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Module 103: The Heart, Lungs and Blood > Theme 2: Lecture 2 - Platelets and Haemostasis > Flashcards

Theme 2: Lecture 2 - Platelets and Haemostasis Flashcards

1
Q

What is the endothelium?

A

Layer of cells lining inner surface of all vessel walls and have a huge total surface area

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2
Q

What is the function of the endothelium?

A
  • Controls blood fluidity and flow
  • Controls size of blood vessel
  • When intact: contributes to preventing clots
  • When injured: promotes local clotting on exposed basement membrane
  • Signals inflammatory cells to areas needing defence/repair
  • Gate-keeper between blood and tissues
  • Actively controls extravasation of fluid, cells & molecules
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3
Q

What is haemostasis

A

process which causes bleeding to stop

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4
Q

What does the endothelium secrete under normal conditions

A

Inhibitors of haemostasis

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5
Q

What does the endothelium secrete when injured

A

von Willebrand factor (and stops secreting haemostasis inhibitors)

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6
Q

von Willebrand factor

A

a blood protein that is an important trigger for many aspects of clotting

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7
Q

Haemorrhage

A

large amount of blood loss

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8
Q

How do platelets form the primary haemostatic plug due to vessel wall injury

A
  • Platelet adhesion (to endothelium wall)
  • Platelet activation (causes platelets to do a lot of different things)
  • Platelet aggregation (platelets stick together to begin to form a plug)
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9
Q

Examples of vasoconstrictors

A
  • Serotonin
  • ADP
  • Thromboxane A2
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10
Q

What do platelets release in order to aid blood clotting

A

vasoconstrictors and prothrombotic agents

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11
Q

How does vasoconstriction aid in blood vessel repair

A

it slows down blood flow

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12
Q

Virchow’s triad

A

the three types of increased risk for thrombosis:

  • endothelial injury leading to plug formation
  • hypercoagulability
  • venous stasis
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13
Q

Megakaryocyte

A
  • the precursor to platelets
  • Made in the bone marrow
  • 4000/megakaryocyte
  • Polypoid
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14
Q

Polypoid

A

multi nuclueated

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15
Q

Thrombocyte

A

Platelet

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16
Q

Thrombocytopaenia

A

low platelet count in the blood

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17
Q

Normal platelet count (in relation to RBCs)

A

20X < RBCs

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18
Q

Normal platelet size

A

2-3 µm

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19
Q

What happens to platelets when they are activated

A
  • exocytose dense granules
  • change shape
  • increase respiratory rate
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20
Q

Which part of haemostasis is platelet activation required for

A
  • aggregation of platelets

- some coagulation steps

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21
Q

Resting platelet shape

A

smooth and disc shaped

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22
Q

Activated platelet shape

A

irregular shape with many protruding pseudopodia

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23
Q

Where do platelets adhere to

A

exposed collagen in the basement membrane

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24
Q

What dense granules do platelets exocytose when activated

A
  • Serotonin
  • ADP
  • Calcium
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25
Q

What is platelet aggregation stimulated by

A

ADP

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26
Q

Which drug blocks platelet aggregation

A

Prasugrel

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27
Q

How does platelet aggregation occur

A

via fibrinogen

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28
Q

More details of platelet activation

A
  • Extracellular ADP causes activation of the P2Y receptor on the surface of platelets
  • This leads to cation flow inside the platelet
  • Platelets release Thromboxane A2
  • ADP leads to positive feedback on platelets as more ADP is released
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29
Q

Clotting factors

A
  • All circulate as inactive precursors *E

- Most are enzymes, which cleave other factors to activate them

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30
Q

Which clotting factors aren’t enzymes

A

Factor V and Factor VIII

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31
Q

What are Factors V and VIII

A
  • co factors allowing the enzymes to function

- work with factor X

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32
Q

Why is the initial activating factor segregated

A

So that the clotting cascade isn’t constantly activated

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33
Q

Where is tissue factor located

A

behind endothelial cells

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34
Q

Where are the clotting factor precursors (except tissue factor)

A

Circulating in the blood

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35
Q

Thrombosis

A

pathological clotting of the blood that can lead to clogging of a blood vessel

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36
Q

When can thrombosis occur spontaneously

A

where blood flow is slow

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37
Q

How do labs stop blood from clotting

A

with citrate or heparin

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38
Q

Plasma

A

fluid portion of the blood

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39
Q

Serum

A

fluid left after blood clotting

40
Q

How do plasma and serum differ

A

they are almost identical except that serum is missing fibrinogen, clotting factors II, V, VIII

41
Q

embolism

A

abnormal migration of clot (or other intravascular object

42
Q

What are the 2 coagulation cascades

A
  • extrinsic (tissue factor) pathway

- intrinsic (contact activation) pathway

43
Q

Extrinsic pathway

A
  • Requires secretion of tissue factor to occur
  • Initiation of coagulation
  • Tissue factor (under endothelium) + factor VIIa
44
Q

Intrinsic pathway

A
  • All factors/proenzymes are already in place

- Amplification of process through positive feedback

45
Q

How is thrombin activated

A
  • Activated by Factor Xa, but poorly
  • Factor Va is a co-factor for Factor Xa
  • Together they activate Thrombin well
46
Q

What are the pathways to activate factor X

A
  • Extrinsic pathway
  • Intrinsic pathway
  • Thrombin also activates it (positive feedback)
47
Q

Where is there positive feedback in coagulation

A

Thrombin activates co-factors (inactive factor V and VIII) to activate itself

48
Q

What are coagulation factors in the prothrombin group

A

Factors II VII IX X

49
Q

describe the prothrombin coagulation factors

A
  • So called because they act on prothrombin and turn it into thrombin
  • They are Enzymes
  • Vitamin K needed for synthesis
  • Require Ca2+ for activation
  • Stable
50
Q

What are the coagulation factors in the thrombin group

A

Factors I V VIII

51
Q

describe the thrombin coagulation factors

A
  • So called because they are affected by thrombin
  • Thrombin activates them
  • V & VIII are co-factors
  • Factor I is fibrinogen
  • Increased in inflammation, pregnancy & with oral contraceptives
52
Q

Which factor is prothrombin

A

Factor II

53
Q

Which factor is fibrinogen

A

Factor I

54
Q

Which factor is thrombin

A

Activated factor II

55
Q

Which factor is fibrin

A

Activated factor I

56
Q

Why can problems with the liver lead to clotting deficiency

A

Clotting factors are made by the liver

57
Q

Vitamin K

A

-A class of related fat-soluble vitamins
-Is required to synthesize enzyme coagulation factors:
Prothrombin (II), VII, IX, X (calcium dependent proteases)
-Vit K essential for gamma carboxylation (an enzyme reaction) of clotting enzymes

58
Q

Fibrinolysis

A

breaking apart a clot

59
Q

Plasmin

A
  • An enzyme
  • Lyses fibrin – stops / destroys clots
  • Starts as inactive Plasminogen, a protein made by liver
60
Q

What does plasminogen require to mature

A

tissue factor activator (tPA)

61
Q

Where is tissue factor activator located

A

on the surface of endothelial cells

62
Q

Protein C

A
  • Coagulation Inhibitor
  • Starts as an inactive enzyme made by liver
  • Activated on surface of endothelial cells
63
Q

What does Protein C do

A

Inactivates Factor Va and VIIIa

64
Q

Which protein does Protein C work with in inactivate Factor Va

A

Protein S

65
Q

Antithrombin III (and heparin)

A

Peptide in blood made by liver

66
Q

Why does Antithrombin III always work in association with heparin

A

because it’s very inactive itself

67
Q

What does Antithrombin III (and heparin) do

A

Blocks activity of thrombin, Xa and IXa

68
Q

What does heparin do in association with Antithrombin III

A

greatly increases Antithrombin III activity

69
Q

What is heparin reversible by

A

protamine sulfate

70
Q

What does Antithrombin III deficiency cause

A

risk of thrombotic disease

71
Q

what is a recombinant form of Antithrombin III used for medically

A

thrombotic disorders

72
Q

What does vitamin K deficiency result in

A

clotting insufficiency

73
Q

Why is vitamin K deficiency rare

A
  • vitamin K is made by bacteria of large intestine

- Also found in leafy green vegetables (e.g. broccoli)

74
Q

What is vitamin K deficiency caused by

A
  • GI disease
  • no fat absorption
  • Liver disease as this means no bile salts formed
75
Q

What does warfarin do

A
  • prevents recycling of vitamin K

- Depletes active vitamin K after a few days

76
Q

Haemophilia A

A
  • Clotting disorder
  • Affects larger blood vessels
  • Joints, muscles
  • Wounds that bleed for days
  • X linked
77
Q

What causes Haemophilia A

A

congenital lack of factor VIII

78
Q

How is haemophilia A treated

A

Treat with injected purified Factor VIII (expensive, rare)

79
Q

Haemophilia B

A
  • AKA Christmas disease
  • defect of factor IX
  • symptoms as per Haemophilia A
80
Q

Describe how inflammation due do atherogenesis can cause haemostasis

A

-Monocytes enter lesion
-Become macrophages and consume cholesterol esters
-Can become foam cells
-Foam cells can die and release their contents
Which attract more monocytes, cytokines and chemo-attractants
-This leads to inflammation which can cause haemostasis

81
Q

Describe the disease process of atherogenesis from lipid deposits

A
  • LDL deposits lipids in lesion
  • Cholesterol esters are non-aqueous which can make lesion solid / hard
  • Cholesterol esters are oxidized, making oxygen radicals which makes them immunogenic
  • Oxidized lipids are consumed by macrophages
  • Which become Foam Cells which explode and attract more monocytes
82
Q

Describe what happens to the endothelium in atherogenesis

A

-Endothelium expresses chemo attractants for monocytes to find and enter lesion
-When endothelium is lost, collagen stimulates coagulation
-Endothelium normally covers collagen and basement membrane
When endothelium is lost, vessel cannot control its dilation as endothelium normally provides nitric oxide

83
Q

What do anti-platelet agents do

A
  • block platelet activation
  • Prevent clotting in arteries where anticoagulants have limited effects
  • Used in acute coronary syndromes
84
Q

Aspirin

A
  • An anti-platelet agent
  • Cyclo-oxygenase (COX) inhibitor
  • Blocks formation of thromboxane A2 in platelets
  • Lengthens bleeding time
  • Does NOT increase coagulation time
  • Prophylaxis for myocardial infarction
85
Q

Prasugrel

A
  • An anti-platelet agent

- ADP receptor inhibitor

86
Q

Clopidogrel

A
  • An anti-platelet agent

- ADP receptor inhibitor

87
Q

Anti-coagulants

A
  • Block production or activity of clotting factors
  • Used to treat venous disease *E
  • Prevent clotting in veins and in low pressure pulmonary circulation
88
Q

What are anti-coagulants used as a prophylactic for

A
  • DVT

- PE

89
Q

What do heparins do

A
  • An anti-coagulant

- Inhibit coagulation (with AT III) by inhibiting Factor Xa

90
Q

NOACs

A
  • Novel oral anticoagulants

- anti-coagulants

91
Q

Dabigatran

A
  • A NOAC (type of anti-coagulant)

- Thrombin inhibitor

92
Q

Rivaroxaban

A
  • A NOAC (type of anti-coagulant)

- Factor Xa inhibitor

93
Q

Wararfin

A
  • An anti-coagulant
  • Vitamin K antagonist
  • Slow onset (days)
  • Requires monitoring
94
Q

Fibrinolytics

A
  • Drugs used primarily used to dissolve fibrin in arterial disease
  • Used in acute coronary syndromes
95
Q

Give 3 fibrinolytic drugs

A
  • Tissue Plasminogen Activator (tPA)
  • Streptokinase
  • Urokinase

Module 103: The Heart, Lungs and Blood (51 decks)

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