RESPIRATORY: 606 - 607 Flashcards

1
Q

What are pneumoconioses?

A

Chronic occupational exposure to small fibrogenic particles that leads to interstitial fibrosis

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2
Q

Give 4 examples of pneumoconioses.

A
  1. Asbestosis
  2. Coal workers’ pneumoconiosis
  3. Silicosis
  4. Berylliosis
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3
Q

What does pneumoconiosis increase the risk of?

A
  1. Cor pulmonale

2. Caplan syndrome (rheumatoid arthritis and pneumoconioses with intrapulmonary nodules)

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4
Q

What professions are associated with asbestosis?

A

Shipbuilding, roofing, plumbing

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5
Q

Describe the plaques found in asbestosis.

A

Ivory white, calcified pleural plaques

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6
Q

Asbestosis is associated with increased risk of what 2 cancers.

A

Bronchogenic carcinoma&raquo_space; mesothelioma

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7
Q

Does asbestosis tend to affect the upper or lower lobes?

A

Lower

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8
Q

What do asbestos (ferruginous) bodies look like?

A

Golden-brown fusiform rods resembling dumbbells; has iron deposits

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9
Q

What accumulates in macrophages in coal workers’ pneumoconiosis?

A

Carbon

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10
Q

Are the lung in coal workers’ pneumoconiosis shrunken or swollen?

A

Shrunken (from inflammation and fibrosis)

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11
Q

What is another name for coal workers’ pneumoconiosis?

A

Black lung disease

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12
Q

Does coal workers’ pneumoconiosis tend to affect the upper or lower lobes?

A

Upper

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13
Q

What is anthracosis?

A

Asymptomatic condition found in many urban dwellers exposed to sooty air –> collection of carbon laden macrophages in the lung from mild exposure

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14
Q

What is silicosis associated with?

A

Foundries, sandblasting, mines

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15
Q

Describe the pathophysiology of silicosis.

A

Macrophages respond to silica and release fibrogenic factors leading to fibrosis

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16
Q

Why is silicosis thought to relate to increased risk of TB?

A

Silica may disrupt phagolysosomes and impair macrophages increasing susceptibility to TB infection

17
Q

What is the only pneumoconiosis associated with an increased risk of TB?

18
Q

Does silicosis tend to affect the upper or lower lobes?

19
Q

Describe the hilar lymph nodes in silicosis.

A

“Eggshell” calcification

20
Q

What two occupations are at increased risk of berylliosis?

A
  1. Beryllium miners

2. Workers in aerospace industry

21
Q

In what ways is berylliosis similar to sarcoidosis?

A

Both present with noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs

22
Q

Berylliosis increase the risk of what?

A

Lung cancer

23
Q

Describe the pathophysiology in neonatal respiratory distress syndrome.

A

Surfactant deficiency –> increased surface tension –> alveolar collapse

24
Q

What is predictive of neonatal respiratory distress syndrome as a lab test?

A

Lecithin:sphingomyelin ratio < 1.5 in amniotic fluid

25
Why is there a risk of patent ductus arteriosus in neonatal respiratory distress syndrome?
Persistently low O2 tension
26
Therapeutic supplemental O2 for NRDS can result in what sort of damage?
Free radical damage: 1. Retinopathy of prematuriy 2. Bronchopulmonary dysplasia
27
How can we treat neonatal respiratory distress syndrome?
1. Maternal steroids before birth | 2. Artificial surfactant for infant
28
What are 3 risk factors for NRDS?
1. Prematurity 2. Maternal diabetes 3. C-section delivery
29
Why is maternal diabetes a risk factor for NRDS?
Increased sugars --> increased fetal insulin --> insulin inhibits surfactant production
30
Why is C-section delivery a risk factor for NRDS?
Decreased release of glucocorticoids With a normal delivery, there is release of glucocorticoids (stress hormone) which increases production of surfactant and causes already made surfactant to be released by type II pneumocytes into the lung
31
What are some of the clinical features of NRDS?
1. Increased respiratory effort after birth 2. Tachypnea with use of accessory muscles 3. Grunting 4. Hypoxemia with cyanosis 5. Diffuse granularity of lung on X ray
32
What are some of the causes of acute respiratory distress syndrome?
1. Trauma 2. Sepsis 3. Shock 4. Gastric aspiration 5. Uremia 6. Acute pancreatitis 7. Amniotic fluid embolism
33
Describe the pathophysiology in acute respiratory distress syndrome.
Diffuse alveolar damage --> increase alveolar capillary permeability --> protein-rich leakage into alveoli and noncardiogenic pulmonary edema --> eventual formation of intra-alveolar hyaline membrane
34
What are 2 problems resulting from the formation of hyaline membrane?
1. Thickened diffusion membrane leads to hypoxemia and cyanosis 2. Membranes are sticky and increase the surface tension of the air sacs leading to diffuse collapse
35
What is the initial damage of ARDS due to?
Activation of neutrophils induces protease mediated and free radical damage to type I and type II pneumocytes Also activates coagulation cascade
36
Compare FEV1/FVC in normal vs. obstructive vs. restrictive lung disease.
Normal = 80% Obstructive < 80% Restrictive > 80%