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
Q

GOLD Classification - Moderate COPD

A

worsening airflow limitation

50% < FEV1 < 80%,

SOB on exertion

26
Q

GOLD Classification - Severe COPD

A

further worsening airflow limitation

30% < FEV1 < 50%

greater SOB, reduced exercise capacity, repeat exacerbations, which impact quality of life

27
Q

GOLD Classification - Very Severe

A

severe airflow limitation

FEV1 < 30% or FEV1 <50% with chronic respiratory failure

quality of life impaired, exacerbations might be life-threatening

28
Q

Common Chest X-ray findings in patients with COPD

A

retrosternal airspace

bulla - hyperlucency > 1cm with arcuate shadow

barrel chest

hyperlucency

hyperinflation - flat diaphragm

29
Q

Chest CT in those with COPD

A

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
Q

Therapy Goals

A

prevent decline in pulmonary function

prevent exacerbations

maximize physical function/wellness

decrease mortality and increase longevity

31
Q

Pharmacologic Treatments

A

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
Q

Non-Pharmacologic Treatment

A

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
Q

Surgical Procedures for COPD

A

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
Q

Acute Exacerbations of COPD - Definition

A

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
Q

Acute Exacerbations of COPD - Goal

A

reduce frequency and reduce severity

36
Q

Acute Exacerbations of COPD - Prevention

A

smoking cessation

hang hygiene

immunizations

avoidance of triggers

37
Q

Acute Exacerbations of COPD - Hospitalization

A

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
Q

When are antibiotics recommended for Acute Exacerbations of COPD?

A

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
Q

Other Acute Exacerbations of COPD Treatment

A

parenteral steroids

short acting bronchodilators + - short acting anticholinergics

continued maintenance therapy

respiratory therapy

40
Q

Indications for Noninvasive Mechanical Ventilation

A

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
Q

Indications for Invasive Mechanical Respiration

A

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
Q

When to Refer

A

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