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X Clin Med II Exam 2 > Chronic Obstructive Pulmonary Disease > Flashcards

Chronic Obstructive Pulmonary Disease Flashcards

1
Q

General characteristics of COPD

A

Treatable disease characterized by respiratory sxs and airflow limitation

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2
Q

When does an airway disease become COPD?

A

When it is irreversible

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3
Q

Clinical subtypes of COPD

A

Chronic bronchitis
Emphysema
Chronic obstructive asthma

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4
Q

How does a chronic bronchitis pt look?

A

Blue bloater due to cyanosis and overweight body habitus
Hypoxemia and respiratory acidosis
Cor pulmonale from pulm HTN

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5
Q

How does an emphysema pt look?

A

Pink puffers because of pursed-lip breathing, skin colo and thin body habitus

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6
Q

When does a pt have chronic bronchitis?

A

Chronic productive cough for 3 or more months, during 2 consecutive yrs with no other cause

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7
Q

Structural changes in chronic bronchitis

A

Mucous gland enlargement and hypersecretion
Bronchial squamous metaplasia
Loss of ciliary transport

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8
Q

Pathophysiology of chronic bronchitis

A

Inflammation of the bronchial wall and infiltration of the sub-mucosal layer by NEUTROPHILS
Also may be due to chronic bacterial colonization and airway hyper-reactivity

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9
Q

When is the obstruction for chronic bronchitis?

A

Inspiratory and expiratory

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10
Q

What results from the impeded ventilation in chronic bronchitis?

A

Hypoxemia and hypercapnia

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11
Q

Pathophysiology of emphysema

A

Pathologic enlargement of the air spaces distal to the terminal bronchioles due to destruction of the alveolar walls (might be due to too much elastase or too little antitrypsin)

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12
Q

What is neutrophil elastase?

A

Protease enzyme secreted by neutrophils and macrophages during inflammation
Destroys bacteria and host tissue (like elastin)

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13
Q

What is alpha-1 antitrypsin?

A

Inhibitor of neutrophil elastase (so in a deficiency there is a breakdown of lung structure by elastase)

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14
Q

Structural changes in emphysema

A

Reduced alveolar surface area available for gas exchange
Decreased elastic recoil
Loss of alveolar supporting structure leads to airway narrowing

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15
Q

When is the obstruction in emphysema?

A

Mostly exhalation

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16
Q

Hypoxemia and emphysema

A

Not usually significant until later disease severity (due to destruction of the capillary bed that results in reduced diffusing capacity for CO)

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17
Q

Differences between asthma and COPD

A

Inflammatory disorder of the airways mostly due to EOSINOPHILS
Airway hyperreactivity- increased secretions, mucosal edema, constriction of bronchial SM-obstruction
Reversible!

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18
Q

Risk factors for COPD

A 
Cigarette smoking (most common)
Environment/occupation
Second hand smoke exposure
Airway hyper-responsiveness (asthma)
Genetic: alpha-1 antitrypsin deficiency
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19
Q

Why does cigarette smoking lead to COPD?

A

It stimulates elastase enzymatic activity to cause changes in the structures
Causes release of cytotoxic oxygen radicals from WBCs in lung tissue
Amt and duration will contribute to severity

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20
Q

Examples of environmental exposures

A

Air pollution, coal miners, grain handlers, metal molders, workers exposed to dust, cooking with biomass fuels

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21
Q

What is alpha-1 antitrypsin deficiency?

A

Hereditary syndrome resulting in early onset of emphysema (when its younger age-<45)
Process of lung destruction is accelerated in smokers with this

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22
Q

Classic presentation of COPD

A

Dyspnea, chronic cough and sputum production (5th or 6th decade of life)

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23
Q

Common comorbidities of COPD

A

CVD, DM, renal insufficiency, osteoporosis, psych illness, cognitive dysfunction

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24
Q

What physical exam findings might be seen in COPD?

A

Tripod positioning, cyanosis, tobacco staining of the fingers, JVD, accessory muscle use, pursed lip breathing
Lungs: barrel chest, prolonged expiration, increased resonance on percussion, decreased breath sounds/wheezes/crackles
S3 gallop, RV lift
Hepatomegaly
Peripheral edema

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25
Q

What is the use of pursed lip breathing?

A

Ordinary breathing allows for early bronchial collapse on exhalation
This breathing achieves resistance to outflow at the lips so it raises the intrabronchial pressure to keep them open and expel the air easier

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26
Q

What is cor pulmonale?

A

Altered structure (hypertrophy/dilation) or impaired function of the right ventricle that results from pulmonary HTN associated with diseases like COPD (mostly) or of the vasculature, upper airway or chest wall

27
Q

What is required for diagnosis of COPD?

A

Spirometry (also for severity)

28
Q

What other labs can be used in COPD?

A 
CBC (usually to rule out anemia), BNP, metabolic panel, labs etc
Pulse ox
ABD
EKG
Sputum examination
CXR/high resolution CT chest
29
Q

What do we look for in the PFTS for COPD?

A

Forced vital capacity, forced expiratory volume in 1 second and FEV1/FVC ratio (should be 70-80%)

30
Q

What other results are seen on PFTS in COPD?

A

Increased total lung capacity (vital capacity and reserve volume)
If severe emphysema, decreased diffusing capacity of carbon monoxide

31
Q

After what pulse ox do you assess ABG for COPD?

A

<92%
On ABG, see mild to moderate hypoxemia without hypercapnia (when it’s worse, will see respiratory acidosis due to CO2 increase)

32
Q

What are signs of air trapping on CXR?

A

Increased AP diameter, hyperinflation (elongation of lung fields, hyperlucency (dark), flat diaphragms (>1 cm)
Mostly just to exclude other diagnosis

33
Q

What is pathognomonic for emphysema on a CXR?

A

Blebs or bullae

34
Q

What findings on a CXR are suggestive for emphysema?

A

Hyperinflation (maybe bullae)
Flattening of diaphragm
Enlargement of retrosternal space

35
Q

What findings on a CXR are suggestive for chronic bronchitis?

A

Cardiac enlargement, pulmonary congestion, increased lung markings

36
Q

When would you order a chest CT?

A

If the sxs suggest complication of COPB (pneumonia, pneumothorax, large bullae), PE or if might need lung vol reduction surgery

37
Q

What can lead to increased morbidity and mortality in COPD?

A

More exacerbations

38
Q

Suggested tx for Group A

A

Short acting bronchodilator OR SABA + SAMA combo used PRN

39
Q

Suggested tx for Group B

A

Long-acting bronchodilator (LAMA or LABA)

40
Q

Suggested tx for Group C

A

LAMA

41
Q

Suggested tx for Group D

A

LABA + LAMA, or consider ICS + LAMA

42
Q

What do groups B-D always need to have on hand?

A

SABA for symptom control and acute exacerbations

43
Q

What is the mainstay of therapy for COPD?

A

Bronchodilators: inhaled B2 agonists or anticholinergics

Might also improve mucociliayr clearance, diaphragmatic action and cardiac contractility

44
Q

Short acting B2 agonists (SABA)

A

Albuterol (Ventolin, ProAir, Proventil)

2 puffs q4-6 hrs

45
Q

Long acting B2 agonists (LABA)

A

Salmeterol (Serevent) or Formoterol (Foradil)

q12 hr hosing

46
Q

Benefits of B2 agonists

A

Good bronchodilation but no effect on sputum/secretions

SE: palpitations, tachycardia, insomnia, tremors

47
Q

Short acting muscarinic antagonists (SAMA)

A 
Ipratropium bromide  (Atrovent), ipraptropium plus albuterol (Combivent)
2 puffs BID-QID
48
Q

Long acting muscarinic antagonists (LAMA)

A 
Tiotropium bromide (Spiriva), Umeclidinium (Incruse Ellipta)
Once daily
49
Q

Benefits of muscarinic antagonists (anticholinergics)

A

Good bronchodilation, reduce air trapping in the lungs and less cardiac stimulatory effect
SE: dry mouth, metallic taste, HA, cough

50
Q

What is theophylline?

A

A methylxanthine
Used as a bronchodilator in the past and now just used for refractory cases
Toxicity problem: tachycardia, arrhymthmias, seizures, HA, nausea, potential for drug interactions

51
Q

Corticosteroid benefits

A

Advair, Dulera, Symbicort, Breo Ellipta
Reduce mucosal edema/inflammation by inhibiting prostaglandins to decrease secretions
Can increase the responsiveness to beta-adrenergics
SE: oral candidiasis, bruising

52
Q

When do you use antiprotease therapy?

A

For pts with alpha1-antitrypsin deficiency (serum levels <11)
Injections but costly and controversial

53
Q

Options for adjunct therapy to the meds

A

Pulmonary rehab (stage B-D)
Oxygen to increase survival
Lung volume reduction surgery

54
Q

When is supplemental O2 indicated?

A

Chronic dyspnea at rest

PaO2<55 or SaO2<88%

55
Q

Downside to supplemental O2

A

May reduce the drive to breath and cause respiratory acidosis (these pts are driven to breath due to low O2 levels because they are desensitized to high levels of CO2 so when they add O2 they will not breathe)

56
Q

Ways to minimize complications

A

Avoidance of risk factors
Influenza and pneumococcal vaccines (PPPV13 and PCV23)
Regular exercise
Early recognition of pulmonary infection

57
Q

What are early signs of a pulmonary infection?

A

Increased sputum production, fever, worsening dyspnea, fatigue, chest pain, hemoptysis

58
Q

What might you see in an acute exacerbation of COPD?

A

Increased dyspnea, increase in cough frequency/severity, sputum increases or becomes purulent

59
Q

Most common triggers of acute exacerbation of COPD

A 
Respiratory illnesses (rhinoviruses and influenza viruses most common) and pollution
Viruses might lead to secondary bacterial pneumonia
60
Q

Outpatient management of an acute exacerbation

A

Increase dose of SABA (or can add ipratropium)
Oral steroids (40 mg/day x 5 days)
Abx for mod-severe exacerbations
Maybe hospitalization if severe

61
Q

First line abx for acute exacerbation of COPD with an outpatient

A

Macrolide for uncomplicated COPD

Fluoroquinolone for complicated COPD with risk factors

62
Q

Indications for hospitilization with acute exacerbation of COPD

A 
Severe sxs/signs
Severe underlying COPD (FEV1<50%)
Significant comorbidities
Onset of new physical signs (cyanosis, edema, arrhythmias)
Older
Insufficient home support
63
Q

What FEV1/FVC ratio is consistent with obstructive pattern?

A

less than .7

X Clin Med II Exam 2 (6 decks)

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