Physiology 36: Hemostasis And Blood Coagulation

Front 1

Trauma to a blood vessel wall will cause the smooth muscle to ...

Back 1

contract. first reaction to a hemorrhage before any sort of clot can form = reduce blood flow to the area

Front 2

What is thromboxane A2?

Back 2

a vasoconstrictive agent released with blood vessel trauma = reduce blood flow to area of damage = reduced bleeding

Front 3

Platelets are made from what cells made in the bone marrow?

Back 3

megakaryocytes

Front 4

What is thrombosthenin?

Back 4

contractile proteins, along with actin/myosin, found in platelets

Front 5

Function of glycoproteins on platelet surfaces

Back 5

smooth the surface to prevent adhering to normal endothelium, but will bind to damaged endothelium

Front 6

Platelets secrete what factors to encourage more platelet aggregation?

Back 6

ADP and thromboxane A2

Front 7

What do prothrombin activators do?

Back 7

convert prothrombin into thrombin

Front 8

What does thrombin do?

Back 8

converts fibrinogen into fibrin that will form the clot

Front 9

Rate limiting step in blood coagulation?

Back 9

formation of prothrombin activating factors = proportional to damage

Front 10

Prothrombin is made where?

Back 10

liver, needs vitamin K

Front 11

Thrombin converts fibrinogen into fibrin. This fibrin interacts with other fibrin to form the blood clot. What else does thrombin do to help this?

Back 11

activates fibrin stabilizing factor that creates covalent bonds between fibrin

Front 12

What is serum?

Back 12

blood plasma with clotting factors removed. serum cannot clot

Front 13

Clot formation uses a (positive or negative) feedback mechanism?

Back 13

positive, the platelets and fibrin recruit more platelets or fibrin

Front 14

What initiates the formation of prothrombin activator?

Back 14

vessel trauma, irritation, damaged endothelium. extrinsic or intrinsic pathway leads to prothrombin activators

Front 15

What initiates formation of prothrombin activator in the extrinsic pathway?

Back 15

blood vessel damage = tissue factor release

Front 16

Extrinsic pathway:

Back 16

vessel damage > tissue factor > 7 > 10 > 5 > prothrombin activator > thrombin > fibrin > clot

Front 17

What initiates formation of prothrombin activator in the intrinsic pathway?

Back 17

blood trauma or exposure of the blood to collagen or vWF

Front 18

Intrinsic pathway:

Back 18

blood trauma > 12 > 11> 9 + 8> 10

Front 19

Classic hemophilia is a problem with which clotting pathway?

Back 19

intrinsic, factor 8 problem

Front 20

Classic hemophilia is a problem with which clotting factor?

Back 20

8 in the intrinsic pathway

Front 21

What is thrombocytopenia?

Back 21

low levels of platelets leading to poor clotting ability = more bleeding

Front 22

When blood is taken from the body, what happens when we add citrate ion or oxalate?

Back 22

we remove calcium to prevent clotting. citrate/oxalate bind calcium out of the blood

Front 23

Function of thrombomodulin

Back 23

binds thrombin out of the plasma to reduce clotting ability

Front 24

Protein C prevents coagulation by inhibiting which factors?

Back 24

5 and 8

Front 25

Fibrin and antithrombin 3 do what to thrombin particles in the blood?

Back 25

bind them and remove them from the blood

Front 26

Heparin is only an anticoagulant when combined with what factor?

Back 26

3

Front 27

Function of heparin

Back 27

combines with factor 3 (antithrombin) to increase factor 3's ability to remove thrombin form the blood = less clotting

Front 28

Where is heparin mostly made in the body?

Back 28

mast cells

Front 29

Function of plasmin

Back 29

lyse blood clots

Front 30

How does t-PA function to reduce clotting?

Back 30

t-PA activates plasminogen = more plasmin = break up clots

Front 31

What is thrombocytopenia?

Back 31

low levels of platelets leading to poor clotting ability = more bleeding

Front 32

When blood is taken from the body, what happens when we add citrate ion or oxalate?

Back 32

we remove calcium to prevent clotting. citrate/oxalate bind calcium out of the blood

Front 33

Function of thrombomodulin

Back 33

binds thrombin out of the plasma to reduce clotting ability

Front 34

Protein C prevents coagulation by inhibiting which factors?

Back 34

5 and 8

Front 35

Fibrin and antithrombin 3 do what to thrombin particles in the blood?

Back 35

bind them and remove them from the blood

Front 36

Heparin is only an anticoagulant when combined with what factor?

Back 36

3

Front 37

Function of heparin

Back 37

combines with factor 3 (antithrombin) to increase factor 3's ability to remove thrombin form the blood = less clotting

Front 38

Where is heparin mostly made in the body?

Back 38

mast cells

Front 39

Function of plasmin

Back 39

lyse blood clots

Front 40

How does t-PA function to reduce clotting?

Back 40

t-PA activates plasminogen = more plasmin = break up clots

Front 41

What is thrombocytopenia?

Back 41

low levels of platelets leading to poor clotting ability = more bleeding

Front 42

When blood is taken from the body, what happens when we add citrate ion or oxalate?

Back 42

we remove calcium to prevent clotting. citrate/oxalate bind calcium out of the blood

Front 43

Function of thrombomodulin

Back 43

binds thrombin out of the plasma to reduce clotting ability

Front 44

Protein C prevents coagulation by inhibiting which factors?

Back 44

5 and 8

Front 45

Fibrin and antithrombin 3 do what to thrombin particles in the blood?

Back 45

bind them and remove them from the blood

Front 46

Heparin is only an anticoagulant when combined with what factor?

Back 46

3

Front 47

Function of heparin

Back 47

combines with factor 3 (antithrombin) to increase factor 3's ability to remove thrombin form the blood = less clotting

Front 48

Where is heparin mostly made in the body?

Back 48

mast cells

Front 49

Function of plasmin

Back 49

lyse blood clots

Front 50

How does t-PA function to reduce clotting?

Back 50

t-PA activates plasminogen = more plasmin = break up clots

Front 51

3 major causes for excess bleeding

Back 51

vitamin K deficiency, hemophilia, thrombocytopenia

Front 52

Hemophilia is more common in which gender?

Back 52

males

Front 53

What is von Willebrand's disease?

Back 53

defective vWF = less platelet aggregation = more bleeding

Front 54

How do we treat thrombocytopenia?

Back 54

give fresh whole blood with platelets in it; remove spleen (spleen removes platelets)

Front 55

What is an embolus?

Back 55

freely flowing clots

Front 56

Causes of thromboembolus formation

Back 56

hemostasis (slow or pooled blood flow); rough endothelium (atherosclerosis)

Front 57

Heparinase function

Back 57

destroy heparin

Front 58

Warfarin mechanism of action

Back 58

inhibits VKORc1 = less active vitamin K = less clotting factor synthesis

Front 59

Function of VKOR c1

Back 59

activates vitamin K for synthesis of clotting factors

Front 60

Function of vitamin K in clotting factor synthesis

Back 60

carboxylates glutamic acid on clotting factors to activate them

Front 61

What is the PT?

Back 61

prothrombin time; how long it takes to clot.

Front 62

A patient with low levels of prothrombin will have a (faster or slower) prothrombin time?

Back 62

low prothrombin = high PT = slower clotting

Front 63

INR =

Back 63

(PT of patient) / (PT normal)

Front 64

Normal prothrombin time

Back 64

12 seconds