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64 Cards in this Set
- Front
- Back
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functions of normal hemostasis?
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maintain blood in a fluid, clot-free state
induce rapid and localized plug at site of vascular injury |
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thrombosis
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inappropriate activation of normal hemostatic process
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what are hemostasis and thrombosis regulated by?
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platelets, vascular wall and coagulation cascade
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what makes primary hemostasis?
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ECM exposed and platelet aggregation to form a plug
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what makes secondary hemostasis?
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TF released by endothelial cells, coagulation cascade, thrombin, fibrin, more platelets
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what two products of endothelial cells are both vasodilators and inhibitors of platelet aggregation?
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NO and PGI2
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what is protein C activated by and what does it do?
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activated by thrombin with thrombomodulin
cleaves factors V and VIII |
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what does tissue factor pathway inhibitor do?
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inhibits factors VII and X
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what do heparin-like molecules do?
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cofactor with antithrombin III to inactivate thrombin and factor X
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what does tissue-type plasminogen activator(t-PA) do?
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promotes fibrinolytic activity from plasminogen
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when is von Willenbrand factor(vWF) produced and what does it do?
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it is produced all the time and it helps to adhere platelets to collagen and other surfaces
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what do endothelial cells secrete to depress fibrinolysis?
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inhibitors of plasminogen activator (PAI's)
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what do platelet alpha granules contain?
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P-selectin
fibrinogen fibronectin factors V and VIII platelet-derived growth factor transforming growth factor-beta |
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what do platelet beta granules contain?
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adenine nucleotides
ionized calcium histamine serotonin epinephrine |
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what part of vWF helps to adhere platelets to the ECM?
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glycoprotein Ib
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what is ADP's role in coagulation?
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helps platelets adhere to other platelets
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what products secreted by platelets stimulate platelet aggregation?
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ADP, thromboxane A2 and fibrinogen
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what does aspirin do to prevent thrombosis?
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blocks thromboxane A2 synthesis
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what triggers the extrinsic coagulation cascade?
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TF
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where do the coagulation pathways converge?
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factor X
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how is antithrombin induced and what does it do?
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activated by binding to heparin-like molecules
inhibits thrombin and factors IX,X,XI, and XII |
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how does tissue factor pathway inhibitor work?
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complexes to factor X and to TF-VII and inactivates them
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what are the two plasminogen activators?
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urokinase-like PA (uPA)
tissue-type PA (tPA) |
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how does tPA work?
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made by endothelial cells
attached to fibrin |
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what is the Virchow triad?
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three primary influences of thrombus
endothelial injury stasis or turbulent blood flow hypercoagulability |
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aneurysms
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abnormal aortic and arterial dilations
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most common causes of genetic hypercoagulability?
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factor V and prothrombin gene mutations
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defect in factor V mutation?
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glutamine for arginine and 506
cannot be cleaved by protein C |
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defect in prothrombin mutation?
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G to A in 3' untranslated region causes three-fold increase in levels
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what causes hypercoagulability with increasing age?
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increased susceptibility to platelet aggregation and reduced PGI2
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what do lines of Zahn indicate?
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thrombosis at a site of blood flow
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mural thrombi?
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thrombi adhered to the wall of the underlying structure
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where are red thrombi found?
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veins
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risk factors for deep vein thrombosis?
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pregnancy
immobilization malignancy hypercoagulable states obesity |
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what is DIC?
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sudden onset of widespread fibrin thrombi in the microcirculation
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presentation of DIC?
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initial thrombotic disorder evolving in to a serious bleeding disorder
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embolus
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detached intravascular solid, liquid or gaseous mass carried by the blood to a distant site from point of origin
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infarction
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ischemic necrosis of distal tissue
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major sites for arteriolar embolization?
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lower extremities and brain
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what characterizes fat embolism?
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pulmonary insufficiency, neurologic symptoms, anemia and thrombocytopenia
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thrombocytopenia?
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decrease in platelet number
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caisson disease
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persistence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis
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what type of necrosis happens in infarction?
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ischemic coagulative necrosis, except in the brain which is liquefactive
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what organs are most susceptible to infarction?
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kidney and spleen- end arterial
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what cells are particularly vulnerable to hypoxia?
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neurons and myocardial cells
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shock
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hypoperfusion due to reduction in cardiac output or in circulating blood volume
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most common cause of septic shock?
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gram negative bacteria
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what causes anaphylactic shock?
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IgE mediated hypersensitivity response associated with vasodilation and increase vascular permeability
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what produces the effects in septic shock
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bacterial wall lipopolysaccharides
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what other parts are involved in septic shock besides LPS?
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LPS binding protein, CD14, TLR-4
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ascites
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hydroperitoneum
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anasarca
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severe and generalized edema with profound subQ tissue swelling
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transudate
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protein-poor edema
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exudate
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protein-rich edema
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what usually causes generalized increases in venous pressure?
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congestive heart failure
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important cause of albumin loss?
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nephrotic syndrome-leaky glomerular capillary wall and generalized edema
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what causes edema of dependent body parts?
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congestive heart failure
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what causes edema in the whole body?
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liver or kidney dysfunction
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hyperemia
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active process of increased blood flow in a particular tissue
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congestion
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passive process of increased blood flow in a particular tissue
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hematoma
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accumulation of blood within a tissue
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petechiae
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1-2mm hemorrhages in skin, mucous membranes or serosal surfaces due to increased pressure, defective platelet fx, clotting factor deficits
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purpura
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over 3mm hemorrhages due to trauma, vascular inflammation or increased vascular fragility
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ecchymoses
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1-2cm subQ hematomas due to trauma
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