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Path x2 Flashcards

1
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi and bronchioles, caused by destruction of muscle and elastin tissue

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2
Q

Is bronchiectasis reversible?

A

no

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3
Q

What are the two requisite conditions for bronchiectasis?

A

Obstruction and chronic, persistent infections

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4
Q

What is the histological change with bronchiectasis?

A

FIbrosis of the bronchioles, holding them open

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5
Q

What are the three common obstructive causes of bronchiectasis?

A

Tumor
FB
Concretions/secretions

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6
Q

What are the two congenital conditions that cause bronchiectasis?

A

CF
Kartagener’s syndrome
Immunodeficiency

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7
Q

What type of pneumonia causes bronchiectasis? What organism?

A

Necrotizing

Staph Aureus, klebsiella, or TB

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8
Q

What chromosome is responsible in CF?

A

7

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9
Q

Why is there thick mucus with CF?

A

NaCl is pulled inward, opposite of sweat glands

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10
Q

What is the defect with Kartagener syndrome?

A

Structural defect in dynein of cilia

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11
Q

Is Kartagener syndrome AR or AD?

A

AR

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12
Q

What are the histological findings of the cilia with Kartagener syndrome?

A

Loss of the radial spokes

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13
Q

What are the ssx of bronchiectasis? (4)

A

Chronic cough
Foul smelling sputum
Hemoptysis
Dypsnea

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14
Q

What are the complications that can arise from bronchiectasis? (4)

A

Pulmonary HTN
Brain abscesses
Cor pulmonale
Amyloidosis

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15
Q

What is the major, basic issue with restrictive diseases?

A

Fibrosis of the lungs causes problems getting air in

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16
Q

What type of lung disease is kyphoscoliosis?

A

Restrictive

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17
Q

What are the two external causes of restrictive lung diseases?

A

Deformed chest wall

Pleural space filled with stuff

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18
Q

What are the hallmarks of chronic, diffuse interstitial diseases? What is the consequence of this?

A

Reduced compliance d/t inflammation and fibrosis.

Dyspnea results

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19
Q

What happens to TLC with restrictive lung diseases? FEV1? FEV1/FVC?

A

TLC reduced
FEV1 normal-ish
FEV1/FVC normal

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20
Q

What is the typical presentation of interstitial lung diseases? Lung sounds?

A

SOB/hypoxia

Inspiratory crackles

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21
Q

What are the x-ray findings of interstitial lung disease?

A

Diffuse, bilateral infiltrative lesions, or ground glass shadows

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22
Q

What are the complications of interstitial lung diseases?

A

pHTN

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23
Q

What is the end stage result of ILDs?

A

honeycomb lung

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24
Q

What is acute lung injury?

A

Capillary damage causing non-cardiogenic pulmonary edema

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25
Q

What is the clinical presentation of acute lung injury?

A

Abrupt onset of significant hypoxemia and pulmonary infiltrates

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26
Q

What is ARDS?

A

Acute respiratory distress syndrome causing diffuse alveolar capillary damage

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27
Q

What are this histological manifestations of ARDs and acute lung injury?

A

Diffuse alveolar damage

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28
Q

What is the severe sequelae of ARDS?

A

Multisystem organ failure

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29
Q

What is the most common cause of noncardiogenic pulmonary edema?

A

ARDS

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30
Q

What are the three direct injures (from outside) that cause ARDS?

A

Infection
Aspiration
Oxygen toxicity

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31
Q

What are the four major indirect (from inside) causes of ARDS?

A

Shock
Sepsis
Toxins
TRALI

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32
Q

What are the CXR findings of ARDS?

A

bilateral infiltrates on CXR

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33
Q

What happens to pulmonary capillary wedge pressure with ARDS?

A

Is less than 18 mmHg

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34
Q

What happens to PaO2/FiO2 with ALI?

A

Less than 300

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35
Q

What happens to PaO2/FiO2 with ARDS?

A

Less than 200

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36
Q

What is the pathogenesis of ARDS?

A

Uncontrolled activation of acute inflammatory system, leading to an increased vascular permeability and alveolar thickening

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37
Q

What happens to diffusion capacity with ARDS?

A

Decreased

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38
Q

What happens to the surfactant with ARDS?

A

Widespread abnormalities

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39
Q

What causes the inflammation in endothelial cells with ARDS?

A

Complement and TNF-alpha

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40
Q

What causes the destruction of the alveolar capillaries with ARDS?

A

Oxygen radicals
Proteases
Prostaglandins

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41
Q

What is the primary effect of IL-8?

A

Potent PMN chemoattractant

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42
Q

What is the cause of IRDS?

A

Deficiency in pulmonary surfactant causes an increase in vascular permeability and alveolar flooding

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43
Q

What is the role of NO with ARDS?

A

Dilation of the pulmonary vasculature decreases PA pressure and resistance

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44
Q

What is the mortality rate with ARDS?

A

40%

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45
Q

What are the gross characteristics of the lungs with ARDS?

A

Heavy, thick, red, firm

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46
Q

What are the histological characteristics of ARDS? (2)

A

Interstitial and alveolar edema

Hyaline membranes

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47
Q

Transudate or exudate with ARDS?

A

Exudate

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48
Q

What are the three phases of ARDS, and when do they occur?

A
  • Acute exudative: 0-7 days
  • Proliferative phase 1-3 weeks
  • fibrotic/healing 3-4 weeks
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49
Q

What happens in the fibrotic stage of ARDS? (what two cell types are activated)

A

Fibroblastic proliferation and type II pneumocyte hyperplasia

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50
Q

What is the general progression of ARDS?

A
  1. injury = edema
  2. Alveoli collapse, type II pneumocytes increase
  3. Fibrosis
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51
Q

Do patients with ARDS always have fibrosis if they recover?

52
Q

What is TRALI?

A

Anti-HLA or HNA antibodies cause lung collapse

53
Q

What are the four major categories of ILD?

A

Fibrosing
Granulomatous
Eosinophilic
Smoking related

54
Q

What are the three major fibrosing ILDs?

A
  • Usual interstitial pneumonia (UIP)
  • Non-specific interstitial pneumonia (NSIP)
  • Cryptogenic organizing pneumonia (COP)
55
Q

What are the two major granulomatous ILDs?

A
  • Sarcoidosis

- Hypersensitivity pneumonitis

56
Q

What is pneumoconiosis?

A

Inorganic material breathed in

57
Q

What are the two smoking related ILDs?

A

DIP

Respiratory bronchiolitis

58
Q

What is the initial finding of diffuse interstitial disease?

A

Alveolitis with Leukocyte accumulation

59
Q

What is the final stage of diffuse interstitial lung diseases?

A

Fibrotic lung (honeycomb lung)

60
Q

What is the role of M1 macrophages? M2?

A 
M1 = Inflammation
M2 = healing
61
Q

What is the major cell type that is implicated with diffuse interstitial disease?

A

Macrophages

62
Q

What is idiopathic pulmonary fibrosis?

A

Pulmonary disorder of unknown etiology characterized by diffuse interstitial fibrosis

63
Q

What is the histological pattern of idiopathic pulmonary fibrosis?

A

Usual interstitial pneumonia (UIP)

64
Q

What is the term for the interstitial fibrosis with idiopathic pulmonary fibrosis?

A

Cryptogenic fibrosing alveolitis

65
Q

What is the clinical course of idiopathic pulmonary fibrosis?

A

slow, Insidious onset of SOB with non-productive cough

66
Q

What are the complications of late IPF?

67
Q

How do you diagnose IPF?

A

Diagnosis of exclusion

68
Q

What is the prognosis of IPF? What is the treatment?

A

3 year survival

Lung transplant (NOT steroids)

69
Q

What is the current theory of IPF?

A

Repeated cycles of epithelial activation/injury by some agent causes fibrosis

70
Q

What is the major cell type that is upregulated with IPF? Cytokines?

A

Th2
IL-4
IL-5
IL-13

71
Q

What is the hallmark histological finding of IPF? What causes this?

A

Fibroblastic foci

Overwhelming healing

72
Q

What is the main fibrosing component of IPF? What does this do? (3)

A

TGF-beta1

  • Activates fibroblasts and myofibroblasts
  • Reduced telomerase
  • Inhibits caveolin
73
Q

What is the effect of TGF-beta1 on fibroblast caveolin in IPF? What does this cause?

A

TGF inhibits it

Caveolin can no longer inhibit deposition of collagen

74
Q

What are the early findings of IPF? (2)

A

Alveolitis with leukocyte infiltration

“Fibroblastic foci”

75
Q

What is the hallmark of UIP?

A

Patchy, interstitial fibrosis

76
Q

What is the “temporal heterogeneity” seen with IPF?

A

Over time, lungs become more collagenous and less cellular, but occurring at different rates in different places

77
Q

What are the late findings of IPF?

A

Dense fibrosis and collapse of alveolar wall

“honeycomb lung”

78
Q

What causes the honeycomb lung in the end stages of lung diseases?

A

Dense fibrosis and collapse of the alveolar walls, leading to restructuring of airspaces and obliteration of small airways

79
Q

What is the consequence of IPF?

A

cor pulmonale

80
Q

What is the only form of ILD does not respond to steroids, and requires a transplant?

81
Q

True or false: aspiration can lead to honeycomb lung

82
Q

What are the diseases that can lead to honeycomb lung?

A

DAD
IPF
Interstitial granulomatous disease

83
Q

What are the collagen vascular disease that can cause restrictive lung disease?

A

RA
Scleroderma
SLE

84
Q

What restrictive lung disease can be caused by scleroderma?

85
Q

What is the main determinant of the pathogenesis of pneumoconioses?

A

Solubility and size

86
Q

What does pneumoconiosis lead to?

A

Acute Lung Injury

87
Q

What happens to larger particles in pneumoconioses?

A

Resist dissolution, leading to fibrosis

88
Q

What is the physicochemical reactivity of the particles in lungs?

A

Direct tissue damage from releasing free radicals and other chemical groups

89
Q

What is the key endogenous factor that determines the prognosis with pneumoconioses?

A

Capacity of inhaled dusts to stimulate fibrosis

90
Q

What are the three main mediators release by macrophages that cause damage in pneumoconioses?

A

Free radicals
Chemotactic factors
Fibrogenic cytokines

91
Q

What are the initial changes with coal exposure? What about for long term?

A

Emphysema progressing to fibrosis

92
Q

What is the key characteristic of asbestos?

A

Extremely fibrogenic

93
Q

What is anthracosis?

A

Benign buildup of carbon in macrophages d/t pollution

94
Q

What is simple coal workers’ pneumoconiosis (CWP)?

A

1-2 mm Nodules with collagen fibrils, but minimal lung dysfunction.

95
Q

What is complicated CWP? What are the sequelae of this?

A

Progressive/massive fibrosis that leads to compromised lung function

Cor pulmonale from fibrosis and pHTN

96
Q

Is there an increased risk for cancer or TB with CWP?

97
Q

What is the eventual consequence of CWP?

A

Pulmonary massive fibrosis (PMF)

98
Q

What is the “black lung disease”?

A

Disabling respiratory insufficiency d/t massive pulmonary fibrosis

99
Q

What is Caplan syndrome? What does this lead to?

A

Coexistence of rheumatoid arthritis with a pneumoconiosis. Leads to the development of distinctive nodular pulmonary edema

100
Q

What is the most prevalent occupational disease in the world?

101
Q

What is the progression of silicosis?

A

Slowly progressive, nodular fibrosis

102
Q

What are the ssx of silicosis?

A

Progressive SOB and cyanosis

103
Q

What is the pathogenic part of silicosis?

A

Quartz crystal

104
Q

What major cytokine is released when macrophages are exposed to the quartz in silicosis?

A

TNF

TGF beta

105
Q

Are patients with silicosis more susceptible to cancer and/or TB?

A

Yes, to both

106
Q

What are the gross characteristics of silicosis?

A

Concentrically arranged collagenous nodules that begin as small lesions in the upper lungs, but grow

107
Q

What are the histological findings of silicosis? What technique can be used to highlight this?

A

Hyalinized whorls of collagen with scant inflammation

Polarized light

108
Q

What are the serpentines seen with asbestos? How about amphiboles? Which is more pathogenic and is the one associated with mesothelioma?

A 
Serpentines = Flexible curved rods
*Amphiboles* = Straight rods
109
Q

Asbestos was classically seen in whom?

A

Construction yard or shipyard workers

110
Q

Which type of pneumoconiosis causes pleural plaques and this pleural effusions?

A

Asbestosis

111
Q

Which is more of an issue with asbestosis: mesothelioma or lung cancer?

A

Lung cancer develops much sooner

112
Q

What is the histological pattern seen with asbestos? What else is seen?

A

UIP

Fibrosis and asbestos bodies

113
Q

True or false: asbestos increases the risk for cancer systemically

114
Q

What are the characteristics of the asbestos fibers that break through the interstitium to cause diffuse interstitial pulmonary fibrosis?

115
Q

What are asbestos body?

A

Asbestos fibers absorbed by macrophages and coated by hemosiderin

116
Q

What is the general morphology of asbestosis? (what structures are affected/how does it progress)

A

DIffuse pulmonary fibrosis that begins around respiratory bronchioles and progressives to involve alveoli (honeycomb lung)

117
Q

Which generally causes upper lobe fibrosis, and which causes lower lobe fibrosis: asbestosis, silicosis

A 
Silicosis = upper lobe
Asbestosis = lower lobg
118
Q

What is the increase in lung cancer development with asbestos exposure? What about with smoking? What abous with mesotheliomas?

A

5x with exposure
55x with smoking
1000x with mesothelioma

119
Q

What causes the 1000x increase in lung CA with mesothelioma?

A

ROS generation with asbestos fibers

120
Q

What is the clinical course of asbestosis?

A
  • DOE, later at rest.

- Heart and respiratory failure

121
Q

What are the drugs that cause lung fibrosis? (2)

A

Bleomycin

Amiodarone

122
Q

What is the use of bleomycin?

A

Hodgkin’s lymphoma

123
Q

What is the use of methotrexate?

124
Q

What are the drugs that cause hypersensitivity pneumonitis? (2)

A

Methotrexate

Nitrofurantoin

125
Q

What are the two drugs that cause bronchospasm?

A

ASA

Beta blockers

126
Q

What is acute radiation pneumonitis?

A

1-6 months post radiation causes an inflammatory response, and can cause pleural effusions

127
Q

What is chronic radiation pneumonitis

A

Failure of acute radiation pneumonitis to resolve, leading to pulmonary fibrosis

Respiratory (34 decks)

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