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M1 Histopathology Labs with Virtual Slides
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Histopath Lab 6:
Circulatory Derangements II

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Robbins and Cotran Pathologic Basis of Disease 9th Ed.

Suggested Reading:
Pages 113-116 – Edema and Congestion
Pages 122-129 – Thrombosis and Embolism
Pages 129-131 – Infarction
Pages 526-531 – Heart Failure
Pages 540-550 – Ischemic Heart Disease
Pages 697-699 – Pulmonary Embolism/Infarction
Pages 779-780 – Ischemic Bowel Disease
Pages 864-865 – Hepatic Circulatory Disorders


CIRCULATORY DERANGEMENTS II


Slide 47 [WebScope][ImageScope]

Lung: 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, while in other parts of the section (the abnormal area of lung tissue), 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 abnormal area with those in the more normal area. What process is going on in the “filled” area?
  • What is going on at the interface between the normal and abnormal lung tissue?
  • Within a number of pulmonary arterial branches, you’ll note dense blood clots. What is going on at the interface between the vessel wall and the clot? What does this tell you about the duration of the process? Can you think of a clinical situation in which this would occur?
  • 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 and radiologic features of this process we are seeing in this patient’s lung? What are the radiographic manifestations?

 

Slide 48 [WebScope][ImageScope]

Kidney: 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?
  • 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?
  • A side note: road 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. However, in other sections from this patient’s kidney there was a leukocytic reaction and clear-cut infarcts.
  • What are other (i.e., non-renal) manifestations of atheroembolism?

 

Slide 49 [WebScope][ImageScope]

Heart: 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.”

  • How can you distinguish epicardial from endocardial surface?
  • At scanning power, the myocardium has an abnormally mottled appearance with irregular pale patches. Focus on these pale areas. What is going on here?
  • 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 [WebScope][ImageScope] during the first laboratory session. Describe the evolution of a focus of coagulative necrosis into what you see in Slide 49 [WebScope][ImageScope].
  • 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?
  • What sort of clinical scenario would you observe this histopathology in the myocardium?
  • What are the possible consequences of myocardial infarction?

     

Slide 50 [WebScope][ImageScope]

Colon: 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?

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