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Pulmonary Medicine > Bronchiectasis, COPD, Chronic Bronchitis, CF, Emphysema > Flashcards

Bronchiectasis, COPD, Chronic Bronchitis, CF, Emphysema Flashcards

1. Define, compare, and contrast COPD, chronic bronchitis, and emphysema, including signs and symptoms. 2. Compare and contrast emphysema from alpha-1 antitrypsin deficiency with the more commonly encountered emphysema. 3. When given a clinical scenario, develop and defend a differential diagnosis of a person with suspected obstructive pulmonary disease. 4. Outline the approach to the diagnosis of a person with suspected obstructive lung disease. 5. List and discuss risk factors for the deve

1
Q

Abnormal enlargement of air spaces distal to the terminal bronchiole with destruction of their walls and without obvious fibrosis

A

Emphysema

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2
Q

Main cause of emphysema

A

Chronic Cigarette Smoking

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3
Q

Decreased elastic recoil due to destruction of elastin fibers
Oxidant stress
Neurogenic Stimuli

A

Emphysema

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4
Q

Other causes of cigarette smoking

A

Alpha 1 Antitrypsin Dz

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5
Q

When is emphysema commonly seen

A

40+ years old

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6
Q

Emphysemic patients have a slowly progressive

A

Dyspnea (coming to dyspnea at rest)

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7
Q

When looking at the alveolar walls and airspaces of a pt with emphysema, you will see

A

Loss of alveolar walls

Dilation of airspaces

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8
Q

Signs and Symptoms of Emphysema

A
  1. Minimal cough
  2. Scant sputum
  3. Occasional infections
  4. Dyspnea
  5. Often significant weight loss
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9
Q

Patient’s Lab work comes in after presenting with a mild cough and shortness of breath:

  1. Normal serum hemoglobin or polycythemia
  2. Mild hypoxia, especially at night
  3. Normal PaCO2 (Unless FEV1
A

Emphysema

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10
Q

What will show up on a CXR in a patient with Emphysema

A

Barrel Chest, Small Heart, Hyperinflation, Flattened Diaphragms, Possible Bullous Changes

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11
Q

“Pink Puffer”

A

Emphysema

Some patients with severe long-standing chronic bronchitis and emphysema are breathless and have a hyperinflanted chest, but a well maintained PaO2 and low PaCO2. These patients are not cyanosed but are breathless, hence the term “pink puffer”

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12
Q

Pt comes in complaining of a recurrent cough with mucus production most days of the week. This started about 3 years ago, but has since felt more coughing and decides to come in. What dx would you presume?

A

Chronic Bronchitis

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13
Q

Causes of Chronic Bronchitis

A
  1. Globlet Cell Hyperplasia
  2. Mucous Plugging
  3. Airway Obstruction
  4. Sputum Production
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14
Q

The mucus secretions and inflammation in the bronchi tend to narrow the airways and provide an obstacle to airflow, thus increasing the resistance of the airways.

A

Chronic Bronchitis

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15
Q

Signs and Symptoms

A
  1. Sputum production
  2. Frequent infections
  3. Intermittent dyspnea
  4. Hemoptysis
  5. Pedal edema
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16
Q

Physical Exam Findings for Chronic Bronchitis

A
  1. Cyanosis
  2. Wheezing
  3. Weight Gain
  4. Diminished Breath Sounds
  5. Distant Heart Sounds
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17
Q

In Chronic bronchitis, what would you see on a CBC?

A

Red blood cells will be increased due to decreased O2 levels (aka Polycythemia)

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18
Q

In Chronic bronchitis, what would you see with CO2 levels?

A

Increased CO2 levels (aka Hypercapnia)

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19
Q

In Chronic bronchitis, what would you see with O2 levels?

A

Decreased O2 levels (aka Hypoxemia)

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20
Q

A CXR in a patient with Chronic Bronchitis will show

A

Increased bronchovascular markings

Cardiomegaly

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21
Q

“Blue Bloater”

A

Chronic Bronchitis

The PaCO2 has risen, and the PaO2 has fallen. Breathlessness at rest is not prominent, and the patient looks more comfortable than the “pink puffer”; “blue bloaters” have right heart failure, which results in peripheral edema. The combination of this edema and the cyanosis accounts for the term “blue bloater”

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22
Q

A disease state characterized by airflow limitation that is not fully reversible.

Usually a progressive dz assc with abnormal inflammatory response of the lungs to noxious particles of gases

A

Chronic Obstructive Pulmonary Disease

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23
Q

Airflow obstruction in COPD is caused by?

A

Mixture of

  1. Small Airway Disease (Obstructive Bronchiolitis)
  2. Parenchymal Destruction (Emphysema)
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24
Q

Most important thing to know in COPD

A

Irreversible airflow obstruction!

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25
Q

_______ is a disorder, where subsets of patients may have dominant features of chronic bronchitis, emphysema or asthma.

A

COPD

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26
Q

Fourth leading cause of death in the US

A

COPD

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27
Q

COPD is more common in which sex?

A

Male

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28
Q

COPD is more common in:

A
  1. Males
  2. Increasing Age
  3. Lower SES
  4. Hispanics > Whites > AAs
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29
Q

Death assc with COPD has been ______ since 1970.

A

Increasing

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30
Q

What causes COPD?

A
  1. Cigarette Smoking **Most Important
  2. Air pollution
  3. Antiprotease deficiency (alpha-1 antitrypsin)
  4. Occupational exposure (firefighters, jobs around a great deal of dust)
  5. Infection possibly (viral)
  6. Occupational Pollutants (Cadmium, Silica)
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31
Q

Pathophysiology of COPD with Airway Obstruction

A 
Smooth muscle contraction
Bronchoconstriction
Mucus Hypersecretion
Loss of Elastic Recoil
Alteration of Cholinergic Response
Airway Narrowing
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32
Q

Pathophysiology of COPD with Inflammation

A 
Oxidative Stress
Increased Neutrophils
Increased Macrophages
Increased CD8 lymphocytes
Increased IL-8 and TNF-alpha
Protease/Antiprotease Imbalance
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33
Q

Pathophysiology of COPD with Structural Changes

A

Alveolar Destruction
Collagen Deposition
Glandular Hypertrophy
Airway Fibrosis

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34
Q

A patient comes into clinic with a history of COPD, in the lungs would you experience the following:

  1. Mucus Hypersecretion
  2. Neutrophils in Sputum
  3. Squamous metaplasia of epithelium
  4. No basement membrane thickening
  5. Increased Macrophages
  6. Increased CD8 Lymphocytes
  7. Little increase in airways smooth muscle
  8. Mucus gland hyperplasia
  9. Goblet Cell hyperplasia

A. Large Airways
B. Alveoli
C. Small Airways
D. Parenchymal Space

A

A. Large Airways

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35
Q

A patient comes into clinic with a history of COPD, in the lungs would you experience the following:

  1. Inflammatory exudates in lumen
  2. Thickened wall with inflammatory cells, macrophages, CD8 cells, Fibroblasts
  3. Peribronchial fibrosis

A. Large Airways
B. Alveoli
C. Small Airways
D. Parenchymal Space

A

C. Small Airways

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36
Q

A patient comes into clinic with a history of COPD, in the lungs would you experience the following:

  1. Alveolar Wall Destruction
  2. Loss of elasticity
  3. Destruction of Pulmonary Capillary Bed
  4. Increased Inflammatory Cells, Macrophages, CD8 lymphocytes

A. Large Airways
B. Alveoli
C. Small Airways
D. Parenchymal Space

A

D. Parenchymal Space

37
Q

Signs and Symptoms of COPD

A
  1. Dyspnea (progressive, worse with exertion, persistent, “heaviness,” “gasping,” “air hunger”)
  2. Chronic Cough (may be intermittent and unproductive)
  3. Chronic Sputum Production
  4. History of Exposure to Risk Factors
38
Q

What do you do if the signs and symptoms point to COPD?

A

Perform spirometry (PFTs)

39
Q

What do the PFTs look like for a pt with COPD?

A 
FEV1/FVC = < 70 **Most important**
FEV1 = Variable
Total Lung Capacity = Increased
Residual Volume = Increased
Diffusion Capacity
-- If Chronic Bronchitis: Normal
-- If Emphysema: Decreased
40
Q

A suspected COPD patient comes into clinic, and PFTs are ordered. Results come back showing:

FEV1/FVC or equal to 80% predicted

What type of COPD Classification would you put this patient in?

A. Mild
B. Moderate
C. Severe
D. Very Severe

A

A. Mild

41
Q

A suspected COPD patient comes into clinic, and PFTs are ordered. Results come back showing:

FEV1/FVC

A

C. Severe

42
Q

A suspected COPD patient comes into clinic, and PFTs are ordered. Results come back showing:

FEV1/FVC

A

B. Moderate

43
Q

A suspected COPD patient comes into clinic, and PFTs are ordered. Results come back showing:

FEV1/FVC

A

D. Very Severe

44
Q

A suspected COPD patient with a history of chronic respiratory failure, and PFTs are ordered. Results come back showing:

FEV1/FVC

A

D. Very Severe

45
Q

In an adult non-smoking male, FEV1 typically ________ over time at a rate of about _______ per year.

A

Declines

35-40 mL

46
Q

In an adult smoking male, FEV1 typically ________ over time at a rate of about _______ per year.

A

Declines

70-120 mL

47
Q

FEV1 of less than 1 L will have a mean survival rate of 50% at

A

Five years

48
Q

True/False
If you’ve been smoking for 60 years, it would be no benefit to you to quit because you have caused irreversible chronic damage to your lungs.

A

FALSE!

Quitting at any point in time will allow for a better FEV1 than if you continued.

49
Q

What are the goals of therapy for COPD Treatment?

A
  1. To prevent further deterioration in lung function
  2. To alleviate symptoms
  3. To improve performance of daily activities and quality of life
50
Q

Treatment of COPD

A
  1. Smoking Cessation
  2. Bronchodilators (short and long acting)
  3. Inhaled (sometimes oral) steroids
  4. Sometimes Methylxanthines
  5. Vaccination against influenza and pneumonia
  6. Oxygen supplementation
  7. Pulmonary Rehab
51
Q

Short Acting Beta Agonist Medications in COPD

A

Albuterol
Levalbuterol

Used in all stages of COPD

52
Q

Long Acting Beta Agonists Medications in COPD

A

Salmeterol
Formoterol

Used in COPD stages Moderate-Very Severe

53
Q

Anticholinergic Medications in COPD

A

Ipratropium

Tiotropium

54
Q

Inhaled Corticosteroids in COPD

A

Fluticasone
Budesonide

Used in COPD stages Severe-Very Severe

55
Q

Methylxanthine in COPD

A

Theophylline

56
Q

When is Oxygen Therapy an option in COPD patients?

A
  1. Decreased SaO2 with rest, exercise, or sleep
  2. PaO2 ≤55 mm Hg(SaO2 <89%) if cor pulmonale,RV failure, erythrocytosis present

**Very severe stage

Is this objective?

57
Q

Surgical Procedures to improve lung function

A
  1. Bullectomy
  2. Lung Volume Reduction Surgery
  3. Lung Transplant
58
Q

If a patient with COPD has an Acute Exacerbations

A
  1. O2 Therapy
  2. Bronchodilators
  3. Antibiotics
  4. Corticosteroids
  5. Assisted Ventilation
59
Q

What type of genetic disorder is CF?

A

Autosomal Recessive Disorder

60
Q

What transmembrane regulator is genetically affected in CF?

A

CFTR

61
Q

What does CFTR normally do?

A

Regulates and participates in the transport of chloride across epithelial cell and intracellular membranes.

62
Q

Mutation of the CFTR causes

A

Defective Chloride transport and reduced sodium reabsorption resulting in thickened mucous.

63
Q

Where does CF primarily affect?

A

The lungs, but affects all exocrine glands

64
Q

About how many people in the US are affected by CF

A

30,000; 1:3500 births = Cf

65
Q

When being racially insensitive, how many Caucasian people are carried? How any African American people are carriers?

A

1: 25
1: 65

66
Q

CF is considered an _______ pulmonary disorder

A

Obstructive

67
Q

Because the airways get filled with thick mucous secretions, what common types of bacteria get trapped in the lungs of CF patients.

A
  1. Pseudomonas Aeruginosa
  2. Staph Aureus
  3. Haemophilus influenza
68
Q

Common Pulmonary Manifestations

A

Pneumothorax
Cor Pulmonale
Upper Respiratory (Nasal Polyps; Chronic Sinusitis)

69
Q

True/False:

Pancreatic dysfunction including DM, Vitamin Deficiency and Malnutrition are common occurrences in CF.

A

True!

Also, steatorrhea

70
Q

The presence of excess fat in feces. Stools may also float due to excess lipid, have an oily appearance and be especially foul-smelling.

A

Steatorrhea

71
Q

True/False

CF can cause azoospermia and decreased fertility in females.

A

True

72
Q

CF can also cause:

A
  1. Cirrhosis
  2. Portal Hypertension
  3. Cholelithiasis
  4. Nephrolithiasis
73
Q

What organs are commonly affected in CF?

A
  1. Lungs
  2. Sinuses
  3. Skin
  4. Liver
  5. Pancreas
  6. Intestines
  7. Reproductive Organs
74
Q

In the US, how is CF diagnosed?

A
  1. Screening for all newborns
  2. Skin Sweat Testing (>60 meq/L x 2)
  3. Genetic Tests –> More than 900 CF mutations
75
Q

What tests can SUPPORT the dx of CF?

A
  1. Chest Radiography
  2. Pulmonary Function Tests
  3. ABGs: Hypoxemia and Hypercapnia
  4. Sputum Cultures: P. aeruginosa or S. aureus
  5. Pancreatic exocrine insufficiency
76
Q

What is the nonpharmacologic treatment for CF?

A
  1. Mucus mobilization
  2. Pulmonary Rehabilitation
  3. O2 Therapy
  4. Vaccinations
77
Q

What is the pharmacologic treatment for CF?

A
  1. Bronchodilators
  2. Recombinant human deoxyribonuclease (Pulmozyme)
  3. Antibiotics
  4. Glucocorticoids
  5. Azithromycin
78
Q

How do you treat the extrapulmonary diseases assc. with CF?

A
  1. Pancreatic Enzymes
  2. Vitamin Supplementation
  3. Sinusitis Regimens
  4. Treatment of pancreatic endocrine dysfunction
79
Q

Abnormal dilation of the bronchi that results from inflammation and premanent destructive changes in the elastic and muscular layers of the bronchial walls .

A

Bronchiectasis

80
Q

What normally causes Bronchiectasis?

A 
Recurrent Infections
(Staph aureus pneumonia; TB; ABPA (hypersensitivity to aspergillus with intractable asthma, central bronchiectasis, high levels of IgE))
81
Q

True/False:

Bronchiectasis only happens in middle aged to older people.

A

False, it can also occur in young people

  1. 50% of all cases of Bronchiectasis in young people = CF
  2. Also in Alpha 1 Antitrypsin Deficiency
  3. Immotile Cilia (Kartgener’s) Syndrome (Sinusitis, Situs inversus, infertility)
82
Q

A 45 year old female comes into clinic today presenting with cough, blood streaked sputum and potential onset of clubbing on the hands. Given a history of pneumonia, what would your presumed diagnosis be?

A. COPD
B. Alpha-1 Antitrypsin Deficiency
C. Bronchiectasis
D. Chronic Bronchitis

A

C. Bronchiectasis

83
Q

Preferred imaging for suspected Bronchiectasis?

A
  1. HRCT

2. CXR MAY show Bronchiectasis, however not necessarily

84
Q

What will PFTs show for a patient with Bronchiectasis?

A

Varying degrees of obstruction

85
Q

Treatment for Bronchiectasis?

A

10-14 days of amoxicillin/clavulanic acid, trimethoprin/sulfamethoxazole for acute infections

Suppressive Therapy considered in some with recurrent infections

Bronchodilators

Chest Physical Therapy

86
Q

Alpha-1 Antitrypsin

A

Inhibitor of Neutrophil Elastase

Neutrophil elastase is an enzyme that breaks down elastin in the lungs, which causes destruction of the alveolar wall.

87
Q

Alpha-1 Antitrypsin Deficiency can cause symptoms similar to what disease/condition?

A

Emphysema

88
Q

How do you distinguish between emphysema and alpha-1 antitrypsin?

A

Age? Refer for genetic testing?

Pulmonary Medicine (14 decks)

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