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30 Cards in this Set
- Front
- Back
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What do Protein C and Protein S do?
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These are Vit K dependent proteins that inactivate the cofactors Va and VIIIa and help to control coagulation
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Intrinsic pathway cascade
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Activated by factor XII (Hageman facotr),--> XI --> IX --> VIII --> X
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Extrinsic pathway cascade
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Tissue factor activates factor VII (needs Vit k) --> IX --> X
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Which factor shows up in both clotting cascades?
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Factor IX
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What is the test for intrinsic pathway clotting?
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Partial thromboplastin time (PTT). If you have deficeincies in this pathway the time it takes will be longer.
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What is the test for extrinsic pathway clotting?
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Prothrombin time (PT). Normal is 10-12 sec. Values >2 sec longer than this are abnormal.
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What drug acts on the intrinsic pathway to prevent clotting?
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Heparin, although its mostly used in heparin locks in hospitals and dialysis centers
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What drugs act on extrinsic pathway to prevent clotting?
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Coumadin, which is an anti-Vitamin K drug and Pradaxa (dabigatran) which blocks thrombin activation
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What is INR?
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Its basically just a standardized way of expressing PT. Normal is 0.9 to 1.1.
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When should you discontinue an anti-clotting drug pre-op?
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Never, you just titrate them to get down in the 2 range on INR
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What is the Virchow triad?
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It comprises three things that predispose to thrombus formation 1) Endothelial injury 2) Stasis or turbulence of blood flow 3) Blood hyper-coagulability
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What type of thrombosis is caused by turbulence?
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Cardiac and arterial thrombosis
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What type of thrombosis is caused by stasis?
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Venous thrombosis
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What is the single most important factor in thrombus formation?
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Endothelial injury or integrity
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What are the most common sites for arterial thorombus formation?
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1) Coronary 2) Cerebral 3) Femoral
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What are the most common areas for venous thrombi (phlebothrombosis)?
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Veins of the lower extremities
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Under what circumstances do thrombi form on heart valves?
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Infective, non-bacterial, and Libman-Sacks endocarditis
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Effect of Rheumatic heart disease on thrombus formation
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The heart valves get destroyed and become areas of turbulent blood flow where clots can easily form
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Characterize disseminate intravascular coagulation (DIC)
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Not a primary disease, widespread thrombin activation and micro thrombi are formed. This consumes all the platelets and clotting factors and the pt will bleed. Organ failure eventually
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What is the origin of 99% of emboli?
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They come from some part of a dislodged thrombus.
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What are the potential consequences of thromboembolic events?
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Ischemic necrosis of down-stream tissue due to infarction from vascular blockage
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Where do most pulmonary emboli originate from?
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Usually from a deep leg vein thrombosis above the level of the knee
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What is systemic thromboembolism?
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It refers to emboli traveling within the arterial circulation. 80% arise from intracardiac mural thrombi. Usually end up in lower extremeties
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What are the 4 classifications of infarcts?
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Red (hemorrhagic), white (anemic), septic (bacterial), and bland
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Where do red infacrts occur?
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In venous occlusions and loose tissues such as the lung. Also in tissues with dual circulation like the lung and small intestine
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Where do white infarcts occur?
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In arterial occlusions and in solid organs like the heart, spleen, and kidney
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What is the dominant histologic characteristic of infarction?
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Ischemic coagulative necrosis
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What are the 3 major causes of shock?
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Cardiogenic, hypovolemic, and septic(they are all characterised by hyopersion)
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What are the cytokines involved in endotoxic shock?
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TNF, IL-1, and IL-6/IL-8. This constitutes 70% of septic shock cases.
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Which organs show greatest cellular damage from shock?
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Brain, heart, lungs, kidneys, adrenals, and GI tract
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