Occupational & Traumatic Disorders Flashcards

1
Q

Define acute respiratory distress syndrome

A

Manifestation of severe acute lung injury

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2
Q

Define acute lung injury

A

Abrupt onset of hypoxemia and bilateral pulmonary infiltrates in the absence of heart failure

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3
Q

Both ARDS & ALI involve inflammation-associated increases in _______.

A
  1. pulmonary vascular permeability
  2. edema
  3. epithelial cell
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4
Q

Define diffuse alveolar damage (DAD)

A

Histologic manifestation of ARDS/ALI

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5
Q

Describe the pathophysiology of ARDS/ALI

A

Injury → neutrophil recruitment & endothelial activation/injury → release of proteases, ROS → leakage of proteins into alveoli → hyaline membrane → interference w/gas exchange.

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6
Q
A
  • blue arrow: collapsed alveoli
  • black arrows: hyaline membranes formed due to damage (these interfere with gas exchange & decrease lung compliance)
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7
Q
A

Organizing phase of ALI/ARDS. About one week after the initial injury, fibroblasts begin to proliferate within the alveolar walls.

  • Yellow arrow: scattered residual alveoli containing proteinaceous fluid
  • Yellow circle: alveolar wall which is thickened by loosely arranged fibroblastic tissue (i.e. granulation tissue).
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8
Q

ARDS/ALI clinical presentation

A
  1. Tachypnea
  2. Dyspnea → hypoxemia
  3. Respiratory acidosis (⇡ PCO2)

(mechanical ventilators often become necessary)

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9
Q

Prognosis of ARDS/ALI

A

40% mortality

(survivors may heal with fibrosis → chronic pulmonary disease)

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10
Q

CXR findings of ARDS/ALI

A

Diffuse bilateral infiltrates

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11
Q

Define pneumoconiosis

A

Lung disease caused by the inhalation of mineral or organic dust or chronic or vapors

(typically occupational disease)

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12
Q

Many cases of pneumoconiosis results in _______.

A

pulmonary fibrosis

(regulations limiting worker exposure have decrease this)

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13
Q

List 4 factors that increase the likelihood of pneumoconiosis development

A
  1. Amount of dust retained in the lungs
  2. particle size of 1-5 micrometers in diameter
  3. Particle solubility
  4. genetics
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14
Q

The most common chronic occupational disease in the world

A

Silicosis

(type of pneumoconiosis)

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15
Q

Define silicosis

A

Fibrosing lung disease caused by inhalation of silicon dioxide (silica) particles

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16
Q

most commonly implicated particle in silicosis

A

Quartz

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17
Q

Silica occurs in both crystalline and amorphous forms. _____ is more fibrogenic. ______ is more pathogenic.

A
  • Crystalline
  • Amorphous
18
Q

Pathogenesis of silicosis

A

macrophages phagocytize a silica particle → become activated → inflammatory mediators released → fibrosis

19
Q
A

Silicosis

(Black Arrow: dense fibrosis)

20
Q
A

silicotic nodule composed of dense collagenous fibrous connective tissue

(these coalesce)

21
Q
A

Silicotic nodule w/birefringent silica particles

22
Q

3 Occupations at risk for silicosis

A
  1. miners
  2. Sand blasters
  3. Quartz stone cutters
23
Q

CXR findings for silicosis

A

Fine nodularity in the upper zones of the lung

24
Q

silicosis is associated with an increased susceptibility to ______

A

tuberculosis

(“slow to kill” disease; most patients do not developed dyspnea until they have massive fibrosis)

25
Define asbestos
a family of hydrated silicates that form fibers
26
Occupational exposure to asbestos is linked to ______(6).
1. pleural plaques 2. Pleural effusion 3. Pulmonary interstitial fibrosis (asbestosis) 4. Lung carcinoma 5. Mesothelioma 6. Laryngeal, ovarian malignancies
27
The oncogenicity related to asbestos-related disease is due to the _____.
Generation of free radicals and adsorption of carcinogens on to the fibers
28
asbestosis
29
Define asbestosis
interstitial fibrosis due to asbestos exposure
30
Asbestos bodies (golden-brown beaded batons)
31
pleural plaques due to asbestos exposure
32
Define hypersensitivity pneumonitis
Immune-mediated lung disorders caused by exposure to inhaled organic antigens (bacterial, fungal or animal proteins)
33
Hypersensitivity pneumonitis is also known as
Extrinsic allergy alveolitis (important to recognize these disorders early)
34
Farmer's lung: source of antigen
Thermophilic actinomycetes spores in warm moist air
35
Pigeon breeder's lung: source of antigen
Proteins from serum, excreta or feathers of birds
36
Humidifier lung: source of Antigen | (air conditioner)
thermophilic bacteria and heated water reservoirs
37
hypersensitivity pneumonitis pathogenesis: type III hypersensitivity
complement and Igs in vessel walls
38
Hypersensitivity pneumonitis pathogenesis: Type IV hypersensitivity (delayed type: after 2-3 days)
noncaseating granulomas
39
Hypersensitivity pneumonitis clinical symptoms: acute attack (4)
1. Fever 2. Dyspnea 3. Cough 4. Leukocytosis
40
CXR findings: hypersensitivity pneumonitis
Interstitial infiltrates
41
Hypersensitivity pneumonitis: Long-term exposure symptoms
Progressive respiratory failure with a restrictive pattern
42
hypersensitivity pneumonitis: noncaseating interstitial granuloma containing a Langhans giant cell (yellow arrow) consistent with a type IV hypersensitivity reaction. (If exposure to the offending antigen persists, then the patient can go on to develop interstitial fibrosis, obliterative bronchiolitis and honeycombing).