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
Q

Define asbestos

A

a family of hydrated silicates that form fibers

26
Q

Occupational exposure to asbestos is linked to ______(6).

A
  1. pleural plaques
  2. Pleural effusion
  3. Pulmonary interstitial fibrosis (asbestosis)
  4. Lung carcinoma
  5. Mesothelioma
  6. Laryngeal, ovarian malignancies
27
Q

The oncogenicity related to asbestos-related disease is due to the _____.

A

Generation of free radicals and adsorption of carcinogens on to the fibers

28
Q
A

asbestosis

29
Q

Define asbestosis

A

interstitial fibrosis due to asbestos exposure

30
Q
A

Asbestos bodies (golden-brown beaded batons)

31
Q
A

pleural plaques due to asbestos exposure

32
Q

Define hypersensitivity pneumonitis

A

Immune-mediated lung disorders caused by exposure to inhaled organic antigens (bacterial, fungal or animal proteins)

33
Q

Hypersensitivity pneumonitis is also known as

A

Extrinsic allergy alveolitis

(important to recognize these disorders early)

34
Q

Farmer’s lung: source of antigen

A

Thermophilic actinomycetes spores in warm moist air

35
Q

Pigeon breeder’s lung: source of antigen

A

Proteins from serum, excreta or feathers of birds

36
Q

Humidifier lung: source of Antigen

(air conditioner)

A

thermophilic bacteria and heated water reservoirs

37
Q

hypersensitivity pneumonitis pathogenesis: type III hypersensitivity

A

complement and Igs in vessel walls

38
Q

Hypersensitivity pneumonitis pathogenesis: Type IV hypersensitivity

(delayed type: after 2-3 days)

A

noncaseating granulomas

39
Q

Hypersensitivity pneumonitis clinical symptoms: acute attack (4)

A
  1. Fever
  2. Dyspnea
  3. Cough
  4. Leukocytosis
40
Q

CXR findings: hypersensitivity pneumonitis

A

Interstitial infiltrates

41
Q

Hypersensitivity pneumonitis: Long-term exposure symptoms

A

Progressive respiratory failure with a restrictive pattern

42
Q
A

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).