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Pulmonology > Lecture 16, 18: Occupational Lung Disease and Pathology > Flashcards

Lecture 16, 18: Occupational Lung Disease and Pathology Flashcards

1
Q

Pneumoconiosis

A

Lung disease secondary to dust inhalation

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2
Q

Mechanisms of aerosol deposition: 3, by particle size (large –> small)

A

Impaction (filtered by nose, >5 um), sedimentation (small airways 1-5 um), diffusion (alveoli

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3
Q

Silicosis: who? how long?

A

Sandblasters, rock miners, quarry workers, stonecutters; ~20 years unless very heavy dose

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4
Q

Silicosis: pathogenesis

A

Silica particles phagocystosed by alveolar macrophages –> apoptosis –> alveolitis and fibrosis –> SILICOTIC NODULE

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5
Q

Two stages of silicosis

A
  1. Simple (small nodules) –> 2. Complicated (nodules coalescent)
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6
Q

What lung zone more affected in silicosis?

A

Upper lung zone

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7
Q

How does silicosis usually present (predominant symptom)

A

Dyspnea

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8
Q

Someone with silicosis is particularly susceptible to…

A

Infections with mycobacteria (perhaps due to impaired macrophage function)

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9
Q

Pneumoconiosis (CWP): who?

A

Coal miners

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10
Q

CWP: pathogenesis

A

Dust engulfed by macrophages –> aggregate around respiratory bronchioles –> broncholes dilate –> focal dust emphysema

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11
Q

Simple CWP

A

Coal macules (aggregation of dust and macrophages around respiratory bronchioles with little tissue reaction) and coal nodules (above + collagen)

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12
Q

Complicated CWP (progrssive massive fibrosis)

A

Coalesced nodules: bulky, irregular, well-defined, heavily pigmented black tissue masses

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13
Q

CWP: symptoms according to type

A

Simple –> few symptoms w/ preserved pulmonary function; Complicated –> pronounced symptoms

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14
Q

Abestos: who? how long?

A

People who work with insulation, shipyard and construction workers, and brake linings; 10-20 years

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15
Q

Asbestos-related lung disease (3)

A
  1. Asbestosis; 2. Pleural disease (mesothelioma); 3. Lung cancer
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16
Q

Asbestosis: pathogenesis

A

Clearence of fibers differs based on size; short –> phagocytosed and drained into pleural space; longer –> incompletely phagocytosed and become core of asbestos body, fibrosis throughout alveolar walls

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17
Q

Characteristic finding of asbestosis. What does it look like?

A

Asbestos body; rod-shaped body with clubbed ends that appears yellow-brown in stained tissue due to iron

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18
Q

Where in the lung does asbestosis have its largest affect?

A

Lung bases and subpleural regions

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19
Q

Asbestosis: radiology (include advanced cases findings)

A

Pattern of linear streaking that is generally most prominent at the lung bases; advanced cases can have cyst formation and honeycombing; often associated pleural disease

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20
Q

Asbestosis: pleural findings (2)

A

Diffuse pleural thickening and plaques

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21
Q

T/F: Pleural plaques related to asbestos exposure are malignant

A

False: non-malignant, assymptomatic

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22
Q

Berylliosis: who?

A

Workers in aerospace, nuclear weapons and electronics industries

23
Q

Berrylliosis: pathogenosis

A

Hypersensitivity to beryllium –> granulomas

24
Q

What does berrylliosis mimic?

A

Sarcoidosis

25
Q

First line treatment for pneumoconiosis

A

Removing occupasional exposure

26
Q

Hypersensitivity pneumonitis (HP): definition

A

Result of immunologic phenomena directed against an antigen

27
Q

Steps of hypersensitivity pneumonitis (3)

A
  1. Repeated antigen exposure –> 2. Immunologic sensitiziation of host to antigen –> 3. Immune-mediated damage to lung
28
Q

How is HP typically categorized?

A

Acute, subacute, and chronic

29
Q

HP: pathogenesis

A

Exposed to antigen –> Th1 (acute) and Th2 (subacute/chronic) response –> inflammation, tissue damage, fibrosis

30
Q

HP involves what types of immune responses?

A

Type 1, Type 3, Type 4

31
Q

Type 1

A

Allergic response/asthma due to IgE binding of sensitized mast cells –> degranulation

32
Q

Type 2

A

Antibody-initiated –> direct binding of antibody to surface molecules (autoimmunity)

33
Q

Type 3

A

Antibody-initiated –> formation of immune complexes which are deposited (autoimmunity)

34
Q

Type 4

A

T-cell dependent starting with primed T cells –> inflammation and T cell-mediated (CD8+) cytotoxicity

35
Q

With HP, can you simply test for IgG antibodies?

A

Nope: not sensitive or specific

36
Q

HP: pathology (triad)

A

Triad: cellular bronchiolitis (airway-centered inflammation), organizing pneumonia, scattered, small, non-necrotizing granulomas

37
Q

Acute HP: clinical features

A

4-12 hours after exposure with viral-like respiratory symptoms (cough, dyspnea, chest tightness, fevers, chills, malaise) with tachypnea, rales

38
Q

PFTs reveal what kind of defect with Acute HP?

A

Restrictive ventilatory defect

39
Q

Acute HP: treatment

A

Remove exposure to inciting antigen

40
Q

Chronic HP: clinical features

A

Insidious development of dyspnea, cough, and systemic features (fatigue, loss of appetite, weight loss) with tachypnea, rales, clubbing

41
Q

PFTs reveal what kind of defect with Chronic HP?

A

Restrictive (fibrotic), obstructive, (reduced airway diameter) or combined

42
Q

Chronic HP: treatment (besides removing antigen)

A

Corticosteroids

43
Q

Definition of a restrictive lung disease

A

Reduced TLC

44
Q

Definition of an obstructive lung disease

A

Less than 0.7 FEV1 / FVC ratio

45
Q

What is a Ferruginous body

A

General term referring to any inorganic substance with a coating of iron and protein (graphite, ceramic, iron, etc)

46
Q

What is an Asbestos body

A

Ferruginous body formed on an asbestos fiber—characterized by a clear internal core and beaded ferruginous coating

47
Q

Asbestos causes what pulmonary parenchymal fibrosis (the term) which leads to what end-stage fibrosis (the term)

A

Asbestosis –> honeycomb lung

48
Q

Describe the fibrosis progression of asbestosis

A

Begins around respiratory bronchioles and alveolar ducts and extends distally until it causes honeycomb lung; begins lower lube and subpleurally –> moves to middle and upper

49
Q

Silicosis is marked by what major finding? What do these cause?

A

Silicotic nodule; enlarge and eventually obstruct airways and blood vessels

50
Q

What does the silicotic nodule look like grossly? Where are they found at first?

A

Stellate shape at the edges; found in upper lung and hilar lymph nodes

51
Q

What does the silicotic nodule look like microscopically?

A

Small nodules of fibroblasts and histiocytes with silica (under polarization, this can be visualized), that become less cellular and more hyalinized with time

52
Q

What can silicosis lead to?

A

Progressive massive fibrosis

53
Q

Coal workers’ pneumoconiosis begins as what and then progresses to what…(%)

A

Simple CWP: coal macules/nodules –> 10% develop progressive massive fibrosis

54
Q

What is Caplan syndrome

A

Rheumatoid arthritis AND pneumoconiosis cause rapidly developing nodular pulmonary lesions histologically identical to rheumatoid nodules more commonly seen in soft tissue

Pulmonology (21 decks)

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