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Flashcards in Pneumoconiosis Deck (44):
1

pneumoconiosis

the accumulation of mineral dusts inciting tissue reactions that range from minimal reversible stromal reactions to interstitial fibrosis that results in permanent scarring

2

silicosis

a chronic lung disease due to inhalation of crystalline silica (usually quartz)

characterized by progressive parenchymal nodules and pulmonary fibrosis

upper lobe disease

3

epidemiology of silicosis

most prevalent chronic occupational lung disease worldwide

risk is directly proportional to particle concentration, duration of exposure, and silica content of different rock types

4

Describe the common histologic features of pneumoconiosis

1) acellular hyalinized collagen

2) layered collagen

3) thick capsule

5

factors that increase dust deposition in the lung

exertion

younger age

close proximity to sources of dust

acute or chronic lung disorders

6

fast phase clearance

half-time of 3.0 +/ 1.6 hrs

mucociliary clearance

does not remove all particles deposited in the larger airways

7

slow phase clearance

half-time of 109 +/- 78 days

depends on lung scavenger cells (macrophages)

8

pathogenesis of mineral dust pulmonary toxicity

injury due to dust particle inhalation

silica engulfed by macrophages to form nodules

mitochondria - ROS/RNS and DNA damage

apoptosis and fibrotic response

scarring of the lungs

9

chronic silicosis

characterized by nodules that are typically located in the peribronchial regions with interstitial extension

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common CXR findings of chronic silicosis

small 1-3 mm nodules

symmetrical bilateral upper lobes

calcified nodules

hilar LN with eggshell clacification

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pulmonary function test for chronic silicosis

often normal early

later on will have - decreased lung volumes and diffusion capacity

eventual airway obstruction

12

progressive massive fibrosis

a state of silicosis where nodules expand and coalesce into large massis that can undergo necrosis

13

acute silicosis

characterized by diffuse fluid-filled alveolar spaces that consist of eosinophilic proteinaceous and surfactant-containing material

14

pathology of acute silicosis

alveolar proteinosis, poorly formed nodules, intersitial infiltrates

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acute silicosis CXR

alveolar pattern - ground glass

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HRCT of acute silicosis

"crazy paving" - ground glass + septal thickening

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management of silicosis

avoidance

no established treatment - lung transplant

treat mycobacterial infections as silica impairs alveolar macrophages

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"angel wing" appearance

the symmetrical appearance of PMF

19

coal worker's pneumoconiosis

also called "black lung" or "antraco-silicosis"

due to chornic exposure to coal dust, graphite, and other forms of carbon

black nodules

carbon is less fibrogenic than quartz

20

pathology of coal workers' pneumoconiosis

greater dust burden

black lung nodules (randomly arranged)

black lymph nodes

centrilobular emphysema

coal-laden alveolar macrophages

coal macules can develop into PMF if many coalesce

21

clinical manifestations of CWP

simple, complicated, and PMF

chronic bronchitis is a more prominent feature

an acute onset form of the disease does not occur

advanced disease can have cough, SOB, and cor pulmonale

Caplan's Syndrome

22

simple CWP

most common and typically occurs after low-dose coal exposure for more than 20 years

relatively asymptomatic but can develop cough and sputum production

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characteristic HRCT findings in CWP

focal emphysema

punctate opacities

subpleural nodules

PMF

cavitating masses

diffuse interstitial pulmonary fibrosis

bronchiectasis

24

PFT in CWP

restricted lung volumes

reduced DLCO

mixed restricted/obstructive defects

 in PMF, severe mixed restriction and obstruction

not as bad as silicosis

also no cancer risk!

25

treatment of CWP

no established treatment

look out for complicating mycobacterial infections

26

asbestos-related diseases

asbestos naturally occurs in silicate fibers, ideal for construction

long latency of 15-40 years from exposure to disease

cause nonmalignant and malignant inflammatory pulmonary diseases

27

asbestos fiber types

serpentine and amphibole fibers

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serpentine asbestos fibers

curly-stranded, curved structures

95% of insulation is chrysotile, which is a type of serpentine fiber

not as bad as amphibole fibers

29

amphibole asbestos fibers

straight, rod-like fibers

more harmful than serpentine fibers

amphibole hypothesis - crocidolite is especially more carcinogenic and fibrogenic

accumulate more readily in the distal lung parenchyma, not as effectively cleared

30

Describe the mechanism underlying free radical generation by asbestos fibers.

due to reactions occurring on surface of the mineral dusts

mitochondrial dysfunction and activation of AMs or neutrophils attempt to take upf fibers

coated with iron inside the macrophages and become ferruginous bodies

asbestos body is used to define coated fibers where the core fiber is asbestos

31

How does asbestos fibers proomte pulmonary toxicity?

induce AM mitochondrial H2O2 production via a Rac1-dependent mechanism

ROS production activates NALP3 inflammasomes that trigger inflammatory signaling

32

asbestos-induced pleural plaques

discreet collagenous material along parietal pleura of the mid-lower ribs and diaphragm

latency is greater than 20 years

prevalence varies with intensity of exposure

long fibers are retained in the parietal pleura and can block the stomata

fairly specific to asbestos exposure and rarely affects PFTs

33

clinical manifestations of asbestos exposure

benign asbestos pleural effusions (BAPE)

pleural plaques

rounded atelectasis

malignant mesothelioma

asbestosis

lung cancer

34

rounded atelectasis

a distinct form of pleural/parenchymal thickening that is characterized by its major radiographic inding, the "comet tail sign"

as pleural fibrosis progresses, it can entrap the underlying healthy lung and bronchovascular tissue

35

malignant mesothelioma

rare tumor caused by all forms of asbestos

no synergy with tobacco smoke

latency period of > 30 years

36

clinical manifestation of malignant mesothelioma

male predominant, insiduous onset

nonspecific symptoms such as fever, weight loss, night sweats, and fatigue

dyspnea, nonpleuritic chest pain, and cough may also occur

stain positive for vimentin, keratin, and calretinin

37

management of malignant mesothelioma

cisplatinum +/- pemextred -> 9-12 month survival

chemo, radiation, and surgery -> median survival 22 months

38

favorable prognostic signs of malignant mesothelioma

< 5% of total body weight loss

tumor confined to the ipsilateral pleura

epithelioid histology

good performance status

platelets < 400,000

age < 60

39

asbestosis

slowly progressive, diffuse pulmonary fibrotic process

present with exertional dyspnea

20 year latency period

pleural plaques present in 80-90%

similar IPF findings but with plaques

PFTs show decreased lung volumes and DLCO below normal

end-inspiratory bibasilar crackles, clubbing, and cor pulmonale

40

diagnosis of asbestosis

a reliable exposure history

an appropriate latency period

characteristic chest radiograph of HRCT interstitial abnormalities

reduced lung volumes and/or DLCO

end-inspiratory crackles

**unlike IPF, asbestosis is slowly progressive

41

What are the two most common causes of hard metal lung disease?

beryllium and cobalt

42

berylliosis

identical to sarcoid clinically, radiographically, and pathologically

an important early marker is the proliferation of T lymphocytes proliferating in the lung and the blood

up to 10 years of latency

PFT shows reduced volumes and DLCO

slow decline that can result in cor pulmonale

43

treatment for berylliosis

steroids are administered

elimination of further exposure

high correlation between berylliosis and lung cancer

44

cobalt-associated disease

airway obstruction that resembles occupational asthma

acute interstitial pneumonitis with features of hypersensitivity pneumonitis

chronic diffuse interstitial fibrosis

characteristic diagnostic feature is the presence of odd-appearing giant multinucleated cells