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MHD Pulm Heme Block > Pulm Path I > Flashcards

Pulm Path I Flashcards

1
Q

What are type I pneumocytes for?

A

-gas exchange

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2
Q

What are type II pneumocytes for?

A
  • secrete surfactant

- stem cells

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3
Q

What do alveolar macrophages do?

A

ingest foreign matter

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4
Q

What are endothelial cells for?

A

-line blood vessels, gas exchange

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5
Q

Mucociliary escalator

A
  • Goblet cells secrete mucus

- Cilia and goblet cells exist till the end of the respiratory bronchioles

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6
Q

Where does lung begin to grow?

A

From the foregut as a laryngotracheal tube during the 4th week. It undergoes dichotomous branching at that point.

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7
Q

The Lung’s stages of development

A
  • Embryonic
  • Pseudoglandular
  • Canalicular
  • Saccular
  • Alveolar
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8
Q

Clinical presentation of lung agenesis or hypoplasia

A
  • dec. intrathoracic space and breathing movements

- associated with prolonged oligohydramnios

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9
Q

What are some trachea or bronchial anomalies?

A
  • atresia
  • stenosis
  • fistulas
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10
Q

What is bronchogenic cyst?

A

foregut buds that become separated and disconnected from the tracheobronchial tree
-enlarges progressively, forming a cystic mass

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11
Q

What is congenital cystic adenomatoid Malformation?

A

-Also known as [Congenital Pulmonary Airway Malformation] (CPAM)
-Hamartomatous lesions = usually lower lobes
Type 1 - 5 (type 1 most common)
-Classification based on size and level of origin of cysts

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12
Q

What is a hamartoma?

A

Benign, focal malformation composed of tissue elements normally found at that site, but which are growing in a disorganized mass

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13
Q

Pulmonary sequestration

A

Discrete mass of lung tissue without connection to the airway system

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14
Q

Resorption shifts the mediastinum [away or toward] the affected lung?

A

Towards

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15
Q

Compression shifts the mediastinum [away or toward] the affected lung?

A

Away

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16
Q

Where do items tend to lodge in the lung?

A

Right Lower lobe

17
Q

Signs/symptoms of Acute Lung Injury (ALI)

A
  • Acute onset of dyspnea
  • Hypoxemia
  • Development of bilateral pulmonary infiltrates in absence of cardiac failure
  • SEVERE ALI CAN PROGRESS TO ARDS
18
Q

Acute Respiratory Distress (ARDS) Signs/Symptoms

A
  • rapid onset of resp. insufficiency
  • cyanosis
  • severe arterial hypoxemia (refractory to oxygen therapy)
  • possible progression to multisystem organ damage
19
Q

ARDS Synonyms

A
  • Adult resp. distress syndrome
  • Acute lung injury?
  • Traumatic wet lung
  • Noncardiogenic pulmonary edema
  • Adult hyaline membrane disease
20
Q

Etiology of ARDS

A
  • sepsis
  • diffuse pulmonary infections
  • gastric aspiration
  • mechanical trauma, head injuries
21
Q

Etiology of ARDS (with mnemonic)

A

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

22
Q

ARDS Onset

A

24 - 72 hours after precipitating event

23
Q

Approach to ARDS Dx

A

clinical history, imaging studies (x-ray, CT), bronchoscopy

24
Q

Treatment for ARDS

A

treat underlying condition and supportive care

25
Q

ARDS on histology is known as:

A

Diffuse Alveolar Damage

26
Q

Histology of ARDS

A
  • pneumoncyte and endothelial cell necrosis
  • edema
  • Hyaline membrane formation
  • Organizing interstitial fibrosis and type 2 pneumocyte proliferation
27
Q

Two possible outcomes of ARDS

A
  • Restoratoin of normal lung architecture

- Progression to fibrosis (endstage honeycomb fibrosis)

28
Q

Phases of ARDS on pathology

A
  • Early exudative phase (acute)
  • Subacute proliferative phase (organizing)
  • Fibrotic phase (late)
29
Q

Neonatal Respiratory Distress (NRD) Syndrome synonyms

A
  • Infant Resp. Distress syndrome (IRDS)
  • Resp. Distress syndrome of newborn
  • Hyaline membrane disease
30
Q

Etiology of NRDS

A
  • Fetal injury during delivery
  • aspiration of blood or amniotic fluid
  • cord compression
  • excessive sedation of mother
  • hyaline membrane disease (most common)
31
Q

Predisposing factors to NRDS

A
  • prematurity
  • maternal diabetes
  • C-section
32
Q

Main problem in NRDS

A

Insufficient pulmonary surfactant production resulting in failure of lungs to inflate after birth

33
Q

Surfactant characteristics

A
  • synthesized in type II pneumocyte
  • Composed of phosphatidylcholine (lecithin)
  • stabilizes lung by reducing surface tension
  • production starts as early as 20 weeks, but not enough till 34 weeks
34
Q

Treatment of NRDS

A
  • Delay labor if possible to allow lung maturity
  • administer exogenous surfactant
  • assess fetal lung maturation (Lecithin:sphingomyelin ratio over 2:1
35
Q

Acute Interstitial Pneumonia is also known as:

A

Harman-Rich syndrome

36
Q

Acute Interstitial Pneumonia clinical presentation

A
  • adults with influenza-like illness followed by SOB
  • clinically similar to ARDS but no known cause
  • death usually within 2 months
  • histologically: brisk interstitial fibroblastic proliferation

MHD Pulm Heme Block (11 decks)

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