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56 Cards in this Set
- Front
- Back
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What is hemostasis? |
Physiological process that lead to the stoppage of bleeding from an injured vessel |
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3 stages of hemostasis |
1. Vascular construction 2. Formation of the plates plug/ temporary clot through platelets aggregation |
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Final stage of hemostasis |
Blood coagulation/ formation of definitive clot |
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What is the first and 2nd steps in vascular constriction? |
1. Reflex Vasoconstriction 2. Platelets arrival and release of vasoconstriction mediators . 3. Release of Prostacyclin ( vasodilation) from endothelium. |
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What does reflex vasoconstriction do? |
Provides temporary slowing down of the blood flow. |
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Vasoconstriction mediators |
1. Platelets release Thromboxane A2 (TXA2) =vasoconstriction 2. Serotonin = vasoconstriction 3. Endothelin is potent vasoconstrictor 4. Prostacyclin (Prostaglandin) from endothelium Prostacyclin=vasodilation is released to Prevent platelets from aggregating in uninjured areas. |
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Function of prostacyclin ( prostaglandin) |
Can vasoconstrict or vasodilate |
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Stages of formation of platelets plugs |
1. Platelets ( Alpha and Dense granules). 2. Von Willebrand factor ( transports factor VIII) released from endothelium to help with adhesion to collagen fibers. 3. Thromboxane and ADP activates and signals platelets to come to the area. 4. Platelets arrive and accumulate. 5. Fibrinogen binds to platelets receptor sites to form loose plug. Platelets plug.
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Alpha granules include |
Clotting factors and adhesion proteins. P Selectin • Fibrinogen Von Willebrand Factor (VWF) Factor V • Factor VIlI Platelet Factor IV (heparin bindin • Fibronectin Platelet Derived Growth Factor (PDGF) Transforming Factor-alpha (TGF- alpha) |
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Dense granules include |
• ADP • ATP • Calcium • Histamine ( vasoconstriction mediators) Serotonin Epinephrine |
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Blood coagulation cascades? |
Intrinsic: slower 1-6 min Activated in circulation by Factor XII Extrinsic: Rapid: trauma at vessel site which releases Tissue Factor and activates Factor VII. |
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Terminal factor in intrinsic system ( blood or vessel injury) and extrinsic system ( tissue factor) ? |
Factor X |
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What activates prothrombin? |
Factor X + Ca ++ ions |
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Prothrombin converts to … |
Thrombin |
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What activities fibrinogen? |
Back (Definition) |
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Stable clot in the vessel? |
Fibrin ( monomer to polymer). |
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Organ plays major role in blood clotting factors? |
Liver |
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Natural anticoagulation factors? |
Protein C, S, antithrombin |
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Factors produced by hepatocytes in a liver? |
Fibrinogen Prothrombin Factors: V, VIl, IX, X, xI, xII |
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What factors inactivates Protein C? |
Factor V, VIII helps to decrease the amount of thrombus formation |
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Protein C deficiency causes? |
Increased risk of thrombosis or thromboemboly. |
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Function of protein S? |
Acceleration function of protein C |
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Fibrinogen is needed for ? |
For activation of Pro-coagulation factor of Fibrin for clot formation |
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Prothrombin is needed for.. |
Conversion of thrombin |
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Antithrombin is needed for |
Inactivates coagulation factors to neutralize Thrombin |
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Lack of Protein C and S causes … |
Hypercoagubility state / higher risk of developing thromboemboly |
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Vitamin K helps to synthesize? |
Vitamin K Synthesis:
II, VII, IX, X Prothrombin Protein C |
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Clot dissolution is known as? |
Fibrinolysis |
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Plasminogen is activated by? |
Plasminogen activator |
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Plasminogen converts to … |
Plasmin to break the clots ( Factors V, VII, VII, Prothrombin, Fibrinogen). |
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Plasmin inactivated by… |
Plasmin alpha inhibitor |
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Thrombocytosis |
Hypercoagulability state- increased platelets function |
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Types of thrombocytosis |
Primary - nothing underlying ( Defect of thrombopoietin receptor; Causes increased levels of free thrombopoietin) Secondary- smth causes problems ( Seen with disease states that increase thrombopoietin) |
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Secondary Thrombocytosis causes? |
CA, RA, chronic inflammatory infection, causes of tissues damage. |
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Something that stimulates trombopoietin to… |
Increase amount of RBC |
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Normal feedback system |
Platelets decreased - Increased Unbound TPO Stimulates Megakaryocytes Production Platelets Increased • Decreased unbound TPO Inhibition of Megakaryocyte Production |
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Primary Thrombocytosis main cause? |
Myeloproliferative disorder Stem cells makes more platelets than balance system can handle on a negative feedback Can be the cause of defects on the platelets receptor- inhibiting ability of TPO to attach to the receptor- free TPO- unbound TPO is going to stimulate bone marrow to make more megakaryocytes to increase the platelets |
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Increased numbers of platelets and their form causing |
Causes increased risk of blood clots and because of the abnormal form - bleeding |
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Protein C and S made in a liver is to … |
To anticoagulate , to inactivate clotting factors Protein C Inactivates Factor V and VIlI Protein S Accelerates the action of Protein C |
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Goal of Protein C, S ? |
To prevent blood clots in a body Goal: Prevent thromboembolism |
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Protein C and S deficiency causes? |
• Increased risk for blood clots |
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What is Factor V Leiden? |
It’s a mutation in the blood clotting Factor V Because of the mutation protein C cannot shut it down Factor V Leiden resistant to protein C and will not respond Causes risks of blood clots. Risk population: Pregnancy |
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Protein C deficiency caused by ? |
Congenital Liver failure Vitamin K deficiency Malignancy |
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Protein S deficiency causes? |
Autoimmune disorder |
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Treatment for Inherited Hypercoagulability Disorders |
Anticoagulation treatment |
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Acquired Hypercoagulabilit Causes |
Immobility MI Cancer Smoking Surgery Obesity Heart failure Especially cancer Hormone replacement Oral contraception |
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Coagulation factor deficiencies-inherited |
Von Willebrand Hemophilia A ( factor VIII deficiency) |
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Von Willebrand hallmark |
Hereditary Can’t form clots/ Clotting Cascade interrupted Transports factor VIII Risk at bleeding ( nose bleed, dental procedure) Bleeding in the presence of normal platelet counts- hallmark |
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Hemophilia A Factor 8 deficiency |
Hereditary X Linked Recessive Affects males Spontaneous bleeding in soft tissue/GI Tract |
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Factor 8 and Coagulation Factor Deficiencies-Inherited |
You have to differentiate is it a primary true deficiency in hemophilia A of factor 8 or is it a secondary as a result of Von Willebrand. |
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If it’s a hemophilia A , liver and endothelial lining are not making factor 8. Not enough factor 8 being made- primary cause. |
If it’s plenty of factor 8 being made and it’s a transport problem . It becames a secondary cause as deficiencies in Von Willebrand. |
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Acquired Bleeding Disorders Vitamin K deficiency Clotting factors not working |
Reasons: Not enough vitamin k in a diet Intestinal problem ( bacteria will not be present to break down for Vit K) Use of antibiotics ( destroyed intestinal flora) Liver disease ( liver can’t store vitamin k) Can be seen in newborns ( they don’t have established intestinal flora) Factors II, VII, IX, X not functional |
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Bleeding Associated with Platelet Disorders Thrombocytopenia=LOW PLATELETS Causes |
Primary immune thrombocytopenic purpura ( idiopathic thrombocytopenia purpura) is a result of antibody attack glycoproteins on platelets Autoimmune disorder Receptors involved: 3 B 1B 3 A These receptors are targeted for destruction. It will caUse an excessive amount of platelets distraction and will cause thrombocytopenia. |
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Purpura |
Discoloration on the skin because of platelets distraction Risks of bleeding gums, Nose bleed Menstrual bleeding GI bleeding |
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Disseminated Intravascular Coagulation : problems |
1. Excessive amount of coagulation 2. Excessive amount of bleeding |
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Coagulation part of DIC |
Increased bleeding Excessive coagulation
Tissue injury • Obstetric complications • Malignant neoplasms • Infections (especially gram-negative sepsis) • Trauma • Surgery • Burns • Hypotension ENDOTHELIAL CELL INJURY • Infections • Immune complex deposition • Burns • Hypoxia • Acidosis • Shock • Vasculitis Activation of both clotting cascades - excessive clotting. Thrombin generation. Thrombin goes unchecked. excessive amount of fibrin production. Fibrin will produce clots: • Ischemic tissue injury • Microangiopathic hemolytic anemia ( intravascular). DIC causes the destruction of natural coagulants: Anti- Thrombin III. With excessive amount of clotting, plasmin (fibrinolysis) gets activated. Plasmin will destroy clotting factors ( V, VIII, fibrinogen, platelets). No more left for other clotting mechanisms- people will bleed. |
