Lecture 16, 18: Occupational Lung Disease and Pathology Flashcards Preview

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

Flashcards in Lecture 16, 18: Occupational Lung Disease and Pathology Deck (54):
1

Pneumoconiosis

Lung disease secondary to dust inhalation

2

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

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

3

Silicosis: who? how long?

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

4

Silicosis: pathogenesis

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

5

Two stages of silicosis

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

6

What lung zone more affected in silicosis?

Upper lung zone

7

How does silicosis usually present (predominant symptom)

Dyspnea

8

Someone with silicosis is particularly susceptible to...

Infections with mycobacteria (perhaps due to impaired macrophage function)

9

Pneumoconiosis (CWP): who?

Coal miners

10

CWP: pathogenesis

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

11

Simple CWP

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

12

Complicated CWP (progrssive massive fibrosis)

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

13

CWP: symptoms according to type

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

14

Abestos: who? how long?

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

15

Asbestos-related lung disease (3)

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

16

Asbestosis: pathogenesis

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

17

Characteristic finding of asbestosis. What does it look like?

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

18

Where in the lung does asbestosis have its largest affect?

Lung bases and subpleural regions

19

Asbestosis: radiology (include advanced cases findings)

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

20

Asbestosis: pleural findings (2)

Diffuse pleural thickening and plaques

21

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

False: non-malignant, assymptomatic

22

Berylliosis: who?

Workers in aerospace, nuclear weapons and electronics industries

23

Berrylliosis: pathogenosis

Hypersensitivity to beryllium --> granulomas

24

What does berrylliosis mimic?

Sarcoidosis

25

First line treatment for pneumoconiosis

Removing occupasional exposure

26

Hypersensitivity pneumonitis (HP): definition

Result of immunologic phenomena directed against an antigen

27

Steps of hypersensitivity pneumonitis (3)

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

28

How is HP typically categorized?

Acute, subacute, and chronic

29

HP: pathogenesis

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

30

HP involves what types of immune responses?

Type 1, Type 3, Type 4

31

Type 1

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

32

Type 2

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

33

Type 3

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

34

Type 4

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

35

With HP, can you simply test for IgG antibodies?

Nope: not sensitive or specific

36

HP: pathology (triad)

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

37

Acute HP: clinical features

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

38

PFTs reveal what kind of defect with Acute HP?

Restrictive ventilatory defect

39

Acute HP: treatment

Remove exposure to inciting antigen

40

Chronic HP: clinical features

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

41

PFTs reveal what kind of defect with Chronic HP?

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

42

Chronic HP: treatment (besides removing antigen)

Corticosteroids

43

Definition of a restrictive lung disease

Reduced TLC

44

Definition of an obstructive lung disease

Less than 0.7 FEV1 / FVC ratio

45

What is a Ferruginous body

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

46

What is an Asbestos body

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

47

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

Asbestosis --> honeycomb lung

48

Describe the fibrosis progression of asbestosis

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

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

Silicotic nodule; enlarge and eventually obstruct airways and blood vessels

50

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

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

51

What does the silicotic nodule look like microscopically?

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

52

What can silicosis lead to?

Progressive massive fibrosis

53

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

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

54

What is Caplan syndrome

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