1. Atherosclerosis is a disease of large and medium-sized muscular arteries Characteristics: endothelial dysfunction vascular inflammation buildup of lipids‚ cholesterol‚ calcium and cellular debris within the intima of the blood vessel wall. The build up results in atheroma (plaque formation). It is a fatty deposit in the intima of an artery‚ resulting from atherosclerosis. Atheroma/Plaque is made up of: fatty substances Cholesterol Waste products from cells Calcium
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Stroke Pathophysiology Sid Shah‚ MD Pathophysiology of Stroke Sid Shah‚ MD Page 2 of 14 Stroke Pathophysiology Introduction The two major mechanisms causing brain damage in stroke are‚ ischemia and hemorrhage. In ischemic stroke‚ which represents about 80% of all strokes‚ decreased or absent circulating blood deprives neurons of necessary substrates. The effects of ischemia are fairly rapid because the brain does not store glucose‚ the chief energy substrate and is incapable of anaerobic
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INTRODUCTION Cardiovascular disease‚ currently the leading cause of death and illness in the United States‚ Europe and most developed countries‚ is fast growing to become the preeminent health problem worldwide (Murray & Lopez‚ 1997). Atherosclerosis is a progressive disease of the large and intermediate-sized arteries characterized by accumulation of lipids and fibrous elements which cause development of fatty lesions called atheromatous plaques on the inside surfaces of the arterial walls;
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The body health depends in keeping body fluid in balance‚ which distribute between intravascular in blood vessels‚ and extravascular which can be inside the cell (intracellular fluid) or between the cells called (interstitial fluid). Edema occurs when the interstitial volume has increased due to fluid leaks from capillaries or tiny blood vessels to interstitial space‚ then the space will expand cause edema.[1] To understand the mechanism clearly‚ fluid dynamic control should be considered‚ the hydrostatic
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Atherosclerosis is a disease affecting the arterial blood vessel and it is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries. Theses plaques begin to form when a vessel receives tiny injuries‚ usually at a point of branching. In turn these plaques gradually thicken and harden with fibrous material‚ cells‚ and other deposits‚ restricting the lumen (opening) of the vessel and reducing blood flow to the tissues‚
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blood vessel by an embolus (undissolved material carried by the blood and impacted in some part of the vascular system‚ as thrombi or fragments of thrombi‚ tissue fragments‚ clumps of bacteria‚ protozoan parasites‚ fat globules‚ or gas bubbles)‚ or thrombus (a clot that forms in and obstructs a blood vessel‚ or that forms in one of the chambers of the heart) formation. PVD causes either acute or chronic ischemia [ih-skee-mee-uh] (lack of blood supply). The symptoms of PVD are: • Claudication - pain
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Tesla is hemodynamically stable‚ without evidence of left atrial thrombus or heart failure. Her CHA2DS2-VASc score is at 6‚ which requires medication for stroke prevention with an anticoagulant (Epocrates‚ 2018). Ms. Tesla will be given a prescription for apixaban‚ an oral anticoagulant used for the prevention of stroke
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Factor V Leiden is a mutation of one of the clotting factors in the blood called Factor V. This mutation can increase your chance of developing abnormal blood clots (thrombophilia)‚ usually in your veins. Most people who have this particular disorder never develop any signs or symptoms. Your doctor will most likely suspect you have Factor V Leiden if you’ve had one more incident of thrombosis (blood clot) or a pregnancy loss. This disorder can be inherited if your family has a history of Factor V
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Because heparin is an anticoagulant‚ it is also called antithrombotic because it works to prevent the formation of a clot or thrombus. All anticoagulants work in the clotting cascade but so at different points. This specific drug prevents conversion of fibrinogen to fibrin and prothrombin by enhancing inhibitory effects of antithrombin III. Heparin works by binding to antithrombin
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number and % of RBC’s and HgB usually from blood loss or extreme erythrocyte destruction and malformation. It causes dyspnea‚ pallor‚ palpitation‚ fatigue‚ and hypotension. Embolus: foreign substance travels through blood stream (air‚ clot‚ fat). Thrombus: blood clot in blood vessel‚ usually caused by slow blood circulation‚ immobility‚ or changes in vessel walls. Hematoma: localized clotted mass of blood usually from traumatic injury causing blood vessel to rupture. Contusion: bruise-minor hematoma
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