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Applied Biochemistry > Blood Coagulation and Wound Healing > Flashcards

Blood Coagulation and Wound Healing Flashcards

1
Q

what is the process of blood clotting/ coagulation? (6)

A

injury/rupture to blood vessel
blood vessel around wound constricts (reduces blood flow to the damaged area)
activated platelets stick to the injury site
platelets become sticky and clump together to form a platelet plug
platelets and damaged tissue release clotting factors
blood clotting mechanism to form fibrin which acts like a mesh to stop the bleeding

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2
Q

primary hemostasis

A

vasoconstriction and platelet response

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3
Q

what mediates platelet aggregation at the site of injury in primary hemostasis (4)

A

platelet receptors
platelet-derived agonists
platelet-derived adhesive proteins
plasma-derived adhesive proteins

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4
Q

secondary hemostasis

A

clotting cascade

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5
Q

what does secondary hemostasis consist of?

A

the cascade of coagulation serine proteases that culminates in cleavage of soluble fibrinogen by thrombin

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6
Q

Thrombin cleavage generates insoluble fibrin that forms a cross-linked fibrin mesh at

A

the site of an injury

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7
Q

fibrin generation occurs simultaneously to

A

platelet aggregation

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8
Q

what do clotting factors do

A

convert prothrombin to thrombin

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9
Q

what does thrombin do

A

convert fibrinogen to fibrin (insoluble)

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10
Q

damaged blood vessel

A

injury to vessel lining triggers the release if clotting factors

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11
Q

formation of platelet plug

A

vasoconstriction limits blood flow and platelets form a stick plug

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12
Q

development of clot

A

fibrin strands adhere to the plug to form an insoluble clot

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13
Q

platelets release important signaling molecules upon initial binding to

A

collagen

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14
Q

Platelets that stick to collagen undergo a release reaction, in which they secrete (3)

A

ADP, serotonin, and thromboxane A2

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15
Q

Serotonin and thromboxane A2 cause

A

vasoconstriction

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16
Q

platelet plug process

A

ADP and thromboxane A2 attract other platelets and make them stick to the growing mass of platelets that are stuck to the collagen in the broken vessel

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17
Q

what can platelets secrete?

A

serotonin

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18
Q

what does serotonin cause?

A

blood vessels to spasm, decreasing blood flow to that area

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19
Q

the initial binding of platelets to vWF is mediated by

A

glycoproteins that are necessary for platelet tethering (ex. loosely bound), but do not promote strong adhesion (ex. GPlb amd la are not enough, even in conditions of high shear)

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20
Q

firm adhesion of platelets to the sub endothelial is mediated by a glycoprotein called

A

GP2B/3A

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21
Q

the GP2B/3A integrins on resting platelets bind

A

poorly to its ligands

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22
Q

GP2B/3A intern ligands (2)

A

vWF or fibrinogen

23
Q

upon platelet activation (by GPV1), GPV2B/3A undergoes a conformational change that reveals a previously hidden binding site for

A

vWF or fibrinogen

24
Q

activated GP2B/3A binds to vWF at the subendothelial surface to promote

A

strong adhesion to the vessel wall

25
Q

primary aggregation

A

strong adhesion to the vessel wall

26
Q

what does GP2B/3A binding to fibrinogen play a role in?

A

platelet-platelet interactions

27
Q

AGGREGOMETER TRACINGS record the aggregation of platelets in platelet-rich plasma in response to

A

an aggregating agent

28
Q

in these cases, the aggregating agents are (2)

A

collagen and two concentrations of ADP

29
Q

The initial increase in light transmission is due to

A

dilution by the agent, the small downward deflection to a change in platelet shape and the subsequent increase to aggregation

30
Q

With collagen there is a lag before ADP is secreted by the platelets to cause aggregation; when ADP is supplied directly the effect is

A

faster

31
Q

The effect of a low concentration of ADP is reversed as enzymes

A

destroy ADP

32
Q

The extrinsic pathway is activated by

A

external trauma that causes blood to escape from the vascular system

33
Q

is the intrinsic or extrinsic pathway faster?

A

extrinsic

34
Q

what factor does the extrinsic pathway involve?

A

7

35
Q

The intrinsic pathway is activated by (5)

A

trauma inside the vascular system, and is activated by platelets, exposed endothelium, chemicals, or collagen

36
Q

what factors does the intrinsic pathway use? (4)

A

12
10
9
8

37
Q

common pathway

A

when the intrinsic and extrinsic pathways meet and finish the pathway of clot production

38
Q

what factors are involves in the common pathway? (4)

A

1
2
5
10

39
Q

The coagulation factors are generally

A

serine proteases

40
Q

serine proteases act by

A

cleaving downstream proteins

41
Q

The exceptions are (4)

A

tissue factor, FV, FVIII, FXIII

42
Q

Tissue factor, FV and FVIII are —, and Factor XIII is a —

A

glycoproteins

transglutaminase

43
Q

The coagulation factors circulate as

A

inactive zymogens

44
Q

The coagulation cascade is therefore classically divided into .

A

three pathways

extrinsic, intrinsic, common

45
Q

fat soluble vitamins (4)

A

D
E
A
K

46
Q

the platelet plug that initially forms is not ..

A

strong enough by itself to fully prevent further bleeding

47
Q

a fibrin mesh is laid down to

A

further reinforce and strengthen the platelet plug

48
Q

what is cross linking of fibrin catalyzed by?

A

transglutaminase or factor 13

49
Q

In circulation, plasminogen adopts a —, activation-resistant conformation

A

closed

50
Q

Upon binding to clots, or to the cell surface, plasminogen adopts an open form that can be converted into

A

active plasmin

51
Q

plasminogen can be converted to active plasmin by a variety of enzymes, including (4)

A

tissue plasminogen activator (tPA), urokinase plasminogen activator (uPA), kallikrein, and factor XII (Hageman factor)

52
Q

Fibrin is a cofactor for plasminogen activation by

A

tissue plasminogen activator

53
Q

Urokinase plasminogen activator receptor (uPAR) is a cofactor for plasminogen activation by

A

urokinase plasminogen activator

Applied Biochemistry (52 decks)

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