Pulm Path I Flashcards
What are type I pneumocytes for?
-gas exchange
What are type II pneumocytes for?
- secrete surfactant
- stem cells
What do alveolar macrophages do?
ingest foreign matter
What are endothelial cells for?
-line blood vessels, gas exchange
Mucociliary escalator
- Goblet cells secrete mucus
- Cilia and goblet cells exist till the end of the respiratory bronchioles
Where does lung begin to grow?
From the foregut as a laryngotracheal tube during the 4th week. It undergoes dichotomous branching at that point.
The Lung’s stages of development
- Embryonic
- Pseudoglandular
- Canalicular
- Saccular
- Alveolar
Clinical presentation of lung agenesis or hypoplasia
- dec. intrathoracic space and breathing movements
- associated with prolonged oligohydramnios
What are some trachea or bronchial anomalies?
- atresia
- stenosis
- fistulas
What is bronchogenic cyst?
foregut buds that become separated and disconnected from the tracheobronchial tree
-enlarges progressively, forming a cystic mass
What is congenital cystic adenomatoid Malformation?
-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
What is a hamartoma?
Benign, focal malformation composed of tissue elements normally found at that site, but which are growing in a disorganized mass
Pulmonary sequestration
Discrete mass of lung tissue without connection to the airway system
Resorption shifts the mediastinum [away or toward] the affected lung?
Towards
Compression shifts the mediastinum [away or toward] the affected lung?
Away
Where do items tend to lodge in the lung?
Right Lower lobe
Signs/symptoms of Acute Lung Injury (ALI)
- Acute onset of dyspnea
- Hypoxemia
- Development of bilateral pulmonary infiltrates in absence of cardiac failure
- SEVERE ALI CAN PROGRESS TO ARDS
Acute Respiratory Distress (ARDS) Signs/Symptoms
- rapid onset of resp. insufficiency
- cyanosis
- severe arterial hypoxemia (refractory to oxygen therapy)
- possible progression to multisystem organ damage
ARDS Synonyms
- Adult resp. distress syndrome
- Acute lung injury?
- Traumatic wet lung
- Noncardiogenic pulmonary edema
- Adult hyaline membrane disease
Etiology of ARDS
- sepsis
- diffuse pulmonary infections
- gastric aspiration
- mechanical trauma, head injuries
Etiology of ARDS (with mnemonic)
A - aspiration, acute pancreatitis, air/amniotic fluid embolism
R - radiation
D - drug overdose, DIC, drowning
S - shock, sepsis, smoke inhalation
ARDS Onset
24 - 72 hours after precipitating event
Approach to ARDS Dx
clinical history, imaging studies (x-ray, CT), bronchoscopy
Treatment for ARDS
treat underlying condition and supportive care
ARDS on histology is known as:
Diffuse Alveolar Damage
Histology of ARDS
- pneumoncyte and endothelial cell necrosis
- edema
- Hyaline membrane formation
- Organizing interstitial fibrosis and type 2 pneumocyte proliferation
Two possible outcomes of ARDS
- Restoratoin of normal lung architecture
- Progression to fibrosis (endstage honeycomb fibrosis)
Phases of ARDS on pathology
- Early exudative phase (acute)
- Subacute proliferative phase (organizing)
- Fibrotic phase (late)
Neonatal Respiratory Distress (NRD) Syndrome synonyms
- Infant Resp. Distress syndrome (IRDS)
- Resp. Distress syndrome of newborn
- Hyaline membrane disease
Etiology of NRDS
- Fetal injury during delivery
- aspiration of blood or amniotic fluid
- cord compression
- excessive sedation of mother
- hyaline membrane disease (most common)
Predisposing factors to NRDS
- prematurity
- maternal diabetes
- C-section
Main problem in NRDS
Insufficient pulmonary surfactant production resulting in failure of lungs to inflate after birth
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
Treatment of NRDS
- Delay labor if possible to allow lung maturity
- administer exogenous surfactant
- assess fetal lung maturation (Lecithin:sphingomyelin ratio over 2:1
Acute Interstitial Pneumonia is also known as:
Harman-Rich syndrome
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
