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MHD > Normal Lung, Congenital Abnormalities, Acute Lung Injury, and RDS > Flashcards

Normal Lung, Congenital Abnormalities, Acute Lung Injury, and RDS Flashcards

1
Q

How are the bronchi structurally distinct from the bronchioles?

A

Bronchi have submucosal glands and cartilage.

Bronchioles do not

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2
Q

In the primary bronchi, what are the layers from lumen –> cartilage?

A 
Lumen
Pseudostratified columnar epithelium
Lamina propria
Muscularis
Submucosa (with glands)
Cartilage
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3
Q

Describe the normal sequence from terminal bronchioles –> alveoli?

A 
Terminal bronchioles
Respiratory bronchioles
Alveolar duct
Alveolar sac
Alveoli
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4
Q

What is the main function of type I pneumocytes?

A

Gas exchange

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5
Q

What is the main function of type II pneumocytes?

A

Surfactant production

Can divide and regenerate type I cells in cases of injury

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6
Q

What is the main function of the mucociliary escalator?

A

Goblet cells secrete mucus and cilia rhythmically beat upwards to push mucus out of airway

Reaches as far down as the respiratory bronchioles

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7
Q

What might be a cause of lung agenesis or hypoplasia?

A

Oligohydramnios (kidney agenesis) –> low amniotic fluid –> bad lung development

Could also result from decreased intrathoracic space

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8
Q

What are Bronchogenic cysts?

A

Foregut buds that become disconnected from the tracheobronchial tree, enlarge over time, and form a cystic mass

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9
Q

What is CCAM? What is seen on gross imaging of lungs? Histology?

A

Congenital Cystic Adenomatoid Malformation

See multiloculated cysts all over the lungs, replacing the entire lobes

The alveoli are lined by epithelium more similar to bronchiole epithelium (much thicker)

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10
Q

What is pulmonary sequestration? What are the consequences of this happening?

A

Discrete mass of lung tissue without connection to the airway system
May be intralobar or extralobar

Lots of mucus will plug up the mucosa
Inflammation
Recurrent respiratory infections

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11
Q

What are some causes of atelectasis in adults?

A

Resorption
Compression
Contraction

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12
Q

Describe Resorption Atelectasis

A

Some obstruction in the respiratory tract blocks some alveoli. That part of the lung resorbs inward and shrinks.

Mediastinum shifts TOWARDS the affected lung

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13
Q

Describe Compression Atelectasis

A

Something in the pleura (air, effusion) is compressing the lung space

Mediastinum shifts AWAY from the affected lung

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14
Q

Describe Contraction Atelectasis

A

Lung parenchyma is destroyed and you get fibrosis of the lung

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15
Q

Describes the different types and the pathophysiology of Pneumothorax

A

Could be spontaneous or traumatic

Causes compression, collapse, and atelectasis, leading to respiratory distress

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16
Q

If a solid object is aspirated, which bronchus is is most likely to fall down? Which lobe is it likely to end up in?

A

Likely to fall down R mainstem bronchus and lodge in the R lower lobe

17
Q

What is the most common cause of pulmonary edema?

A

L sided heart failure

18
Q

What is the normal weight of a lung?

A

350-450 g

19
Q

What does pulmonary edema look like on histology?

A

All the normal air spaces are pink with fluid. Vessels are highly congested

20
Q

What are the three main characteristics of acute lung injury (non-cardiogenic pulmonary edema)?

A
  • Acute onset dyspnea
  • Hypoxemia
  • Bilateral pulmonary infiltrates in absence of cardiac failure
21
Q

What is ARDS?

A

Acute Respiratory Distress Syndrome

Rapid onset of life threatening respiratory insufficiency
Cyanosis
Severe arterial hypoxemia
May progress to organ failure

22
Q

List the common causes of ARDS

A

A- Aspiration, Acute Pancreatitis, Air/Amniotic fluid embolism
R- Radiation
D- DIC, drugs, drowning
S- Sepsis, shock, smoke inhalation

23
Q

How do you treat ARDS?

A

Treat the cause and give the patient symptomatic management

24
Q

ARDS is a clinical term. What do pathologists say to describe the same phenomenon?

A

DAD = Diffuse Alveolar Damage

25
Q

Describe the pathogenesis of Acute Lung Injury

A

Macrophages enter, release TNF and IL-8.
PMNs are recruited, they degranulate, producing proteases and leukotrienes.

Causes injury to endothelial cells, leading to protein leakage in the alveolar space.
Hyaline membrane forms

26
Q

How does ARDS appear on histological stain?

A

Hyaline membrane formation around the alveolar spaces (smudgy pink crayon appearance)

Septa are widened

27
Q

How does ARDS progress over time?

A

Over time, progresses to a late proliferative and a fibrotic stage

28
Q

What is the primary cause of neonatal respiratory distress syndrome?

A

Deficient surfactant production

29
Q

What are some predisposing factors to neonatal RDS?

A

Prematurity
Maternal diabetes
C-section

30
Q

What is the main function of surfactant?

A

Reduce surface tension in the alveoli, keeping them inflated

31
Q

About when should the fetus be producing sufficient amounts of surfactant?

A

34 weeks gestation

32
Q

How can surfactant production be measured prenatally?

A

Look at the amniotic fluid L:S (lethicin:sphingomyelin) ratio
Above 2:1 means the baby is ready for delivery

33
Q

Describe the pathogenesis of Neonatal RDS

A

No surfactant production leads to atelectasis. V/Q mismatch in the lung will cause pulmonary vasoconstriction. Leads to hypoxia and acidosis.

Endothelial and epithelial damage occur, leading to plasma leak and buildup of hyaline membranes

34
Q

How does maternal diabetes affect neonatal RDS?

A

High glucose levels lead to high insulin production from the fetal pancreas, which may decrease surfactant production

35
Q

How do glucocorticoids affect neonatal RDS?

A

Babies delivered by C section are not subjected to the stress (and glucocorticoid release) associated with vaginal delivery. The glucocorticoids increase production of surfactant, so babies delivered by C section do not have that stimulus to make more surfactant

36
Q

How do you treat neonatal RDS?

A

Best to prevent it by delaying delivery as long as you can to allow for fetal lung maturity. Once the infant is born, you can give exogenous surfactant to treat

37
Q

What is Acute Interstitial Pneumonia? When is it diagnosed?

A

You cannot diagnose this disease until you have ruled out all other causes.

Has the same histology and clinical features as acute ARDS

MHD (57 decks)

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