IPLab:Lab 4:Thrombosis - Revision history

Peter Anderson: /* Images */

2020-07-08T19:23:11Z

‎Images

Peter Anderson: /* Images */

2020-07-08T19:20:51Z

‎Images

Peter Anderson: /* Images */

2020-07-08T19:14:20Z

‎Images

Peter Anderson: /* Autopsy Findings */

2020-06-24T01:58:42Z

‎Autopsy Findings

Peter Anderson: /* Clinical Summary */

2020-06-24T01:58:35Z

‎Clinical Summary

Seung Park at 16:11, 3 January 2014

2014-01-03T16:11:48Z

Seung Park: /* Images */

2013-08-30T01:31:12Z

‎Images

Seung Park at 02:58, 22 August 2013

2013-08-22T02:58:20Z

Seung Park at 14:58, 21 August 2013

2013-08-21T14:58:26Z

Peter Anderson at 14:28, 21 August 2013

2013-08-21T14:28:58Z

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 <gallery heights="250px" widths="250px">
 File:IPLab4Thrombosis1.jpg|This is a gross photograph of thrombosed coronary artery (arrows).
-File:IPLab4Thrombosis2.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
+File:IPLab4Thrombosis2x.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
 File:IPLab4Thrombosis3.jpg|This is a higher-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque.
 File:IPLab4Thrombosis4.jpg|This is another high-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque. Note the presence of cholesterol crystals.

@@ Line 7: / Line 7: @@
 <gallery heights="250px" widths="250px">
 File:IPLab4Thrombosis1.jpg|This is a gross photograph of thrombosed coronary artery (arrows).
-File:IPLab4Thrombosis2b.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
+File:IPLab4Thrombosis2.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
 File:IPLab4Thrombosis3.jpg|This is a higher-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque.
 File:IPLab4Thrombosis4.jpg|This is another high-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque. Note the presence of cholesterol crystals.

@@ Line 7: / Line 7: @@
 <gallery heights="250px" widths="250px">
 File:IPLab4Thrombosis1.jpg|This is a gross photograph of thrombosed coronary artery (arrows).
-File:IPLab4Thrombosis2.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
+File:IPLab4Thrombosis2b.jpg|This is a low-power photomicrograph of thrombosed coronary artery. The thrombus (1) completely occludes the vessel. Note the layering of the thrombus. The fibrous cap is ruptured (arrow) and there is hemorrhage into the atherosclerotic plaque. Note the cholesterol crystals in the plaque.
 File:IPLab4Thrombosis3.jpg|This is a higher-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque.
 File:IPLab4Thrombosis4.jpg|This is another high-power photomicrograph of the ruptured fibrous cap (arrows) with hemorrhage (1) into the atherosclerotic plaque. Note the presence of cholesterol crystals.

← Older revision		Revision as of 01:58, 24 June 2020
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	At autopsy the heart weighed 500 grams. There was massive acute myocardial infarction (about 2 days old) involving the posterior left ventricle, interventricular septum, and right ventricle from apex to base. The infarct was transmural, and there was a small rupture in the soft infarcted area at the apex. There were 1200 mL of blood within the right pleural cavity, probably secondary to this rupture. The coronary arteries showed moderate to severe atherosclerosis throughout the coronary tree.		At autopsy the heart weighed 500 grams. There was massive acute myocardial infarction (about 2 days old) involving the posterior left ventricle, interventricular septum, and right ventricle from apex to base. The infarct was transmural, and there was a small rupture in the soft infarcted area at the apex. There were 1200 mL of blood within the right pleural cavity, probably secondary to this rupture. The coronary arteries showed moderate to severe atherosclerosis throughout the coronary tree.
−
−	~~== Autopsy Findings ==~~
−
−	The heart weighed 500 grams. There was massive acute myocardial infarction (about 2 days old) involving the posterior left ventricle, interventricular septum, and right ventricle from apex to base. The infarct was transmural, and there was a small rupture in the soft infarcted area at the apex. There were 1200 mL of blood within the right pleural cavity, probably secondary to this rupture. The coronary arteries showed moderate to severe atherosclerosis throughout the coronary tree.

	== Images ==		== Images ==

@@ Line 1: / Line 1: @@
 == Clinical Summary ==
-This 83-year-old white male was admitted with the chief complaint of chest pain. He had been awakened the previous night with dull chest pain which was retrosternal and radiated through to his back. The pain was associated with sweating, nausea, and vomiting and could not be relieved by antacids. Nitroglycerin gave prompt relief. Following admission he developed cardiac arrhythmias. His AST was found to be 130 IU/L. In the early morning of the day after admission, he developed severe epigastric pain and several episodes of tachycardia (150-160 beats per minute) and later cardiac standstill. He expired less than a day after admission. There was a history of hypertension and diabetes.
+At autopsy the heart weighed 500 grams. There was massive acute myocardial infarction (about 2 days old) involving the posterior left ventricle, interventricular septum, and right ventricle from apex to base. The infarct was transmural, and there was a small rupture in the soft infarcted area at the apex. There were 1200 mL of blood within the right pleural cavity, probably secondary to this rupture. The coronary arteries showed moderate to severe atherosclerosis throughout the coronary tree.
 == Autopsy Findings ==

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 File:IPLab4Thrombosis10.jpg|This is a high-power photomicrograph of the luminal surface of a re-canalized vessel. Note that the vessel lumen is lined by endothelial cells (arrows).
 </gallery>
 == Study Questions ==

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 === Images ===
-* [http://peir.path.uab.edu/library/index.php?/tags/34-coronary_artery PEIR Digital Library: Coronary Artery Images]
+* [{{SERVER}}/library/index.php?/tags/34-coronary_artery PEIR Digital Library: Coronary Artery Images]
 * [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html WebPath: Cardiovascular Pathology]

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 * <spoiler text="What is the source for the fibroblasts and endothelial cells that are present in organizing thrombi?">Organization of a thrombus involves a process similar to the normal healing response. First there is inflammation with macrophages that phagocytose the thrombotic material. Then fibroblasts and endothelial cells from the vessel wall and the vasa vasorum of the vessel migrate into thrombotic material. This process results in a picture similar to granulation tissue in a healing wound.</spoiler>
 * <spoiler text="Does recanalization of a thrombus results in normal blood flow to the tissue?">Usually not. The recanalized lumen is not very large and by the time the thrombus is recanalized, the tissue supplied by that artery is usually already dead. Any blood flow down this vessel will help to accelerate the wound healing process in the tissue downstream.</spoiler>
 {{IPLab 4}}
 [[Category: IPLab:Lab 4]]

← Older revision		Revision as of 14:28, 21 August 2013
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		+	== Clinical Summary ==
		+
		+	This 83-year-old white male was admitted with the chief complaint of chest pain. He had been awakened the previous night with dull chest pain which was retrosternal and radiated through to his back. The pain was associated with sweating, nausea, and vomiting and could not be relieved by antacids. Nitroglycerin gave prompt relief. Following admission he developed cardiac arrhythmias. His AST was found to be 130 IU/L. In the early morning of the day after admission, he developed severe epigastric pain and several episodes of tachycardia (150-160 beats per minute) and later cardiac standstill. He expired less than a day after admission. There was a history of hypertension and diabetes.
		+
		+	== Autopsy Findings ==
		+
		+	The heart weighed 500 grams. There was massive acute myocardial infarction (about 2 days old) involving the posterior left ventricle, interventricular septum, and right ventricle from apex to base. The infarct was transmural, and there was a small rupture in the soft infarcted area at the apex. There were 1200 mL of blood within the right pleural cavity, probably secondary to this rupture. The coronary arteries showed moderate to severe atherosclerosis throughout the coronary tree.
		+
	== Images ==		== Images ==
	<gallery heights="250px" widths="250px">		<gallery heights="250px" widths="250px">