Edema and Congestion ( Robbins 5th Ed., p. 93-98) or (Robbins 6th Ed., p. 113-117)
1. Define edema and discuss the four major pathophysiologic categories of edema. (see Robbins 5th Ed., Table 4-1, p. 94) or (Robbins 6th Ed., Table 5-1, p. 114)
2. Distinguish between inflammatory and noninflammatory edema; define exudate vs. transudate.
3. Describe the secondary causes (e.g., hyperaldosteronism) that contribute to edema.
4. List the important clinical states associated with generalized or localized edema and the factors that underlie each condition.
5. Define the terms hyperemia, active and passive congestion; give examples of each.
6. Describe the causes of and morphologic changes in chronic passive congestion of the lungs, liver, and spleen.
Hemostasis ( Robbins 5th Ed., p. 99-105) or (Robbins 6th Ed., p. 119-124)
1. Describe the process of primary and secondary hemostasis, including the role of platelets, vessel wall, and coagulation.
2. List the thrombogenic and anti-thrombogenic properties of the endothelium.
3. Describe the general scheme of the coagulation cascade.
4. List the four categories of plasma coagulation proteins (proenzymes, enzymes, cofactors, and structural)
5. Describe the role of the four categories of plasma coagulation proteins and their interaction with phospholipid surfaces in the coagulation sequence.
6. List the factors that limit coagulation.
7. Describe the three pathways by which proteins involved in coagulation are degraded. Be familiar with the key antagonists in each category.
Thrombogenesis ( Robbins 5th Ed., p. 105-110) or (Robbins 6th Ed., p. 124-129)
1. Describe the three major factors that predispose to thrombosis.
2. Compare and contrast the factors that predispose to venous vs. arterial thrombosis.
3. What are the inherited and acquired factors that predispose to hypercoagulability? What is "lupus anticoagulant" and what are the clinical features associated with this "anticoagulant"?
4. Describe the clinical settings in which arterial, cardiac chamber, and venous thrombosis occur.
5. What is the proper usage of the terms:
a. mural thrombusb. vegetations
c. thrombophlebitis
6. Describe the morphologic features of thrombi.
7. Describe the possible fates of thrombi. see (Robbins 5th Ed., Figure 4-18, p. 108) or (Robbins 6th Ed., Figure 5-14, p. 128)
Infarction ( Robbins 5th Ed., p. 114-116) or (Robbins 6th Ed., p. 132-133)
1. Define an infarct. What is the most common setting in which infarcts occur?
2. Describe the tissue changes that occur in an infarct.
3. How do anatomic patterns of arterialvenous blood supply influence the outcome of tissue injury following vascular occlusion?
Thromboembolic Disease; Pulmonary thromboembolism ( Robbins 5th Ed., p. 111-114) or (Robbins 6th Ed., p. 129-132)
1. Define thrombus, clot, and embolus.
2. List the clinical states that are associated with increased risk of venous thrombosis. Describe the pathophysiologic basis of such associations.
3. List the most common sites of venous thrombosis, including sites that are the sources of clinically significant pulmonary thromboemboli.
4. Relate the outcome of pulmonary thromboembolism to the size of the embolus and the number of emboli.
5. Describe the clinical consequences of pulmonary thromboembolism and their approximate frequency.
6. Describe the events that lead to shock following major pulmonary embolism.
7. List examples of clinical conditions that give rise to fat embolism, air embolism, and amniotic fluid embolism.
1. (Robbins 5th Ed., p. 93-110, 114-116) or (Robbins 6th Ed., p. 113-129, 132-133)
2. Images in Fluid and Hemodynamics Case Studies folder: Case 1
A 65-year-old male presented to the emergency room with a recent (1-day) history of severe chest pain radiating to the left arm. He is suspected to have had a "heart attack." Coronary angiography reveals a complete occlusion of the left anterior descending branch about 2 cm from its origin. He is given a therapeutic dose of recombinant human tissue plasminogen activator (TPA). This treatment restores coronary blood flow and the chest pain improves. Simultaneously he is started on 1 tablet of aspirin per day.
Seven days later he notes swelling of both legs and feet and is found to have pitting edema of the legs, his liver is somewhat enlarged, and his neck veins (jugular) appear full. He is given diuretics and asked to consume a salt-restricted diet. Because of considerable weakness, he remains in bed most of the time. A few days later, he develops sudden pain in the lower right part of the chest, which is aggravated by taking a deep breath. Physical examination reveals that his left leg has now developed more swelling than the right. X-ray of the chest shows a faint shadow in the peripheral part of the right lower lobe of the lung. Intravenous heparin is started. Two days later he becomes very breathless and dies suddenly.