1 - COPD/tobacco Flashcards

1
Q

COPD is characterized by? what cells involved?

A

inflammation: neutrophils = driving force (vs asthma which is eosinophilic)

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2
Q

COPD as a spectrum of pathology?

A

emphysema and chronic bronchitis

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3
Q

what is emphysema

A

abnormal, permanent dilatation of airspaces distal to terminal bronchioles, accompanied by alveolar wall destruction without fibrosis

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4
Q

pink puffers vs. blue bloaters

A

P = emphysema. B = chronic bronchitis

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5
Q

pink puffers: who? why? cor pulmonale?

A

individuals with predominance of emphysema: they maintain normal O2/CO2 until late, so thin and cachetic since they’re expending so much energy. cor pulmonale occurs late.

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6
Q

chronic bronchitis: how is it defined?

A

clinically: productive cough (>250 mL/day) for at least 3 months per year for 2 consecutive years, with air flow obstruction

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7
Q

blue bloaters: who? why? cor pulmonale?

A

pathological process localized to bronchi, these ppl don’t do extra work so hypercapnic and hypoxemic, cor pulmonale develops early

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8
Q

co morbidities of COPD? most will die from?

A

weight loss, muscle wasting/weakness, systemic effects like osteoporosis, anemia, depression, cardiac disease. most die of cardiac causes.

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9
Q

diagnosis of COPD?

A

use symptoms (cough, sputum, dyspnea) with exposure to risk factors (tobacco, occupation, pollution, family hx) –> then do spirometry to confirm COPD

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10
Q

genetics of COPD?

A

only 1/5 smokers develop COPD so there is some genetic susceptibility or resistance to COPD. some will develop emphysema, some get chronic bronchitis.

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11
Q

only known genetic defect that leads to COPD? how?

A

A1AT deficiency: minimizes injury caused by proteolytic enzymes released by neutrophils. deficiency = can’t protect against it = COPD more likely

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12
Q

who do we screen for A1At deficiency?

A

ppl with COPD >65 years, or with smoking history less than 20 pack years

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13
Q

who should be screened for COPD?

A

smoker/ex smoker > 40 with: regular cough, regular phlegm, simple chores make them SOB, wheezing with exertion or at night, frequent colds that persist longer

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14
Q

classification of impairment of lung function?

A

all have FEV1/FVC less than 0.7: then by % predicted to stage mild, moderate, severe or very severe

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15
Q

X rays for diagnosing COPD?

A

not helpful. only thing related to hypertension: flattening of hemi diaphragm on lateral view

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16
Q

objectives of COPD treatment

A

relieving symptoms, improve QoL, prevent/manage exacerbations

17
Q

approach to COPD management

A

smoking cessation/exercise/education + PRN short acting bronchodilators. then with increasing severity: long acting bronchodilators, pulmonary rehabilitation, inhaled corticost. with LABA, oxygen, then surgery

18
Q

3 non pharmacologic COPD therapies

A

vaccinations, smoking cessation, exercise/pulm. rehabilitation

19
Q

bronchidilators: what works better? what does it or not do?

A

long acting better, and better if you use early in disease course. doesn’t influence lung function but will relieve symptoms, improve exercise tolerance, and reduce rates of exacerbations

20
Q

use of inhaled corticosteroids in COPD?

A

not alone: used in combination with LABA –> decrease exacerbations but doesn’t change loss of FEV1