Pulm Path I Flashcards

(36 cards)

1
Q

What are type I pneumocytes for?

A

-gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are type II pneumocytes for?

A
  • secrete surfactant

- stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do alveolar macrophages do?

A

ingest foreign matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are endothelial cells for?

A

-line blood vessels, gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mucociliary escalator

A
  • Goblet cells secrete mucus

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The Lung’s stages of development

A
  • Embryonic
  • Pseudoglandular
  • Canalicular
  • Saccular
  • Alveolar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical presentation of lung agenesis or hypoplasia

A
  • dec. intrathoracic space and breathing movements

- associated with prolonged oligohydramnios

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some trachea or bronchial anomalies?

A
  • atresia
  • stenosis
  • fistulas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is bronchogenic cyst?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pulmonary sequestration

A

Discrete mass of lung tissue without connection to the airway system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Towards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
ARDS on histology is known as:
Diffuse Alveolar Damage
26
Histology of ARDS
- pneumoncyte and endothelial cell necrosis - edema - Hyaline membrane formation - Organizing interstitial fibrosis and type 2 pneumocyte proliferation
27
Two possible outcomes of ARDS
- Restoratoin of normal lung architecture | - Progression to fibrosis (endstage honeycomb fibrosis)
28
Phases of ARDS on pathology
- Early exudative phase (acute) - Subacute proliferative phase (organizing) - Fibrotic phase (late)
29
Neonatal Respiratory Distress (NRD) Syndrome synonyms
- Infant Resp. Distress syndrome (IRDS) - Resp. Distress syndrome of newborn - Hyaline membrane disease
30
Etiology of NRDS
- Fetal injury during delivery - aspiration of blood or amniotic fluid - cord compression - excessive sedation of mother - hyaline membrane disease (most common)
31
Predisposing factors to NRDS
- prematurity - maternal diabetes - C-section
32
Main problem in NRDS
Insufficient pulmonary surfactant production resulting in failure of lungs to inflate after birth
33
Surfactant characteristics
- 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
Treatment of NRDS
- Delay labor if possible to allow lung maturity - administer exogenous surfactant - assess fetal lung maturation (Lecithin:sphingomyelin ratio over 2:1
35
Acute Interstitial Pneumonia is also known as:
Harman-Rich syndrome
36
Acute Interstitial Pneumonia clinical presentation
- 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