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PSL301 > Lecture 5: Blood Clotting > Flashcards

Lecture 5: Blood Clotting Flashcards

1
Q

What gives rise to platelets?

A

megakaryocytes

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2
Q

___ are needed for blood clotting

A

platelets

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3
Q

How do megakaryocytes give rise to platelets?

A

Edges of megakaryocyte break off to form platelets (cell fragments)

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4
Q

Megakaryocytes are…

A

giant cells with many copies of DNA in the nucleus

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5
Q

Half life of platelets?

A

10 days

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6
Q

____ increases platelet numbers by…

A

thrombopoietin

stimulating production of platelets

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7
Q

How is blood clotting regulated? (3 phases)

A
  1. vascular phase
  2. platelet phase
  3. coagulation phase
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8
Q

Vascular phase

A

Exposed collagen & tissue factors cause vasoconstriction of the damaged blood vessel. Vasoconstriction minimizes blood loss.

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9
Q

Vascular phase controlled by…

A

nervous system & muscles (neurogenic & myogenic control)

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10
Q

Vasoconstriction in vascular phase prolonged by…

A
  1. Serotonin
  2. Endothelin-1
  3. Thromoboxane A2
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11
Q

Platelet phase

A
  1. Collagen exposed to blood stream; bind platelets passing by in the blood
  2. Factors released from trapped platelets attract more platelets
  3. Platelets aggregate to form plug
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12
Q

What makes von Willebrand factor?

A

endothelial cells

platelets

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13
Q

What does von Willebrand factor bind to?

A

collagen

platelets

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14
Q

What are the factors released from platelets?

A

ADP
PAF (platelet activating factor)
serotonin
thromboxane

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15
Q

When are factors released from platelets?

A

during platelet phase

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16
Q

What does serotonin and thromboxane cause?

A

vasoconstriction

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17
Q

What do activated platelets look like?

A

spiky outer surface

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18
Q

Purpose of activating platelets?

A

they can adhere to each other better

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19
Q

What do inactivated platelets look like?

A

disk-like cell fragments

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20
Q

What prevents platelet adhesion/activation during normal situations?

A

Vasodilators:
NO
Prostacyclin

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21
Q

What releases NO and prostacyclin

A

endothelium

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22
Q

Prostacyclin is made up of…

A

Prostaglandin I2, PGI2

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23
Q

Why is aspirin given after mild heart attacks?

A

Precursor for thromboxane is arachidonic acid.
Enzyme cyclooxygenase cleaves ADA -> PGH2 -> thromboxane.
Aspirin stops CO activity, so thromboxane can’t be made.
Since thromboxane is used to vasoconstrict & aggregate platelets, these don’t happen as easily.

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24
Q

Function of von Willebrand factor?

A
  • link platelet with collagen
  • draw platelet into exposed collagen area
  • keep VII in circulation longer
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25
Q

What happens during vascular phase?

A

vasoconstriction

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26
Q

What happens during platelet phase?

A

Platelets are actively trying to stop bleeding (loose platelet plug)

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27
Q

What happens during coagulation phase?

A
  • Proper blood clot forms via coagulation cascade

- Fibrinogen -> fibrin

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28
Q

Fibrin

A

Long strand of fibre that reinforces loose platelet plug

One piece of fibrinogen

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29
Q

Inactive form of fibrin

A

fibrinogen

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30
Q

What do all the factors released from platelets cause?

A

platelet aggregation

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31
Q

What are the effects of thromboxane?

A

Constriction

Platelet aggregation

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32
Q

Cyclooxygenase catalyses what reaction?

A

arachidonic acid -> PGH2

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33
Q

What can PGH2 become?

A

Prostaglandins
Thromboxane
Prostacyclin

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34
Q

Why is prostacyclin activity not affected when aspirin is taken?

A

Endothelial cells can still make more CO

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35
Q

What is the sturdiest form of fibrin?

A

covalent cross-links

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36
Q

What enzyme cleaves fibrinogen to fibrin?

A

thrombin

37
Q

is fibrin soluble / insoluble?

A

insoluble

38
Q

How does fibrin become cross-linked?

A

Factor XIII & Ca++ catalysed

39
Q

Summary of coagulation cascade

A
  1. Contact activation pathway
  2. Tissue factor pathway
  3. Common pathway

1->3 or 2->3

40
Q

Intrinsic pathway

A

Contact activation pathway

41
Q

extrinsic pathway

A

tissue factor pathway

42
Q

trigger for intrinsic pathway

A

collagen in bld vessels exposed due to injury

43
Q

What is the function of ADP?

A

Attract more platelets to damaged area

44
Q

Trigger for extrinsic pathway

A

Damaged tissue exposes thromboplastin

45
Q

What does factor XI and factor VII activate?

A

Factor X (common pathway)

46
Q

What activates prothrombin activator?

A 
Factor X
Factor III
Factor V
Ca++
PF3
PL
47
Q

Purpose of prothrombin activator?

A

prothrombin -> thrombin

48
Q

What activates factor XIII?

A

Thrombin

49
Q

What is the beginning of the common pathway?

A

active factor X

50
Q

Where are many plasma factors used for blood clotting made?

A

liver

51
Q

Cascade of intrinsic pathway

A
  1. Exposed collagen activates factor XII
  2. Factor XII & Ca++ activate Factor XI
  3. Factor XI & Ca++ activate factor IX
  4. Factor IX, factor VIII, Ca++, PL activate factor X
52
Q

what regulates levels of factor VIII?

A

von Willebrand factor (keeps VIII around for longer)

53
Q

Vit K needed for the synthesis of…

A

thrombin
VII
IX
X

54
Q

What drugs blocks the action of vit K?

A

Coumadin / Warfarin

-> less blood clotting

55
Q

What vitamin helps blood clotting?

A

vit K

56
Q

Cascade of extrinsic pathway

A
  1. Factor III from thromboplastin activate Factor VII
  2. VII + III activate IX
  3. III and VII // Ca++ // PL -> activates X

Positive feedback:
X activates VII

57
Q

vWf disease (symptoms)

A

problem with quality or quantity of vWf

problem with blood clotting

58
Q

Which areas are most affected by the lack of vWf?

A

areas w/ small number of capillaries (skin, GI, uterus)

59
Q

treatment for vWf disease?

A

protein that releases vasopressin to endothelial cells: stimulate release of vWf

60
Q

Hemophilia A need to be injected with…

A

VIII

61
Q

Hemophilia B due to deficiency in…

A

IX

62
Q

Symptoms of hemophilia

A

internal and external bleeding that doesn’t stop easily

63
Q

which pathway is still active in those with haemophilia?

A

Extrinsic, but not enough to have normal blood clotting efficiency

64
Q

Purpose of plasmin

A

fibrin -> fibrin fragments (easy to break up and remove)

65
Q

Which enzymes are responsible for the formation of plasminogen -> plasmin?

A

Thrombin

tPA

66
Q

What enzymes are used for fibrinolysis (anticoagulants)?

A
  1. plasmin
  2. tPa
  3. TFPI
  4. Antithrombin
  5. Protein C
67
Q

tPA released by…

A

damaged endothelium (released very slowly)

68
Q

precursor of plasmin

A

plasminogen

69
Q

Thrombin has positive feedback on…

A
  1. VII activation
  2. VIII activation
  3. IX activation
  4. XI activation
  5. V activation
70
Q

What activates protein C?

A

thrombin -> (catalysed by protein S)

71
Q

function of protein C?

A
  1. stop activation of VIII

2. stop activation of V

72
Q

function of TFPI?

A

stop VII activation

73
Q

function of antithrombin?

A
  1. stop IX activation
  2. stop X activation
  3. stop XI activation
  4. stop XII activation
  5. stop thrombin
74
Q

TFPI

A

tissue factor pathway inhibitor

75
Q

Where is plasminogen / plasmin released from?

A

liver

76
Q

Where is tPA released from?

A

many tissues

77
Q

Where is TFPI released from?

A

endothelium

78
Q

Where is antithrombin released from?

A

liver

79
Q

Where is protein c released from?

A

liver

80
Q

tPA is activated by…

A

not activated

81
Q

TFPI is activated by…

A

not activated

82
Q

Antithrombin is activated by…

A

heparin

83
Q

Haemorrhagic stroke

A

Blood vessel in brain bursts, and blood leaks into brain

84
Q

Stroke

A

Blood clot gets stuck in artery going into brain

85
Q

Thrombus

A

blood clot attached to vessel wall (less O gets to tissues)

86
Q

Embolus

A

Floating blood clot

87
Q

tPA

A

tissue plasminogen activator

88
Q

What is a treatment for stroke?

A

tPA given within 3-4 after a stroke

this breaks down the blood clot

89
Q

When is tPA not administered as a treatment for a stroke?

A

Haemorrhagic stroke

Will make the bleeding worse

PSL301 (29 decks)

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