Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med II Unit II > 2 COPD > Flashcards

2 COPD Flashcards

1
Q

Highest prevalence of COPD is among…

A

65-74 year olds

Men and women affected almost equally

Morbidity increases with age and is greater in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition:

A

Chronic obstructive pulmonary disease is a common, PREVENTABLE and TREATABLE disease that is 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three clinical subtypes of COPD?

A

Chronic Bronchitis (predominant)

Emphysema (predominant)

Chronic Obstructive Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Patients with Chronic Bronchitis are described as…

A

“Blue Bloaters” due to CYANOSIS and OVERWEIGHT body habitus

Hypoxemia and respiratory acidosis more common

Cor pulmonale from pulmonary HTN (b/c problems with both getting air in and out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Patients with Emphysema are described as …

A

“Pink Puffers” because of pursed-lip breathing, skin color, and thin body habitus

Use a lot of accessory muscles to breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Chronic bronchitis is defined as a chronic productive cough for ____________ with no other cause.

A

3 or more months during 2 consecutive years

Leads to structural changes:
• Mucous gland enlargement —> hyper secretion
• Bronchial squamous metastasis
• Loss of ciliary transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

In Chronic Bronchitis, inflammation of bronchial wall and infiltration of sub-mucosal layer is caused by ________

A

Neutrophils (vs eosinophils in asthma)

Chronic bacterial colonization and airway hyper-reactivity are thought to play an important role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Obstruction in chronic bronchitis is ….

A

Both inspiratory and expiratory

Hypoxemia and hypercapnia result form impeded ventilation

There is less parenchymal damage than emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathologic enlargement of the air spaces distal to the terminal bronchioles due to destruction of the alveolar walls

A

Emphysema

Destructive process not clearly understood (may be too much elastase or too little antitrypsin activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Protease enzyme secreted by neutrophils and macrophages during inflammation

A

Neutrophil elastase - it destroys bacteria and host tissue (ie - elastin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

An inhibitor of neutrophil elastase

A

Alpha-1 Antitrypsin

When in deficiency there is breakdown of the lung structure by elastase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe what happens to the alveoli in emphysema

A

Reduced alveolar surface area available for gas exchange

Decreased elastic recoil

Loss of alveolar supporting structure = airway narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Obstruction in emphysema is …

A

Mostly during exhalation

Not associated with significant hypoxemia until later in disease severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Destruction of capillary beds in emphysema results in …

A

Reduced DLCO (diffusing capacity for carbon monoxide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic inflammation in asthma is primarily mediated by…

A

Eosinophils

Airway hyper-reactivity —> increased secretions, mucosal edema, constriction of bronchial smooth muscle —> airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Is asthma reversible or irreversible?

A

Reversible!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most common risk factor for COPD

A

Cigarette smoking - 80% of COPD patients, most have smoked at least 20 cigarettes a day for 20 or more years

Other risk factors:
• Environment/occupation
• Second hand smoke exposure
• Airway hyper-responsiveness (asthma)
• Genetic RF: alpha-1 antitrypsin deficiency (<1% of all cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does cigarette smoking cause COPD?

A

Stimulates elastase enzymatic activity, causing degenerative changes in elastin and alveolar structures

Causes release of cytotoxic oxygen radicals from WBCs in lung tissue

Amount and duration contribute to disease severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Examples of environmental exposures that can lead to COPD

A

Air pollution

Coal miners

Grain handlers

Metal molders

Workers exposed to dust

Cooking with biomass fuels (1/3 of the world)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A hereditary syndrome resulting in the early onset of emphysema (<1% of US cases)

A

Alpha-1 antitrypsin deficiency

Features of emphysema present at a younger age (≤45)

AAT is a protease inhibitor - inhibits elastase and several other proteolytic enzymes

The process of lung destruction is accelerated in smokers with AAT deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Classic presentation of COPD

A

Dyspnea, chronic cough, and sputum production

Sx onset in 5th or 6gh decade of life

Most common early symptom is DYSPNEA ON EXERTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Common comorbidities of COPD

A

CVD (HTN, CAD, stroke)

DM

Renal insufficiency

Osteoporosis

Psychiatric illness

Cognitive dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Gross physical exam findings in emphysema

A

Tripod positioning

Cyanosis

Tobacco staining of fingers (because the idiot is still smoking)

JVD, use of accessory muscles (neck and shoulder)

Pursed lip breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why do patients with emphysema purse their lips?

A

In COPD, ordinary breathing allows early bronchial collapse on exhalation

Pursed-lip breathing achieves resistance to outflow at the lips, raising intrabronhial pressure, keeping the bronchi open. More air can thus be expelled.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

More specific physical exam findings in Emphysema

A

Lungs:
Barrel chest (increased AP diameter)
Prolonged expiration
Increased resonance on percussion (b/c of air trapping)
Decreased breath sounds (distant), wheezing, and crackles at base

Heart:
S3 gallop (if cor pulmonale), RV lift

ABD:
Hepatomegaly, pulm HTN if cor pulmonale

Ext:
Muscle wasting, peripheral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Altered structure (hypertrophy or dilation) and/or impaired function of the RIGHT ventricle that results from pulmonary HTN associated with diseases of the lung, vasculature, upper airway, or chest wall

A

Cor Pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most common cause of cor pulmonale

A

COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Diagnostic study required for the diagnosis of COPD

A

Spirometry

Will also do a CBC, BNP, cardiac enzymes, metabolic panel, AAT but spirometry is diagnostic

Other tests: Pulse ox, ABG, EKG, sputum exam, CXR/HRCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

The amount of air forcefully exhaled during maximal forced expiration

A

Forced Vital Capacity (FVC)

Normal is 80-120%

Compared to Forced Expiratory Volume in 1 second (FEV1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the FEV1/FVC ratio?

A

% of FVC expired in 1 sec

Normal is 70-80%

31
Q

How does spirometry diagnosis of COPD work?

A

First perform a pre and post-bronchodilator spirometry test
(FEV1/FVC <0.7 is consistent with an obstructive pattern)

Next review post-bronchodilator FEV1% predicted to determine GOLD grade I-IV

32
Q

In addition to FEV1/FVC < 0.7 and a decreased FEV1, COPD patients will have:

A

Increased Total Lung Capacity (TLC) due to air trapping

If severe emphysema, will also have decreased Diffusing Capacity of Carbon Monoxide (DLCO) because there’s not good air exchange occurring in capillary beds

33
Q

What will you see on CBC in COPD patients?

A

Usually normal but useful to rule out anemia as cause of dyspnea

Chronic bronchitis pt may have polycythemia secondary to chronic hypoxia

Leukocytosis may be present during acute exacerbations of COPD

34
Q

How to use Pulse Oximetry in COPD patients

A

If <92%, assess further with arterial blood gas

Arterial Blood Gas really only done inpatient
• Usually mild to moderate hypoxemia without hypercapnia (CO2 retention)
• As disease progresses hypoxemia worsens and CO2 increases (respiratory acidosis)

35
Q

When should you do a sputum culture on COPD patients?

A

When in-patient and unresponsive to initial abx treatment

36
Q

Possible EKG findings in COPD

A

Tachycardia

R atrial enlargement

R axis deviation and/or RVH

37
Q

Pathognomonic CXR findings for emphysema

A

Blebs (focal areas of blackness) or Bullae (larger blebs)

38
Q

Why do we do a CXR in COPD?

A

Obtain to exclude other diagnoses and assess for comorbities

See signs of air trapping - increased AP diameter, hyperinflation, hyperlucency, flat diaphragms

Blebs or bullae

Perivascular or peribronchial markings may be present in chronic bronchitis

39
Q

CXR findings more suggestive of emphysema

A

Hyperinflation (possibly with bullae)
Flattening of diaphragms
Enlargement of retrosternal air space

40
Q

CXR findings more suggestive of chronic bronchitis

A

Cardiac enlargement
Pulmonary congestion
Increased lung markings

41
Q

Do we need to do a chest CT on COPD patients?

A

Helpful but not needed for routine Dx

Obtain if SSx suggest a complication of COPD (PNA, pneumothorax, large bullae), alternate Dx (PE), or if considering lung volume reduction surgery (HRCT)

42
Q

GOLD strategy for staging

A

Step 1 - Determine if obstructive pattern (FEV1/FVC ratio < 0.7)

Step 2 - Determine severity (GOLD Grade 1-4, based on percent FEV1)

Step 3 - Assess symptoms (use patient rating scale)

Step 4 - Determine exacerbation risk (use frequency of exacerbations in past year)

43
Q

What are the four GOLD grades?

A

GOLD 1 = Mild (FEV1 ≥ 80% predicted)

GOLD 2 = Moderate (50% ≤FEV1, <80% predicted)

GOLD 3 = Severe (30% ≤FEV1, <50% predicted)

GOLD 4 = Very Severe (FEV1 <30% predicted)

44
Q

How to use number of exacerbations to determine further risk of exacerbation

A

0-1 exacerbations in the past 12 months = Low risk

2 or more exacerbations OR 1 hospitalization for COPD = High risk

45
Q

How do you prevent progression in COPD?

A

Stop smoking, you idiot!

46
Q

How do you relieve symptoms in COPD?

A

Pharmacotherapy/pulm rehab/Oxygen

Improve exercise tolerance

Manage/prevent exacerbations

Reduce mortality

47
Q

3 min counseling for smoking cessation can increase quit rate by…

A

5-10%

48
Q

Management of COPD for Group A patients (Gold 1-2, 0-1 exacerbations, mMRC 0-1)

A

Short-acting bronchodilator OR

SABA + SAMA combo used PRN

49
Q

Management of COPD for Group B patients (Gold 1-2, 0-1 exacerbations, mMRC 2+)

A

Long-acting bronchodilator (LAMA or LABA)

50
Q

Management of COPD for Group C patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 0-1)

A

LAMA

51
Q

Management of COPD for Group D patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 2+)

A

LABA + LAMA, consider ICS + LABA

52
Q

Mainstay of treatment for COPD

A

Inhaled ß2-agonists and anticholinergics (short and long acting)

Besides bronchodilation, may provide other effects such as ability to improve mucociliary clearance, diaphragmatic action, and cardiac contractility

53
Q

Examples of short acting ß2 agonists (SABAs)

A

Albuterol (Ventolin, ProAir, Proventil)

Usual dose = 2 puffs q4-6 hours (also available in neb form)

54
Q

Examples of Long-acting ß2-agonists (LABA)

A

Salmeterol (Serevent)
Formoterol (Foradil)

q12h dosing - every day, not for rescues

55
Q

Side effects of ß2 agonists

A

Palpitations
Tachycardia
Insomnia
Tremors

56
Q

Examples of anticholinergic bronchodilators

A

Short-acting:
• Ipratropium bromide (Atrovent) - most common
• Ipratropium plus albuterol (Combvent)
• 2 puffs BID-QID, also in neb form

Long-acting:
• Tiotropium bromide (Spiriva) - once daily
• Umeclidinium (Incruse Elliot’s) - once daily

Good bronchodilation, reduces air trapping in lungs, less cardiac stimulation

57
Q

Side effects of anticholinergics

A

Dry mouth
Metallic taste
HA
Cough

58
Q

Examples of LAMA+LABA combo meds

A

Used in category C/D disease

Bevespi Aerosphere - BID
Utibron Neohaler - BID
Stiolto Respiratory - QD
Anoro Ellipta - QD

59
Q

Drug that was the standard bronchodilator for many years, but tendency now to avoid use except in refractory cases

A

Theophylline - a methylxanthine

No long used commonly b/c lots of SE and drug interactions

Debate over benefits:
• Theophylline toxicity common problem
• Can cause tachycardia, arrhythmias, seizures, HA, nausea
• Potential for drug-drug interactions

60
Q

Examples of corticosteroids

A

Advair, Dulera, Symbicort, Breo Ellipta
(Inhaled form is available alone or in combo with LABA)

Reduces mucosal edema/inflammation by inhibiting prostaglandins —> decreased secretions

Increases responsiveness to beta-adrenergics

61
Q

Side effects of corticosteroid use

A

Oral candidiasis (pt ed=rinse mouth after use)

Bruising

Increased risk of URI

Kind of out of favor now b/c not as effective

62
Q

Treatment for alpha1 antitrypsin deficiency

A

Antiprotease replacement therapy in the form of weekly or monthly injections

Used in patients with serum alpha-1 antitrypsin levels <11uM)

Treatment is costly and controversial

63
Q

Examples of adjunct therapy for COPD patients

A

Pulmonary rehab (if GOLD stage B-D) - patient ed, exercise training, nutritional counseling and psychosocial support

Oxygen - increases survival (but only if used ≥ 12 hours per day)
• Goal: O2 saturation > 90% during rest, sleep, and exertion

Lung volume reduction surgery —> improved lung recoil

64
Q

Why do we use supplemental O2 in COPD patients?

A

Long-term continuous oxygen therapy prolongs survival (min 12 hours/day)

Indicated if chronic dyspnea at rest PaO2 ≤ 55 mmHg or SaO2 ≤ 88%

Caution - high flow O2 may reduce drive to breath and cause resp acidosis (maintain O2 sat 90-92%)

65
Q

What do we do to minimize complications/exacerbations in COPD patients?

A

Educate ALL COPD patients about avoidance of risk factors

Influenza vaccination

Pneumococcal vaccination (PPV13 and PCV23)

Regular exercise

Early recognition of pulmonary infection (increased sputum production, fever, worsening dyspnea, fatigue, chest pain, hemoptysis)

66
Q

How do we define an acute exacerbation of COPD?

A

Acute change in patient’s baseline dyspnea, cough, or sputum that is beyond normal variability, and sufficient to warrant a change in therapy

Increased dyspnea
Increase in cough frequency/severity
Sputum increases or becomes purulent

67
Q

Why do we care about acute exacerbations of COPD

A

Because they contribute to high mortality

68
Q

70% of acute exacerbations are caused by…

A

Respiratory illnesses

Pollution also common

69
Q

Viral infections that most commonly lead to COPD exacerbations

A

Rhinovirus and influenza

Viral most common, but may lead to secondary bacterial pneumonia

70
Q

Most common bacterial pathogens causing pneumonia secondary to viral infections

A

H flu, Strep pneumo, Moraxella catarrhalis, Mycoplasma pneumo, and Pseudomonas (if hospitalized recently or recent abx use)

71
Q

Outpatient management of an acute exacerbation includes…

A

Increased dose of short-acting bronchodilators (B2 agonist, add Ipratropium if not already taking)

Oral steroids - 40 mg/day x 5 days (reduces recovery time and hospital time)

Abx (for mod-severe exacerbations)

Consider hospitalization if severe

72
Q

Meds used in uncomplicated COPD exacerbation with no risk factors (Age <65, FEV1 > 50, <3 exacerbations/year, No cardiac disease)

A

Advanced macrolide (azithromycin, clarithromycin) OR

Cephalosporins OR

Doxy OR

Bactrim

73
Q

Meds used in complicated COPD exacerbations with 1 or more risk factors (age >65, FEV1<50, ≥3 exacerbations/year, cardiac disease)

A

Fluoroquinolone (levofloxacin) OR

Augmentin

If at risk for pseudomonas, use cipro and get sputum culture

74
Q

Indications for hospitalization in COPD exacerbations

A

Severe SSx

Severe underlying COPD (FEV1<50%)

Onset of new physical signs (cyanosis, edema, new arrhythmia)

Failure to respond to initial med mgmt

Older age

Insufficient home support

Clin Med II Unit II (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions