Acute Lung Injury

Question 1

How does the status of cardiopulmonary function deteremine the damage that is done to lung tissue by embolization?

Answer 1

Adequate C/P function:
• Bronchial Artery Supply should be enough to keep tissue distal to the infarction alive.

Inadequate C/P function:
• Infarction

Question 2

How do you know a clot is premortum?

Answer 2

Lines of Zahn - alternating lines of fibrin and blood clots

Question 3

What is seen here?

Answer 3

Question 4

What is seen here?

Answer 4

Question 5

What happens to lung tissue around 48 hours after infarct?

Answer 5

Tissue becomes a paler red-brown from conversion of hemoglobin to hemosiderin by macrophages that eventually progresses to form a scar

Question 6

What is seen here?

Answer 6

A non-thrombotic emboli that has resulted from cellulose buildup resulting in plug formation in this small artery

Question 7

What is seen here?

Answer 7

Bone marrow embolus that may result from bone trauma.
• Note the fat and hypercellularity that are tale-tale signs that this is bone marrow.

Question 8

What kind of embolus is seen in patients who die as a result of resuscitation?

Answer 8

Bone/Fat emboli from cracking ribs

Question 9

What is shown here?
• what should you worry about?

Answer 9

Amniotic Fluid Embolus - often results in DIC and death. Note teh keratin debris that can be seen throughout the tissue.

Question 10

What is seen here?

Answer 10

Question 11

What are some hemodynamic vs. intrinsic reasons for edema in the lungs?

Answer 11

Hemodynamic:
Heart Failure - edema from increased HYDROSTATIC pressure
Liver Disease - edema from decreased ONCOTIC pressure

Intrinsic - Microvascular Injury:
• Infections
• Inhaled smoke and other gases
• Shock

Question 12

What key features are highlighted by the arrows in this picture?
• what is it showing?

Answer 12

Right: Alveolar Macrophages
Middle: Exudate (protein stains pink)
Left: Engorged capillaries

This is the microscopic appearance of pulmonary edema.

Question 13

What causes the formation of heart failure cells?

Answer 13

• In chronic pulmonary congestion as is seen in CHF, alveolar macrophages ingest blood from microhemorrhages that take place from high pressure. These hemosiderin laden macrophages are known as heart failure cells.

Question 14

How does ARDS manifest histologically?

Answer 14

Histologically we see Diffuse Alveolar Damage (DAD)

Question 15

What are the steps and key mediators in the formation of hyaline membranes in ARDS?

Answer 15

1. endothelial activation and release of TNF
2. TNF recruits neutrophis that secrete macrophage inhibitor factor (MIF) which amplifies inflammatory response
3. Hyaline Membranes of protein form as a result of Hyaline Membrane damage
4. TGF-ß and PDGF are key in the proceeding fibrotic process in which Edema and Hyaline membranes receed only to be replaced by collagen.

Question 16

What is shown here? Is the process Acute or Chronic?
• how do you know?

Answer 16

Chronic Diffuse Alveolar Damage, we know its chronic because the trichrome stain stains collagen blue. TGF-ß and PDGF cause fibrosis and collagen deposition AFTER the acute phase of the disease is over.

Question 17

This is from a patient who had ARDS. Was this biopsy taken soon after the attack or later?

Answer 17

This shows hyaline membrane formation so the biopsy was likely taken soon after disease.

Question 18

What is shown here?

Answer 18

Neonatal Respiratory Distress Syndrom.

Question 19

Diffuse Alveolar Damage primarily affect which pulmonary function?

Answer 19

DAD typically affects DIFFUSION OF GASES

Question 20

How is edematous fluid removed from the lungs?

Answer 20

Via lymphatics, lymphatics always drain the interstitium

Question 21

Following pulmonary thromboembolism, what is the most important factor in the development of pumonary infarction?

Answer 21

Congestive Heart Failure

Question 22

What is the most common cause of cor pulmonale?

Answer 22

Pulmonary Emboli