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| ability to stop bleeding from blood vessels that have been injured. |
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| formation of a solid mass from the constituents of blood within living blood vessels or the heart. Involves interaction of blood vessel walls, formed elements of the blood and the blood clotting system (platelets and coagulation cascade leading to formation of a fibrin clot), and a feedback mechanism to prevent excessive clot formation (fibrinolysis, plasminogen system, anti-thrombin III). |
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| clotting of blood either within or outside of a vessel (hematoma, test tube) due solely to activation of the coagulation sequence. |
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| Contributors to normal hemostasis |
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Definition
| platelets, vascular wall and coagulation cascade |
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| Platelet contribution to hemostasis |
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Definition
| Adhere to ECM via glycoprotein1b receptor to vWF, leads to activation (secretion of granule contenets, changes in shape, and activation of receptors). Receptors cross-link with fibrinogen (aggregation), and fibrin deposition cements plug in place. |
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| vascular wall contribution to hemostasis |
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Definition
| contains factors for coagulation, exposure leads to activation of platelets |
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| coagulation cascade contribution to hemostasis |
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Definition
| tissue factor initiates coagulation cascade, thrombin coverts fibrinogen to fibrin, restricted to sites of vascular injury |
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| 3 major factors predisposing to thrombosis |
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Definition
Injury to endothelium
Alteration in normal blood flow Alterations in the blood (hypercoagulability) |
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| by toxins, hypertension, inflammation or metabolic products |
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| Alterations in blood flow |
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Definition
| stasis or turbulence (due to aneurysms or atherosclerotic plaque) |
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| hypercoagulability, either primary (factor V leiden, increased prothrombin synthesis, antithrombin II deficiency) or secondary (bed rest, tissue damage, malignancy) |
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Definition
| are typically relatively rich in platelets because endothelial injury leads to platelet activation. They are usually superimposed on a ruptured atherosclerotic plaque or due to other vascular injuries |
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Definition
| frequently propagate some distance toward the heart, forming a long case within the vessel lumen that is prone to give rise to emboli. An increase in activity of coagulation factors is involved in the gensis of most venous thrombi, with platelet activation playing a secondary role. These thrombi form in the sluggish venous circulation and tend to contain more enmeshed red cells |
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| microscopic or gross apparent laminations that represent pale platelet and fibrin layers alternating with darker red cells, they are only found in thrombi that form in flowing blood, can distinguish antemortem thrombosis from the nonlaminated clots that form in the postmortem state |
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Term
| White (coagulation) Thrombi |
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Definition
| arise in rapidly moving arterial or cardiac circulation. Are composed of alternating layers of fibrin and platelets, with only a few trapped red cells. The layering results in lines of Zahn. |
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Definition
| form in vessels with sluggish blood flow, such as veins. They have tangled fibrin layers and large amounts of coagulated blood. Usually their primary origin is firmly attached to the underlying endothelium. |
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| attached to the inner wall of the heart |
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| completely obstructing a vessel |
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| attached to the heart valves |
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| Four events following the development of a thrombus |
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Definition
| Propagation, embolization, dissolution, organization and recanalization |
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| Thrombi can enlarge vai accretion of additional platelets and fibrin, increasing the odds of vascular occlusion or embolization |
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| part of all of the thrombus is dislodged and transported elsewhere in the vasculature |
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Definition
| fibrinolytic system can rapidly shrink and dissolve newly formed clots. |
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| Organization and recanalization |
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Definition
| older thrombi becomes organized by ingrowth of endothelial cells, smooth muscle cells, and fibroblasts. can lead to an aneurysm. |
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| Clinical Significance of a Thrombi |
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Definition
| is dependent on location and size of thrombus, age of patient, accompanying disorders. |
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Term
| Disseminated Intravascular Coagulation |
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Definition
| is an acquired thrombo-hemorrhagic disorder occurring as a secondary complication of a variety of conditions, such as obstetric complications, infections, neoplasms, massive tissue injury. |
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Definition
| Is characterized by activation of the coagulation sequence that leads to the formation of microthrombi throughout the microcirculation of the body. As a consequence, there is consumption of platelets, fibrin, and coagulation factors and, secondarily, activation of fibrinolytic mechanisms. Hemorrhage may resuls from depletion of the elements required for hemostasis. Clinically there is multiple site bleeding, such as from nose, mouth, rectum, IV sites.Usually all laboratory findings related to coagulation are abnormal. Treatment is directed at control of the underlying disorder. |
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| Blockage of a coronary artery due to a thromboembolus results in death of heart muscle, which is characterized by |
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| Initiation of DIC can be caused by all of the following EXCEPT |
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A 76 year old man was admitted to hospital with abdominal pain, fever, and leukocytosis. He was diagnosed with acute diverticulitis, an inflammatory disease of the colonic wall that occurs when the weakened walls of these diverticuli perforate. Antibiotics were administered, but his condition rapidly worsened as colonic bacteria seeded into the peritoneal cavity, causing diffuse peritonitis. Emergency surgery was performed to remove a portion of the descending colon. His post-operative course was complicated by acute pancreatitis, gram-negative bacterial sepsis, and disseminated intravascular coagulation (DIC). He became disoriented 2 days after surgery, and died 4 days later.
The development of DIC in this patient was most likely related to which of the following? |
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Definition
| Induced expression of tissue factor by endothelium and mononuclear phagocytes, as a consequence of exposure to bacterial endotoxin |
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| Induced expression of tissue factor by endothelium and mononuclear phagocytes, as a consequence of exposure to bacterial endotoxin |
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| Which artery is the most common site of occlusive arterial thrombosis? |
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