Hemostasis, Hemophilia, Vit K

Question 1

tertiary hemostasis

Answer 1

-aka blood coagulation

Question 2

intrinsic pathway

Answer 2

-aka contact activation pathway
-initiated from the blood itself after exposure of
the blood to collagen from a traumatized blood vessel

Question 3

extrinsic pathway

Answer 3

• aka tissue activation pathway
• more important
• started by tissue injury and release of tissue factor, III

Question 4

common pathway

Answer 4

-fibrinogen -> fibrin (via thrombin)

Question 5

thrombin

Answer 5

• acts on fibrinogen to create fibrin monomer which can interact with other fibrin monomers to form fibrin fibers
• 4 molecules reomoved from fibrinogen -> fibrin

Question 6

fibrinogen

Answer 6

-fibrin precursor (needs peptides removed to make fibrin monomer)

Question 7

hemophilia A

Answer 7

• inherited coagulation disorder, intrinsic pathway
• cofactor VIII -> less Xa formed -> less thrombin
• treatment: missing factor VIII (recombinant factors) or blood transfusions

Question 8

hemophilia B

Answer 8

• inherited coagulation disorder, intrinsic pathwat
• cofactor IX -> less Xa formed -> less thrombin
• -treatment: missing factor IX (recombinant factors) or blood transfusions

Question 9

anticoagulants

Answer 9

• Agents that decrease Ca2+
• coumains (vit K antagonists)
• heparin and derivatives
• antithrombin-like agents (bind to thrombin, medicinal leeches = hirudin, bivalirudin)

Question 10

tissue plasminogen activator

Answer 10

• activating plasminogen activator to plasmin (Plasmin can be effective in dissolving intravascular clots)
• Within 3 hours it can improve recovery odds of: pulmonary ebolism, myocardial infarction, stroke
• risk of hemorrhage

Question 11

hemostasis

Answer 11

prevention of blood loss

Question 12

vit K

Answer 12

• a co-factor in the production of an unusual amino acid, γ-carboxyglutamate (gla)
• Gla residues are part of Vitamin K-dependent proteins (VKDP)
• Addition of Gla residues confers on these proteins their capacity to bind to phospholipid surfaces in the presence of Ca2+

Question 13

proteases

Answer 13

• endopeptidases
• exist in zymogen/inactive form
• synthesized in liver (except III, tissue factor and some VIII, antihemophylic globulin)
• present in low concentrations (except pro-thrombin, II = 1microM, and fibrinogen, I = 10microM)

Question 14

protease cofactors

Answer 14

-also require activation

Question 15

coagulation factors

Answer 15

-generally serine proteases

Question 16

tissue factor

Answer 16

-a combination of phospholipids and lipoproteins released from damaged tissue that act as a proteolytic enzyme

Question 17

HMWK

Answer 17

• High Molecular Weight Kininogen
• bound to prekallikrein and factor XII
• attracked to negatively charged surfaces such as injured blood vessel

Question 18

IXa-VIIIa-phospholipid-Ca2+ complex

Answer 18

• aka tenase
• activate X to Xa
• where extrinsic and intrinsic pathways collaborate to start common pathway

Question 19

VKDP

Answer 19

Vitamin K-dependent proteins
– Intrinsic pathway: Factors IX
– Extrinsic pathway: Factor VII
– Common pathway: Factor II = Prothrombin and factor X
– Anti-coagulation factors: Protein C and Protein S

Question 20

vit K deficiency

Answer 20

-inefficient coagulation and bleeding

Question 21

vit K depletors

Answer 21

• Warfarin/Coumadin, Dicoumarol
• inhibit production and recycling of vit K
• prescribed for elderly at risk for thrombosis for prolonged anticoagulant treatment

Question 22

heparin sulfate

Answer 22

• facilitates the interaction of antithrombin with thrombin
• > inhibits prothrombin conversion to thrombin
• > inhibits thrombin action on fibrinogen

Question 23

vWF

Answer 23

-Von Willebrand Factor