CIRCULATORY DERANGEMENTS II

Slide 47 [WinLab] [Mac] [WinHome]

Lung: Pulmonary Arterial Emboli and Infarct

This lung came from a 77-year-old woman who was incapacitated by advanced Alzheimer’s disease and confined to bed.

• Under the lowest powers, you’ll note that the alveoli in part of the section appear to contain air or variable amounts of edema, while in other parts of the section, the alveoli are filled by something more substantial. Under higher magnification, the material that is obliterating alveoli appears to be blood in varying stages of disintegration.

• Compare the alveolar septa in the “filled” area with those in the more normal area. What is it that allows you to conclude that the pulmonary parenchyma is actually necrotic in this area of density?

• In and around this infarcted zone, there is irregular leukocyte infiltration in response to the necrosis, and in one set of sections (trade sections-looking for the one with a more triangular outline) there is a zone of organization at the margin of the infarct.

• Within a number of pulmonary arterial branches, you’ll note dense blood clots. In most instances, there is ingrowth of capillaries and fibroblasts at the periphery of the clots. What does this tell you about the duration of the process?

• Can you tell from the histopathologic features whether these clots are thrombi or emboli? What gross features would be helpful? What do the clinical circumstances suggest? Can you relate the patient’s history to what you see on the slides?

• What are the clinical manifestations of pulmonary emboli and infarcts? What are the radiographic manifestations?

Slide 48 [WinLab] [Mac] [WinHome]

Kidney: Atheroemboli

This kidney was obtained at autopsy of a 62-year-old woman who died following coronary artery bypass surgery.

• Scan the slide systematically, directing your attention to arterial branches throughout the section. In some of them, even under low power, you’ll note “cholesterol clefts” the spaces left when large cholesterol crystals are dissolved during tissue processing. How can these be distinguished from “ordinary” atherosclerosis involving the vessels?

• In most of the vessels, the cholesterol crystals are surrounded by a loose fibrous tissue that fills the vessel lumen, and here and there is a multinucleated giant cell nuzzling a crystal. What does this tell you about the age of some of these atheroemboli?

• Broad zones of the renal parenchyma have a washed-out appearance due to extensive karyolysis in tubular epithelium. Much of this could be post-mortem autolytic change; but in some sections, there is a trace of leukocytic reaction suggesting that some of the changes represent early infarct. (Other sections from this patient’s kidneys did show clear-cut infarcts.)

• What do you suppose was the anatomic source of these renal atheroemboli? Although many atheroembolic episodes are spontaneous, some are iatrogenic. What in this patient’s history suggests triggering of atheroembolism by a medical procedure?

• What are other (i.e., non-renal) manifestations of atheroembolism? Risk factors for these?

Slide 49 [WinLab] [Mac] [WinHome]

Heart: Organizing and Older Myocardial Infarcts

This portion of left ventricular wall came from a 68-year-old man who had a long history of ischemic heart disease, including many episodes of angina pectoris and several “heart attacks.”

• Looking at the slide at scanning power, how would you know that it was taken from the left ventricle and not from the right ventricle or either atrium? How can you distinguish epicardial from endocardial surface?

• Note, also, at scanning power, that the myocardium has an abnormally mottled appearance with irregular pale patches. These are the abnormal areas upon which to concentrate your microscopic attention.

• Under the lowest powers, you’ll note that the cardiac muscle has largely vanished from the pale areas. Each of these areas is occupied, instead, by connective tissue with a scattering of macrophages and perhaps a few lymphocytes.

• Many of the macrophages contain granules of brown pigment. What might be the origin(s) of this pigment?

• The abnormal areas are of slightly different ages. How can you tell this histologically?

• Each of these areas represents a later stage of ischemic necrosis, which initially would have been similar in appearance to what you observed in Slide 2 [WinLab] [Mac] [WinHome]. In fact, remains of necrotic fibers are still present in some of the areas. See if you can describe the evolution of a focus of coagulative necrosis into what you see in Slide 49 [WinLab] [Mac] [WinHome].

• What do you think caused the ischemia in this myocardium? How do you account for the fact that different foci of damage in the same sector of ventricular wall seem to be of different ages?

• If you scan the epicardial surface, you’ll note occasional clumps of fibrin, with a sparse infiltrate of leukocytes in the subjacent connective tissue. This sort of fibrinous pericarditis is sometimes seen in association with myocardial infarction. What might be the clinical manifestation of such a process?

• What are the possible consequences of myocardial infarction?

Slide 50 [WinLab] [Mac] [WinHome]

Colon: Ischemic Changes (“Ischemic Colitis”)

This specimen was obtained at the autopsy of an 82-year-old woman who died of intractable cardiac failure.

• Under the lowest powers, identify the various layers of the colonic wall. Note that there is a sort of gradient of abnormality, ranging from a generally normal muscularis propria to a severely damaged mucosa. (Ischemia which is not total often produces this gradient of damage; while total ischemia generally leads to transmural infarction.)

• Identify areas of mucosa that are more or less intact. If you follow from these intact areas to neighboring areas, you’ll note that the crypts disappear, sometimes leaving ghosts of a few epithelial cells. The lamina propria in these areas is stuffed with fibrin and diffusely infiltrated by leukocytes -- reactions to the infarcted epithelium.

• The inflammatory reactions and associated hemorrhage extend focally into the submucosa, which is also markedly edematous. What is the gross and the roentgenographic representation of these changes?

• In what situations would one encounter ischemic changes like these in the colon?

• What would be the clinical manifestations and the possible sequelae?