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2 - CPR (pulmonary) > Respiratory Pathology - 1 > Flashcards

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
Q

Where are pulmonary sequestrations usually found?

A

Left lower lung lobe

26
Q

What 2 things categorize pulmonary sequestrations?

A
  1. NO connection to tracheobronchial tree

2. Independent arterial supply (NOT pulmonary vasculature)

27
Q

What 2 things categorize pulmonary sequestrations?

A
  1. NO connection to tracheobronchial tree

2. Independent arterial supply (not pulmonary vasculature)

28
Q

What are the unique things about Intralobar Pulmonary Sequestrations?

A
  • Occurs in children/adults

= Budding of lung tissue occurs BEFORE pleura is established

29
Q

What are Intralobar pulmonary sequestrations prone to?

A

Infections and abscesses because there is a lack of airway perfusion

30
Q

What are the unique things about Extralobar pulmonary sequestrations?

A
  • Occurs after birth and with other congenital anomalies

= Budding occurs AFTER pleura is established

31
Q

Atelectasis

A

Acquired incomplete expansion of lung parenchyma

32
Q

Acquired incomplete expansion of lung parenchyma

A

Atelectasis

33
Q

What are 3 types of Atelectasis?

A
  1. Resorption (obstructive)
  2. Compression
  3. Contraction
34
Q

Pink material (interstitial, proteinaceous fluid) in alveolar spaces

A

Pulmonary edema

35
Q

Pulmonary edema can be caused by pressure gradients. What are the 2 options?

A
  • Pushing out (increased hydrostatic pressure)

- Leaking out (decreased oncotic pressure)

36
Q

What are examples of when Pulmonary edema due to pressure gradients can occur?

A
  • Pushing out = LEFT SIDED HEART FAILURE

- Leaking out = hypoalbuminemia

37
Q

What else besides pressure gradients can cause pulmonary edema?

A
  • Alveolar wall injury - pneumonia/sepsis, smoke, aspiration
  • High altitude
  • Brain injury
38
Q

With pulmonary edema there is increased blood in the capillaries. What will this result in?

A

Microhemorrhage

= Scattered hemosideren laden Macrophages in the alveoli that are known as HF cells

39
Q

With pulmonary edema there is increased blood in the capillaries. What will that result in?

A

Microhemorrhage

= Scattered hemosideren laden Macrophages in alveoli that are known as HF cells

40
Q

Acute Lung Injury

A

Acute onset
Hypoxemia
Bilateral infiltrates
No signs of cardiac failure

41
Q

Acute Respiratory Distress Syndrome

A

Worsening hypoxemia

42
Q

Diffuse Alveolar Damage

A

Histologic manifestations of ARDS

43
Q

What are the stages of ARDS?

A

Stage 1 = Exudative
Stage 2 = Proliferative
Stage 3 = Fibrotic

44
Q

Stage 1 ARDS

A

Exudative

- Edema, hyaline membranes, neutrophils

45
Q

Stage 2 ARDS

A

Proliferative

- fibroblast proliferation, early fibrosis

46
Q

Stage 3 ARDS

A

Fibrotic

- Fibrosis and loss of alveolar architecture

47
Q

After stage 3 ARDS, what are the options?

A

Resolution of normal structure/function OR

Fibrosis = IRREVERSIBLE destruction of structures

48
Q

What makes up hyaline membranes?

A

Edema + fibrin + cell debris

49
Q

With ARDS, what happens in the cascade?

A
  • Endothelial activation
  • Neutrophils move into alveolus
  • Fluid accumulates in alveolus
    = Formation of hyaline membranes
50
Q

What makes up hyaline membranes?

A

Edema + fibrin + cell debris

2 - CPR (pulmonary) (26 decks)

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