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M1 Histopathology Labs with Virtual Slides
The University of Michigan Medical School
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Histopath Lab 1:
Cell and Tissue Injury I

INSTRUCTORS: First click here to
map a drive, then open all of the
WinLab links by clicking this link.

Robbins and Cotran Pathologic Basis of Disease 9th Ed.

Suggested Reading:
Pages 41-44 – Necrosis
Pages 62 – Steatosis
Pages 496-501 – Atherosclerosis
Page 359-360 – Cytomegalovirus
Pages 847-849 – Hemochromatosis
Page 997 – Condyloma


Slide 1 [WebScope][ImageScope]

Liver: 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.

  • What feature(s) unique to liver allow identification of this tissue histologically?
  • Note the cytoplasmic vacuolization of the hepatocytes in a pattern of either multiple small vacuoles or one huge vacuole per cell.
  • Knowing that these vacuoles are the result of lipid accumulation, how do you account for the fact that the vacuoles appear to be empty?
  • What is the diagnosis?
  • How would you confirm that the vacuoles were filled with lipid? Name another substance that could accumulate intracytoplasmically and appear as “empty” vacuoles in routine H&E stained slide preparations?
  • What might lead to this liver condition? Would you expect this condition to be reversible?
  • 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 [WebScope][ImageScope]

Heart: 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.

  • What features allow the histologic identification of this tissue as myocardium?
  • Within the section are broad areas of necrotic myocardium alternating with normal myocardium. How can you distinguish histologically between viable and dead (necrotic) myocytes?
  • The hordes of small cells that produce a blue streaking of these necrotic areas (low power). What are these cells called?
  • How can you tell that what you’re looking at is truly necrosis and not simply post-mortem autolysis?
  • What pattern of necrosis is exemplified by this slide? What is the most common cause? What is another name for this?
  • While this patient was still alive, what serum enzyme changes might have been detected? Can you account for elevated blood levels of these enzymes?
  • Can you predict in general histologic terms what would have happened to this tissue over time had this patient survived? (Slide 49 [WebScope][ImageScope] will illustrate some of this.)


Slide 3 [WebScope][ImageScope]

Spleen: This spleen is from a 28-year-old patient who died of a systemic infection.

  • How can you identify this tissue as spleen?
  • Scan this section under the lowest power of your microscope. 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.
  • 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!)
  • What pattern of necrosis is exemplified by this slide? What sort of etiologic agents might cause this? How would you go about distinguishing between these various agents found either at autopsy or in a surgically resected specimen?
  • How would infectious agents reach the spleen?
  • What is the usual fate of caseous areas?


Slide 4 [WebScope][ImageScope]

Brain: 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.

  • How can you tell histologically that this tissue is from the central nervous system?
  • Inspect the section under scanning power and note that there are 3 straight-cut edges of the tissue (top, right, bottom) and one curved, convoluted portion (gyrus) on the left. Concentrate your attention to the latter area.
  • Under scanning power, you’ll note portions of the gyrus 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.
  • 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.
  • In the setting of ischemic injury to the brain (i.e., a “stroke”), what pattern of necrosis takes place?
  • What would an area of cerebral infarct look like a year or so later?


Slide 5 [WebScope][ImageScope]

Omentum: This omental adipose tissue 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).

  • 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 necrotic?
  • This is a case of enzymatic fat necrosis. Can you account for the fact that the cytoplasm of the dead cells appears purplish and does not appear “empty” like that of normal adipocytes? Injury to which organ would lead to this scenario?
  • On the outer surface of the largest tissue fragment, there is a layer of fibrin and neutrophils. This is consistent with a fibrinopurulent exudate (to be further discussed during subsequent lectures/labs pertaining to inflammation).
  • 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.
  • Supplementary slide (Slide 6): For sake of comparison, a quick look at Slide 6 [WebScope][ImageScope] 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 background, normal adipocytes. These spaces are “puddles” of cytoplasmic lipid from smashed adipocytes. What kind of cells are at the periphery of these puddles (hint: these cells are trying to “gobble” up the fat)? What cells are these derived from?
  • Finally, note that in the absence of exposure to pancreatic enzymes (Slide 6), the dead adipose tissue looks very different than in Slide 5 [WebScope][ImageScope].


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