Term
List the three mechanisms by which hemostasis is accomplished. |
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Definition
Hemostasis, the cessation of bleeding 1. rapid constriction of the injured vessel to reduce flow through the vessel 2. clumping of platelets to form a plug on the injured surface of the blood vessel 3. clot formation |
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Term
List three factors in the clotting cascade that are not enzymes. |
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Definition
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Term
List the physical characteristics of fibrinogen. |
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Definition
Fibrinogen is a protein with 45 nm length, 9 nm maximum diameter, and a molecular weight of 340,000. It contains three nodules (globular regions) connected by two rods (α-helical regions). It is comprised of six polypeptide chains. Two sets of three unlike chains, α2 β2γ2 ,are linked head to head and side to side by disulfide bonds near their amino terminal regions. |
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Term
| Which activations need Ca++ and PL |
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Definition
X→Xa IX→IXa VIIa + TF(III)→ VIIa-TF(IIIa) Promothrombin→ Thrombin |
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Term
| What can VIIa-TF(IIIa) activate |
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Definition
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Term
What can thrombin activate? |
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Definition
Fibrogenin→Fibrin V VII VIII XIII |
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Term
| What can kallikrein-HMK activate? |
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Definition
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Term
| Which factors have their Glu residues converted to Gla |
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Definition
II(Prothrombin) VII IX X Same places that need Ca++ and PL |
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Term
| How is Glu converted to γ-carboxyglutamyl (Gla)? |
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Definition
Vitamin K serves as a cofactor for a liver microsomal enzyme that carboxylates peptide bound glutamyl (Glu) residues and converts them to γ-carboxyglutamyl (Gla) residues. |
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Term
| What is the significance of γ-carboxyglutamyl (Gla)? |
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Definition
They are carboxy ends which bind to Ca++ which in turn bind with the platelets. This keeps the Factors in the areas that they need to be in. |
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Term
| What do the drugs Bishydroxycoumarn (Dicoumarol) and Warfarin (Coumadin) do? |
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Definition
Inhibits vitamin K cycle. Regulates clotting by reducing the amount a carboxylation that occurs on the vitamin K dependant proteins(II, VII, IX, X)(2+7=9...10) |
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Term
| What drug is used in rat poison? What happens when they get into children? |
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Definition
Warfarin(Coumadin) If child swallows it they could have persisting problems after treatment because it can be stored as fat and come out again later. |
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Term
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Definition
Plasma protein that inactivates Thrombin. Forms irreversible complexes with thrombin factor XIIa and other stuff and inactivates them. |
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Term
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Definition
Found in Mast cells lining the walls of blood vessels. Increase the formation of Antithrombin-Thrombin complexes. |
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Term
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Definition
γ-carboxyglutamic acid(Gla) containing proteins inactivates clotting factors VIIIa and Va. Activated by Thrombin, when it is bound to Thrombomodulin. |
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Term
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Definition
A γ-carboxyglutamic acid(Gla) containing protein that acts as a cofactor for activated protein C. |
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Term
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Definition
Vitamin K-dependent plasma protein(has Gla) PZ inhibits coagulation by serving as a cofactor for plasma PZ-dependent protease inhibitor. The complex inactivates factor Xa. |
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Term
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Definition
An inhibitor of a variety of proteases, including the clotting factors which are serine proteases. |
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Term
Lipoprotein-associated coagulation inhibitor (LACI) |
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Definition
Inactivates the Factor VIIa-TF-Xa complex; also known as tissue factor pathway inhibitor (TFPI). |
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Term
Genetic risk factors for Thrombosis |
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Definition
Antithrombin III Protein C Protein S Factor V Leiden Factor II 20210A Excessive fibrinogen |
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Term
| Dietary risk factor for Thrombosis |
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Definition
Factor VIIa is significantly increased after consumption of a high fat meal. |
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Term
| Deficiancy of Antithrombin III |
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Definition
Risk factor for Thrombosis An autosomal dominant deficiency of antithrombin III has been reported in several families. |
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Term
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Definition
Risk factor for Thrombosis For cases of venous thrombosis in individuals under 45 years of age, 4% are due to protein C deficiency. |
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Term
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Definition
For cases of venous thrombosis in individuals under 45 years of age, 5% are due to protein S deficiency. |
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Term
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Definition
A genetic defect such that Factor Va is not inactivated by Protein C; occurs in 3% of the population in Western countries. |
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Term
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Definition
A change in prothrombin mRNA (G--->A) that leads to increased messenger stability and increased levels of prothrombin and thrombosis. |
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Term
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Definition
Leads to thrombosis Exhibited in some patients |
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Term
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Definition
The obstruction of blood vessels by detached clots. It is observed to a greater extent in women taking oral contraceptives than in other women. The pill has been reported to cause a decrease in antithrombin III. |
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Term
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Definition
Formation of a clot in a coronary artery damaged by atherosclerosis leading to loss of blood supply to parts of the heart muscle. |
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Term
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Definition
The special case where pulmonary vessels are obstructed due to a detached clot. |
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Term
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Definition
Formation of a clot in the veins of the legs leading to obstruction of venous drainage. |
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Term
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Definition
Loss of blood supply to the brain due to a thrombus. |
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Term
| How is Heparin used in the treatment of clots? |
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Definition
It increases the affinity of Antithrombin III to Thrombin. Immediate effect but does not stop already formed clots. |
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Term
| How are Coumarins (warfarin and dicoumarol) used to treat clots? |
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Definition
Used in patients prone to abnormal venous clot formation; slower acting, but longer lasting inhibitors of clotting compared with heparin. In humans, resistance to warfarin is only a problem if one needs anticoagulant therapy. |
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Term
| How is Aspirin used to treat clots? |
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Definition
At low concentrations, aspirin inhibits formation of thromboxane A2, a stimulant for platelet aggregation. At high concentrations, aspirin induces a decrease of the plasma concentrations of vitamin K dependent clotting factors. (II, VII, IX, X) |
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Term
| How does Clopidogrel (Plavix) used to treat clots? |
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Definition
Inhibitor of ADP-induced platelet aggregation. Clopidogrel irreversibly modifies the platelet ADP receptor and inhibits ADP binding. |
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Term
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Definition
An abnormal fibrinogen is produced. Leads to bleeding. |
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Term
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Definition
Hereditary combined deficiency of the vitamin K-dependent clotting factors (II, VII, IX, X) is a very rare autosomal recessive bleeding disorder. |
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Term
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Definition
Hemophilia is a category of diseases characterized by abnormal or excessive bleeding resulting from deficiency or absence of a clotting factor. Classic: Deficiency in factor VIII |
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Term
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Definition
Autosomal dominant disorder Leads to impaired platelet adhesion. vWF and factor VIII circulate together in a noncovalent complex. A deficiency of vWF will result in increased degradation of factor VIII. |
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Term
| What deactivates Plasmin? |
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Definition
| (fish symbol)2- antiplasmin |
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Term
| What can activate Plasminogen→ Plasmin? |
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Definition
TPA: Major one. Serine protease. Has an affinity for Fibrin so it should be near by when needed. Streptokinase: NOT made in the body. Complexes with it to activate it. Urokinase: Made in the KIDNEY. Activated by factor XII |
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Term
| What inavtivate t-PA(TPA)? |
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Definition
Plaminogen Activator Inhibitors PAI-1, PAI-2 |
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Term
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Definition
It dialates the blood vessel to make it more permeable. More blood can get through. Lowers blood pressure. Vascular peptide in plasma. |
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Term
| How is Bradykinin synthesized? |
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Definition
Kininogen→ Bradykinin (kallikrein is enzyme) Kininogen is a large polypeptide and is cleaved by kallikrein and the 9bp that are removed are called Bradykinin. A kallikrein not located in the plasma will cleave it at a different place and make it bigger. |
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Term
| How is Bradykinin inactivated? |
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Definition
| A lung peptidase removes 10% (Phe-Arg) from it. |
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