What is the organ? Describe What do you see. Gross Heart, view of the tricuspid valve from the right atrium The valve are obscured by the presence of large irregular and friable masses of thrombi, also called vegetations.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
What is the organ?
Describe What do you see.
Gross Heart, view of the tricuspid valve from the right atrium The valve are obscured by the presence of large irregular and friable masses of thrombi, also called vegetations
The vegetations are formed due to an underlying damage to the valvular endocardium (endocarditis) by organisms (bacteria, fungi) that gain access to the venous circulation, (in intravenous drug abusers via use of nonsterile needles). The microorganisms reach the tricuspid valve, causing inflammation (endocardial injury), thus allow infected thromboi (or vegetations) to form.
Describe what do you see.
low-power micrograph Heart, coronary artery - Angiography & radiograph The left frame shows marked narrowing as seen by angiography. The right shows the histology of the narrowing.
There is marked thickening of the intima due to coronary atherosclerosis( it is a disease of the intima and the process is characterized by lipid deposition in the intimal layer followed by laying down of collagen and calcification).. The red mass in the narrowed lumen is a postmortem clot.
Describe what do you see
The lumen of the coronary artery is completely occluded by a dark red thrombus. Thrombosis in general results from damage to the endothelium. The most common and the most important cause of arterial thrombosis is atherosclerosis.
Describe what do you see
A fresh thrombus is attached to the damaged endothelium. In some parts of the thrombus, there is formation of new capillary channels. This process, called recanalization, can restore blood flow. Note that the media is thinned, secondary to compression by the thickened intima.
-What are other causes of arterial
thrombosis?Arterial thrombosis is caused by injury to the endothelium. In addition to
-What is the thrombus made of?
Fibrin, platelets, and red cells
Arterial thrombosis is caused by endothelial damage (eg, atherosclerosis or vasculitis);
venous thrombosis is caused by stasis (sluggishness) of blood flow.
Both types of vessels are affected in hypercoagulable states such as antithrombin or protein C deficiency.
-What conditions predispose to venous thrombosis?
Venous stasis caused by prolonged immobilization (eg, in hospitalized patients after surgery) or by congestive heart failure.
-What is the most common symptom associated with such venous thrombi?
There are no symptoms in about 50% of cases. Local pain and edema occur in the remaining cases.
Organization with recanalization.
If more than 60% of the pulmonary circulation is obstructed by emboli, the patient is at a high risk of sudden death due to acute right heart failure (cor pulmonale) or shock (cardiovascular collapse).
High power Lung, infarct
The alveolar septa are prominent, due to marked congestion of the capillaries. The alveolar lumens contain pale-staining edema fluid.
The fluid in pulmonary edema is a transudate (ie, it is protein poor, has low specific gravity, and does not contain inflammatory cells). Edema in inflammation is an exudate.
patient with ischemic heart disease can develop failure of the left ventricle and, eventually, of the right ventricle, giving rise to congestive heart failure. Because of impaired venous return to the heart, the neck veins become distended, the liver becomes enlarged, and fluid collects in interstitial spaces (edema).
The patient infectived with with gram-negative Bactria will develop septicemia. The shock will result from release from the bacteria of endotoxins that triggered the release of inflammatory mediators such as IL-1 and tumor necrosis factor (TNF).
TNF plays an important role in the development of septic shock by promoting the release of IL-1, IL-6, IL-8, and nitric oxide, thus initiating a cytokine cascade. These mediators, in low to moderate quantities, may lead to local inflammation and systemic effects, such as fever. When present in higher quantities, however, they promote the development of shock by causing systemic vasodilation, impaired myocardial contractility, and widespread endothelial injury, which may lead to DIC.
Compare the thinned and discolored cerebral cortex on the left side to the relatively preserved cortex on the right side