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CELL AND TISSUE INJURY I
Slide 1 [WinLab] [Mac] [WinHome]
Liver: Steatosis (“fatty infiltration,” etc.)
This slide is from the liver of a 54-year-old alcoholic who died of heart disease. At autopsy, the liver was enlarged (2800 gm, as compared to the expected normal of 1700 gm), and had a paler than usual color, almost uniformly throughout the organ. A few small foci were mottled and darker.
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What feature(s) unique to liver allow identification of this tissue histologically?
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Note the cytoplasmic vacuolization of the hepatocytes in a pattern of either multiple small vacuoles or one huge vacuole per cell.
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Knowing that these vacuoles are the result of lipid accumulation, how do you account for the fact that the vacuoles appear to be empty?
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What other substances could accumulate intracytoplasmically and appear as “empty” vacuoles in routine preparations such as this? How would you go about distinguishing these various substances?
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What might lead to hepatic steatosis? To lipid accumulation in other organ?
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Would you expect hepatic steatosis to be reversible?
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A detail in passing: You’ll note grossly that the narrower end of the section has a deeper color (corresponding to the mottled gross foci mentioned above). Many of the hepatocytes in this area have died; and associated with the dead hepatocytes are many polymorphonuclear neutrophils, which have irregular lobulated nuclei. Patches of hemorrhage are also evident, along with brownish blotches of pigment deposited as an artifact of fixation.
Slide 2 [WinLab] [Mac] [WinHome]
Heart: Coagulative Necrosis (myocardial infarct)
This 63-year-old patient had a “heart attack” approximately 2 days prior to his demise.
The immediate cause of his death was an irreversible cardiac arrhythmia.
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Within the section are broad areas of necrotic myocardium alternating with normal myocardium. How can you distinguish histologically between viable and dead myocytes? How can you tell that what you’re looking at is truly necrosis and not simply post-mortem autolysis?
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Why does this pattern of necrosis qualify as “coagulative” necrosis?
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The hordes of small cells that produce a blue streaking of these necrotic areas (low power)
are almost exclusively neutrophils responding to the dead tissue.
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What is the most common cause of coagulative necrosis? What is another name for an area of coagulative necrosis produced by ischemia?
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While this patient was still alive, what serum enzyme changes might have been detected?
Can you account for elevated blood levels of these enzymes?
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Can you predict in general histologic terms what would have happened to this tissue over time had this patient survived? (Slide 49 [WinLab] [Mac] [WinHome] will illustrate some of this.)
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When coagulative necrosis occurs in an area in which the dead tissue is exposed to saprophytic, putrefactive microbes, the result is gangrene. Slide 7 [WinLab] [Mac] [WinHome] shows skin and soft tissue from a partly gangrenous foot. At one end of the section, everything is dead; at the other end, mostly alive. In between is a neutrophilic inflammatory reaction. Although not visible here, there are many bacteria growing in the necrotic tissue.
Slide 3 [WinLab] [Mac] [WinHome]
Spleen: Caseous Necrosis
This spleen is from a 28-year-old patient who died of a systemic infection.
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How can you identify this tissue as spleen?
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Scan this section under the lowest power of your microscope. You’ll quickly spot the lymphocytes clustered around small vessels, but then search for pale pink areas, each surrounded by a light-staining cellular halo. Under higher power you’ll note that the pale
areas consist largely of granular cell debris -- a mix of cytoplasmic “crumbs,” karyorrhectic particles, and disintegrating cells. Grossly visible masses of this dead material appear cheesy, hence this form of necrosis is called caseous.
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The halo of pale staining cells around each caseous area consists of so-called epithelioid cells (modified macrophages) with occasional multinucleated giant cells (derived from macrophages). These cells constitute the inflammatory reaction, which qualifies as “granulomatous.” (More at a later time about this!)
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What sort of etiologic agents might lead to the presence of caseating granulomas such as in this spleen? How would you go about distinguishing between these various agents found either at autopsy or in a surgically resected specimen?
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How would infectious agents reach the spleen?
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What is the usual fate of caseous areas?
Slide 4 [WinLab] [Mac] [WinHome]
Brain: Liquefactive Necrosis (cerebral infarct)
This section of brain is from a 68-year-old patient who suffered embolic occlusion of cerebral arterial branches a couple of weeks prior to death.
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How can you tell histologically that this tissue is from the central nervous system?
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Inspect the section under scanning power and note that there are 3 straight-cut sides and one curved, convoluted portion. Concentrate your attention on the latter area.
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Under scanning power, you’ll note portions of the gyri in this section appear pale and “rarefied.” Under high power, you’ll see that the brain substance has begun to disappear in these areas, leaving a fluid which appears as “space” in this section.
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Associated with these areas are many macrophages -- large mononuclear cells with granular material in their cytoplasm. Some of this material is debris from the brain substance which is undergoing necrosis while the coarse brown material is hemosiderin derived from red blood cells breaking down in the area.
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Grossly, an area of dead brain gradually softens as it progressively “liquefies.” What would an area of cerebral necrosis look like a year or so later?
Slide 5 [WinLab] [Mac] [WinHome]
Omentum: Enzymatic Fat Necrosis
This specimen is from a 32-year-old patient with a history of severe abdominal pain prior to death. At autopsy her omental and mesenteric adipose tissue was seen to contain chalky, 1-3 mm flecks (visible on the section).
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Under the scanning power of your microscope, note the peculiarly altered purplish nodules of adipose tissue, each surrounded by an inflammatory reaction. Under high power, compare the adipose tissue within the purplish areas with that in the more normal omentum. How do you know that the purplish areas are dead? In addition to the halo of inflammatory cells around each necrotic zone, there is a layer of fibrin and PMNs along the outer surface of the largest tissue fragment.
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Can you account for the fact that the cytoplasm of the dead cells does not appear “empty” like that of normal adipocytes? This sort of change requires exposure of the adipose tissue to pancreatic enzymes. Under what circumstances might such exposure occur?
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It should be noted in passing that there are other ways to kill adipose tissue -- e.g., ischemia, trauma, etc. Ischemic-necrotic adipose tissue would manifest coagulative necrosis. See if you can imagine the microscopic appearance of such an area. A quick look at Slide 6 [WinLab] [Mac] [WinHome] will show you the appearance of traumatic fat necrosis. This specimen, skin and adipose, is from a mastectomy specimen. The patient had had a breast biopsy, prior to the mastectomy (i.e., surgical trauma). Note the “spaces” in the adipose tissue that are much larger than the adipocytes. These spaces are “puddles” of cytoplasmic lipid from smashed adipocytes. At the margins of the puddles, you can see macrophages (“lipophages”) drinking it all in. Note that in the absence of exposure to pancreatic enzymes, the dead adipose tissue looks very different than in Slide 5 [WinLab] [Mac] [WinHome].
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