Blood Vessels
General
1. Understand the general properties of vascular endothelial and smooth muscle cells. Understand how these cells respond to injury (Robbins 5th Ed., p. 469-472) or (Robbins 6th Ed., 495-497).
Atherosclerosis
1. Describe the natural history of coronary artery atherosclerosis and the associated clinical syndromes. What level of obstruction defines critical stenosis (Robbins 5th Ed., p. 524-528) or (Robbins 6th Ed., p. 550-554)?
2. List four key risk factors for atherosclerosis (Robbins 5th Ed., p. 474-476) or (Robbins 6th Ed., p. 503-507). How do atherosclerotic lesions cause clinical events (Robbins 5th Ed., p. 484) or (Robbins 6th Ed., p. 498-499)?
3. Describe the basic structure of an atherosclerotic plaque. Describe the gross and microscopic appearance of atherosclerotic plaques (Robbins 5th Ed., p. 476-479) or (Robbins 5th Ed., p. 499-503).
4. List factors that are important in the initiation and growth of atherosclerotic plaques. Understand the roles of endothelial cells, smooth muscle cells, macrophages, and platelets in plaque formation (Robbins 5th Ed., p. 479-483) or (Robbins 6th Ed., p. 507-509).
5. List the ways that lipoprotein oxidation contributes to the formation of atherosclerotic plaques (Robbins 5th Ed., p. 481-482) or (Robbins 6th Ed., p. 508).
6. Compare and contrast atherosclerosis, Monkeberg's medial calcific sclerosis, and arteriolosclerosis (Robbins 5th Ed., p. 484, 488-489) or (Robbins 6th Ed., p. 498).
Heart
General
1. Review the blood supply of the heart, including the regions supplied by each coronary artery and the meaning of "dominant" coronary artery (Robbins 5th Ed., p. 467-469, 517-519) or (Robbins 6th Ed., 494-495, 545).
Heart failure
1. Define heart failure. List at least two causes of systolic dysfunction. List at least 2 causes of diastolic dysfunction. (Robbins 5th Ed., p. 519-522, see Figure 12-1) or (Robbins 6th Ed., p. 546-550, see Figure 13-2).
2. Compare and contrast the morphology and consequences of pressure overload vs volume overload (Robbins 5th Ed., p. 520-521) or (Robbins 6th Ed., p. 547-549).
3. Compare and contrast the causes and consequences of right and left heart failure (Robbins 5th Ed., p. 522-523) or (Robbins 6th Ed., p. 549-550).
Ischemic Heart Disease
1. Define ischemia. List causes of impaired oxygen supply, increased oxygen demand (Robbins 5th Ed., p. 524) or (Robbins 6th Ed., p. 550-551).
2. List the clinical syndromes associated with ischemic heart disease. Understand the role of the following (Robbins 5th Ed., p. 524-528) or (Robbins 6th Ed., p. 551-554):
a. fixed coronary obstructionb. coronary thrombosis
c. acute plaque change
d. vasospasm
3. What morphologic changes are associated with (Robbins 5th Ed., p. 524-528, Table 12-3) or (Robbins 6th Ed., p. 551-554, Table 13-2):
a. stable anginab. unstable angina
c. variant angina
d. myocardial infarction
4. What are the pathologic correlates of sudden death? (5th Ed., p. 541) or (Robbins 6th Ed., p. 564).
5. Define acute myocardial infarction. List the sequential effects of ischemia (Robbins 5th Ed., p. 531, Table 12-4) or (Robbins 6th Ed., p. 556, Table 13-3. Describe the timing of the wave front of irreversible myocardial damage after total coronary artery occlusion, and the implications for the success of thrombolytic interventions (5th Ed., p. 532) or (Robbins 6th Ed., p. 556-559).
6. How long does it take for a typical infarct to be grossly recognizable to a trained pathologist? How long does it take before histopathologic changes are recognizable in an infarct? (5th Ed., p. 532-536) or (Robbins 6th Ed., p. 557-561)?
7. Describe how an evolving myocardial infarction can be altered by thrombolysis and reperfusion (Robbins 5th Ed., p. 535-537) or (6th Ed., p. 559-561). What pathologic changes are common in reperfused infarcts? (Robbins 5th Ed., p. 535-537) or (Robbins 6th Ed., p. 559-561).
8. Compare and contrast transmural and subendocardial infarction (Robbins 5th Ed., p. 529, 531, 533-534) or (Robbins 6th Ed., p. 554, 556-559).
9. Compare and contrast tests of CK and LD with regard to timing, sensitivity, and specificity in acute myocardial infarction (AMI). Describe how sequential tests for CK-MB are used in the clinical setting to rule out AMI. When is CK-MB unreliable in ruling out AMI? Describe the major tissue sources of the three CK isoenzymes (CK-MM, CK-MB, and CK-BB) (Robbins 6th Ed. p. 561).
10. Describe the specificity and time course of troponin as it relates to the diagnosis of acute myocardial infarction (Robbins 6th Ed. p. 561).
11. List important complications of acute myocardial infarction. When is the patient at greatest risk for myocardial rupture?
1. (Robbins 5th Ed., p. 467-469) or (Robbins 5th Ed., p. 494-495)(this review of normal vascular structure will be helpful for understanding the material in this section), (Robbins 5th Ed., p. 473-484, 488-489, 517-522, 524-541) or (Robbins 6th Ed., p. 498-510, 514-515, 543-549, 550-564)
2. Images 1-7 relate to the case; 8-13 are related to other objectives
A 40 year-old diabetic was evaluated in the emergency room for chest pain. She had a history of hypertension, and a 30 pack year smoking history. Her medications included antihypertensives and cholesterol-lowering agents. She had a prior admission several years ago for a small uncomplicated myocardial infarct. She had angina for many years, averaging one bout of angina a week. Her usual angina lasted 10-15 minutes and was relieved by nitroglycerine. A cardiologist attempted angioplasty several years ago. This procedure relieved her symptoms for six months but eventually exercise-induced angina returned. There were no clinical changes until two weeks prior to her emergency room admission, when she began having daily anginal attacks that lasted 30 minutes or more. In the hour prior to her admission she had awakened with severe chest pain, nausea, and dyspnea. There had been severe unrelenting pain for 45 minutes and it had not been relieved by nitroglycerine. HR 105. BP 100/50 (her usual BP runs about 155/95). Temp. 100 F. One examiner described her as obese and diaphoretic (sweating profusely), with pale skin and labored respirations. Rales were heard over both lung fields. An EKG and serial cardiac enzymes were ordered.
Lab Values - Case 1
|
|
IU |
ng/ml |
|
ng/ml |
|
Admission |
150 |
3 |
20 |
<0.4 |
|
8 hours |
320 |
8 |
25 |
0.8 |
|
16 hours |
500 |
30 |
60 |
10.4 |
|
24 hours |
750 |
30 |
80 |
22.0 |
|
48 hours |
300 |
18 |
60 |
14.0 |
|
72 hours |
80 |
2 |
25 |
9.3 |
|
Normal |
38-120 |
0-3 |