratory symptoms AND measurable obstructive airflow limitation

by definition NOT completely reversible

common, preventable, and treatable, but not curable

characterized by emphysema, chronic bronchitis, and sometimes asthma

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5
Q

What is the irreversible pathophysiology of COPD?

A

fibrosis and narrowing of the airways

loss of elastic recoil due to alveolar destruction

destruction of alveolar support that maintains patency of small airways

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6
Q

What is the reversible pathophysiology of COPD?

A

inflammatory cells, mucus, and plasma exudate in bronchi

smooth muscle contraction in peripheral and central airways

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7
Q

What affects will COPD have on Pulmonary Vasculature? Which lab finding will indicate this?

A

Vascular intimal hyperplasia – thickening of alveolar-capillary barrier due to inflammation, mucus, and exudate

Chronic hypoxic vasoconstriction can lead to smooth muscle hypertrophy/hyperplasia

Alveolar destruction leads to loss of adjacent capillaries

Lab: low diffusion capacity (DLCO): measures CO and quantifies gas diffusion across alveolar-capillary membrane

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8
Q

Chronic Bronchitis

A

productive cough for more than 3 months in duration in each of two successive years

may occur in absence of airflow obstruction

due to airway thickening and decreased mucociliary activity

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9
Q

Emphysema

A

abnormal and permanent enlargement of and damage to the walls of the alveoli without obvious fibrosis

can exists without airflow obstruction, but is more common among patients who have moderate or severe airflow obstruction

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10
Q

Asthma

A

chronic airway inflammation and airway hyperresponsiveness

recurrent episodes of wheezing, breathlessness, chest tightness, and coughing; particularly at night or in the early morning

episodes are reversible either spontaneously or with treatment; COPD is NOT reversible

reactive airway – greater than 12 percent improvement in FEV1 with bronchodilator

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11
Q

In order to diagnose COPD, the patient must have….

A

measurable airflow obstruction that is not completely reversible

people with chronic bronchitis, emphysema, or both are not considered to have COPD unless they have measurable airflow obstruction

patients with airflow obstruction due to diseases that have a known etiology or a specific pathology are NOT considered to have COPD

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12
Q

Risks

A

cigarette smoking - leading cause; 38% of COPD patients are current smokers and 37% are former smokers

long-term exposure to other irritants - air pollution, chemical fumes, cooking fumes, dusts

alpha-1 antitrypsin deficiency (AATD)

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13
Q

Apha-1 Antitrypsin Deficiency (AATD)

A

hereditary deficiency or absence of the alpha-1 anti-trypsin protein in the blood

produced by the liver, protects elastin in the lungs from inflammation and inhaled irritants

low AAT occurs because the AAT is abnormal and cannot be released from the liver

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14
Q

Low alpha-1 antitrypsin in the blood leads to….

High alpha-1 antitrypsin leads to….

A

low - lung disease (emphysema)

high - liver disease (cirrhosis)

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15
Q

What types of patients should you suspect have alpha-1 antitrypsin deficiency?

A

suspect alpha-1 antitrypsin deficiency in patients with cirrhosis or lung disease, especially if it is more serious than expected or in those younger than 40

 DNA Genotype as follow-up: MM normal, MS or MZ carriers, ZZ or SZ have AATD

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16
Q

Symptoms

A

constant coughing – smoker’s cough

shortness of breath while doing everyday activities

inability to breathe easily or take a deep breath

excess mucus production – coughed up as sputum

wheezing

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17
Q

What test is required for diagnosing COPD?

A

spirometry

18
Q

Exam Findings or Sings

A

odor of tobacco

coughing

increased work of breathing or pursed-lip breathing, especially during minimal activity

prolonged expiration

wheezing or forced expiration (whistle) - sometimes airways are too tight to even produce a whistle

hyperinflation - increased resonance or percussion, diminished breath sounds, distant heart sounds, increased AP diameter (barrel chest), and depressed diaphragm

yellow/brown nicotine and tar stains on fingers

cachexia - loss of weight, muscle atrophy, fatigue, weakness, and significant loss of appetite

19
Q

What will the FEV1/FVC be?

A

less than 70% after bronchodilators

20
Q

What will the total lung capacity be?

A

normal or increased

21
Q

What will the residual volume be?

A

normal or increased

22
Q

What method is used for determining COPD severity?

A

GOLD Staging

severity of functional impairment based on FEV1 doesn’t always correlate well

air trapping (RV and TLC) and reduction of DLCO may be more accurate reflectors of impact on daily functioning

23
Q

GOLD Classification for COPD - first confirm …..

A

FEV1/FVC <70% and not reversible by bronchodilators

24
Q

GOLD Classification - Mild COPD

A

mild airflow limitation

FEV1 > 80% predicted

with or without chronic symptoms

25
GOLD Classification - Moderate COPD
worsening airflow limitation 50% < FEV1 < 80%, SOB on exertion
26
GOLD Classification - Severe COPD
further worsening airflow limitation 30% < FEV1 < 50% greater SOB, reduced exercise capacity, repeat exacerbations, which impact quality of life
27
GOLD Classification - Very Severe
severe airflow limitation FEV1 < 30% or FEV1 <50% with chronic respiratory failure quality of life impaired, exacerbations might be life-threatening
28
Common Chest X-ray findings in patients with COPD
retrosternal airspace bulla - hyperlucency > 1cm with arcuate shadow barrel chest hyperlucency hyperinflation - flat diaphragm
29
Chest CT in those with COPD
mostly to assess for emphysema and to rule out bronchiectasis & others focal lucencies scattered in lungs often predominates in upper zones of each lobe may reveal large bullae or blebs associated loss of vasculature in areas of emphysema
30
Therapy Goals
prevent decline in pulmonary function prevent exacerbations maximize physical function/wellness decrease mortality and increase longevity
31
Pharmacologic Treatments
bronchodilators steroids combination of long-acting bronchodilators and steroid formulations phosphodiesterase-4 inhibitor (roflumilast) oxygen chronic macrolide therapy in selected individuals with frequent exacerbations consider treatment for asthma/atopic/allergic component as well
32
Non-Pharmacologic Treatment
smoking cessation – never too late education, self-management pulmonary rehab nutrition vaccination end of life and palliative care treatment of hypoxemia (oxygen) treatment of hypercapnia, or elevated CO2, (biPAP or other NIV)
33
Surgical Procedures for COPD
Lung volume reduction surgery: considered in pts with upper-lobe emphysema Bronchoscopic lung volume reduction: for advanced emphysema Bullectomy: open lung or VATS resection of large bullae Lung transplant: high post-op mortality Not common
34
Acute Exacerbations of COPD - Definition
o worsening of respiratory symptoms (dyspnea, cough, and/or sputum production) over the course of hours to days that is outside of usual day-to-day variability
35
Acute Exacerbations of COPD - Goal
reduce frequency and reduce severity
36
Acute Exacerbations of COPD - Prevention
smoking cessation hang hygiene immunizations avoidance of triggers
37
Acute Exacerbations of COPD - Hospitalization
severe symptoms: worsening of resting dyspnea, high respirations, hypoxia, confusion, drowsiness acute respiratory failure: respirations greater than 30, increased work of breathing, either hypoxic or hypercapnic onset of new physical signs (cyanosis, peripheral edema) failure of exacerbation to respond to initial medical management presence of serious comorbidities (heart failure, EKG changes, high troponin) insufficient home support more aggressive antibiotics and steroids early
38
When are antibiotics recommended for Acute Exacerbations of COPD?
Increased dyspnea Increased sputum volume Increased sputum purulence OR If patient requires mechanical ventilation for AECOPD (either invasive or noninvasive) Really relies on sputum; color of sputum doesn’t matter, unless it is a change
39
Other Acute Exacerbations of COPD Treatment
parenteral steroids short acting bronchodilators + - short acting anticholinergics continued maintenance therapy respiratory therapy
40
Indications for Noninvasive Mechanical Ventilation
At least one of the following: Resp acidosis: PaCO2>45mmHg AND pH <7.35 Severe dyspnea with clinical signs of respiratory fatigue Persistent hypoxemia despite supplemental oxygen therapy
41
Indications for Invasive Mechanical Respiration
Unable to tolerate NIV or NIV failure S/p resp or cardiac arrest Diminished consciousness, psychomotor agitation uncontrolled by sedation Massive aspiration Persistent inability to remove resp secretions Severe hemodynamic instability without response to fluids & pressors Severe ventricular or supraventricular arrhythmias Life-threatening hypoxemia in pts unable to tolerate NIV
42
When to Refer
A1AT deficiency or known FH of AATD Restrictive pattern on PFTs Any finding that seems worse than you expect (eg severe ↓DLCO in someone with mild obstruction) Rapid progression of symptoms Frequent exacerbations despite whatever you’re doing for them Pulmonary nodules (esp if multiple – malignancy until proven otherwise) Adenopathy noted on imaging Whenever you are considering the use of less common treatments