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36 Cards in this Set

  • Front
  • Back
What is hemostasis?
Hemostasis is the arrest of bleeding, in a healthy vessel anti-clotting factors predominate, in an injured vessel pro-clotting factors predominate.
What is the result of uncontrolled bleeding disorders?
Hemorrhage, causing hypotension, and shock.
What is the result of uncontrolled hypercoagulability disorders?
Thrombus formation, which embolizes, and causes an infarct.
What are the 3 components of hemostasis?
Components of hemostasis: a) Vascular wall (endothelial cells and ECM) b) Platelets c) Coagulation cascade
What are the 4 steps in hemostasis, including cause and response?
4 steps: 1) Injury causes transient vasoconstriction. 2) Primary response creates the reversible platelet primary hemostatic plug. 3) Secondary response creates the permanent platelet and fibrin secondary hemostatic plug. 4) Counter regulation limits coagulation to the site of injury.
Describe the 1st step of hemostasis.
Injury leads to transient vasoconstriction mediated by neurogenic factors and endothelin from endothelial cells. ECM (specifically collagen) exposure leads to the rest.
Describe the 2nd step of hemostasis
Platelets adhere to ECM (collagen) and activate, secrete α and dense core granules, and aggregate in the primary plug.
Describe the 3rd step of hemostasis
Endothelial cells secreted tissue factor activates the coagulation cascade at the platelet surface. Thrombin cleaves fibrinogen to fibrin, which forms the permanent plug with platelets.
Describe the 4th step of hemostasis
Endothelial cells secrete tissue plasminogen activator (t-PA) to lyse fibrin, and thrombomodulin to block further coagulation, limiting the hemostatic response.
What cells are responsible for hemostasis (in the broader definition)?
Endothelial cells
What is the anti-thrombotic action of endothelial cells?
Antithrombotic: Thrombin binds to cells receptors, or thrombomodulin. The cell produces: ADPase, which degrades ADP (thrombosis mediator), and PGI 2 and NO which prevent thrombosis and cause vasodilation. Thrombomodulin causes Protein C to degrade Factor V and VIII from the cascade. Heparin-like molecules bind antithrombin III, which degrades thrombin, Factor IX-XII. // Summarized: cell: ADPase, PGI, NO. // Thrombomodulin: causes Protein C to degrade factor V and VIII. // Heparin-like molecules: antithrombin III: degrades thrombin, Factor IX and X.
What is the Pro-thrombotic action of endothelial cells?
Prothrombotic: von Willebrand factor (vWF) is secreted, aiding the binding of platelets to collagen. CK (TNF, IL-1, endotoxins) cause tissue factor (TF) release, which activates factors IX and X. tPA inhibitor (PAI) is released to block fibrinolysis. >> Summary: vWF: platelets bind collagen. /// CK: TF: IX and X /// PAI blocks tPA.
What is contained in platelet α and dense core granules?
Granules: 1) α granules: fibrinogen, fibronectin, cofactors V and VIII, platelet factor 4, PDGF, TGF α 2) dense core granules: serotonin, epinephrine, histamine, ADP, ATP, Ca2+.
What endothelial factor aids platelet adherence? What is secreted?
vWF. Receptor agonists, α and dense core granules, Ca2+ , ADP, phospholipids surface.
What mediators are active in primary platelet plug formation?
vWF, Ca2+ , ADP, thromboxane 2 (TXA2, aspirin inhibited) cause primary plug formation.
How is the permanent plug formed? What is the effect of fibrin split products (FSP)
Fibrinogen is activated by thrombin to fibrin and FSP. Platelets plus fibrin form the permanent plug. ADP causes the GpIIb-IIIa receptors on platelets to bind fibrinogen and coagulate. FSP and thrombin cause neutrophil and monocyte adhesion.
Of the coagulation factors, which is most associated with bleeding disorders (number and name)? Which is the Liden factor, associated with deep vein thrombosis?
VIII, Antihemophilic factor. V, proaccerin.
What are the general players in the coagulation cascade?
zymogens, proteases, cofactors, Ca2+ , phospholipid surface.
Describe the Intrinsic pathway in the coagulation cascade.
Intrinsic: XII (Hageman factor) is activated by kallikrein, XII activates XI, which (plus VIII cofactors and Ca2+) activates X. 2)
Describe the Extrinsic pathway in the coagulation cascage.
Extrinsic: VIII (plus TF and Ca2+) activates X.
Describe the Common pathway in the coagulation cascade.
Common: X (plus phospholipid, Ca2+, and cofactor V) activates II (prothrombin) to thrombin (IIa), which activates fibrinogen (I) to fibrin (Ia), and XIII aids cross linking.
What is the inhibitory activity of antithrombin III?
Antithrombin III : binds heparin like molecules on endothelial cells: blocks Thrombin, IX, X, XI, and XII (IX-XII).
What is the inhibitory activity of Thrombomodulin?
Thrombomodulin on endothelial cell surface: binds thrombin: activates protein C, inactivates V and VIII.
What is the inhibitory activity of tPA? What blocks tPA?
tPA: activates plasminogen to plasmin, which lyses fibrin clots to FSP. Plasminogen activator inhibitor (PAI) blocks tPA.
What is the effect of FSP?
FSP are chemotactic for inflammatory cells, such as neutrophils and monocytes.
What is the Virchow triad, for thrombus in a vessel without gross injury?
Virchow triad: 1) Endothelial injury 2) Blood flow disturbance (stasis or turbulence). Clotting factors concentrate, platelets reach the endothelial wall because laminar flow is disturbed. 3) Hypercoagulability
What are some causes of abnormal blood flow?
Arterial bifurcations, aneurysms, occlusions (atherosclerotic plaque/stenosis), MI, hyperviscosity (sickle cell, etc.).
What are 4 primary (genetic) causes of hypercoagulatibility?
Primary hypercoagulatibility: a) Factor V (Liden) mutation, causing Protein C resistance. B) Prothrombin mutation c) Antithrombin III deficiency d) Protein C or S deficiency
5 secondary (acquired) causes?
Secondary hypercoagulatibility: a)Bed rest/immobilization. B) Oral contraceptives c) Tumor products d) Age: causes decreasd PGI2. e) High molecular weight heparin: causes HIT: heparin antibodies form, bind heparin-like proteins on platelets, which are activated, clotting ensues.
What is a characteristic shared by all thrombi in high flow areas?
Zahn lines, of alternating fibrin and platelets/RBCs.
Describe a cardiac thrombus?
Intracardiac thrombus, often is mural.
Describe an arterial thrombus? How does it propagate?
Arterial thrombus elongates retrograde. Causes occlusion and infarct.
Describe a venous thrombus?
Venous thrombi frequently appear in lower extremities (DVT), can embolize, elongate in direction of flow, towards the heart. Less fibrin strands, more RBCs, causing a gel like thrombus.
When a venous thrombus embolizes to the pulmonary trunk branches and lodges on a bifurcation, what is the resulting often fatal condition?
Saddle Thrombus.
What are the 4 fates of thrombi?
Thrombus fates: a) Propagation b) Resolution: fibrinolysis c) Embolization: boom! d) Organization: become connective tissue
What is the presentation and end result of disseminated intravascular coagulation (DIC)?
Secondary to a diseases state, systemic microscopic thrombi exhaust coagulation products, and activate fibrinolysis, leading to a bleeding disorder state. Diffuse petechiae throughout the body.