Lecture 16, 18: Occupational Lung Disease and Pathology

Question 1

Pneumoconiosis

Answer 1

Lung disease secondary to dust inhalation

Question 2

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

Answer 2

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

Question 3

Silicosis: who? how long?

Answer 3

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

Question 4

Silicosis: pathogenesis

Answer 4

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

Question 5

Two stages of silicosis

Answer 5

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

Question 6

What lung zone more affected in silicosis?

Answer 6

Upper lung zone

Question 7

How does silicosis usually present (predominant symptom)

Answer 7

Dyspnea

Question 8

Someone with silicosis is particularly susceptible to…

Answer 8

Infections with mycobacteria (perhaps due to impaired macrophage function)

Question 9

Pneumoconiosis (CWP): who?

Answer 9

Coal miners

Question 10

CWP: pathogenesis

Answer 10

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

Question 11

Simple CWP

Answer 11

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

Question 12

Complicated CWP (progrssive massive fibrosis)

Answer 12

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

Question 13

CWP: symptoms according to type

Answer 13

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

Question 14

Abestos: who? how long?

Answer 14

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

Question 15

Asbestos-related lung disease (3)

Answer 15

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

Question 16

Asbestosis: pathogenesis

Answer 16

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

Question 17

Characteristic finding of asbestosis. What does it look like?

Answer 17

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

Question 18

Where in the lung does asbestosis have its largest affect?

Answer 18

Lung bases and subpleural regions

Question 19

Asbestosis: radiology (include advanced cases findings)

Answer 19

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

Question 20

Asbestosis: pleural findings (2)

Answer 20

Diffuse pleural thickening and plaques

Question 21

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

Answer 21

False: non-malignant, assymptomatic

Question 22

Berylliosis: who?

Answer 22

Workers in aerospace, nuclear weapons and electronics industries

Question 23

Berrylliosis: pathogenosis

Answer 23

Hypersensitivity to beryllium –> granulomas

Question 24

What does berrylliosis mimic?

Answer 24

Sarcoidosis

Question 25

First line treatment for pneumoconiosis

Answer 25

Removing occupasional exposure

Question 26

Hypersensitivity pneumonitis (HP): definition

Answer 26

Result of immunologic phenomena directed against an antigen

Question 27

Steps of hypersensitivity pneumonitis (3)

Answer 27

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

Question 28

How is HP typically categorized?

Answer 28

Acute, subacute, and chronic

Question 29

HP: pathogenesis

Answer 29

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

Question 30

HP involves what types of immune responses?

Answer 30

Type 1, Type 3, Type 4

Question 31

Type 1

Answer 31

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

Question 32

Type 2

Answer 32

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

Question 33

Type 3

Answer 33

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

Question 34

Type 4

Answer 34

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

Question 35

With HP, can you simply test for IgG antibodies?

Answer 35

Nope: not sensitive or specific

Question 36

HP: pathology (triad)

Answer 36

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

Question 37

Acute HP: clinical features

Answer 37

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

Question 38

PFTs reveal what kind of defect with Acute HP?

Answer 38

Restrictive ventilatory defect

Question 39

Acute HP: treatment

Answer 39

Remove exposure to inciting antigen

Question 40

Chronic HP: clinical features

Answer 40

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

Question 41

PFTs reveal what kind of defect with Chronic HP?

Answer 41

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

Question 42

Chronic HP: treatment (besides removing antigen)

Answer 42

Corticosteroids

Question 43

Definition of a restrictive lung disease

Answer 43

Reduced TLC

Question 44

Definition of an obstructive lung disease

Answer 44

Less than 0.7 FEV1 / FVC ratio

Question 45

What is a Ferruginous body

Answer 45

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

Question 46

What is an Asbestos body

Answer 46

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

Question 47

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

Answer 47

Asbestosis --> honeycomb lung

Question 48

Describe the fibrosis progression of asbestosis

Answer 48

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

Question 49

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

Answer 49

Silicotic nodule; enlarge and eventually obstruct airways and blood vessels

Question 50

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

Answer 50

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

Question 51

What does the silicotic nodule look like microscopically?

Answer 51

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

Question 52

What can silicosis lead to?

Answer 52

Progressive massive fibrosis

Question 53

Coal workers' pneumoconiosis begins as what and then progresses to what...(%)

Answer 53

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

Question 54

What is Caplan syndrome

Answer 54

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