1. Hemodynamic Tutorial

2. Describe what you see?

3. What are other causes of arterial thrombosis?
Vasculities.
Trauma
What is the thrombus made of?
Fibrin, platelets, and red cells.

4. What causes arterial thrombosis? ...venous thrombosis?
Arterial thrombosis is caused by endothelial damage (eg, atherosclerosis or vasculitis);
venous thrombosis is caused by stasis (sluggishness) of blood flow.
Both types of vessels are affected in hypercoagulable states such as antithrombin or protein C deficiency.

5. What are the various fates of thrombi?
Propagation, embolism, dissolution, and organization with recanalization.
Which of these fates is clinically most significant in the arterial circulation vs. the venous circulation?
The most significant problem with arterial thrombi is propagation leading to luminal obstruction, resulting in infarction of the tissue supplied. Important examples include myocardial and cerebral infarction. In contrast, the most significant problem with venous thrombi is the possibility of potentially fatal embolization into the pulmonary circulation.

7. What is the difference between a postmortem clot and a thrombus?
Postmortem clots are not attached to endothelium;
they are gelatinous, rubbery, dark red at the ends and yellowish elsewhere.
Thrombi are attached to endothelium and are traversed by pale grey fibrin strands that can be seen on cut section; they are more firm but fragile.

8. What do you see her
The well-defined pale area in the acute myocardial infarct represents coagulative necrosis. It is surrounded by a red area of reactive hyperemia. In contrast, the ill-defined pale area in the old myocardial infarct represents a fibrous scar.

9. What is the organ? What do you see here?

10. The congestion and accompanying sinusoidal dilatation are maximum in and around central veins and decrease progressively toward portal triads

11. The alveolar septa are prominent, due to marked congestion of the capillaries. The alveolar lumens contain pale-staining edema fluid.

12. What is the pathogenesis of pulmonary edema?
Left ventricular failure (eg, caused by a myocardial infarct) causes pump failure, and secondarily there is impaired flow of blood from the lung to the left atrium. This causes increased hydrostatic pressure in pulmonary alveolar capillaries and subsequent transudation of fluid into alveoli.
Pulmonary edema in other cases may also result from damage to alveolar capillaries (eg, in adult respiratory distress syndrome).

13. How does this type of edema differ from that seen in acute inflammation?
The fluid in pulmonary edema is a transudate (ie, it is protein poor, has low specific gravity, and does not contain inflammatory cells).
Edema in inflammation is an exudate.

14. What are the cells seen here?

15. What do you see here?

17. Why are some infarcts red and others pale?
Red infarcts result from hemorrhage into the necrotic area. This is likely to occur in tissues that have a loose texture and dual blood supply (eg, lung); by contrast, pale infarcts occur in compact tissues and those in which the collaterals do not readily refill the necrotic area (eg, heart).

18. What is the most common symptom of pulmonary embolism?
There are usually no symptoms. Most pulmonary emboli (60-80%) are clinically silent because of their small size and because of the dual blood flow through the bronchial circulation. With time, these emboli organize and are incorporated into the vessel wall.

19. How and when does pulmonary thromboembolism cause sudden death?
If more than 60% of the pulmonary circulation is obstructed by emboli, the patient is at a high risk of sudden death due to acute right heart failure (cor pulmonale) or shock (cardiovascular collapse).

20. When does pulmonary thromboembolism result in infarction?
The possibility of developing pulmonary infarction is higher in a previously diseased lung, especially in the setting of sluggish bronchial arterial flow or prior pulmonary congestion due to left heart failure.