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MHD 1 > L77-L80 Pulmonary > Flashcards

L77-L80 Pulmonary Flashcards

1
Q

What three concerns can be detected by PFTs and what technique is used?

A
  1. Obstruction - Spirometry
  2. Restriction - Lung Volume Determination
  3. Diffusion Defect - Diffusion Capacity Measurement
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2
Q

How are the measurements taken in spirometry reported?

A
  1. Flow-Volume Loop

2. Volume-Time Curve

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3
Q

What data points can be garnered from the Flow-Volume Loop?

A 
Total Lung Capacity (TLC)
Residual Volume (RV)
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4
Q

What data points can be garnered from the Volume-Time Curve?

A

Forced Expiratory Volume in 1 Second (FEV1)

Forced Vital Capacity (FVC)

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5
Q

What happens to the Flow-Volume Loop in obstruction?

A

Scooped Loop appearance - less flow at any given moment due to narrowed airways

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6
Q

What happens to the Volume-Time Curve in obstruction?

A

Delayed raise in the curve

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7
Q

How is obstruction defined numerically?

A

Reduced ratio of FEV1:FVC

Normal: >0.8 (age 20-39), >0.7 (age 60-80)

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8
Q

What determines the severity of an obstruction?

A

FEV1 % predicted value

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9
Q

What determines the reversibility of an obstruction?

A

FEV1 increases by 200 mL and 12% with a bronchodilator

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10
Q

What determines hyperreactivity in obstruction?

A

FEV1 decreases by 20% in response to methacholine (bronchoconstrictor)

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11
Q

Discuss the difference between lower and upper airway obstruction.

A

Lower: airflow is relatively normal at high lung volumes; obstruction worsens during exhalation, results in gradually decreasing airflow

Upper: airflow is reduced even at high lung volumes (when bronchioles should be maximally open)

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12
Q

What is the difference between fixed and variable upper airway obstructions?

A

Fixed: intra-thoracic pressure changes do NOT affect the degree of obstruction (both loops are flat); obstruction may be either intra- or -extra-thoracic

Variable: intra-thoracic pressure changes do affect the degree of obstruction (one loop is flat, one is normal)

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13
Q

What happens to intrathoracic pressure upon inspiration? Expiration?

A

Inspiration: lowers
Expiration: raises

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14
Q

Which part of the Flow-Volume loop is affected in an extra-thoracic obstruction? Intra-thoracic obstruction?

A

Extra-thoracic: inspiratory limb affected

Intra-thoracic: expiratory limb affected

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15
Q

What are the three lung volumes important in restrictive disease?

A
  1. TLC
  2. RV
  3. FRC
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16
Q

What determines TLC?

A

Elastic recoil

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17
Q

What determines FRC?

A

Balance between elastic recoil of the lung (in) and the chest wall (out)

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18
Q

What is RV?

A

Volume of gas trapped due to airway closure at the end of forced expiration

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19
Q

What does a decreased TLC indicate?

A

Restrictive process (interstitial lung disease, chest wall disease, neuromuscular disease)

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20
Q

What does an increased TLC indicate?

A

Hyperinflation (loss of elastic recoil, emphysema)

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21
Q

What does an increased RV indicate?

A

Gas trapping (any obstructive process)

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22
Q

What are the three categories of restrictive lung disease?

A
  1. Interstitial lung disease
  2. Chest wall disease
  3. Neuromuscular disease
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23
Q

What is the primary problem in interstitial lung disease and how do we measure it?

A

Increased lung elastic recoil

Decreased TLC

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24
Q

What is the primary problem in chest wall disease and how do we measure it?

A

Decreased chest wall elastic recoil

Decreased TLC

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25
Q

What happens to various volumes in obesity?

A

Reduced chest wall recoil
Mild obesity - reduced FRC
Severe obesity - reduced TLC

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26
Q

What happens to lung volumes in neuromuscular disease?

A

Decreased TLC
Increased RV
Normal FRC

Prove by measuring strength of inspiratory and expiratory force

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27
Q

How is diffusion capacity measured?

A

Inhale known [CO], which diffuses easily across alveolar and capillary membranes and binds easily with Hgb

Measure exhaled [CO]

DL = [CO inhaled] - [CO exhaled]

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28
Q

What is a normal DL CO?

A

25 mL/min/mmHg

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29
Q

What are causes of reduced DL CO?

A

Loss of alveoli (emphysema and interstitial lung disease), loss of blood flow to alveoli (pulmonary HTN), anemia

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30
Q

What are causes of increased DL CO?

A

Alveolar hemorrhage, CHF, polycythemia

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31
Q

Suspect ___ when DL CO is low but spirometry, lung volumes, and Hgb are normal.

A

Pulmonary HTN

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32
Q

If FEV1:FVC Ratio is <0.70, think ___.

A

Obstruction

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33
Q

If TLC is < 80% predicted, think ___.

A

Restriction

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34
Q

If DLCO is <80% predicted, think ___.

A

Diffusion defect

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35
Q

If PFT’s are normal, what is not ruled out?

A

Asthma or mixed defects

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36
Q

What causes obstructive sleep apnea?

A

Upper airway obstruction; thoracic effort maintained

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37
Q

What causes central sleep apnea?

A

Failure of the brain to initiate respiration; thoracic effort interrupted

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38
Q

What happens in obesity-hypoventilation syndrome?

A

Obstructive sleep apnea + hypoventilation when awake

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39
Q

How is sleep apnea diagnosed?

A

Polysomnography (sleep study)

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40
Q

What is the apnea-hypopnea index (AHI)?

A

Combined number of 10-second episodes per hour of apnea and hypopnea (partial reduction in airflow)

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41
Q

What are risk factors for obstructive sleep apnea?

A
  1. Obesity
  2. Neck circumference (>17”)
  3. HTN
  4. Males
  5. Increasing age
  6. Smoking
  7. Retrognathia
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42
Q

What are risk factors for central sleep apnea?

A
  1. CHF

2. CNS disease

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43
Q

What are consequences of fragmented sleep in apnea?

A
  1. Daytime hypersomnolence (measure with Epworth sleepiness scale)
  2. Intellectual impairment
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44
Q

What are consequences of repeated episodes of hypoxia in apnea?

A
  1. Pulmonary HTN

2. Polycythemia

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45
Q

Why are their cardiovascular effects of sleep apnea?

A

Breathing stops, saturation levels drop and are sensed by carotid bodies, SNS activated, repeated cycle

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46
Q

What is lead-time bias?

A

Diagnosis of disease is made earlier in the screened group, resulting in an apparent increase in survival time, although the time of death is the same in both groups

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47
Q

What is length-time bias?

A

The probability of detecting disease is related to the growth rate of the tumor. Aggressive, rapidly growing tumors have a short potential screening period. Unless screening tests are repeated frequently, patients with aggressive tumors are more likely to present with symptoms. More slowly growing tumors have a longer potential screening period and are more likely to be detected when asymptomatic. As a result, a higher proportion of “indolent” tumors is found in the screened group, causing an apparent improvement in survival.

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48
Q

What is overdiagnosis bias?

A

Extreme form of length-time bias; detection of indolent tumors in the screened group produces apparent increases in # of cases.

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49
Q

What are the current USPSTF guidelines for lung cancer screening?

A

B recommendation - annual screening with low-dose CT in adults 55-80 y/o who have a 30 pack-year smoking history and currently smoke or have quit within the past 15 years. Stop screening once a person has not smoked for 15 years or develops a health problem that substantially limits life expectancy or the ability or willingness to have curative lung surgery.

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50
Q

What are the three broad etiologies of dyspnea?

A
  1. Cardiac
  2. Pulmonary
  3. Other (renal, anemia, neuromuscular)
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51
Q

Obstruction involves increased ___ and ___ lungs. Restriction involves abnormal ___ and ___ lungs.

A

Airway resistance; large

Elastic recoil; small

52
Q

Compare the lung sounds heard in obstruction vs. restriction.

A

Obstruction: wheezing
Restriction: crackles

53
Q

How is asthma treated, broadly?

A
  1. Relievers (PRN, bronchodilators)

2. Controllers (regular, anti-inflammatory)

54
Q

What are the first line “relievers” for asthma treatment?

A
  1. Albuterol
  2. Pirbuterol
    (Beta agonists)
55
Q

What are the second line “relievers” for asthma treatment?

A
  1. Levalbuterol (beta-agonist)

2. Ipratropium (anti-cholinergic)

56
Q

What are the first line “controllers” for asthma treatment?

A

Inhaled corticosteroids (beclomethasone, budesonide, ciclesonide, fluticasone, mometasone)

57
Q

What are common and rare side effects of inhaled corticosteroids?

A
  1. Oral-pharyngeal (candida)
  2. HPA axis suppression
  3. Bone problems
  4. Cataracts
58
Q

What are the second line “controllers” for asthma treatment?

A

In addition to inhaled corticosteroids:

  1. Long-acting beta-agonists (Salmeterol, Formoterol)
  2. Anti-leukotrienes (Montelukast, Zafirlukast, Zileutin)
59
Q

What are some less common treatments for asthma?

A
  1. Cromolyn (mast cell stabilizer)
  2. Theophylline
  3. Anti-cholinergics
  4. Omalizumab
60
Q

What is the last resort for asthma treatment?

A

Chronic oral steroids

61
Q

What are the 3 most common causes of chronic cough?

A
  1. Cough-variant asthma
  2. Post-nasal drip
  3. GERD
62
Q

What is Reactive Airway Dysfunction Syndrome?

A

“Big bang” exposure leading to asthma (no prior asthma), treated with steroids

63
Q

What is Samter’s triad?

A

Syndrome caused by aspirin sensitivity:

  1. Asthma
  2. Nasal polyposis
  3. ASA sensitivity
64
Q

How is aspirin sensitivity treated?

A

Anti-leukotrienes

65
Q

What is Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

Asthma with central bronchiectasis, migratory pulmonary infiltrates, peripheral eosinophilia, high IgE to Aspergillus

66
Q

What is the key feature of emphysema?

A

Permanent distention of the distal air spaces with destruction of alveolar septa

67
Q

What is the key feature of chronic bronchitis?

A

Excessive sputum production

68
Q

How does COPD present?

A

Insidious onset of dyspnea and cough with minimal day to day variability

69
Q

What is seen on PFT’s with COPD?

A
  1. Obstruction with minimal bronchodilator response
  2. Hyperinflation
  3. Reduced diffusing capacity
70
Q

What is the medication treatment for COPD?

A
  1. Short-acting bronchodilators (anti-cholinergics, beta-agonists, combination)
  2. Long-acting bronchodilators (anti-cholinergics, beta-agonists)
  3. Other: corticosteroids, azithromycin, theophylline
71
Q

What is the staging and treatment of COPD Stage 0?

A

“At risk”
Normal spirometry
Smoking cessation

72
Q

What is the staging and treatment of COPD Stage 1?

A

“Mild COPD”
FEV1/FVC <0.70, but normal FEV1
Short-acting bronchodilators

73
Q

What is the staging and treatment of COPD Stage 2?

A

“Moderate COPD”
FEV1 50-80% predicted
Long-acting bronchodilator

74
Q

What is the staging and treatment of COPD Stage 3?

A

“Moderately severe COPD”
FEV1 30-50% predicted
Maybe add inhaled corticosteroids

75
Q

What is the staging and treatment of COPD Stage 4?

A

“Severe COPD”
FEV1 <30% predicted
Maybe methylxanthines

76
Q

What is the only thing that can prolong life in COPD?

A

Long-term oxygen therapy (only works in patients who are hypoxic)

77
Q

Check ___ levels in all patients with COPD.

A

Alpha-1-anti-trypsin

78
Q

What is the primary pathology of bronchiectasis?

A

Permanent abnormal dilation of the bronchi

79
Q

What is Cole’s vicious cycle of inflammation?

A
  1. Bacterial colonization
  2. Neutrophil inflammation (proteases)
  3. Airway destruction and distortion (bronchiectasis)
  4. Abnormal mucus clearance
    Repeat
80
Q

What are the bacteria commonly seen in bronchiectasis?

A

GN: P. aeruginosa, H. influenzae, M. catarrhalis
GP
NTM

81
Q

What are the symptoms of bronchiectasis?

A
  1. SOB/DOE

2. Daily copious sputum production

82
Q

What is seen on PFT in Bronchiectasis?

A

Obstruction

83
Q

What is seen CXR/CT in Bronchiectasis?

A
  1. Signet ring sign - internal diameter of the bronchus is larger than that of its accompanying vessel
  2. Tram tracking - bronchus fails to taper in the periphery of the chest
84
Q

What is the treatment for bronchiectasis?

A
  1. Airway clearance therapy (CPT, 7% hypertonic saline, bronchodilators)
  2. Antibiotic therapy (suppressive vs. eradication)
  3. Anti-inflammatory therapy (inhaled corticosteroids, macrolides)
85
Q

What are the main interstitial lung diseases?

A
  1. Sarcoid
  2. Hypersensitivity pneumonitis
  3. Idiopathic pulmonary fibrosis
  4. TB
  5. Fungal
  6. Aspiration/Asbestosis
  7. Connective tissue diseases/Cancer
  8. Eosinophilic Granuloma
  9. Drugs (amiodarone, nitrofurantoin, bleomycin)
  10. Pneumoconioses
86
Q

How does interstitial lung disease present?

A

Dyspnea and cough

87
Q

What are the signs of interstitial lung disease?

A

Crackles, small lungs, +/- clubbing

88
Q

What is seen on CXR in interstitial lung disease?

A

Reduced volumes

Interstitial markings

89
Q

What is seen on PFT in interstitial lung disease?

A

Decreased TLC

90
Q

What are the treatments for IPF?

A

Pirfenidone and Nintedanib

91
Q

Normally, the pleural space contains less than ___ of fluid.

92
Q

What is a pleural effusion?

A

Excess pleural fluid accumulation

93
Q

Which part of the pleura is innervated?

94
Q

Discuss the arterial and venous supply of the visceral pleura.

A

Arterial: bronchial and pulmonary arteries
Venous: through pulmonary veins to LA

95
Q

Discuss the arterial and venous supply of the parietal pleura.

A

Arterial: aortic intercostals
Venous: through IVC to RA

96
Q

What does primary left heart failure cause?

A

Pulmonary edema, pleural effusions, and/or both

97
Q

What does pulmonary arterial HTN cause?

A

Cor pulmonale, no pulmonary edema or effusions

98
Q

What creates the sub-atmospheric pleural pressure?

A

Elastic recoil of the lung pulling in and elastic recoil of the chest wall pulling out

99
Q

What can cause an increase in the filtration coefficient, leading to excess pleural fluid formation?

A

Infection, inflammation, cancer

100
Q

What can cause an increase in the capillary hydrostatic pressure, leading to excess pleural fluid formation?

A

LV failure

101
Q

What can cause an decrease in the pleural hydrostatic pressure, leading to excess pleural fluid formation?

A

Atelectasis

102
Q

What can cause an decrease in the capillary osmotic pressure, leading to excess pleural fluid formation?

A

Nephrotic syndrome, cirrhosis, malnutrition

103
Q

What are some symptoms of pleural effusions?

A

Asymptomatic
Pain
Dyspnea
Respiratory failure

104
Q

What are some signs of pleural effusions?

A

Dullness to percussion
Decreased breath sounds
Tactile fremitus
Egophony

105
Q

What are some CXR findings of pleural effusions?

A
  1. Blunting of the angle
  2. Meniscus
  3. White-out + shift of mediastinum away
  4. Lateral decubitus layering
  5. Loculations (adhesion between parietal and visceral pleura, creates a trapped chamber of fluid)
106
Q

What are the Light’s Criteria for exudates?

A
  1. Total pleural protein/Total serum protein >0.5, or
  2. Pleural LDH/Serum LDH >0.6, or
  3. Pleural LDH >200 (or 2/3 upper normal)
107
Q

What are the Revised Criteria for exudates?

A
  1. Pleural LDH > 200 (or 2/3 upper normal), or

2. Pleural cholesterol >45

108
Q

What is on the differential for transudative effusions?

A
  1. CHF
  2. Cirrhosis
  3. Nephrotic syndrome
  4. Atelectasis
  5. Hypothyroidism
  6. PE (15%)
  7. Peritoneal dialysis
109
Q

What is on the differential for exudative effusions?

A
  1. Cancer
  2. Infections (empyema)
  3. Parapneumonic effusions
  4. PE (85%)
  5. Connective tissue diseases
  6. Esophageal rupture
  7. Drug-induced disease (hydralazine)
  8. Post-MI
  9. Post-pericardiotomy
  10. Uremia
  11. Asbestos
  12. Meig’s syndrome (ovarian cancer with malignant effusions)
  13. Yellow nail syndrome
  14. Hemothorax
  15. Chylothorax (ruptured thoracic duct)
110
Q

What else can be tested in the pleural fluid?

A

pH - normally slightly higher than serum due to active HCO3 transport; low pH may be seen in infection, malignancy, and esophageal rupture

Glucose - low in RA, B, cancer, empyema

111
Q

Lots of PMNs on CBC indicate what in pleural effusion? Lots of lymphocytes?

A

Acute infection

TB or fungus

112
Q

Elevated adenosine deaminase (ADA) is indicative of ___.

113
Q

Elevated amylase is indicative of ___ or ___.

A

Pancreatitis and/or esophageal rupture

114
Q

Pattern: exudative, lymphocytic, <5% mesothelial cells, +ADA

115
Q

Pattern: exudative, lymphocytic, RBC’s, +/- low pH/glucose, large

A

Malignant effusion

116
Q

Pattern: small, unilateral, exudative, +/- bloody

A

PE 85% of the time

117
Q

Pattern: left-sided, low pH, high amylase

A

Esophageal rupture

118
Q

Pattern: bloody, +/- associated with pneumothoraces/hemoptysis

A

Endometriosis

119
Q

Pattern: underlying cirrhosis, transudative, R>L sided, rapid re-accumulation

A

Hepatic effusions

120
Q

Pattern: milky effusions

A
  1. Chylothorax (triglycerides >110)
  2. Pseudochylothorax (triglycerides >100 and cholesterol >200)
  3. Empyema
121
Q

What can be used to treat loculations?

A

Thrombolytics

122
Q

What is air in the pleural space?

123
Q

What happens in a PT?

A

Air enters the pleural space until Ppl = Patm, lung collapses inward, and chest wall expands

124
Q

What are signs of a PT?

A

Unilateral hyperinflation
Decreased breath sounds
Tactile fremitus
Hyperresonance

125
Q

What is seen on CXR in a PT?

A

Hyperlucent lung fields
Lack of lung markings
Thin white pleural line
Shift of mediastinum (tension)

MHD 1 (58 decks)

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