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PP > Lecture 9 - Intro To Haemostasis > Flashcards

Lecture 9 - Intro To Haemostasis Flashcards

1
Q

What is haemostasis?

A

Maintenance of fluid status in normal vessels whilst permitting rapid formation of a haemostatic clot at a sit of vascular injury

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2
Q

What are the 3 components of haemostasis?

A

Vascular wall

Platelets

Coagulation cascade:
-Coagulation factors
-Anticoagulant factors

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3
Q

What is the basic aim of normal haemostasis?

A

Stopping bleeding following trauma to blood vessel

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4
Q

What are the 3 general processes of stopping normal bleeding?

A

Vessel wall contracts
Platelet plug forms
Fibrin clot forms to stabilise

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5
Q

How does vessel size relate to bleeding from the vessel?

A

larger vessel = more bleeding

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6
Q

What cells are platelets made from?

A

Megakaryocytes

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7
Q

Where are megakaryocytes/platelets made?

A

In the bone marrow

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8
Q

What is the normal platelet count?

A

150 - 400 x 10^9/L

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9
Q

What 3 stages do platelets go through when a vessel is injured?

A

Adhesion
Activation
Aggregation (Forms platelet clot)

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10
Q

How do platelets adhere to blood vessels?

A

Collagen from tunica adventitia exposed

Von Willebrand factor produced by vascular endothelial cells binds to platelets binding the platelets to the collagen fibres adhering them

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11
Q

When platelets are activated what do they secrete?

A

Granules containg:
-Fibrinogen
-ADP
-Thromboxane
-Some coagulation factors
And more substances to activate other platelets

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12
Q

What is platelet aggregation?

A

When platelets cross link to form a platelet plug

Platelet plug adds some stability but is quite weak

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13
Q

What is the role of collagen in platelets action?

A

Binds platelets to vessel wall

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14
Q

What is the role of Von Willebrand factor?

A

To get platelets to adhere to the collagen

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15
Q

What is the role of ADP and Thromboxane?

A

Cause platelets to interact and form a platelet plug

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16
Q

What is the role of Thrombin?

A

Converts fibrinogen to fibrin

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17
Q

Why is formation of fibrin important?

A

It is insoluble so is what forms the stable clot

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18
Q

What is a zymogen?

A

A proenzyme (enzyme that is not active)

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19
Q

What is the clotting cascade aiming to produce?

What is the point of producing this?

A

Thrombin

Thrombin needed to convert fibrinogen into fibrin

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20
Q

Why does fibrinogen need to be converted into fibrin?

A

Fibrinogen is soluble
Fibrin is insoluble

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21
Q

Why do natural anticoagulants exist?

A

To carefully balanced the clotting cascade to prevent over clotting

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22
Q

What are the 2 pathways of the clotting cascade that lead to the common pathway?

A

Intrinsic pathway (contact activation pathway

Extrinsic pathway (tissue factor pathway)

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23
Q

What do both the intrinsic pathway and the extrinsic pathway produce which is the common insertion point into the common pathway?

A

Factor X (10)

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24
Q

What does Factor X (10) do in the common pathway?

A

Convert prothrombin to thrombin

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25
Q

Where are most the coagulation factors made?

A

The Liver

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26
Q

What are the 3 coagulation tests for clotting defects?

A

APTT (Activated partial Thromboplastin time)
PT (Prothromin time)
TT (Thrombin time)

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27
Q

What pathways does PT (prothrombin time) measure?

A

Extrinsic pathway

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28
Q

The function of what clotting factor is assed by PT (extrinsic pathway)?

A

Factor VII

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29
Q

What pathway is the (Activated partial thromboplastin time) APTT measuring the functioning of?

A

Intrinsic pathway

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30
Q

What does increased/abnormal APTT and PT indicate?

A

Problem in common pathway
(From factor X downwards)

Usually deficient Factor V, X, thrombin an fibrinogen

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31
Q

What does Thrombin clotting time measure?

A

Conversion of fibrinogen to fibrin via action of thrombin

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32
Q

If somebody has Haemophilia A or B what anticoagulation test is abnormal?

A

APTT (activated partial thromboplastin)

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33
Q

What happens to the vessel wall when damaged?

A

Vasoconstriction (Reduce blood flow/bleeding)

Producing Von Willebrand factor (so platelets stick to the collagen)

Exposure of platen and tissue factor initiates activation of clotting factors

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34
Q

What is the goal of haemostasis?

A

Make a clot
Control clotting
Break down clot

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35
Q

What 3 natural anticoagulants?

A

Protein C
Proteins S
Antithrombin

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36
Q

What Factors does Protein C inactivate?

A

Factor VIIIa
Factor Va

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37
Q

How is protein S related to Protein C?

A

Proteins S is a cofactor for protein C

Protein S must be activated in order for Protein C to be activated

38
Q

What vitamin is the synthesis of Protein C and Protein S dependant on?

A

Vitamin K dependant

39
Q

What does Antithrombin inactivate?

A

Thrombin
Other clotting factors

40
Q

What activates Antithrombin?

A

Heparin

41
Q

What is the function of Antithrombin on the body as a whole ?

A

Prevents spread of clot (rapidly inactivates travelling clotting factors)

42
Q

Where does Tissue Factor Pathway Inhibitor act?

A

Start of Extrinsic pathway inhibiting Factor VII
Extrinsic pathway = tissue factor activation pathway

43
Q

What is Fibrinolysis?

A

Break down of the final clot

44
Q

What takes place in fibrinolysis?

A

Plasminogen converted to plasmin
Plasmin breaks down clot forming D-Dimers

45
Q

What is the clinical significance of measuring D-Dimers in the blood?

A

Indicates clotting is taking place

46
Q

What causes bleeding disorders?

A

Abnormalities in:
-Vessel wall
-Platelets
-Coagulation factors

47
Q

What is Thrombocytopenia?

A

Deficiency of platelets in the blood resulting in bleeding into the tissues, bruising and slow blood clotting after injury

48
Q

What are the signs of Thrombocytopenia?

A

Purpura
Petechiae
Mucosal bleeding
Epistaxis
Menorrhagia

49
Q

What are the signs of Thrombocytopenia?

A

Purpura
Petechiae
Mucosal bleeding
Epistaxis
Menorrhagia

50
Q

What is Purpura?

A

Haemorrhages in skin

51
Q

What is petechiae?

A

Red dots/rash on skin

52
Q

What is epistaxis?

A

Nose bleeds

53
Q

What is menorrhagia?

A

Heavy menstrual periods

54
Q

On a basic level, how does Thrombocytopenia happen?

A

Decreased production
Increased consumption

55
Q

What are some causes of decreased production of platelets?

A

Marrow aplasia
Megaloblastic anaemia
Sepsis

56
Q

What are some immun causes of thrombocytopenia?

A

Immune Thrombocytopenic Purpura

Thrombotic Thrombocytopenic Purpura

57
Q

What is Immune Thrombocytopenic Purpura?

A

Low platelet count with a normal bone marrow and any other cause of low platelets has been ruled out

58
Q

What is Thrombotic Thrombocytopenic Purpura?

A

Many small blood clots forming in small vessels are ounce the body

Leads to platelets and RBCs being used up and consumed

59
Q

What are some non immune causes of thrombocytopenia?

A

Haemolytic-uraemic syndrome (HUS)

Hypersplenism

Disseminated Intravascular Coagulation

60
Q

What’s characteristic of Haemoytic-uraemia syndrome (HUS)?

A

Low RBCs
Acute kidney injury
Low platelets

61
Q

Who often get Haemoytic-uraemia syndrome?

A

Children more than adults
Associated with E.Coli infection

62
Q

What are the symptoms of Haemoytic-uraemia syndrome?

A

Bloody diarrhoea
Fever
Vommiting
Weakness
Kidney failure
Low platelets

63
Q

How does Hypersplenism cause Thrombocytopenia?

A

Enlarged overactive spleen removes too many platelets from blood

(Bone marrow tries to proliferate more to compensate)

64
Q

What are the 3 most common congenital Coagulation factor disorders?

A

Haemophilia A
Haemophilia B
Von Willebrand’s disease

64
Q

What are the 3 most common congenital Coagulation factor disorders?

A

Haemophilia A
Haemophilia B
Von Willebrand’s disease

65
Q

What type of genetic inheritance are both forms of Haemophilia?

A

X linked recessive

66
Q

What Factor is lacking in Haemophilia A?

A

Factor VIII

67
Q

Why in Haemophilia A is APTT longer but PT normal?

A

Factor VIII is normally present in intrinsic pathway which is measured by APTT

PT measures the extrinsic pathway (factor VII)

68
Q

How is Haemohillia A treated?

A

Recombinant Factor VIII

69
Q

What Factor is deficient in Haemophilia B?

A

Factor IX

70
Q

Why is APTT prolonged but PT normal with Haemophilia B?

A

Factor IX involved in intrinsic pathway

71
Q

What is the only way to distinguish between Haemophilia A and B and why?

A

Presence of Factor VIII or IX

Both have same results of prolonged APTT and normal PT

72
Q

How does Haemophilia present?

A

Prolonged bleeding post dental extraction
Muscle haematomas
Life threatening post operative an post traumatic bleeding
Easy bruising
Mass haaemorrhaging

73
Q

What type of disease is Von WIllebrand disease?

A

Autosomal dominant

74
Q

What is reduced in Von Willebrand disease?

A

Reduced platelet adhesion to vessel walls
Reduced Factor VIII

75
Q

How does Von Willebrand Disease present?

A

Spontaneous nose bleeds
Excessive wound bleeding
Menorrhagia

76
Q

What do vessel wall abnormalities usually lead to?

A

Easy bruising
SPontaeous small vessel bleeds
Mainly from skin but can be mucous membranes

77
Q

What are 2 examples of vessel wall abnormalities?

A

Ehlers Danlos (connective tissue disorders)

Scurvy

78
Q

What is Disseminated Intravascular coagulation (DIC)?

A

Lots of small blood thrombi form and get broken down
Platelets and clotting factors get consumed
When actually need to form clots (Haemostasis) you can so you haemorrhage

79
Q

What would the levels of fibrinogen and D dimers be in someone with DIC and why?

A

Low fibrinogen
High D dimers

Lots of fibrinogen converted to fibrin due to overactive clotting
Lots of fibrolysis happening so high D-Dimers

80
Q

There is always a trigger to cause DIC, what are some?

A

Malignancy
Massive tissue injury (burns)
Infections (gram - sepsis)
Massive haemorrhage
Obstetric cause (amniotic fluid embolism, preeclampsia)

81
Q

What are Thrombophilias?

A

Congenital or acquired defects of haemostasis which can increase a patients risk of thrombosis

82
Q

What is a congenital cause of thrombophilia?

A

Deficient in anticoagulants

83
Q

What is more likely to happen in antiphospholipid syndrome?
Who is more likely to get this defect?

A

Clot development
A thrombophilia

Afro-Caribbean’s, Hispanics, Asians and Native Americans

84
Q

What are some Anticoagulant drugs?

A

Vitamin K inhibitors (Warfarin)
Direct oral anticoagulants
Heparin

85
Q

What are some Direct oral anticoagulants?
How do they work?

A

Dabigatran
Rivaroxaban
Apixaban

Rivaroxaban and Apixaban inhibit Factor X, this means that less prothrombin is converted to thrombin so less fibrinogen to fibrin

86
Q

Why is warfarin being moved away from as an anticoagulant?

A

Needs constant patient monitoring

87
Q

What are 2 anti platelet drugs?

A

Aspirin
Clopidogrel

88
Q

How does Aspirin act as an anti platelet drug?

A

Blocks formation of Thromboxane
Therefore preventing formation of platelet plug

89
Q

How does Clopidogrel act as an anti platelet drug?

A

Blocks ADP produced by platelets
Preventing the formation of the platelet plug

90
Q

What is the main risk of anticoagulants?

A

BLEEDING

91
Q

What is the most common Inherited Thrombophilia in Caucasians?

What type of inheritance?

A

Factor V Leiden

Autosomal dominant

PP (20 decks)

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