IPLab:Lab 4:Mural Thrombus: Difference between revisions - Pathology Education Instructional Resource

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File:IPLab4MuralThrombus7.jpg|This high-power photomicrograph of thrombus demonstrates more clearly the components of the layers--the pale regions which contain primarily platelets (degranulated platelets) with some fibrin (1), and the red areas which contain RBCs, some leukocytes, and fibrin (2).

</gallery>

== Study Questions ==

* <spoiler text="Why do mural thrombi form on the endocardium of the heart after a myocardial infarction?">The infarct produced necrosis and inflammation. Also, the infarcted ventricular wall is akinetic and/or dyskinetic (bulges outward during systole). Thus, the blood in the ventricle tends to form thrombi on the surface of the infarcted endocardium.</spoiler>

* <spoiler text="List the sequence of events leading to mural thrombus formation.">* Platelets bind to damage endocardium and release ADP, 5-HT, thromboxane and platelet factor 4.

* This results in recruitment of more platelets and more degranulation of platelets with activation of the clotting cascade.

* Thrombin is activated leading to fibrin polymerization.

* This process results in the development of a platelet-fibrin thrombus.</spoiler>

* <spoiler text="What are possible sequelae of these mural thrombi?">The thrombotic material may break off and go to the brain or kidney (the two most likely sites since they get so much blood flow) or any arterial system.</spoiler>

[[Category: IPLab:Lab 4]]

@@ Line 17: / Line 17: @@
 File:IPLab4MuralThrombus7.jpg|This high-power photomicrograph of thrombus demonstrates more clearly the components of the layers--the pale regions which contain primarily platelets (degranulated platelets) with some fibrin (1), and the red areas which contain RBCs, some leukocytes, and fibrin (2).
 </gallery>
+== Study Questions ==
+* <spoiler text="Why do mural thrombi form on the endocardium of the heart after a myocardial infarction?">The infarct produced necrosis and inflammation. Also, the infarcted ventricular wall is akinetic and/or dyskinetic (bulges outward during systole). Thus, the blood in the ventricle tends to form thrombi on the surface of the infarcted endocardium.</spoiler>
+* <spoiler text="List the sequence of events leading to mural thrombus formation.">* Platelets bind to damage endocardium and release ADP, 5-HT, thromboxane and platelet factor 4.
+* This results in recruitment of more platelets and more degranulation of platelets with activation of the clotting cascade.
+* Thrombin is activated leading to fibrin polymerization.
+* This process results in the development of a platelet-fibrin thrombus.</spoiler>
+* <spoiler text="What are possible sequelae of these mural thrombi?">The thrombotic material may break off and go to the brain or kidney (the two most likely sites since they get so much blood flow) or any arterial system.</spoiler>
 {{IPLab 4}}
 [[Category: IPLab:Lab 4]]