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Flashcards in Headley - COPD Deck (27):

COPD is a disease state characterized by all of the following except:

A. Airflow limitation that is fully reversible.

B. Mucus hypersecretion in the airways.

C. Smooth muscle hyperplasia of airway walls.

D. Fibrosis of airway walls.

E. Inflammation characterized by CD8 lymphocytes,                        neutrophils, and macrophages.

A. Airflow limitation that is fully reversible -> this describes ASTHMA


What is the definition of COPD?

- Chronic obstructive pulmonary disease

- Disease state characterized by airflow limitation that is not fully reversible

- Airflow limitation is usually progressive and associated with abnormal chronic inflammatory response of the lungs to noxious particles or gase

- Exacerbations & comorbidities contribute to the overall severity in individual patients


What are the 4 defining characteristics of COPD?

- Reduced FEV-1 

- Reversibility <15%, fixed 

1. Reversibility in asthma: INC in FEV-1 and FVC by more than 200 mL or 15% with bronchodilator 

- Noxious particles/gases: cigarette smoke, coal dust, pollution, biomass fuels 

- Amplified immune response: macros, neutros, CD8+, remodelling of airways, destruction of parenchyma 



What are the mechs underlying airflow limitation in COPD (2)?

- Small airway disease: airway inflammation and fibrosis, luminal plugs, INC airway resistance (narrow airways) 

- Parenchymal destruction: loss of alveolar attachments, decreased elastic recoil


Which statement is true about COPD?

A. COPD is the seventh leading cause of death worldwide.

B. In the past 20 years, death rates from COPD among females in the USA has doubled.

C. COPD death rates are very high in those under the age of 45 years and COPD death rates decline steeply with increasing age.

D. In the past 20 years, death rates from COPD among males in the USA has doubled.

- B. In the past 20 years, death rates from COPD among females in the USA has doubled.

- Women started smoking later than men (in the 1960's) 



How have COPD age-adjusted death rates changed in the last 50 years?

- They have increased (see graph)


What is the epi of COPD in the US and the world?

- 3rd leading cause of death in the USA and worldwide (behind heart disease, cancer, and cerebrovascular disease) and is estimated to remain the fourth leading cause of death through 2030

- Affects more than 12% of the US population (24 million adults) and accounts for > 120,000 deaths each year

- In 2000, the WHO estimated 2.74 million deaths worldwide from COPD


How have COPD rates changed in the last 50 years?

- Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 (see attached image) 


What is the cost of COPD (billions)?

- Direct Medical Cost: $29.5     

- Total Indirect Cost: $20.4

- Total Cost: $49.9


What is the biggest risk factor for COPD? What are other risk factors?

- Cigarette smoking is the primary cause of COPD

- In the US 47.2 million people (28% of men and 23% of women) smoke

- WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025

1. In low- and middle-income countries, rates are increasing at an alarming rate



How is FEV-1 affected by age? COPD?

- FEV-1 40-60%: predicted associated with exertional dyspnea (yellow arrow)

- FEV-1 <30%: associated with disability (red arrow)

- FEV-1 <1 liter: 5-year mortality 50%

- People can lose as much as 5x their normal decline in FEV-1 if they continue smoking

- REMEMBER these numbers


What are the clinical features of COPD?

- Typically smokers: mean 20 cigarettes/day for 20 years 

1. Smokers with < 10-15 pack years rarely devo COPD

- Symptoms in 40’s w/productive cough or acute chest illness; DOE in 50's or 60's

- History of wheezing, dyspnea often leads to an erroneous diagnosis of asthma

- Presence of irreversible airflow obstruction due to chronic bronchitis and/or emphysema

- Spirometry: post-bronchodilator FEV1/FVC < 70% confirms persistent airflow limitation -> need to dx as COPD

- May include a reversible, or "asthmatic" component 

- Some pts w/long history of asthma may devo irreversible airflow obstruction indistinguishable from COPD


How do you diagnose COPD?

- Symptoms: shortness of breath, chronic cough, sputum 

Risk factor exposure: tobacco, occupation, indoor/outdoor pollution 

Spirometry: REQUIRED to establish diagnosis 


Describe the cough characteristic of COPD.

- Intermittent at first but usually becomes progressive throughout the day (referred to as a “smoker’s cough”)

- Usually productive of sputum but may be non-productive

- Cough syncope (temporary LOC due to fall in BP, i.e., fainting) or cough-related rib fractures may occur in advanced cases 


Describe the sputum production characteristic of COPD.

- Intermittent at first (usually in the morning) but usually becomes present throughout the day

- Sputum is usually tenacious and mucoid and in small quantities (20-30 ml/d up to 100 ml/d)

- A change in sputum color (purulent-yellow or green) or volume suggests an infectious exacerbation

- Production of sputum for 3-months in 2 consecutive years is clinical definition of chronic bronchitis (KNOW THIS -> will be on test)


What is the clinical definition of chronic bronchitis?

Production of sputum for 3-months in 2 consecutive years 


Describe the dyspnea characteristic of COPD.

- Usually PROGRESSIVE; becomes persistent over time

- At onset, occurs during exercise (climbing stairs, walking up hills) and may be avoided by appropriate behavioral changes (using an elevator, decreasing physical activity).

- As disease progresses, elicited even during minimal exertion or rest

- Quantification of dyspnea w/Modified Research Council Dyspnea scale indicated bc it predicts QOL, survival

- NOTE: ask your patients what will happen if they DO walk – they may instinctively avoid these things, and therefore not know it causes them to have shortness of breath 


What things might you note, or be looking for, on the physical exam of a COPD patient?

- Inspection for signs of airflow limitation, hyperinflation, and impairment of the mechanics of breathing:

1. Wheezing on auscultation w/slow or forced breaths

2. Prolongation of forced expiratory time

3. Barrel chest deformity (chronic hyperinflation)

4. Pursed lip breathing (hyperinflation) -> creates back pressure (like PEEP)

5. Low diaphragm position (hyperinflation)

6. DEC intensity (distant or muffled) heart and breath sounds (chronic hyperinflation)

7. Chest/abdominal wall paradoxical movements

8. Use of accessory muscles (intercostal, SCM)

9. In-drawing of lower intercostal interspaces


What are some of the systemic signs of COPD that can be seen on physical exam?

- Heart auscultation: may show signs of cor pulmonale (R. heart failure), like split S2 or pulmonary/tricuspid murmurs 

JVD, liver enlargement, and peripheral edemamay be due to cor pulmonale or severe hyperinflation

Loss of muscle mass and peripheral muscle wasting: are consistent with malnutrition and/or skeletal muscle dysfunction
- Cyanosis or bluish color: of the mucosal membranes may indicate hypoxemia


How can you test the airflow limitation in COPD?

Spirometry: should be performed in all pts suspected of COPD

- Bronchodilator reversibility: should be performed to exclude asthma, establish the best lung function, and to estimate prognosis -> spirometry pre- and post- bronchodilator (does it improve)

1. Reversibility: INC in FEV-1 or FVC by 200 mL or 15% (from baseline) 


What is the GOLD classification system for?

- To classify severity of airflow limitation in COPD

- In patients with FEV1/FVC < 0.70:

1. GOLD 1: Mild              FEV1 > 80% predicted      

2. GOLD 2: Moderate      50% < FEV1 < 80% predicted

3. GOLD 3: Severe          30% < FEV1 < 50% predicted

4. GOLD 4: Very Severe   FEV1 < 30% predicted

*Based on Post-Bronchodilator FEV1


How can you test lung volumes and gas exchange in COPD patients?

Static lung volumes (TLC, RV, RV/TLC) INC in advanced COPD -> useful in pts w/advanced disease and those being considered for surgery 

- DLCO: reduced in COPD pts w/predominant emphysema (but not those that predominantly have chronic bronchitis, which is more of an airway disease) -> may be useful to exclude asthma and to stratify patients for lung resection

1. Only going to happen with destruction of alveoli


How do you assess for risk of exacerbations in COPD?

- Use history of exacerbations and spirometry: 

1. Two or more exacerbations w/in last year OR 

2. FEV-1 <50% of predicted value are indicators of HIGH RISK

- More exacerbations = greater risk


What is an exacerbation of COPD?

- An acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations AND leads to a change in medication 


What are the consequences of COPD exacerbations (5)?

- Negative impact on QOL 

- Impact on symptoms and lung function 

- Increased economic costs

- Increased mortality 

- Accelerated lung function decline

- NOTE: want to try and minimize exacerbations in patients 


What are some additional tests you could order for COPD patients (other than spirometry and DLCO)?

- CXR should be performed to detect bullous disease and to exclude other diseases such as pneumonia, cancer, CHF, pleural effusions, and pneumothorax

- Oximetry and arterial blood gas: pulse oximetry or ABG’s can be used to evaluate a patient’s oxygen saturation and need for supplemental oxygen therapy

- Alpha-1 antitrypsin deficiency screening: perform when COPD develops in patients of Caucasian descent under 45 years or with a strong family history of COPD


Who should be tested for a deficiency in alpha-1-anti-trypsin? What is the test for?

- Should be measured in young pts (30's-40's) who devo COPD and have strong family hx of COPD 

- Accounts for < 1% of cases

- Normal allele is Pi MM (chromosome 14)

1. 90% of deficient peeps are homozygous (Pi ZZ) for Z allele; other rare forms are Pi SZ, Pi null null or Pi null-Z

Testing for deficiency in Alpha-1-anti-trypsin :

nDeficiency usually seen in Caucasians of northern European descent; more rare in Asians or African-Americans but should be tested.
nPatients rarely develop COPD without smoking.
nAlpha-1-anti-trypsin replacement therapy is associated with reduced mortality and a slowing of decline in lung function (FEV1) compared to no treatment.