Respiratory Pathology - 1 Flashcards

1
Q

What 2 things does the normal fetal lung development require?

A
  1. Space in the thoracic cavity

2. Ability of fetus to inhale amniotic fluid with chest wall movements

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2
Q

What 2 things does the normal fetal lung development require?

A
  1. Space in the thoracic cavity

2. Ability of fetus to inhale amniotic fluid with chest wall movements

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3
Q

What is the respiratory tract histology features?

A
  • Ciliated respiratory epithelium
  • Smooth muscle
  • Submucosal glands
  • Cartilage
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4
Q

What is the predominant histo in the respiratory system?

A

Lung parenchyma - bronchiole, alveoli, pneumocytes

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5
Q

What do Type 1 pneumocytes do?

A

Gas exchange

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6
Q

What do Type 2 pneumocytes do?

A

Produce surfactant and replace Type 1 pneumocytes

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7
Q

What do Alveolar pores (of kohn) do?

A

Allow aeration but also bacteria, cells, fluid to travel between alveoli

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8
Q

Pulmonary Hypoplasia can be caused by decreased space in the thoracic cavity. What is an example of when that occurs?

A

Diaphragmatic hernia

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9
Q

Pulmonary Hypoplasia can be caused by an impaired ability of the fetus to inhale. What are 3 examples of when that can occur?

A
  • Oligohydramnios (decreased fluid/renal agenesis)
  • Airway malformation (tracheal stenosis)
  • Chest wall motion disorders (arthrogryposis)
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10
Q

What is the outlook for pulmonary hypoplasia?

A

High mortality especially if the lung weight is < 40%

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11
Q

What are Foregut Cysts?

A

Detached outpouchings of foregut - can be respiratory, esophageal or gastroenteric

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12
Q

Where are foregut cysts commonly seen?

A

Along hilum and mediastinum

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13
Q

Is the histology of foregut cysts the same as the tissue that surrounds it?

A

Yes

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14
Q

What are possible complications of foregut cysts?

A

Rupture, airway compression, infection

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15
Q

Treatment for Foregut cysts?

A

Excision is curative

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16
Q

CPAM

A

Congenital Pulmonary Airway Malformation

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17
Q

What is CPAM?

A

Arrested development of pulmonary tissue with the formation of intrapulmonary cysts

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18
Q

What is CPAM?

A

Arrested development of pulmonary tissue with the formation of intrapulmonary cystic masses

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19
Q

What does CPAM depend on?

A

Stage of arrest

  • stage 0 = trachebronchial
  • stage 1 = bronchial
  • stage 2 = bronchiolar
  • stage 3 = alveolar duct
  • stage 4 = distal acinar
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20
Q

CPAM communicates with?

A

Tracheobronchial tree and pulmonary vasculature

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21
Q

How is CPAM detected?

A

Fetal ultrasound

22
Q

What are possible complications of CPAM?

A

Deadly due to hydrops or pulmonary hypoplasia

Infected later on

23
Q

What are the 2 types of Pulmonary Sequestrations?

A

Intralobar

Extralobar

24
Q

What are pulmonary sequestrations?

A

NONfunctioning lung tissue that forms an accessory lung bud

25
Where are pulmonary sequestrations usually found?
Left lower lung lobe
26
What 2 things categorize pulmonary sequestrations?
1. NO connection to tracheobronchial tree | 2. Independent arterial supply (NOT pulmonary vasculature)
27
What 2 things categorize pulmonary sequestrations?
1. NO connection to tracheobronchial tree | 2. Independent arterial supply (not pulmonary vasculature)
28
What are the unique things about Intralobar Pulmonary Sequestrations?
- Occurs in children/adults | = Budding of lung tissue occurs BEFORE pleura is established
29
What are Intralobar pulmonary sequestrations prone to?
Infections and abscesses because there is a lack of airway perfusion
30
What are the unique things about Extralobar pulmonary sequestrations?
- Occurs after birth and with other congenital anomalies | = Budding occurs AFTER pleura is established
31
Atelectasis
Acquired incomplete expansion of lung parenchyma
32
Acquired incomplete expansion of lung parenchyma
Atelectasis
33
What are 3 types of Atelectasis?
1. Resorption (obstructive) 2. Compression 3. Contraction
34
Pink material (interstitial, proteinaceous fluid) in alveolar spaces
Pulmonary edema
35
Pulmonary edema can be caused by pressure gradients. What are the 2 options?
- Pushing out (increased hydrostatic pressure) | - Leaking out (decreased oncotic pressure)
36
What are examples of when Pulmonary edema due to pressure gradients can occur?
- Pushing out = LEFT SIDED HEART FAILURE | - Leaking out = hypoalbuminemia
37
What else besides pressure gradients can cause pulmonary edema?
- Alveolar wall injury - pneumonia/sepsis, smoke, aspiration - High altitude - Brain injury
38
With pulmonary edema there is increased blood in the capillaries. What will this result in?
Microhemorrhage | = Scattered hemosideren laden Macrophages in the alveoli that are known as HF cells
39
With pulmonary edema there is increased blood in the capillaries. What will that result in?
Microhemorrhage | = Scattered hemosideren laden Macrophages in alveoli that are known as HF cells
40
Acute Lung Injury
Acute onset Hypoxemia Bilateral infiltrates No signs of cardiac failure
41
Acute Respiratory Distress Syndrome
Worsening hypoxemia
42
Diffuse Alveolar Damage
Histologic manifestations of ARDS
43
What are the stages of ARDS?
Stage 1 = Exudative Stage 2 = Proliferative Stage 3 = Fibrotic
44
Stage 1 ARDS
Exudative | - Edema, hyaline membranes, neutrophils
45
Stage 2 ARDS
Proliferative | - fibroblast proliferation, early fibrosis
46
Stage 3 ARDS
Fibrotic | - Fibrosis and loss of alveolar architecture
47
After stage 3 ARDS, what are the options?
Resolution of normal structure/function OR | Fibrosis = IRREVERSIBLE destruction of structures
48
What makes up hyaline membranes?
Edema + fibrin + cell debris
49
With ARDS, what happens in the cascade?
- Endothelial activation - Neutrophils move into alveolus - Fluid accumulates in alveolus = Formation of hyaline membranes
50
What makes up hyaline membranes?
Edema + fibrin + cell debris