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*MHD Exam 6 > Pulmonary Path I > Flashcards

Pulmonary Path I Flashcards

1
Q

What is the difference between the type I and type II cells in alveoli?

A
  • Type I: squamous pneumocytes, responsible for gas exchange

- Type II: granular pneumocytes, secrete surfactant

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2
Q

How does the bronchial tree develop embryologically?

A

It develops as an outgrowth from the foregut and undergoes progressive dichotomous branching. (laryngotracheal tube –> tracheal buds –> bronchial buds –> further bifurcation/branching)

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3
Q

What is CCAM?

A

Congenital Cystic Adenomatoid Malformation (CCAM) - hamartomatous lesions, usually of the lower lobes; multiloculated cysts replace most of the lung parenchyma

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4
Q

Congenital hypoplasia is associated with:

A
  • prolonged oligohydramnios (decreased amniotic fluid production)
  • decreased intrathoracic space (leading to cystic disease and diaphragmatic hernia)
  • decreased breathing movements (leading to anencephaly and MSK disorders)
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5
Q

Acute lung injury is a spectrum of bilateral pulmonary damage which manifests as:

A
  • acute onset dyspnea
  • hypoxemia
  • development of bilateral pulmonary infiltrates in the absence of cardiac failure
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6
Q

What are the 2 main categories of the clinical causes of ALI?

A
  • Direct injury (pneumonia, aspiration, trauma, fat embolism, inhalation injury, reperfusion injury, drug overdose, near drowning)
  • Indirect injury (sepsis, severe trauma with shock, acute pancreatitis, drug overdose, uremia, DIC)
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7
Q

What is the etiology of ARDS?

A
  • A: aspiration, acute pancreatitis, air/amniotic fluid embolism
  • R: radiation
  • D: drug overdose, DIC, drowning
  • S: shock, sepsis, smoke inhalation
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8
Q

What are the phases of ARDs?

A
  • Early exudative phase (acute)
  • Subacute proliferative phase (organizing)
  • Fibrotic phase (late)
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9
Q

What are the classic signs of ARDS?

A

tachypnea, dyspnea, and cyanosis (due to hypoxemia); absence of cardiac dysfunction
*acute onset (within 24-72 hours of precipitating event)

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10
Q

What is seen on histology in ARDS?

A
  • hyaline membranes composed of dead pneumocytes, endothelial cells, and plasma proteins
  • widened septa with sparse inflammation
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11
Q

What happens (histologically/pathologically) during the late proliferative and fibrotic stages of ARDS?

A

more macrophages fill into the alveolar spaces; alveolar septa become widened due to deposition of fibrotic and proteinaceous material

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12
Q

The histologic manifestation of ARDS is ___________.

A

Diffuse Alveolar Damage (DAD)

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13
Q

What are the causes of respiratory distress in newborns?

A
  • hyaline membrane disease/RDS* (most common)
  • fetal injury during delivery
  • aspiration of amniotic fluid and blood
  • cord compression
  • excess sedation of the mother
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14
Q

What is the fundamental abnormality in RDS?

A

insufficient pulmonary surfactant production by immature lungs, resulting in failure of lungs to inflate after birth (disease of prematurity)

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15
Q

Surfactant can be secreted as early as ____ weeks gestation but is not produced in sufficient amounts until ____ weeks gestation.

A

20; 34

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16
Q

Describe the series of events that occur when surfactant is deficient.

A

increased alveolar surface tension –> resistance of alveoli to inflation –> surface collapse/atelectasis –> stress on alveolar wall leading to alveolar injury –> DAD/NRDS

17
Q

What are the predisposing factors to NRDS?

A
  • prematurity* (biggest factor)
  • maternal diabetes (insulin decr. production of surfactant)
  • C-section
18
Q

What is surfactant synthesis modulated by?

A
  • glucocorticoids (increase production)
  • insulin (decreases production)
  • labor (induces production)
  • prolactin
  • thyroxine
  • TGF-β
19
Q

How can NRDS be prevented?

A
  • delaying labor (if possible) to permit fetal lung maturity
  • prophylactic administration of exogenous surfactant to infants less than 28 weeks
  • assess maturation of fetal lungs via amniotic fluid and assays (lecithin:sphingomyelin ratio, or lamellar body counts)
20
Q

What is the difference in pathophysiology between ARDS and NRDS?

A
  • ARDS: imbalance of pro- and anti-inflammatory mediators

- NRDS: surfactant deficiency

21
Q

What is the difference in treatment of ARDS and NRDS?

A
  • ARDS: treating underlying cause + supportive care

- NRDS: CPAP, surfactant replacement, ventilator

22
Q

What are the potential long-term complications of the oxygen therapy used in NRDS?

A
  • retrolental fibroplasia (can lead to blindness)

- bronchopulmonary dysplasia (chronic, characterized by large alveoli)

23
Q

What are the acquired causes of atelectasis?

A
  • resorption/obstruction (asthma, COPD, bronchiectasis, aspiration, post-op patients)
  • compression (effusions, air, tumors, CHF)
  • contraction (fibrosis of lungs/pleura)
24
Q

Pneumothorax is most commonly associated with which conditions?

A

emphysema, asthma, TB

25
Q

What are the FIRST airways that participate in gas exchange?

A

respiratory bronchioles

26
Q

How do the primary bronchi differ from the trachea?

A

the primary bronchi have discontinuous cartilaginous plates, whereas the trachea has a C-shaped ring of cartilage

27
Q

How do the bronchioles differ from the trachea and bronchi?

A

Bronchioles lack cartilage and submucous glands.

28
Q

Which type of epithelium is found in the terminal bronchioles?

A

simple cuboidal

29
Q

The mucus escalator function is negatively affected by:

A
  • Smoking
  • Dusts
  • Low humidity
  • Mucostasis
  • Ciliary dyskinesia
30
Q

What is the most common tracheal or bronchial congenital anomaly?

A 
Type C (esophageal atresia with distal tracheoesophageal fistula): 
-Causes blind ending esophagus w/ infant choking on formula and persistently choking
31
Q

Which cytokines are chemotactic for PMNs?

A

TNF and IL8

32
Q

What are the mediastinal shifts associated with the different types of atelectasis?

A
  • Resorption/obstruction (asthma, COPD, bronchiectasis, aspiration): mediastinum shifts toward affected lung
  • Compression (effusions, air, tumors): mediastinum shifts away from affected lung

*MHD Exam 6 (20 decks)

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