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

Lecture 22 Blood coagulation and wound healing Flashcards

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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
What functions to hold enzymes onto the surface of the cell membrane?
Carboxyglutamate | Allow membrane interactions to continue pathways
26
What are the fat soluble vitamins?
- Vitamin D - Vitamin E - Vitamin A - Vitamin K
27
What are the vitamin K dependent clotting factors?
- II - VII - IX - X
28
When does fibrin start laying down a meshwork to reinforce the clot?
As soon as the platelet first attaches | - (highly organized cross link mesh of fibrin)
29
Why does the fibrin clot eventually need to go away?
In pulmonary vessels clot could break off and go to brain | Could cause stroke
30
What degrades fibrin polymer?
Plasmin
31
What activates plasminogen so it can break down fibrin?
Factors XIa, XIIa, Kallikrein
32
What are the stages of wound healing?
- Hemostasis - Inflammation - Proliferative - Remodeling
33
Hemostasis
within minutes of post injury, platelets aggregate at the injury site to form a fibrin clot which acts to control bleeding (restricting blood flow)
34
Inflammatory phase
- 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
35
Proliferative phase
- Angiogenesis - collagen deposition - Granulation tissue formation - Epithelization - Wound contraction
36
Remodeling phase
- Collagen is remodeled and realigned along tension force lines and cells no longer needed are removed by apoptosis
37
What drives the wound healing process to jump from one stage to the next?
Growth factors
38
System has anticoagulants to stop clotting process.
these are small inhibitors and cant proceed with process after this occurs
39
How do citrate anticoagulants prevent clotting?
They bind to calcium in the blood and there is now no regulation of the binding and the cascade cannot begin.
40
Prothrombin Test
- 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
Prothrombin Time (PT)
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
Prothrombin Time
- 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
INR of 1.1 or below
Normal
44
An INR range of 2-3
Effective therapeutic range for people taking warafin for disorders such as atrial fibrillation or a blood clot in leg or lung
45
When the INR is higher than the recommended range
It means that your blood clots more slowly than desired and a lower INR means your blood clots more quickly than desired
46
Drugs that precent coagulation or blood thinners
- Warfarin - Pradaxa - Xarelto - Eliquis - Plavis
47
Warfarin
- Competitively inhibits the Vitamin K epoxide reductase complex 1 (VKORC1) - can deplete functional vitamin K reserves
48
VKORC1
an essential enzyme for activating vitamin K
49
Hemophilia A
- X linked recessive - Decreased synthesis of Factor 8 - treat with recombinant Factor 8
50
Hemophilia B
- X-linked recessive - Decreased synthesis of Factor 9 - Treat with recombinant Factor 9 - Christmas disease
51
Scott syndrome
a bleeding disorder caused by defective scrambling of membrane phospholipids
52
Kallikrein mutations
- 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
Glanzmann's thrombasthenia
- (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
Von Willebrand Disease
- 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
Bernard Soulier Syndrome
- 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
Other clotting factor gene mutations
Factor V, II, VII, X, XIII
57
Factor VII
Activated by thrombin in the presence of Ca2+
58
Factor X
activated on surface of activated platelets by tenase complex and factor VIIa in presence of tissue factor and Ca2+
59
Factor IX
activated by factor XIa in presence of Ca2+
60
Factor XI
activated by factor XIIa
61
Factor XII
- binds to exposed collagen at site of vessell wall injury | - activated by high MW kininogen and kallikrein
62
Factor XIII
- Activated by thrombin in presence of Ca2+; stabilizes fibrin clot by covalent cross linking
63
Cofactors of coagulation
- Factor VIII - Factor V - Factor III Tissue Factor
64
Regulatory elements
- Von willebrand factor - Protein C - Protein S - Thrombomodulin - Antithrombin III
65
Factor VIII
- activated by thrombin | - factor VIIIa is a cofactor in the activation of factor X by factor IXa
66
Factor V
- Activated by thrombin | - factor Va is a cofactor in the activation of prothrombin by factor Xa
67
Factor III Tissue Factor
Subendothelial cell surface glycoprotein that acts a cofactor for factor VII
68
Von willebrand factor
- Associated with subendothelial tissue | - serves as a bridge between platelet, glycoprotein GPIb/IX and collagen
69
Protein C
- Activated to protein Ca by thrombin bound to thrombomodulin - Then degrades factors VIIIa and Va
70
Protein S
- Acts as a cofactor of protein C | - both proteins contain gla residues
71
Thrombomodulin
- Protein on the surface of endothelial cells | - Binds thrombin which then activates protein C`
72
Antithrombin III
- Most important coagulation inhibitor | - Controls activities of thrombin, and factors IXa, Xa, XIa, and XIIa
73
What anticoagulant medication targets thrombin?
Pradaxa
74
What anticoagulant medication targets factor Xa?
Xarelto and Eliquis
75
Is warfrin a rapid acting medication?
No it takes several days to see effects | - INR levels should be monitored
76
What are the rapid acting anticogulants?
- Pradaxa - Xarelto - Eliquis
77
TPA
- broad spectrum effect of breaking up clot | - bleeding risk
78
Plasmin
- breaks up clot locally | - no bleeding risk
79
Scott syndrome
- a bleeding disorder caused by defective scrambling of membrane phospholipids - dont have phosphotidal serine
80
Kallikrein mutations
-can survive pretty well bc extrinsic pathway compensates
81
Glanzmanns
defect in gpIIb-IIIa glycoprotein | - bruise easily
82
VWF disease
- no VWF | - cant form platelet plug
83
Bernard souiler syndrome
- heavy and prolonged menstral cycles
84
Factor 5 diseases
- less than 10% of normal levels of coagulation factor 5 in their blood - abnormal bleeding - has to be inherited with 2 copies
85
Factor II mutations
- prthrombin thrombophilia - base change in gene - too much thrombin - leads to too much clotting
86
Factor VII mutations
- abnormal bleeding | - not related to amount of factor 7 just not functioning properly
87
Factor 10
- deficiency of factor 10 causes not clotting
88
Factor 8 mutations
- 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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