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Biochemistry (Cole) > Lecture 22 Blood coagulation and wound healing > Flashcards

Lecture 22 Blood coagulation and wound healing Flashcards

1
Q

Blood clotting (Coagulation) steps

A
  • Injury/rupture to blood vessel
  • Blood vessel around would constricts (reduces blood flow to injured area)
  • Activated platelets stick to the injury site
  • Platelets become sticky and clump together to form platelet plug
  • Platelets and damaged tissue release clotting factors (factor VIII)
  • Blood clotting mechanism to form fibrin which acts like a mesh to stop the bleeding
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2
Q

Hemostasis

A

the stopping of blood flow

2 types (primary and secondary)

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3
Q

Primary hemostasis

A

-Vasoconstriction and platelet response

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4
Q

What is platelet aggregation at the site of injury mediated by?

A
  • Platlete derived agonists
  • Platelet derived Adhesive proteins
  • Plasma derived adhesive proteins
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5
Q

Secondary Hemostasis

A
  • clotting cascade
  • Cascade of coagulation serine proteases that culminates in the cleavage of soluble fibrinogen by thrombin (into fibrin)
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6
Q

Is fibrin soluble?

A

No, fibrin is insoluble and forms a clot.

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7
Q

When does fibrin generation occur?

A

Simultaneously to platelet aggregation

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8
Q

What cleaves fibrinogen to turn into insoluble fibrin?

A

thrombin

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9
Q

What do platelets release when they stick to collagen at the injury site?

A
  • ADP
  • Serotonin
  • thromboxane A2
  • (stored as dense granules)
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10
Q

What causes vasoconstriction?

A

Serotonin and Thromboxane A2

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11
Q

What attracts other platelets to stick together and form the platelet plug?

A

ADP

Thromboxane A2

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12
Q

Serotonin Biosynthesis

A

Tryptophan –> 5HTP –> Serotonin 5 hydroxytryptamine (5HT)

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13
Q

What is the first step in platelet aggregation?

A

Binding to VWF

- induces a conformational change on GPIIb/IIIa to bind to fibrinogen

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14
Q

Extrinsic pathway

A

The extrinsic pathway is activated by external trauma that causes blood to escape from the vascular system. This pathway is quicker than the intrinsic pathway. It involves factor VII

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15
Q

Intrinsic Pathway

A

Activated by the trauma inside the vascular system and is activated by platelets, exposed endothelium, chemicals , or collagen.
Slower than the extrinsic but more important

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16
Q

What activates the intrinsic pathway?

A
  • platelets
  • exposed endothelium
  • collagen
  • chemicals
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17
Q

What factors are involved in the intrinsic pathway?

A
  • XII
  • XI
  • IX
  • VIII
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18
Q

Common pathway

A
  • Both pathways meet and finish the pathway of clot production in what is know as the common pathway.
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19
Q

What factors are involved in the common pathway?

A
  • I
  • II
  • V
  • X
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20
Q

What the coagulation factors generally?

A

Serinen proteases

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21
Q

What factors are glycoproteins?

A
  • Factor V

- Factor VIII

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22
Q

Why is Ca important in the intrinsic and extrinsic pathways?

A
  • Need calcium and phospholipids to activate factor X

- thrombin then turns fibrinogen into fibrin

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23
Q

Factor 1

A

Fibrinogen

-Cleaved by thrombin

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24
Q

Factor II

A

Prothrombin

ACtivated on surface of activated platelets by prothrombinase complex

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25
Q

What functions to hold enzymes onto the surface of the cell membrane?

A

Carboxyglutamate

Allow membrane interactions to continue pathways

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26
Q

What are the fat soluble vitamins?

A
  • Vitamin D
  • Vitamin E
  • Vitamin A
  • Vitamin K
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27
Q

What are the vitamin K dependent clotting factors?

A
  • II
  • VII
  • IX
  • X
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28
Q

When does fibrin start laying down a meshwork to reinforce the clot?

A

As soon as the platelet first attaches

- (highly organized cross link mesh of fibrin)

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29
Q

Why does the fibrin clot eventually need to go away?

A

In pulmonary vessels clot could break off and go to brain

Could cause stroke

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30
Q

What degrades fibrin polymer?

A

Plasmin

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31
Q

What activates plasminogen so it can break down fibrin?

A

Factors XIa, XIIa, Kallikrein

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32
Q

What are the stages of wound healing?

A
  • Hemostasis
  • Inflammation
  • Proliferative
  • Remodeling
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33
Q

Hemostasis

A

within minutes of post injury, platelets aggregate at the injury site to form a fibrin clot which acts to control bleeding (restricting blood flow)

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34
Q

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
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35
Q

Proliferative phase

A
  • Angiogenesis
  • collagen deposition
  • Granulation tissue formation
  • Epithelization
  • Wound contraction
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36
Q

Remodeling phase

A
  • Collagen is remodeled and realigned along tension force lines and cells no longer needed are removed by apoptosis
37
Q

What drives the wound healing process to jump from one stage to the next?

A

Growth factors

38
Q

System has anticoagulants to stop clotting process.

A

these are small inhibitors and cant proceed with process after this occurs

39
Q

How do citrate anticoagulants prevent clotting?

A

They bind to calcium in the blood and there is now no regulation of the binding and the cascade cannot begin.

40
Q

Prothrombin Test

A
  • Take citrated plasma and add calcium back and also thromboplastin
  • This evaluates the presence of prothrombin (II), factors X, V, and VII and fibrinogen
  • Add calcium and clot forms
41
Q

Prothrombin Time (PT)

A

is a test used to help detect and diagnose a bleeding disorder or excessive clotting disorder; the internation normalized ration (INR) is calculated from a PT result and is used to monitor how well the blood-thinning medication (warfin) is working to prevent blood coagulation

42
Q

Prothrombin Time

A
  • measure of the integrity of the extrinsic and final common pathways of the coagulation cascade.
  • This consists of tissue factor and factors VII, II (prothrombin) V, X and fibrinogen.
43
Q

INR of 1.1 or below

A

Normal

44
Q

An INR range of 2-3

A

Effective therapeutic range for people taking warafin for disorders such as atrial fibrillation or a blood clot in leg or lung

45
Q

When the INR is higher than the recommended range

A

It means that your blood clots more slowly than desired and a lower INR means your blood clots more quickly than desired

46
Q

Drugs that precent coagulation or blood thinners

A
  • Warfarin
  • Pradaxa
  • Xarelto
  • Eliquis
  • Plavis
47
Q

Warfarin

A
  • Competitively inhibits the Vitamin K epoxide reductase complex 1 (VKORC1)
  • can deplete functional vitamin K reserves
48
Q

VKORC1

A

an essential enzyme for activating vitamin K

49
Q

Hemophilia A

A
  • X linked recessive
  • Decreased synthesis of Factor 8
  • treat with recombinant Factor 8
50
Q

Hemophilia B

A
  • X-linked recessive
  • Decreased synthesis of Factor 9
  • Treat with recombinant Factor 9
  • Christmas disease
51
Q

Scott syndrome

A

a bleeding disorder caused by defective scrambling of membrane phospholipids

52
Q

Kallikrein mutations

A
  • LAck of functional plasma kallikrein protein does not generally cause any symptoms because another process called the extrinsic coagulation pathway can compensate for the impaired intrinsic coagulation pathway.
53
Q

Glanzmann’s thrombasthenia

A
  • (GpIIb-IIIa def.)
  • Frequent nosebleeds and may bleed from the gums
  • Excessive bleeding following injury, trauma, or surgery
  • Affected women may may have excessive blood loss during pregnancy and childbirth
54
Q

Von Willebrand Disease

A
  • easy bruising, long-lasting nosebleeds, and excessive bleeding or oozing following an injury,, surgery, or dental work
  • Mild forms may became apparent only when abnormal bleeding occurs following surgery or serious injury
55
Q

Bernard Soulier Syndrome

A
  • GpIb
  • Bruise easily and have an increased risk of nosebleeds
  • Abnormally heavy bleeding following minor injury or surgery or even without trauma (spontaneous bleeding)
56
Q

Other clotting factor gene mutations

A

Factor V, II, VII, X, XIII

57
Q

Factor VII

A

Activated by thrombin in the presence of Ca2+

58
Q

Factor X

A

activated on surface of activated platelets by tenase complex and factor VIIa in presence of tissue factor and Ca2+

59
Q

Factor IX

A

activated by factor XIa in presence of Ca2+

60
Q

Factor XI

A

activated by factor XIIa

61
Q

Factor XII

A
  • binds to exposed collagen at site of vessell wall injury

- activated by high MW kininogen and kallikrein

62
Q

Factor XIII

A
  • Activated by thrombin in presence of Ca2+; stabilizes fibrin clot by covalent cross linking
63
Q

Cofactors of coagulation

A
  • Factor VIII
  • Factor V
  • Factor III Tissue Factor
64
Q

Regulatory elements

A
  • Von willebrand factor
  • Protein C
  • Protein S
  • Thrombomodulin
  • Antithrombin III
65
Q

Factor VIII

A
  • activated by thrombin

- factor VIIIa is a cofactor in the activation of factor X by factor IXa

66
Q

Factor V

A
  • Activated by thrombin

- factor Va is a cofactor in the activation of prothrombin by factor Xa

67
Q

Factor III Tissue Factor

A

Subendothelial cell surface glycoprotein that acts a cofactor for factor VII

68
Q

Von willebrand factor

A
  • Associated with subendothelial tissue

- serves as a bridge between platelet, glycoprotein GPIb/IX and collagen

69
Q

Protein C

A
  • Activated to protein Ca by thrombin bound to thrombomodulin
  • Then degrades factors VIIIa and Va
70
Q

Protein S

A
  • Acts as a cofactor of protein C

- both proteins contain gla residues

71
Q

Thrombomodulin

A
  • Protein on the surface of endothelial cells

- Binds thrombin which then activates protein C`

72
Q

Antithrombin III

A
  • Most important coagulation inhibitor

- Controls activities of thrombin, and factors IXa, Xa, XIa, and XIIa

73
Q

What anticoagulant medication targets thrombin?

A

Pradaxa

74
Q

What anticoagulant medication targets factor Xa?

A

Xarelto and Eliquis

75
Q

Is warfrin a rapid acting medication?

A

No it takes several days to see effects

- INR levels should be monitored

76
Q

What are the rapid acting anticogulants?

A
  • Pradaxa
  • Xarelto
  • Eliquis
77
Q

TPA

A
  • broad spectrum effect of breaking up clot

- bleeding risk

78
Q

Plasmin

A
  • breaks up clot locally

- no bleeding risk

79
Q

Scott syndrome

A
  • a bleeding disorder caused by defective scrambling of membrane phospholipids
  • dont have phosphotidal serine
80
Q

Kallikrein mutations

A

-can survive pretty well bc extrinsic pathway compensates

81
Q

Glanzmanns

A

defect in gpIIb-IIIa glycoprotein

- bruise easily

82
Q

VWF disease

A
  • no VWF

- cant form platelet plug

83
Q

Bernard souiler syndrome

A
  • heavy and prolonged menstral cycles
84
Q

Factor 5 diseases

A
  • less than 10% of normal levels of coagulation factor 5 in their blood
  • abnormal bleeding
  • has to be inherited with 2 copies
85
Q

Factor II mutations

A
  • prthrombin thrombophilia
  • base change in gene
  • too much thrombin
  • leads to too much clotting
86
Q

Factor VII mutations

A
  • abnormal bleeding

- not related to amount of factor 7 just not functioning properly

87
Q

Factor 10

A
  • deficiency of factor 10 causes not clotting
88
Q

Factor 8 mutations

A
  • hemophilia A
  • most common form of bleeding disorder
  • most are single nucleotide changes but some large deletions or rearrangements

Biochemistry (Cole) (25 decks)

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