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Clinical Medicine II > COPD > Flashcards

COPD Flashcards

(48 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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
what is a COPD pts hx like?
SOB, cough, wheeze, cig smoking
26
what do COPD pts have a tendency of retaining that you will see on labs?
bicarb | -have a tendency to obtain bicarb even more than asthma pt b/c obstruction is not reversible
27
why would you do a CXR for COPD pt?
to rule out other causes of symptoms
28
what type of pulmonary test do you do for COPD patients?
pulmonary function test
29
what is the cornerstone of diagnostic evaluation of COPD?
PFTs, particularly spirometry
30
what is DLCO?
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
what conditions decrease the DLCO?
- Anemia - Emphysema, pulmonary HTN, recurrent PE - Interstitial lung disease
32
what does DLCO help distinguish in obstructive disease?
helps distinguish b/w emphysema & chronic bronchitis/asthma
33
what does DLCO help distinguish in restrictive lung disease?
helps distinguish b/w interstitial lung disease and other causes of restrictive lung disease (kyphosis)
34
what lab data is there for COPD?
serum bicarb (CO2) - identifies chronic hypercapnia in chronic disease alpha-1-antitrypsin (AAT) deficiency - esp. in ≤45 years
35
what lab data is used to rule out other causes of dyspnea?
hemoglobin (when anemic can be fatigued) BNP (rule out CHF)
36
what are expected spirometry results for obstructive lung disease?
- 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
what are expected spirometry results for restrictive lung disease?
- FEV1 is reduced - FVC is reduced - FEV1/FVC ratio is normal - TLC is reduced - DLCO differentiates between intrinsic lung diseases and other causes
38
what is the non-pharm management of COPD?
-Smoking cessation - Reduction in risk factors - Vaccinations to prevent pneumo and flu - Oxygen therapy - Pulmonary rehab
39
what is the pharmacologic management of COPD?
Short acting bronchodilators - SABA - albuterol (proair), Levalbuterol (Xopenex) - SAMA - ipratropium (Atrovent) Combo SABA + SAMA Combivent (SABA + Ipratropium) - Most commonly used - Have found that people do better on this than those who just use albuterol
40
what is the first line txt for newly diagnosed COPD?
SABA or SAMA or Combo of SABA + SAMA (Combivent)
41
what does the presentation of an acute exacerbation of COPD look like?
- 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
what is seen on exam of acute exacerbation of COPD?
- Respiratory distress - Accessory muscle tripod use - Tripod position - Pursed lips - Hypoxia - Tachypnea - Wheezing - Poor air movement - Crackles if pneumonia
43
what is the txt of acute COPD exacerbation?
- 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) - abx (if pt requires hospitalization or has infection) - cover atypical organisms (Levo, Azithromycin)
44
treatment of hospital admission for COPD
- 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
who to hospitalize for COPD flare?
- 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
when do you consider adding maintenance medications for COPD?
- Frequent chronic symptoms - Frequent exacerbations - Disease progression
47
what are the maintenance medications for COPD?
-LABA (salmeterol 1 puff inhaled BID) -LABA + Inhaled glucocorticoid combo (salmeterol/fluticasone (Advair) 1 puff BID) -LAMA (tiotropium (Spiriva)) End stage disease: - Chronic steroids - Chronic oxygen
48
what is the result when COPD pts retain CO2 in severe disease?
respiratory acidosis

Clinical Medicine II (10 decks)

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