Difference between revisions of "IPLab:Lab 4:Atheromatous Emboli"

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(Autopsy Findings)
 
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== Clinical Summary ==
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This 71-year-old male was admitted to the hospital with dry gangrene of the left great toe. Subsequently, he was found to have a poorly differentiated adenocarcinoma of the left upper lobe of the lung. He developed a perforation of a duodenal ulcer with generalized peritonitis and died five days after admission.
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Gross examination of the aorta revealed severe atherosclerosis with extensive mural thrombus formation. Recent infarcts were noted in the spleen and in the left kidney. An old posterior myocardial infarct was noted. The left iliac artery also appeared to be almost totally occluded. A whitish-tan tumor was noted in the apical portion of the left upper lobe of the lung with metastases in the carinal and hilar lymph nodes.
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== Images ==
 
== Images ==
 
<gallery heights="250px" widths="250px">
 
<gallery heights="250px" widths="250px">
File:IPlab4AtheromatousEmboli1.jpg|This is a gross photograph of the aorta from this patient opened lengthwise with the luminal surface visible. Note the rough surface with ulcerations and adherent thrombotic material. There is a mild dilation (aneurysm) at the distal aorta just at the bifurcation with an accumulation of thrombus.
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File:IPLab4AtheromatousEmboli1.jpg|This is a gross photograph of the aorta from this patient opened lengthwise with the luminal surface visible. Note the rough surface with ulcerations and adherent thrombotic material. There is a mild dilation (aneurysm) at the distal aorta just at the bifurcation with an accumulation of thrombus.
File:IPlab4AtheromatousEmboli2.jpg|This is a closer view of the luminal surface of the aorta from the previous image. The rough, ulcerated surface and the thrombotic material can be easily seen in this image.
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File:IPLab4AtheromatousEmboli2.jpg|This is a closer view of the luminal surface of the aorta from the previous image. The rough, ulcerated surface and the thrombotic material can be easily seen in this image.
File:IPlab4AtheromatousEmboli3.jpg|This is a low-power photomicrograph of kidney tissue. Several blood vessels can be identified at the corticomedullary junction (arrows).  
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File:IPLab4AtheromatousEmboli3.jpg|This is a low-power photomicrograph of kidney tissue. Several blood vessels can be identified at the corticomedullary junction (arrows).  
File:IPlab4AtheromatousEmboli4.jpg|This higher-power photomicrograph of one of the arcuate arteries reveals a cholesterol embolus. Note the needle-shaped space (arrow) within the lumen of this artery (arrow) which represents the space occupied by the cholesterol crystal that was dissolved away during histologic processing.
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File:IPLab4AtheromatousEmboli4.jpg|This higher-power photomicrograph of one of the arcuate arteries reveals a cholesterol embolus. Note the needle-shaped space (arrow) within the lumen of this artery (arrow) which represents the space occupied by the cholesterol crystal that was dissolved away during histologic processing.
File:IPlab4AtheromatousEmboli5.jpg|This is another view of this vessel with an atherosclerotic embolus. Note the cholesterol clefts (1) and thrombotic material (2) that occlude this artery.  
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File:IPLab4AtheromatousEmboli5.jpg|This is another view of this vessel with an atherosclerotic embolus. Note the cholesterol clefts (1) and thrombotic material (2) that occlude this artery.  
File:IPlab4AtheromatousEmboli6.jpg|A mesenteric artery also had an atherosclerotic embolus. Again note the cholesterol clefts and thrombotic material that occlude this artery.  
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File:IPLab4AtheromatousEmboli6.jpg|A mesenteric artery also had an atherosclerotic embolus. Again note the cholesterol clefts and thrombotic material that occlude this artery.  
 
</gallery>
 
</gallery>
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== Virtual Microscopy ==
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=== Kidney: Atheromatous Emboli ===
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<peir-vm>IPLab4AtheromatousEmboli</peir-vm>
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=== Normal Kidney ===
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<peir-vm>UAB-Histology-00114</peir-vm>
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== Study Questions ==
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* <spoiler text="What is the cause of atheromatous emboli?">Ulcerated or complex atherosclerotic plaques rupture and release cholesterol and other material into the blood stream. These materials lodge in vessels downstream. Ulceration or rupture of atherosclerotic plaques is part of the normal progression of atherosclerosis.</spoiler>
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* <spoiler text="What happens when atherosclerotic material embolizes?">When the atherosclerotic plaque ruptures collagen, cholesterol esters and necrotic material are exposed to the blood stream. This initiates thrombus formation. So, in addition to the cholesterol embolizing to distal vessels, thrombosis is also initiated and can obstruct vessels.</spoiler>
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* <spoiler text="What other types of material can embolize and cause clinical problems?">Probably 99% of all emboli are thromboemboli. Other materials that can embolize are: fragments of bone or bone marrow, fat, tumor cells, foreign bodies such as bullets, and bubbles of air or nitrogen.</spoiler>
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== Additional Resources ==
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=== Reference ===
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* [http://emedicine.medscape.com/article/1950759-overview eMedicine Medical Library: Noncoronary Atherosclerosis]
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* [http://emedicine.medscape.com/article/460428-overview eMedicine Medical Library: Cholesterol Embolism]
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* [http://www.merckmanuals.com/professional/hematology_and_oncology/thrombotic_disorders/overview_of_thrombotic_disorders.html Merck Manual: Thrombotic Disorders]
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=== Journal Articles ===
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* Scolari F, Ravani P.  [http://www.ncbi.nlm.nih.gov/pubmed/20381857 Atheroembolic renal disease].  ''Lancet'' 2010 May 8;375(9726):1650-60.
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=== Images ===
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* [{{SERVER}}/library/index.php?/tags/52-kidney PEIR Digital Library: Kidney Images]
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* [http://library.med.utah.edu/WebPath/ATHHTML/ATHIDX.html WebPath: Atherosclerosis and Thrombosis]
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* [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html WebPath: Cardiovascular Pathology]
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* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html WebPath: Renal Pathology]
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== Related IPLab Cases ==
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* [[IPLab:Lab 1:Kidney Infarction|Lab 1: Kidney: Infarction (Coagulative Necrosis)]]
  
 
{{IPLab 4}}
 
{{IPLab 4}}
  
 
[[Category: IPLab:Lab 4]]
 
[[Category: IPLab:Lab 4]]

Latest revision as of 02:01, 24 June 2020

Clinical Summary[edit]

This 71-year-old male was admitted to the hospital with dry gangrene of the left great toe. Subsequently, he was found to have a poorly differentiated adenocarcinoma of the left upper lobe of the lung. He developed a perforation of a duodenal ulcer with generalized peritonitis and died five days after admission.

Gross examination of the aorta revealed severe atherosclerosis with extensive mural thrombus formation. Recent infarcts were noted in the spleen and in the left kidney. An old posterior myocardial infarct was noted. The left iliac artery also appeared to be almost totally occluded. A whitish-tan tumor was noted in the apical portion of the left upper lobe of the lung with metastases in the carinal and hilar lymph nodes.

Images[edit]

Virtual Microscopy[edit]

Kidney: Atheromatous Emboli[edit]

Normal Kidney[edit]

Study Questions[edit]


Additional Resources[edit]

Reference[edit]

Journal Articles[edit]

Images[edit]

Related IPLab Cases[edit]

Mural thrombosis is the formation of multiple thrombi along an injured endocardial wall.

A thrombus is a solid mass resulting from the aggregation of blood constituents within the vascular system.

Plural of embolus. An embolus is something that blocks the blood flow in a blood vessel. It may be a gas bubble, a blood clot, a fat globule, a mass of bacteria, or other foreign body. It usually forms somewhere else and travels through the circulatory system until it gets stuck.