COPD Flashcards

1
Q

increased retrosternal airspace on lateral film caused by

A

COPD: hyperinflation

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2
Q

increased AP diameter

flattened diaphragm

A

advanced COPD

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3
Q

treatment of COPD exacerbation with dsypnea + wheeze (r/o PE, CHF, MI)

A

antibiotic if lots of sputum: if mild, PO Abx for pneumococcus, h. influenzae, morxella most common bacteria, if severe: add for G- bacteria: klebsiella, psuedomonas
short-acting bronchodilator: B agonist + anticholinergic
systemic CS: ↓ duration of exacerbation, may ↓ risk relapse
O2 if sat

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4
Q

prevention of COPD exacerbation

A

quit smoking: pulm function declines more rapidly if smoker, reduce rate of further deterioration - can equate to nonsmoker rate, ↓ risk comorbidities: CV disease and cancer
inhaled bronchodilator (stage 1: short-acting for PRN for exacerbations (albuterol, ipatropium), stage 2: add long-acting (salmeterol, tiotropium))
inhaled CS: (fluticasone), add if stage 3 or higher: ↓ frequency of exacerbations
influenza (↓ frequency and complications of exacerbations) + pneumococcal vaccines (smokers and those with CLD)
O2: add if stage 4 if evidence of hypoxia (spo2 15 h/day

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5
Q

prevention of COPD exacerbation

A

long-acting bronchodilator
inhaled CS
influenza + pneumococcal vaccines

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6
Q

diff dx: dyspnea + wheezing

A

asthma: onset early in life, +/- smoking, episodic exacerbation, return to baseline
COPD: onset mid to late life, long smoking hx, slowly progressive, can be a complication of asthma too

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7
Q

management for ANY patient with dyspnea: COPD or asthma exacerbation

A

*ABC
*ventilate when: reduced level of consciousness causing unprotected airway, increased work of breathing is tiring, inadequate SpO2
*check for hypoxic signs: SpO2 or ABG, cyanosis of perioral region or digits
*meds:
O2
bronchodilator: inhaled B2 agonist (albuterol) reduces obstruction +/- anticholinergic (ipatropium) synergist with B agonist, RAPID effect
systemic steroids (PO, IM, or IV): reduce airway inflammation, DELAYED effect (takes hrs)

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8
Q

types of COPD

A

chronic bronchitis: cough + sputum production most days for at least 3 mo during last 2 consecutive years
emphysema: dyspnea caused by enlargement of respiratory bronchioles and alveoli caused by destruction of lung tissue

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9
Q

inflammation of airways, lung tissue, vessels
airway obstruction:
NOT fully REVERSIBLE
progressive
associated with chronic bronchitis, emphysema, or both

A

COPD

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10
Q

etiology of COPD

A

smoking
second hand smoke
dust or chemical occupational exposure
α1 antitrypsin deficiency: emphysema

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11
Q

clinical course of COPD

A

initial: daily productive cough (white, thick mucous)
exacerbations (viral or bacterial): worsening cough, clear to yellow/green mucous, wheezing
years later (FEV1 has reduced by 50%): dyspnea (primary presenting symptom), progresses from only with significant exertion, to any exertion, to rest
hyperinflation (later finding): barrel chest, ↓ BS, ↓ heart sounds, flattened diaphragm, expiratory wheeze with prolonged expiratory phase, bullae: parenchymal destruction

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12
Q

diagnostic test of lung function

A

spirometry

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13
Q

partially reversible airway obstruction spirometry:asthma

A

FEV1: ↑ by at least 12% or 200 mL

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14
Q

stage 1 COPD

A

mild: short-acting B agonist PRN

FEV1/FVC 80% predicted

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15
Q

stage 2 COPD

A

moderate: add long-acting B agonist

FEV1/FVC

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16
Q

stage 3 COPD

A

severe: add inhaled CS

FEV1/FVC

17
Q

stage 4 COPD

A

very severe: add O2

FEV1/FVC

18
Q

↑ RA pressure and RV EDP → liver congestion, jugular venous distention, peripheral edema (pitting)

A

cor pulmonale: complication of COPD

19
Q

counsel on smoking cessation before symptomatic COPD b/c

A

once symptomatic patient’s FEV1 will be reduced by 50%