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CPR Exam 2 > Pulmonary Pathology Part 1 > Flashcards

Pulmonary Pathology Part 1 Flashcards

1
Q

What are the requirements for normal fetal lungs to develop?

A
  • Space in thoracic cavity

- Ability to inhale (chest wall must be able to move and enough material must be present to inhale)

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2
Q

What is the process of airway breathing?

A
  • Larger airways conduct air to the terminal acinar units for proper gas exchange
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3
Q

Why does gas exchange occur in the terminal acinar units?

A
  • There are thin walls with high vascularity
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4
Q

What is most of the lung volume made up of?

A
  • Pulmonary parenchyma
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5
Q

What does the normal structure of the alveolar space consist of?

A
  • Capillaries with associated endothelium
  • Type 1 pneumocytes where gas exchange occurs
  • Type 2 pneumocytes that produce surfactant and can replace type 1 pneumocytes during times of destruction
  • Alveolar pores which allow aeration but also bacteria/cells/exudate to travel between cells
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6
Q

What are the alveolar pores of Kohn?

A
  • Holes that allow the travel of small material like bacteria, cells, or exudate
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7
Q

What are some congenital pulmonary anomalies?

A
  • Pulmonary hypoplasia
  • Foregut cysts
  • Congenital pulmonary adenomatoid malformation (CPAM/CCAM)
  • Pulmonary sequestration
  • Tracheoesophageal fistuila
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8
Q

What is pulmonary hypoplasia?

A
  • Reduced space in the thoracic cavity causes the lungs to be underdeveloped
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9
Q

What is another congenital defect can cause pulmonary hypoplasia?

A
  • Diaphragmatic hernia (viscera is taking up space in thoracic cavity)
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10
Q

What are some causes of pulmonary hypoplasia?

A
  • Oligohydramnios (renal agenesis)
  • Airway malformation (tracheal stenosis)
  • Chest wall motion disorders
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11
Q

What is the mortality of pulmonary hypoplasia?

A
  • Up to 95%

- If lung weight is <40%, immediate death occurs

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12
Q

What is a foregut cyst?

A
  • A detached outpouching of foregut
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13
Q

Where is a foregut cyst typically seen?

A
  • Along hilum and mediastinum
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14
Q

When are foregut cysts found?

A
  • Often found incidentally, usually when there is complication
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15
Q

What are some complications of foregut cysts?

A
  • Rupture
  • Infection
  • Airway compression
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16
Q

What is the cure for foregut cysts?

A
  • Excision of the cyst
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17
Q

What is congenital pulmonary adenomatoid malformation (CPAM)?

A
  • “Arrested development” of pulmonary tissue with formation of intrapulmonary cystic masses
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18
Q

Where are CPAMs found?

A
  • They communicate with the tracheobronchial tree
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19
Q

How are CPAMs found?

A
  • Fetal ultrasound
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20
Q

What is the mortality with CPAMs?

A
  • Could be deadly due to hydrops or pulmonary hypoplasia

- Could be asymptomatic throughout childhood can get infected later in life

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21
Q

What are pulmonary sequestrations?

A
  • Non-Functioning lung tissue that forms as an aberrant accessory “lung bud”
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22
Q

Where would a pulmonary sequestration typically be found?

A
  • Region of the left lower lobe
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23
Q

What is a pulmonary sequestration typically characterized by?

A
  • Lack of connection to the tracheobronchial tree

- Independent arterial supply

24
Q

Are pulmonary sequestrations intralobar or extralobar? Why?

A
  • Could be either

- Based on whether the budding occurs before or after the pleura is established

25
Q

Who typically presents with an intralobar pulmonary sequestration (ILS)?

A
  • Older children or adults
26
Q

What are some characteristics of an ILS?

A
  • May be difficult to detect due to being inside the lung lobe
  • Lack of airway perfusion makes it susceptible to infection and abscess formation
27
Q

Why can abscesses for in an ILS?

A
  • Lack of O2 to the neutrophils
28
Q

Who typically presents with an extralobar pulmonary sequestration (ELS) ?

A
  • Presents after birth with other congenital anomalies (like cardiac or GI)
29
Q

What are some characteristics of an ELS?

A
  • Looks like a mini lung
  • Has independent vessels, pleura, and possibly airways
  • Comes to attention as mass lesions in the chest or abdomen
30
Q

Do either the ILS or ELS have connections to the pulmonary vasculature or tracheobronchial tree?

A
  • NO
31
Q

What is atelectasis?

A
  • Incomplete expansion of lung parenchyma
32
Q

What are the three types of atelectasis?

A
  1. Resorption
  2. Compression
  3. Contraction
33
Q

What is resorption atelectasis?

A
  • Airway obstruction with gradual resorption of air reduces lung expansion
  • Anything distal to obstruction is where the air is reabsorbed
34
Q

What is compression atelectasis?

A
  • Accumulated material in pleural cavity compresses the lung parenchyma (pneumo/hemothorax)
35
Q

What is contraction atelectasis?

A
  • Fibrotic or other innate restrictive process in the pleura or peripheral lung restricts lung expansion
36
Q

What are some causes of pulmonary edema?

A
  • “Pushing out” (increase in pressure)
  • “Leaking out”
  • Injury to alveolar wall
  • Unsure mechanisms (neurogenic or high altitude)
37
Q

What are some of the physiological mechanisms behind pulmonary edema?

A
  • Increased hydrostatic pressure forces out fluid

- Decreased oncotic pressure loses fluid through equilibrium across a semipermeable membrane

38
Q

Where would we see high altitude pulmonary edema?

A
  • In people that went hiking in the mountains

- Most notoriously seen in people who climbed Everest and waited to stand on peak

39
Q

What is seen on histology in pulmonary edema?

A
  • Pink proteinaceous material in alveolar spaces due to congestion
40
Q

What is seen in pulmonary edema due to heart failure?

A
  • Microhemorrhage occurs in congested areas

- There are scattered hemosiderin-laden macrophages that accumulate

41
Q

What are “heart failure cells”?

A
  • Hemosiderin-laden macrophages due to their association with pulmonary congestion due to CHF
42
Q

What is the definition of acute lung injury?

A
  • Acute onset
  • Hypoxemia
  • Bilateral infiltrates
  • No evidence of cardiac failure
43
Q

What is the definition of acute respiratory distress syndrome?

A
  • Worsening hypoxia
44
Q

What is the definition of diffuse alveolar damage?

A
  • Histologic manifestation of ARDS
45
Q

What is seen in ARDS?

A
  • Abrupt onset of symptoms
  • Hypoxemia (PaO2/FiO2 <200)
  • Bilateral infiltrates
  • Non-cardiac in nature
46
Q

What is the cellular process of ARDS?

A
  • Endothelial activation
  • Adhesion/extravasation of neutrophils
  • Accumulation of intra-alveolar fluid and formation of hyaline membranes
  • Resolution of injury
47
Q

What are the components of hyaline membranes?

A
  • Edema
  • Fibrin
  • Cell debris
48
Q

What do hyaline membranes do to the aeration?

A
  • Decreased aeration causing hypoxemia (decreased PaO2/FiO2)
49
Q

What are the stages of progression in ARDS?

A
  1. Exudative
  2. Proliferative
  3. Fibrotic
50
Q

What is the exudative phase of ARDS?

A
  • Edema
  • Hyaline membranes
  • neutrophils
51
Q

What is the proliferative phase of ARDS?

A
  • Fibroblast proliferation
  • Organizing pneumonia
  • Early fibrosis
52
Q

What is the fibrotic phase of ARDS?

A
  • Extensive fibrosis

- Loss of normal alveolar architecture

53
Q

What are the two paths that could occur after the proliferative phase in ARDS?

A
  • Resolution

- Fibrosis

54
Q

What happens in the resolution phase of ARDS?

A
  • Restoration of normal cellular structure and function
55
Q

What happens in the fibrosis phase of ARDS?

A
  • Destruction and distortion of normal cellular structure

- Irreversible

56
Q

What is the pathologic diagnosis of ARDS?

A
  • Hyaline membranes
  • Interstitial edema
  • Epithelial necrosis

CPR Exam 2 (12 decks)

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