IPLab:Lab 1:Myocardial Infarction - Revision history

Peter Anderson at 14:26, 16 September 2015

2015-09-16T14:26:40Z

Seung Park at 15:35, 3 January 2014

2014-01-03T15:35:13Z

Seung Park at 01:22, 30 August 2013

2013-08-30T01:22:02Z

Seung Park at 23:31, 18 August 2013

2013-08-18T23:31:19Z

Seung Park at 05:11, 16 August 2013

2013-08-16T05:11:33Z

Seung Park at 03:12, 16 August 2013

2013-08-16T03:12:18Z

Seung Park at 14:49, 15 August 2013

2013-08-15T14:49:48Z

Seung Park at 14:43, 15 August 2013

2013-08-15T14:43:45Z

Seung Park at 14:11, 15 August 2013

2013-08-15T14:11:22Z

Seung Park at 14:08, 15 August 2013

2013-08-15T14:08:37Z

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 == Virtual Microscopy ==
 <peir-vm>IPLab1MyocardialInfarction</peir-vm>
 == Study Questions ==

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 File:IPLab1MyocardialInfarction7.jpg|This high-power photomicrograph contains normal myocytes (1), vacuolated myocytes (2), and infarcted myocytes (3).
 </gallery>
 == Study Questions ==

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 === Images ===
-* [http://peir.path.uab.edu/library/index.php?/tags/43-myocardial_infarct PEIR Digital Library: Myocardial Infarct Images]
+* [{{SERVER}}/library/index.php?/tags/43-myocardial_infarct PEIR Digital Library: Myocardial Infarct Images]
 * [http://library.med.utah.edu/WebPath/CVHTML/CVIDX.html WebPath: Cardiovascular Pathology Images]

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 == Images ==
-<gallery>
+<gallery heights="250px" widths="250px">
 File:IPLab1MyocardialInfarction1.jpg|In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal.
 File:IPLab1MyocardialInfarction2.jpg|This is a low-power photomicrograph of the left ventricular free wall extending from the epicardium (1) to the endocardium (2). The area of infarction is the darker red (hypereosinophilic area) along the subendocardium (3).

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 == Images ==
-{| cellpadding="10"
+<gallery>
-| [[Image:IPLab1MyocardialInfarction1.jpg|frameless]]
+File:IPLab1MyocardialInfarction1.jpg|In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal.
-| In this gross photograph of the heart from this case, note the area of fresh myocardial infarction (arrows) in the anterior portion of the left ventricle and extending into the anterior portion of the interventricular septum. Note that the walls of the left and right ventricle are slightly thicker than normal.
+File:IPLab1MyocardialInfarction2.jpg|This is a low-power photomicrograph of the left ventricular free wall extending from the epicardium (1) to the endocardium (2). The area of infarction is the darker red (hypereosinophilic area) along the subendocardium (3).
-|-
+File:IPLab1MyocardialInfarction3.jpg|This higher-power photomicrograph shows endocardium on the right side of this image. Directly beneath the endocardium is a pale area consisting of cardiac myocytes exhibiting vacuolar degeneration (1). The area of infarction is visible as a hypereosinophilic area (2) and there is a second zone of vacuolated myocytes (3) between the infarct and the normal myocardium (4).
-| [[Image:IPLab1MyocardialInfarction2.jpg|frameless]]
+File:IPLab1MyocardialInfarction4.jpg|This high-power photomicrograph shows the area of infarction on the right (1). There is an area of vacuolated myocytes (2) adjacent to the infarcted myocytes and then normal cardiac muscle to the left (3).
-| This is a low-power photomicrograph of the left ventricular free wall extending from the epicardium (1) to the endocardium (2). The area of infarction is the darker red (hypereosinophilic area) along the subendocardium (3).
+File:IPLab1MyocardialInfarction5.jpg|This high-power photomicrograph shows the endocardium (1) and the area of subendocardial vacuolar degeneration (2). The area of infarction (3) contains some red blood cells.
-|-
+File:IPLab1MyocardialInfarction6.jpg|This high-power photomicrograph demonstrates the border between the vacuolated subendocardial myocytes (1) and the infarcted myocytes (2).
-| [[Image:IPLab1MyocardialInfarction3.jpg|frameless]]
+File:IPLab1MyocardialInfarction7.jpg|This high-power photomicrograph contains normal myocytes (1), vacuolated myocytes (2), and infarcted myocytes (3).
-| This higher-power photomicrograph shows endocardium on the right side of this image. Directly beneath the endocardium is a pale area consisting of cardiac myocytes exhibiting vacuolar degeneration (1). The area of infarction is visible as a hypereosinophilic area (2) and there is a second zone of vacuolated myocytes (3) between the infarct and the normal myocardium (4).
+</gallery>
 == Study Questions ==

← Older revision		Revision as of 03:12, 16 August 2013
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 * [http://www.merckmanuals.com/professional/cardiovascular_disorders/coronary_artery_disease/acute_coronary_syndromes_acs.html Merck Manual: Acute Coronary Syndromes]
-== Journal Articles ==
+=== Journal Articles ===
 * Agnew NM, Pennefather SH, Russell GN.  [http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2044.2002.02469.x/full Isofluorane and coronary heart disease].  ''Anaesthesia'' 2002; 57(4): 338-347
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 == Study Questions ==
-* What type of necrosis is present in this myocardial tissue?
+* <spoiler text="What type of necrosis is present in this myocardial tissue?">Coagulative necrosis.</spoiler>
-<spoiler>Coagulative necrosis.</spoiler>
+* <spoiler text="What are the morphologic characteristics of coagulative necrosis?">Hypereosinophilia, coagulation of cellular proteins, and loss of nuclei (pyknosis, karyolysis, and karyorrhexis).</spoiler>
-* What are the morphologic characteristics of coagulative necrosis?
+* <spoiler text="What causes the vacuolar change seen in the tissue adjacent to this infarct and is this change reversible or irreversible injury?">The vacuolar change (hydropic change) seen in myocytes at the edge of an infarct is a REVERSIBLE CHANGE caused by CELLULAR EDEMA.
-* What causes the vacuolar change seen in the tissue adjacent to this infarct and is this change reversible or irreversible injury?
+At the edge of an infarct the oxygen tension is low (hypoxia) so there is a decrease in oxidative metabolism and an increase in anaerobic glycolysis. Since anaerobic glycolysis is less efficient than aerobic metabolism there are lower ATP levels which result in impaired osmotic regulation. In addition, metabolic metabolites accumulate which further increases the intracellular osmotic load and leads to cellular edema.</spoiler>
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