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Clinical Medicine II > COPD > Flashcards

COPD Flashcards

1
Q

what is the 3rd leading cause of death?

A

COPD

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2
Q

what is COPD?

A

A common preventable (almost always) and treatable disease characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases

-i.e. cig smoke

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3
Q

what are the 3 classifications of COPD?

A

Emphysema (enlargement of air spaces & destruction of lung tissue)

Chronic bronchitis (obstruction of small airways)

Chronic obstructive asthma (basically when asthma is no longer reversible)

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4
Q

what is COPD the result of that asthma isn’t?

A

COPD is usually the result of cig smoking

-NO elevated IgE (like in asthma) - COPD not allergic rxn

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5
Q

at what age is COPD diagnosed vs asthma?

A

COPD is diagnosed at age 50-60s

Asthma diagnosed in childhood

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6
Q

is COPD reversible like asthma?

A

NO!!!

obstruction is either irreversible or partially reversible with bronchodilator therapy

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7
Q

pathophysiology of COPD

A

-Inflammation and <b>fibrosis</b> of the bronchial wall (fibrosis is unique to COPD, not seen in asthma)

-Hypertrophy of the submucosal glands
-Hypersecretion of mucus
-Loss of elastic lung fibers and alveolar tissue
-Results in airway obstruction, decreased surface area for gas exchange, and mismatch of ventilation and perfusion
(Trouble getting air out -> delayed expiratory phase)

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8
Q

does COPD progress despite cessation of smoking?

A

YES!!!

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9
Q

what are common triggers of COPD exacerbations?

A

pulmonary infections (viral URI or pneumonia)

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10
Q

what does COPD often become?

A

a terminal illness -> cause of death

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11
Q

what is COPD associated with?

A

anxiety b/c feel like suffocating

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12
Q

what are risk factors of COPD?

A

<b>-Cig smoking</b>

  • Airway hyper-responsiveness (bronchial constriction in rxn to exposures)
  • Biomass fuel exposure (developing world)
  • Second-hand smoke (probably most common next to cigarette smoking)
  • Ambient air pollution
  • Genetics (alpha-1-anti-trypsin deficiency)
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13
Q

what is alpha-1-anti-trypsin deficiency?

A
  • Genetic predisposition, which is NOT preventable
  • 1% of all cases
  • Think of this in young patients with COPD (<45 years old)
  • Not preventable for these people
  • Usually fatal, short life spans
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14
Q

what is chronic bronchitis?

A
  • Excessive secretion of bronchial mucus
  • <b>Chronic daily productive cough for ≥3 months in each of two successive years without other explanation</b>

-SMOKERS COUGH (hacking & gurgling all the time)

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15
Q

what may chronic bronchitis proceed or follow?

A

the development of airflow limitation

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16
Q

what is seen in chronic bronchitis that isn’t seen in emphysema?

A

fibrosis

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17
Q

what is emphysema?

A

Abnormal and permanent enlargement of the airspaces that is accompanied by destruction of the airspace walls and capillary beds, <b>without obvious fibrosis</b>

-<b>loss of elasticity</b>

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18
Q

what are the 2 types of emphysema?

A

Proximal acinar (centrilobular) & Panacinar

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19
Q

what is proximal acinar (centrilobular) emphysema?

A
  • initial preservation of alveolar ducts and sacs
  • Abnormal dilation or destruction of the respiratory bronchiole
  • Commonly associated with cigarette smoking
  • Can be seen in coal workers’ pneumoconiosis
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20
Q

what is panacinar emphysema?

A
  • involves both bronchioles and alveoli
  • Enlargement or destruction of all parts of the acinus
  • <b>Most commonly associated with alpha-1-antitrypsin deficiency</b>

-Also sometimes found in smokers

21
Q

what are common symptoms of COPD?

A
  • chronic cough
  • sputum production esp with chronic bronchitis (worse in the morning)
  • exertional dyspnea (fatigue)
  • wheezing
  • chest tightness
  • weight gain (d/t to limitation of activity)
  • weight loss in advanced disease
22
Q

what are physical exam findings of COPD?

A
  • Prolonged expiratory phase
  • Expiratory wheezing during acute exacerbations
  • Barrel chest
  • Enlarged lung volumes (poor diaphragmatic excursion)
  • Respiratory distress in severe exacerbation (use of accessory muscles, tripod position, pursed lips)
  • Cyanosis
  • Systemic wasting/significant weight loss (advanced disease)
  • Signs of right heart failure (advanced disease) b/c a cause of R HF is advanced pulm disease
23
Q

what is a pink puffer?

A

EMPHYSEMA PT

  • major complaint is dyspnea
  • cough is rare
  • scant clear mucous
  • pts are thin/weight loss
  • accessory muscle use
  • chest is quiet or soft-pitched wheeze
24
Q

what is a blue bloater?

A

CHRONIC BRONCHITIS PT

  • major complaint is chronic cough
  • mucopurulent sputum
  • frequent COPD exacerbations d/t infections
  • dyspnea mild initially
  • chest is noisy w/rhonchi & wheezing
25
Q

what is a COPD pts hx like?

A

SOB, cough, wheeze, cig smoking

26
Q

what do COPD pts have a tendency of retaining that you will see on labs?

A

bicarb

-have a tendency to obtain bicarb even more than asthma pt b/c obstruction is not reversible

27
Q

why would you do a CXR for COPD pt?

A

to rule out other causes of symptoms

28
Q

what type of pulmonary test do you do for COPD patients?

A

pulmonary function test

29
Q

what is the cornerstone of diagnostic evaluation of COPD?

A

PFTs, particularly spirometry

30
Q

what is DLCO?

A

quantitation of diffusing capacity

  • measurement of the rate of gas transfer from alveolus to the capillary
  • Measured in relation to the driving pressure of CO across the alveolar-capillary membrane
31
Q

what conditions decrease the DLCO?

A
  • Anemia
  • Emphysema, pulmonary HTN, recurrent PE
  • Interstitial lung disease
32
Q

what does DLCO help distinguish in obstructive disease?

A

helps distinguish b/w emphysema & chronic bronchitis/asthma

33
Q

what does DLCO help distinguish in restrictive lung disease?

A

helps distinguish b/w interstitial lung disease and other causes of restrictive lung disease (kyphosis)

34
Q

what lab data is there for COPD?

A

serum bicarb (CO2) - identifies chronic hypercapnia in chronic disease

alpha-1-antitrypsin (AAT) deficiency - esp. in ≤45 years

35
Q

what lab data is used to rule out other causes of dyspnea?

A

hemoglobin (when anemic can be fatigued)

BNP (rule out CHF)

36
Q

what are expected spirometry results for obstructive lung disease?

A
  • FEV1 is decreased
  • FVC is normal
  • FEV1/FVC is decreased (<0.7)
  • Improvement in FEV1 (and ratio) after bronchodilators (more of a response in asthma)
  • DLCO is to distinguish between emphysema and COPD or asthma
37
Q

what are expected spirometry results for restrictive lung disease?

A
  • FEV1 is reduced
  • FVC is reduced
  • FEV1/FVC ratio is normal
  • TLC is reduced
  • DLCO differentiates between intrinsic lung diseases and other causes
38
Q

what is the non-pharm management of COPD?

A

<b>-Smoking cessation</b>

  • Reduction in risk factors
  • Vaccinations to prevent pneumo and flu
  • Oxygen therapy
  • Pulmonary rehab
39
Q

what is the pharmacologic management of COPD?

A

<b>Short acting bronchodilators</b>

  • SABA - albuterol (proair), Levalbuterol (Xopenex)
  • SAMA - ipratropium (Atrovent)

<b>Combo SABA + SAMA Combivent (SABA + Ipratropium)</b>

  • Most commonly used
  • Have found that people do better on this than those who just use albuterol
40
Q

what is the first line txt for newly diagnosed COPD?

A

SABA or SAMA or Combo of SABA + SAMA (Combivent)

41
Q

what does the presentation of an acute exacerbation of COPD look like?

A
  • SOB with exertion
  • Frequent cough usually productive of sputum (if have bronchitis element)
  • Wheezing
  • Often associated with pulmonary infection (URI or pneumo - 70%)
  • Minimal to no improvement with frequent use of rescue inhaler
42
Q

what is seen on exam of acute exacerbation of COPD?

A
  • Respiratory distress
  • Accessory muscle tripod use
  • Tripod position
  • Pursed lips
  • Hypoxia
  • Tachypnea
  • Wheezing
  • Poor air movement
  • Crackles if pneumonia
43
Q

what is the txt of acute COPD exacerbation?

A
  • Oxygen (keep O2 >90% but <96% b/c retain CO2)
  • systemic steroids (Prednisone PO or methylprednisolone IV)
  • short acting bronchodilator (ipratropium & albuterol neb - Duoneb -> better than just albuterol, can give albuterol in b/w doses of Duoneb)
  • <b>abx (if pt requires hospitalization or has infection) - cover atypical organisms (Levo, Azithromycin)</b>
44
Q

treatment of hospital admission for COPD

A
  • Oxygen via nasal cannula keep SaO2 >93 BUT <96
  • Prednisone 60mg PO daily until starting to improve, then taper over 10-14 days (Solumedrol is an alternative)
  • Duoneb q6h while hospitalized
  • Albuterol neb q2h prn SOB/wheeze

-Levofloxacin 750mg PO daily
(Azithromycin is an alternative)

45
Q

who to hospitalize for COPD flare?

A
  • inadequate response to outpatient or ER management (ppl on prednisone & not getting better)
  • marked increase in dyspnea compared to baseline
  • severe underlying COPD (FEV1 = 50% predicted)
  • inability to eat or sleep
  • new cyanosis or hypoxia
  • acute respiratory distress
  • AMS
  • insufficient home support
  • frequent exacerbations
  • high risk comorbidities (pan, arrhythmia, CHF, DM, ARF)
46
Q

when do you consider adding maintenance medications for COPD?

A
  • Frequent chronic symptoms
  • Frequent exacerbations
  • Disease progression
47
Q

what are the maintenance medications for COPD?

A

<b>-LABA</b> (salmeterol 1 puff inhaled BID)
<b>-LABA + Inhaled glucocorticoid combo</b> (salmeterol/fluticasone (Advair) 1 puff BID)
<b>-LAMA</b> (tiotropium (Spiriva))

<b>End stage disease:</b>

  • Chronic steroids
  • Chronic oxygen
48
Q

what is the result when COPD pts retain CO2 in severe disease?

A

respiratory acidosis

Clinical Medicine II (10 decks)

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