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Flashcards in COPD Deck (19):
1

increased retrosternal airspace on lateral film caused by

COPD: hyperinflation

2

increased AP diameter
flattened diaphragm

advanced COPD

3

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

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

4

prevention of COPD exacerbation

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

5

prevention of COPD exacerbation

long-acting bronchodilator
inhaled CS
influenza + pneumococcal vaccines

6

diff dx: dyspnea + wheezing

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

7

management for ANY patient with dyspnea: COPD or asthma exacerbation

*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)

8

types of COPD

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

9

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

COPD

10

etiology of COPD

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

11

clinical course of COPD

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

12

diagnostic test of lung function

spirometry

13

partially reversible airway obstruction spirometry:asthma

FEV1: ↑ by at least 12% or 200 mL

14

stage 1 COPD

mild: short-acting B agonist PRN
FEV1/FVC 80% predicted

15

stage 2 COPD

moderate: add long-acting B agonist
FEV1/FVC

16

stage 3 COPD

severe: add inhaled CS
FEV1/FVC

17

stage 4 COPD

very severe: add O2
FEV1/FVC

18

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

cor pulmonale: complication of COPD

19

counsel on smoking cessation before symptomatic COPD b/c

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