RHS04 - Pulmonary Pathology 2 Flashcards
What is and what causes resorption atelectasis?
If there is a complete obstruction in the bronchi or bronchioles, fresh air will not reach the alveoli. The stagnant air in the alveoli will eventually be resorbed, resulting in collapse of the alveoli which is known as a resorption atelectasis.
What are the clinical findings in resorption atelectasis?
- Fever and dyspnea within 24-36 hours of collapse
- Ipsilateral deviation of trachea
- Ipsilateral diaphragmatic elevation
- Ipsilateral absence of breath sounds and tactile fremitus
What is and what causes compression atelectasis?
Air of fluid accumulation in the pleural cavity causing increased pressure and collapse of the underlying lung tissue.
What are the clinical findings in compression atelectasis?
- Contralateral tracheal and mediastinal shift
What is and what causes contraction atelectasis? How is it fixed?
If a lung becomes fibrotic it won’t be able to expand fully which is known as contraction atelectasis. There is no way to reverse this
What is neonatal atelactasis? What is it AKA?
When a baby is born without enough lung surfactant, breathing becomes extremely difficult due to the increased surface tension and the propensity for the alveoli to collapse on expiration. This is known as neonatal atelactasis, neonatal respiratory distress syndrome, or hyaline membrane disease.
List the major components of lung surfactant. Which cells synthesize these components and how are they stored?
- Phosphatidylcholine (lecithin)
- Phosphatidylglycerol
- Lipoproteins
- Surfactant Proteins A & D (innate immunity)
- Surfactant Proteins B & C (reduce surface tension at air/liquid barrier)
All synthesized by Type 2 Pneumocytes and stored in lamellar bodies
What are the three major causes of neonatal atelactasis?
- Premature Birth - especially before 28 weeks (when surfactant production begins)
- Maternal Diabetes - fetal hyperglycemia stimulates insulin release. Insulin inhibits the production of lung surfactant
- Cesarean Section - labor and vaginal delivery increases stress on the baby which causes an increase in cortisol secretion. Cortisol stimulates lung surfactant production. A C-section prevents this
What are the clinical findings and further complications in neonatal atelactasis?
- Clinical Findings
- Respiratory distress within a few hours of birth
- Hypoxemia and respiratory acidosis
- “Ground Glass” appearance on CXR
- Complications
- Intraventricular hemorrhage (brain ventricles)
- PDA from persistent hypoxemia
- Necrotizing enterocolitis (intestinal ischemia)
- Hypoglycemia (if caused by maternal diabetes)
- O2 therapy can damage lungs and cause cataracts
Describe the key histological finding in neonatal atelactasis and also describe what causes it.
When lung tissue becomes hypoxic, vasoconstriction and hypoperfusion occurs. This leads to both endothelial and epithelial damage which causes plasma to leak into the alveoli. Fibrin begins to form around the necrotic cells forming a pink homogenous membrane known as a hyaline membrane (refer to image).
The appearance of these membranes along with collapsed alveoli are the key histological findings in neonatal atelactasis.
What is the pathogenetic difference between neonatal respiratory distress and acute respiratory distress?
In NRDS, lack of lung surfactant is the cause
In ARDS, inflammation is the cause
What is Acute Respiratory Distress Syndrome (ARDS)? What is it AKA?
ARDS is a rapid onset of the following symptoms, in the absence of heart failure:
- Severe hypoxemia
- Bilateral pulmonary infiltrates
- Often refractory to O2 therapy
AKA - noncardiogenic pulmonary edema, shock lung syndrome, acute lung injury, diffuse alveolar damage
List the major etiologies of ARDS.
- Direct Pulmonary Insult - pneumonia, aspiration, emboli, drowning, oxygen toxicity
- Indirect Pulmonary Insult (from the systemic circulation) - sepsis, trauma with shock, acute pancreatitis, severe burns, transfusion of blood products, uremia, drugs
Describe the pathogenesis of ARDS caused by direct lung injury.
- Alveolar damage is sensed by alveolar macrophages which then secrete TNF, IL-8, and IL-1
- TNF & IL-8 cause capillary endothelium activation causing fluid accumulation in the intersitium and neutrophil recruitment into the alveolus
- The TNF and IL-1 stimulate neutrophils to release PAF, leukotrienes, and proteases resulting in more alveolar damage and edema
Describe the pathogenesis of ARDS caused by indirect lung injury.
- Alveolar capillary endothelial damage/activation occurs which causes accumulation of fluid in the interstitium and neutrophil migration into the alveolus
- Once in the alveolus, the neutrophils release PAF, leukotrienes, and proteases which cause further alvelar damage and edema
Describe the histological appearance of ARDS
Appearance depends upon phase of disease
- Acute (exudative) phase: 0-4 days
- Interstital and intraalveolar edema/hemorrhage
- Necrosis and sloughing of alveolar epithelium
- Hyaline Membranes (refer to image)
- Organizing (proliferative) phase: 4 days to 3 weeks
- Proliferation of Type II pneumocytes
- Organization of fibrin exudates into fibrosis
- Alveolar septal thickening
