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82 Cards in this Set
- Front
- Back
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What is hemostasis2 |
Cellular and biochemical events that keep blood in a liquid state. Prevents blood loss by forming thrombi. |
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What is primary hemostasis |
Started by small injuries to vessels. Vessels contact to seal wound and platelets fill the space by forming a temporary plug. Fibrin, from plasma proteins, strands deposit on the plug to reinforce it. |
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What makes up the vascular intima? |
Endothelial cells lie in elastic lamina and connective tissue. Fibroblasts in the connective tissue produce collagen. Smooth muscle cells lie next to the fibroblasts in the arteries only, not veins. They contract during hemostasis. |
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Coag properties of the vascular intima Vasoconstriction1 Collagen1 E-cells2 What do e-cells coat themselves with1 |
Induces vasoconstriction in the arteries. Collagen binds and activates platelets. E-cells secrete WVF, phospholipids and glycoprotein to make the platelets stick to them. The e-cells coat themselves with p-selectin, an adhesion molecule, to cause platelet and leukocyte binding. |
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Coag properties of the vascular intima/What do the subendothelial (smooth muscle and fibroblasts) secrete1 What does it do1 |
A surface area protein called tissue factor (TF). It activates the cascade through factor VII. |
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Anticoag properties of vascular intima. Prostacyclin1 Nitric oxide1 Heparin1 TFPI1 Thrombomodulin1 |
-Platelet activation inhibitor -Induces vasodilation -Activates antithrombin -Extrinsic pathway inhibitor -Activates protein C pathway, which regulates coag by digesting factors Va and VIIIa |
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Fibrinolytic properties of vascular intima TPA1 PAI-1~1 |
Tissue plasminogen activator binds fibrin and triggers the activation of fibrin-bound plasminogen to form plasmin to digest thrombus Plasminogen activation inhibitor controls TPA. |
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Platelet role in primary hemostasis Adhesion1 Aggregation1 Platelets secrete1 |
Binds to non-platelet surfaces, like the glycoprotein 1b/V/IX on VWF and collagen. Platelets stick to each other with glycoprotein IIb/IIIa. Platelets secrete granule contents during both processes. |
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RBC role in primary hemostasis1 |
Provide bulk and structural integrity to the fibrin clot |
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Monocytes and lymphocytes role in primary hemostasis1 |
In inflammation, provide TF that triggers coagulation |
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Leukocytes role in primary hemostasis |
Promote wound-healing process |
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Secondary hemostasis Procoag1 Serine protease3 |
Could be serine proteases or cofactors. Serine proteases are enzymes of the trypsine family. Made as inactive zymogens and activated by another protease during coag process. The general activation of zymogens is called disseminated intravascular coag (DIC), fatal when acute. |
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Secondary hemostasis/coagulation/Serine protease factors and enzymes7 |
IIa (thrombin), VIIa, IXa, Xa, XIa, XIIa, prekallikrein |
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Secondary hemostasis/procoag/cofactors1 Factors and enzymes4 |
Each cofactor binds to its particular serine protease to make the protease more stable and active. Tissue factor, V, VII, high molecular weight kininogen (HMWK) |
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Secondary hemostasis/procoag/other factors and enzymes6 |
VIII, XIIIa, fibrinogen, calcium, VWF, phospholipids. |
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What does Factor XIIIa do1 |
Crosslinks fibrin to strengthen the fibrin clot. |
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What is VWF What does it do Where is it stored |
A glycoprotein made of several subunits. Stored in Weibel-Palade of the e-cells and alpha granules in platelets. Provides receptor sites for platelets and collagen. |
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Factor VIII Things4 Clin sig2 |
Produced by hepatocytes. Sex-linked. Unstable, unless bound to VWF. Deteriorates quickly. Von Wildebrands disease-Low VWF and VIII. Hemophilia A-Low VIII, but normal VWF. |
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Prothrombin cascade steps |
1) Injury 2) TF exposed, acts as a receptor for VIIa in the presence of a phospholipid and calcium to activate X 3) Xa binds Va on phospholipid surface. This complex activates prothrombin 4) Activated prothrombin is thrombin 5) Thrombin cleaves fibrinopeptides A and B from the fibrinogen molecule to make it fibrin. Fibrin is stabilized by XIIIa. |
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How is Vitamin K significant? |
VII, IX, X and proteins C, S and Z are all Vit K dependent. If there's low Vit K, the factors are released from the liver in a diminished form and can't be used in the cascade. |
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XI deficiency Clin sig1 |
Rosenthal syndrome-Moderate to severe hemorrhage. |
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Prothrombin time test What does it do1 Factors affected5 How does it work1 |
Tests the coagulation factors of the extrinsic pathway. I, II, V, VII and X. A thromboplastin containing TF and Ca is put into the plasma. The complex formed between TF and VII triggers X in the common pathway. |
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Partial thromboblastin time What does it test1 Factors affected8 How does it work1 |
Test coagulation factors of the intrinsic pathway. I, II, V, VIII, IX, X, XI, XII A phospholipid reagent containing a contact activating agent is put into the plasma to trigger the intrinsic pathway. |
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Secondary hemostasis |
Second stage of coagulation where coag proteins are activated in a cascade to produce a fibrin clot. |
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Prolonged PT Clin sig5 |
VII deficiency Vit. K deficiency Protein C and S deficiency Liver disease DIC |
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Decreased PT Clin sig1 |
Too much Vit. K |
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Prolonged aPTT Clin sig7 |
Heparin Any intrinsic factor deficiency Antifactors VIII and X Lupus anticoagulants vWD Hemophilia Liver disease |
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Decreased aPTT Clin sig1 |
DIC |
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What is exposed in primary1 Secondary?1 |
Collagen TF |
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Platelet-poor plasma1 |
A plasma with a very low platelet count. |
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Types of vWD1 Type I2 Type II Type III |
All are autosomal -Low vWF. May/may not show symptoms, nosebleeds. -Bruising, bleeding of the mucosa. -Most severe. Little to no vWF |
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Prothrombin group Procoags and proteins6 Things2 Things1reallylong |
II, VII, IX, X, proteins C, S, Z All structurally resemble prothrombin. All Vit. K dependent because it catalyzes an essential modification on the proteins that allows them to bind to ionic calcium. This bound calcium now allows these proteins to bind neg. charged phospholipids that are essential in coag rxns. |
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Contact/Intrinsic XI cascade steps |
1) A complex of XIIa, HMWK+prekallikrein activate XI 2) XIIa changes the glycoprotein prekallikrein to its active form, kallikrein 3) Kallikrein breaks free from HMWK to make it bradykinin. Meanwhile, if Thrombin does the activating, 4) XIa activates IX 5) IXa activates VIII 6) VIIIa activates X. |
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Tissue plasminogen activator1 |
Activates nearby plasminogen molecules to trigger fibrinolysis, with the formation of fibrin degradation products. |
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Procoagulant1 |
Become activated to form serine proteases or cofactors, which function together to form a localized thrombus. |
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How does tissue factor pathway inhibitor (TFPI) work2 |
From the e-cells, TFPI uses protein S, the cofactor of APC, to inactivcate Xa and binds to the TF/VIIa complex to keep it from further activating other Xa. It provides feedback inhibition because it's not functional until X is activated. Also inhibits IX |
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How does the protein C regulatory system work1long |
In normal vessels, Thrombin binds to the e-cell membrane protein thrombomodulin to make a complex that activates protein C into APC. APC makes a complex with its cofactor, protein S, to inactivate Va and VIIIa. |
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How does antithrombin work1 |
Neutralizes Thrombin and activated IX through XII |
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Thrombolysis cascade steps |
E-cells secrete TPA. TPA with urokinase activate plasminogen to plasmin, a serine protease that breaks down fibrin. |
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What are the things Thrombin acts on? |
V, VIII, IX, and XIII to crosslink the fibrin to make the clot stronger. |
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Leiden factor V mutation |
Inherited. Va resists inactication from protein C complex |
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Hemophilia A1 Hemophilia B1 Things2 |
-Affects VIII -Affects IX -Sex linked. Women not affected. |
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What does heparin cofactor II do?1 |
It inactivcates Thrombin in the presence of heparin |
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How does a Thrombin time test work1 What is it checking1 |
-It introduces Thrombin, so the cascade is bypassed. -It tests the fibrinogen levels |
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What is a reptilase test for1 |
It functions just like a Thrombin time, only for patients on heparin |
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What is a 5-molar urea test1 What does it measure1 |
- -XIII |
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What are the labile factors1 |
V and VIII. The same that the protein C pathway acts on |
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D-dimer |
Assay used to rule out thrombolytic diseases. |
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Alpha 2 antiplasmin |
Rapidly and irreversibly binds free plasmin |
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HUS |
Disease in the kidneys. Starts in the GI tract. Caused by ecoli. |
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Thrombocytopenia vs. Thrombocytosis |
150k-450k vs. Much higher |
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May higglins |
Autosomal dominant |
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Sebastian syndrome |
Inherited autosomal |
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Fechner syndrome |
Same as Sebastian. Deafness, nephritis |
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TAR |
Autosomal recessive |
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What do drugs and alcohol do? |
Reduce platelet production |
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Acute ITP |
In children Abrupt onset Lots of symptoms Caused by viral infections, antibodies producing complexes cause platelet destruction Treated by immunoglobulins |
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Chronic ITP |
20-50 years old Women more than men Brought on by disease Same symptoms Beginning insidiously Antibodies attach to platelets and are removed from circulation by the spleen Treated by immunoglobulins |
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Drug induced |
Hapten and heparin |
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Hypoplasia |
An undevelopment of tissues due to a shortage of cells. |
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Hapten |
A small molecule that can't trigger a response by itself, unless bound to something else. |
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Heparin induced thrombocytopenia (HIT) |
A common side effect of heparin therapy. Platelets bind to pf4, altering pf4, causing neoepitopes (new antigens) to manifest. The immune system produces antibodies to combat them. |
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What role does vWF play in primary and secondary abnormal coagulation |
Pri-the platelets can't adhere. Sec-Problem with VIII. |
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Congenital disorders are caused by? Acquired disorders are caused by? |
Factor deficiency. Brought on by other diseases. |
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How do you distinguish between liver disease and Vit. K deficiency? |
V is specific to liver disease. VII to vir. K deficiency |
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What is DIC caused by |
Low antithrombin levels. Acute-All tests are prolonged. Chronic- Just the d-dimer is prolonged. |
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What must the hemostatic levels in the liver be? |
30% |
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SLE |
Autoimmune. Antibodies attack the body. |
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How does warfarin work. |
Vit. K carboxylates glutamic acid and becomes inactive. Vit. K reductase reactivates it. Warfarin blocks reductase. |
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Which factor inhibitor disorder is the most common |
VIII |
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Thrombosis |
Formation of platelet or fibrin clots, can lead to ischemia or gangrene from anaerobic bacteria eating you. |
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Venous thrombosis vs. Arterial thrombosis |
-Venous is in the leg veins, leads leads to pulmonary embolism. -Arterial is cardiovascular disease and stroke. |
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How does atherosclerotic plaque form? |
Platelets, monocytes and macrophages turn fatty deposits in the vessel lining into fibrous plaque. Suppresses nitric oxide and exposes TF. |
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How can thrombosis be acquired? |
Immobilization/inactivity, diet or homocystenemia. |
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Thrombosis risk factors/ Trousseau syndrome |
Pancreas or colon cancer |
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Thrombosis risk factors/myeloproliferative disorders/ET and PV |
Thrombosis through platelet hyperactivity |
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Thrombosis risk factors/myeloproliferative disorders/promyelocytic leukemia |
DIC caused by progoagulant granules releasing from malignant cells. |
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Thrombosis risk factors/myeloproliferative disorders/Chronic inflammatory diseases |
Elevate fibrinogen and VIII, decrease fibrinolysis. |
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Thrombosis risk factors/myeloproliferative disorders/diabetes mellitus |
Untreated will cause a stroke. |
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Lab evaluation of thrombosis/ antiphospholipid antibodies |
Autoimmune antibodies that bind to protein-phospholipid complexes. Can come as IgA, IgG or IgM. Can be brought on by stroke, vessel disease or miscarriage. |
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Lab evaluation of thrombosis/antiphospholipid antibodies/lupus anticoagulant test profile |
Low reagent phospholipid concentrations are sensitive to LA. Dilute Russell Viper test, dilute thromboplastin time. |
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Lab evaluation of thrombosis/antiphospholipid antibodies/factor V Leiden mutation |
Genetic. Glutamine is replaced with arginine at position 506 of the V molecule. This prevents the hydrolysis of V. This test can also confirm APC resistance. |
