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Pulmonary > PATH: Obstructive and Restrictive Lung Disease > Flashcards

PATH: Obstructive and Restrictive Lung Disease Flashcards

1
Q

List the obstructive lung diseases.

A

1) Emphysema
2) Chronic bronchitis
3) Bronchiectasis
4) Asthma

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2
Q

List the restrictive lung diseases.

A

1) Pneumoconiosis (Coal Worker’s, Silicosis, Asbestosis)
2) Sarcoidosis
3) Pneumonias (various types)

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3
Q

What are the two divisions of obstructive lung disease?

A

Acute and Chronic

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4
Q

True or false: most COPD patients are smokers.

A

TRUE: 80%

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5
Q

True or false: eventually, most smokers develop COPD.

A

FALSE: only 15% of smokers get COPD

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6
Q

When does symptomatic COPD typically occur?

A

Middle age (but is dose dependent, so people who smoke more develop COPD earlier)

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7
Q

True or false: men are more likely to have COPD than women.

A

FALSE: prevalence is approximately equal between sexes

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8
Q

What is emphysema?

A

abnormal permanent enlargement of airspaces due to destruction of the walls (septa) between them—most commonly due to smoking

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9
Q

Who is at an increased risk for development of COPD (accounting for around 40,000 cases in 2 million Americans)?

A

Caucasian Americans with alpha-1-antitrypsin deficiency

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10
Q

Emphysema can be regarded as a disease of destructive ________, inadequate ______ control, and insufficient _______ _______.

A

Emphysema can be regarded as a disease of destructive inflammation, inadequate anti-inflammatory control and insufficient wound repair.

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11
Q

What cytokines are present in the ongoing inflammation of emphysema?

A

IL-8
TNF
Leukotriene B4

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12
Q

Without alpha-1-antitrypsin, what happens to alveolar wall?

A

Without this antiprotease, the alveolar wall becomes destroyed (even in the absence of smoking but emphysema is accelerated in smokers with the deficiency)

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13
Q

List genetic polymorphisms that can lead to inadequate repair of elastin and contribute to the development of emphysema.

A 
High levels of:
MMP-9
MMP-12
Poor repair response to:
TGF-beta
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14
Q

At what point in a breath is a emphysema patient most likely to have collapsed airways? Why?

A

At expiration, the loss of elastic tissue reduces radial traction of the small airways and leads to collapse

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15
Q

How does emphysema lead to pulmonary hypertension?

A

loss of alveolar septal capillaries reduces pulmonary vascular capacitance–making the right heart pump the same amount of blood through a smaller network of vessels ( backing up pressure into the right right)

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16
Q

Emphysema can eventually lead to what disease (progresses from pulmonary HTN)?

A

Right heart failure (cor pulmonale)

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17
Q

Emphysema due to what is typically centriacinar?

A

smoking

Emphysema due to alpha-1-antitrypsin is typically panacinar

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18
Q

Emphysema due to smoking is typically centered around what structure?

A

respiratory bronchioles (spares alveoli)

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19
Q

Emphysema due to smoking is more severe in what lobes?

A

upper (especially apical segments)

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20
Q

Emphysema due to alpha-1-antitrypsin deficiency is more severe in what lobes?

A

lower

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21
Q

What type of emphysema is typical in young adult male smokers with spontaneous pneumothorax?

A

distal acinar and associated with massively enlarged subpleural airspaces (bullae) in upper lobes

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22
Q

What two words describe the microscopic pathology of emphysema?

A

enlarged airspaces

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23
Q

What is the most typical symptom of pure emphysema?

A

insidious onset of progressive dyspnea

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24
Q

What is the FEV1/FVC ratio for emphysema?

A

less than 0.7

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25
Q

What is chronic bronchitis?

A

productive cough for at least 3 months in 2 consecutive years in the absence of a specific diagnosis—mostly due to smoking

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26
Q

What is the pathogenesis of chronic bronchitis?

A

Toxins→ inflammation and hypersecretion of mucous/ hypertrophy of mucous secreting glands→ Obstruction

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27
Q

The inflammation associated with chronic bronchitis involves infiltration of what cell types?

A

CD8 Lymphocytes
Macrophages
Neutrophils

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28
Q

What leads to the mucous hypersecretion associated with chronic bronchitis?

A

T cell cytokines like IL-13 and increased transcription of the MUC5AC gene (MUCking up airways)

leads to hypertrophy of submucosal mucous-secreting glands and bronchial goblet cell hyperplasia

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29
Q

Describe the gross pathology of chronic bronchitis.

A

Bronchial mucosal hyperemia and edema with luminal mucinous or mucopurulent exudate

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30
Q

What will you see under the microscope of lung tissue with acute bronchitis?

A
  • enlargement of submucosal glands
  • lymphocyte infiltration
  • goblet cell metaplasia in bronchioles
  • luminal mucous plugs in bronchioles
  • fibrosis in bronchioles
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31
Q

What is the only sign/symptom of chronic bronchitis?

A

productive cough

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32
Q

How do you diagnose chronic bronchitis?

A

H&P

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33
Q

How do you treat chronic bronchitis?

A
  • Quit Smoking
  • Short-acting, Inhaled Bronchodilators:
    • Beta-2 agonist
    • Anti-cholinergics
  • Long-acting, Inhaled anti-cholinergics
  • Inhaled corticocosteroidds
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34
Q

What is Bronchiectasis?

A

permanent dilation of bronchi due to destruction of muscle and elastic tissue by chronic or recurrent necrotizing infections

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35
Q

What three diseases can lead to the bronchial obstruction and chronic persistent infection that causes bronchiectasis?

A

1) Cystic Fibrosis
2) Immunodeficiency States
3) Kartagener syndrome

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36
Q

What is Kartagener syndrome?

A

rare AR disease causing ciliary impairment

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37
Q

What can lead to localized bronchiectasis?

A

bronchial tumor or necrotizing pneumonia

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38
Q

Describe the gross pathology of bronchiectasis.

A

Dilated bronchi (especially when close to visceral pleural surface); more pronounced in lower lobes

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39
Q

Describe the microscopic pathology of bronchiectasis.

A

scarred, dilated bronchi with intense acute and chronic inflammation

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40
Q

What type of sputum is coughed up with bronchiectasis?

A

copious purulent sputum

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41
Q

How do you diagnose bronchiectasis?

A

CT scan

42
Q

How do you treat bronchiectasis?

A

long-term antibiotics

43
Q

What is the definition of asthma?

A

chronic episodic obstructive airway disease due to reversible bronchoconstriction resulting from hyper-reactivity to various stimuli

44
Q

What type of inflammation occurs in asthma?

A

Th2 type

45
Q

What is involved with the early acute phase of Th2 type inflammation?

A 
IgE
Mast Cells
Histamine
Leukotriene B4
Vagus nerve
46
Q

What is involved with the late acute phase of Th2 type inflammation (4-8 hours after attack and lasting 24 hours max)?

A 
Eosinophils
Neutrophils
Lymphocytes
IL-1, IL-6
TNF
Leukotrienes C4, D4, E4
PGD2
PAF
47
Q

Describe the gross pathology of asthma.

A

Hyperinflated lungs +/- foci of atelectasis

Bronchial mucous plugs due to hypersecretion

48
Q

Describe the microscopic pathology of asthma.

A

Bronchial luminal mucous and lots of neutrophils, the 3 C’s, eosinophils, and submucosal edema (with mixed inflammatory infiltrate)

49
Q

What are the 3 C’s?

A

1) Curschmann’s spirals
2) Charcot-Leyden crystals
3) Creola bodies

50
Q

What are Curschmann’s spirals?

A

small whorled mucous strands twisted in a common direction with a dense refractile coiled or braided core.

51
Q

What are Charcot-Leyden crystals?

A

tiny crystals which are bipyramidal on longitudinal section and hexagonal on cross-section

52
Q

What are Creola Bodies?

A

fragments of degenerated, sloughed respiratory epithelium

53
Q

Describe the 6 changes that occur with airway remodeling.

A

1) Basement membrane thickening (2.5X larger)
2) Submucosal glandular hypertrophy/hyperplasia
3) Muscular wall hypertrophy and hyperplasia
4) Goblet cell metaplasia (and presence in bronchioles)
5) Bronchial epithelial hyperplasia
6) Submucosal thickening with fibrous tissue

54
Q

How do you diagnose asthma?

A

History and Physical; spirometry

55
Q

How do you treat asthma?

A

agonists; inhaled corticosteroids, antibody to IgE

56
Q

What is pneumoconioses?

A

fibrosing restrictive lung diseases caused by inhalation of organic or inorganic particulates or chemical fumes

57
Q

What is coal worker’s pneumoconioses?

A

broad spectrum lung disease due to inhalation of coal dust ranging from asymptomatic non-fibrotic coal dust macules or fibrotic coal nodules to debilitating progressive massive pulmonary fibrosis

58
Q

Black lung disease begins as what?

A

Anthracosis: Ingestion of carbon particles by alveolar macrophages

59
Q

How does black lung disease progress from anthracosis?

A

inflammasome activation and IL-1 (due to non-carbon material in coal) can lead to fibrosis

60
Q

What is the only way to definitively diagnose black lung?

A

lung exam by a pathologist

61
Q

How can you treat black lung disease?

A

transplantation

62
Q

What is silicosis?

A

slowly progressive nodular fibrosing lung disease due to inhalation of silicon dioxide in stone (especially quarts) or coal released by processes that powderize some of it (ex. sandblasting)

63
Q

What is the pathogenesis of silicosis?

A

Ingestion of silica by alveolar macrophages→ release of TNF, IL-1, ROS, TGF-beta, fibronectin→ chronic inflammation

64
Q

Describe the gross pathology of silicosis.

A

discrete palpable grey-tan nodules +/- anthracotic pigment

65
Q

Describe the microscopic pathology of silicosis.

A

nodules of concentrically arranged hyalinized collagen

66
Q

What interesting, yet non-specific feature of silicosis can be seen under the microscope?

A

weakly birefringent particles are visible under polarized light

67
Q

What is asbestosis?

A

slowly progressive pulmonary interstitial fibrosis due to inhalation of asbestos fibers

68
Q

Asbestosis is associated with what conditions?

A

associated with pleural plaques, lung cancers, and mesotheliomas

69
Q

What is a strange feature of the epidemiology of asbestosis?

A

has a long latency so expected to peak in 2024

70
Q

How does asbestosis occur?

A

amphibole type asbestos passes through tissue by gravity (have pointed ends that cannot be broken by macrophages and iron-coated ends that elicit a fibrosing tissue reaponse)

71
Q

Describe the gross pathology of asbestosis.

A

interstitial pulmonary fibrosis (mostly at basal lower lobes), visceral pleural fibrosis, and well-circumscribed round/oval tan/white fibrous plaques on lower parietal pleura and domes of diaphragm

72
Q

Describe the microscopic pathology of asbestosis.

A

interstitial fibrosis and ferruginous bodies of fibers

73
Q

What is sarcoidosis?

A

non-caseating granulomatous multi-system inflammatory disease of unknown cause

74
Q

Where is sarcoidosis most common (body-wise)?

A

most common in lung, lymph node, eye, and skin

75
Q

What is the most likely cause of sarcoidosis?

A

Unknown—but most likely immunologic stimuli→ Th1 CD4 lymphocyte response

76
Q

What is the role of IL-8 in sarcoidosis?

A

acts early as a chemo-attractant of neutrophils

77
Q

Which interleukins promote the Th1 immune response of CD4 lymphocytes?

A

IL-12, IL-18, IL-27

78
Q

Which interleukins mediate the transition to fibrosing inflammation? How?

A

IL-4 (it is a chemoattractant to fibroblasts)

79
Q

Describe the gross pathology of sarcoidosis.

A

small tan non-necrotic granulomas in lymphangitic distribution along bronchovascular bundles and in bilateral hilar LN +/- interstitial fibrosis in lungs

80
Q

Describe the microscopic pathology of sarcoidosis.

A

tight naked granulomas with giant cells (with asteroid bodies and Schaumann bodies) and epitheloid macrophages

81
Q

What is an asteroid body?

A

stellate eosinophilic aggregates of cytoskeletal proteins within vacuoles

82
Q

What is a Schaumann body?

A

laminated basophilic concretion of calcified proteins

83
Q

25% of patients with sarcoidosis have what accompanying sign?

A

skin nodules (granulomas) or erythema nodosum

84
Q

What is the differential diagnosis if you see reticulonodular pulmonary infiltrates and bilateral hilar lymphadenopahty on x-ray?

A

Sarcoidosis
Tb
Histoplasmosis

85
Q

True of false: non-infectious interstitial lung disease is usually chronic.

A

TRUE

86
Q

What is Usual Interstitial Pneumonia?

A

prototype chronic, slowly progressive, fibrosing inflammatory disease of the lungs involving predominantly the septa between air spaces

87
Q

Describe the gross pathology of UIP.

A

fibrosis with large discrete scars worse in periphery and in lower lobes(lung is firmer and greyer)→ honey comb lung

88
Q

Describe the microscopic pathology of UIP.

A

non-uniform patchy interstitial inflammation repair response and fibrosis with temporal heterogeneity

89
Q

What is the hallmark of UIP?

A

fibroblast foci of immature fibrosis bulging into alveoli

90
Q

What is temporal heterogeneity?

A

simulatneous presence of early, intermediate and late fibrosing lesions

91
Q

What is the radiology diagnosis of UIP?

A

asymmetric bilateral irregular reticular(nodular) obacities at the bases and periphery with +/- a little ground-glass, traction bronchiectasis, honeycomb change

92
Q

What is COP?

A

cryptogenic organizing pneumonia (bronchiolitis obliterans–organizing pneumonia) is a rare subacute fibrosing lung disease

93
Q

COP is usually caused by what?

A

necrotizing infection (not cryptogenic)

94
Q

What is the pathological hallmark of COP?

A

Masson bodies= plugs of fibrosing granulation tissue in alveoli and ducts

95
Q

What do you see in a radiograph of COP?

A

bilateral opacities less dense than acute bacterial pneumonia or tumor→ ground glass and possibly air bronchograms

96
Q

How can you treat COP and NSIP?

A

STEROIDS!!

97
Q

What is NSIP?

A

non-specific interstitial pneumonia (but it IS specific)

98
Q

What are the two types of NSIP?

A

Cellular (more inflammatory than fibrotic)

Fibrotic (more fibrotic than inflammatory)

99
Q

What can you see in a radiograph of NSIP?

A

bilateral ground glass opacities

100
Q

When does radiation pneumonitis occur?

A

1-2 months after radiation

101
Q

What is the microscopic pathology of radiation pneumonitis?

A 
Type two pneumocyte hyperplasia
Blood vessel injury
Residual hemosiderin (later)
Interstitial lymphocytes (later)
Active fibroblasts (later)
Interstitial fibrosis (later)
102
Q

What part of the lung is particularly vulnerable to radiation injury?

A

small blood vessels

Pulmonary (34 decks)

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