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Biochem > Blood Coagulation and Wound Healing > Flashcards

Blood Coagulation and Wound Healing Flashcards

1
Q

what are the steps to blood clotting (coagulation)

A

-injury or damage
- vessel contracts
- platelet plug
-fibrin clot

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2
Q

what happens in primary hemostasis

A

-vasoconstriction and platelet response
-platelet aggregation at the site of injury is mediated by platelet receptors, platelet derived agonists, platelet derived adhesive proteins and plasma derived adhesive proteins

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3
Q

what happens in secondary hemostasis

A
  • clotting cascade
  • coagulation of serine proteases that results in cleavage of soluble fibrinogen by thrombin. thrombin cleavage generates insoluble fibrin that forms a cross-linked fibrin mesh at the sit of injury
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4
Q

when does fibrin generation occur

A

simultaneously to platelet aggregation

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5
Q

what happens when platelets bind to collagen

A

-undergo a release reaction where they secrete ADP, serotonin, and TXA2.
-serotonin and TXA2 cause vasoconstriction
-ADP and TXA2 attract platelets and make them stick to the collagen in the broken vessel to make the platelet plug

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6
Q

why is calcium important

A

clotting cascade cant take place without it

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7
Q

what does serotonin come from

A

tryptophan

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8
Q

what is serotonin secreted by

A

enterochromaffin cells

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9
Q

how are platelets formed

A

arachindonic acid is converted into endoperoxides by cyclooxygenase (prostaglandin synthase) which then gets converted into TXA2 by thromboxane synthetase which gets converted into plateletes (TXAB2)

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10
Q

how are endothelial cells formed

A

arachindonic acid is converted into endoperoxides by cyclooxygenase (prostaglandin synthase) which then gets converted into prostacylin by prostacyclin synthase which gets converted into 6 keto PGF 1 alpha (endothelial cells)

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11
Q

what is the initial binding of platelets to vWF mediated by

A

glycoproteins that are necessary for platelet tethering (GPIIb/IIIa) but dont promote strong adhesion

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12
Q

what is responsible for firm adhesion of platelets to the subendothelia

A

GPIIb/IIIa

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13
Q

what happens to GBIIb/IIIa upon platelet activation

A

GBIIb/IIIa undergoes a conformational change that reveals a binding site for vWF or fibrinogen. vWF binds at the subendothelial surface to promote strong adhesion to the vessel wall

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14
Q

what is the delay in platelet activation

A

platelets activate before releasing ADP

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15
Q

what do aggregometer tracings do

A

record the aggregation of platelets in platelet rich plasma in response to an aggregation agent

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16
Q

how does ADP affect platelet aggregation

A

the higher the ADP the longer it can sustain platelet aggregation

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17
Q

what is the extrinsic pathway activated by

A

external trauma that causes blood to escape from the vascular system

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18
Q

what factor is involved in the extrinsic pathway

A

factor 7

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19
Q

which pathway is the clotting cascade is quicker

A

the extrinsic

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20
Q

what is the intrinsic pathway activated by

A

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

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21
Q

what factors are involved in the intrinsic pathway

A

factors 12, 11, and 9

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22
Q

which pathway is the clotting cascade is more important

A

the intrinsic pathway

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23
Q

what factors does the common pathway involve

A

factors 1,2 5, and 10

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24
Q

what does activated partial thromboplastin time test measure

A

the intrinsic pathway

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25
Q

what does the prothrombin time test measure

A

extrinsic pathway

26
Q

what are the fat soluble vitamins

A
  • vitamin D
  • vitamin E
  • vitamin A
  • vitamin K
27
Q

what are the vitamin K dependent factors

A

2, 7, 9, and 10

28
Q

what does the fibrin mesh do

A

laid down to reinforce and strengthen the platelet plug since thats not strong enough itself to prevent further bleeding

29
Q

what catalyzes the crosslinking of fibrin

A

transglutaminase or factor 7

30
Q

where are peptide bonds formed

A

between lysine and glutamine domains of fibrin molecules by transglutaminase

31
Q

how does fibrin polymerization and breakdown occur

A

plasmin breaks peptide bonds and destroys mesh

32
Q

what is plasmin derived from

A

plasminogen

33
Q

what converts plasminogen to plasmin

A

tissue plasminogen activator and urokinase, factor 11a, 12a, and kallikrein

34
Q

what is wound healing

A

complex process in which skin or other tissue repairs itself after injury

35
Q

what are the 4 phases of wound healing

A

-hemostasis
- inflammatory
-proliferative
-remodeling

36
Q

what happens in hemostasis

A

within minutes post-injury, platelets aggregate at the injury site to form a fibrin clot which acts to control bleeding

37
Q

what happens in inflammatory phase

A

bacteria and debris are phagocytosed and removed from the wound site, factors are released that cause migration and division of cells involved in the proliferative phase

38
Q

what happens in the proliferative phase

A

angiogenesis, collagen deposition, granulation, tissue formation, epithelialization and wound contraction

39
Q

what happens in the remodeling phase

A

collagen is remodeled and realigned along tension force lines and cells no longer needed are removed by apoptosis

40
Q

what cells are involved in coagulation

A

platelet/fibrin deposition

41
Q

what cells are involved in the inflammatory phase

A

neutrophil, monocyte, macrophage

42
Q

what cells are involved in the proliferation phase

A

-fibroblast/collagen deposition
-endothelial cell/angiogenesis
- keratinocyte/re-epithelialization

43
Q

what is the plasma form of fibronectin secreted by and what does it do

A

secreted by hepatocytes and modulates platelet function

44
Q

what is the cellular form of fibronectin secreted by and what does it do

A

secreted by cells as part of the ECM and functions as a scaffold protein

45
Q

what is ACD anticoagulant

A

acid citrate dextrose solution- solution of citric acid, sodium citrate and dextrose in water

46
Q

how does citrate work as an anticoagulant

A

citrate in the form of sodium citrate or acid-citrate dextrose is used to disrupt the coagulation cascade and prevent clotting. they bind to the calcium in blood, thus no regulation of binding and cascade cannot begin

47
Q

what is the prothrombin time test used for

A

to help detect and diagnose a bleeding disorder or excessive clotting disorder.

48
Q

what is the INR calculated from and what does it measure

A

calculated from a prothrombin time test and used to monitor how well the blood thinning medication, warfarin, is working to prevent blood coagulation

49
Q

what does the prothrombin time measure

A

the integrity of the extrinsic pathway and final common pathways of the coagulation cascade. consists of tissue factor and factors 7,2,5,10, and fibrinogen

50
Q

what is prothrombin time measured in

A

seconds

51
Q

why is the INR an important tool

A

is allows for easier comparisons of test results from different labs

52
Q

what is a healthy INR

A

1.1 or below

53
Q

what is an effective therapeutic range of INR for people taking warfarin

A

2.0-3.0

54
Q

what does a higher INR mean

A

blood clots more slowly than desired

55
Q

how does warfarin work

A

competetively inhibits the vitamin K epoxide reductase complex 1
- depletes vitamin K reserves and reduced the synthesis of active clotting factors 2,7,9, and 10, coagulation regulatory factors protein C and protein S

56
Q

how can effects of warfarin be neutralized

A

massive doses of vitamin K

57
Q

what targets factor 10a

A

rivaroxaban (xarelto, eliquis)

58
Q

what targets thrombin

A

dabigatran etexilate (pradaxa)

59
Q

what are hemophilia A and B caused by

A

an X-linked recessive genetic mutation

60
Q

what is hemophilia A caused by and how do you treat it

A

caused by decreased synthesis of factor 8 and treat with recombinant factor 8

61
Q

what is hemophilia B caused by and how do you treat it

A

caused by decreased synthesis of factor 9 and treat with recombinant factor 9

62
Q

what form of hemophilia is X-mas disease

A

hemophilia B

Biochem (34 decks)

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