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Pathological Processes * > S5 Haemostasis > Flashcards

S5 Haemostasis Flashcards

1
Q

What are the 3 general principles of haemostasis?

A
  1. Clot production
  2. Clot control
  3. Clot breakdown
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2
Q

What are the essentials for haemostasis?

A
  • blood needs to keep moving
  • platelets
  • coagulation factors
  • anticoagulant factors
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3
Q

Describe the steps in clot initiation, clot formation and fibrinolysis.

A
  1. Vessel wall is damaged (extrinsic)
  2. Platelets aggregate
  3. Coagulation is activate d
  4. Thrombin converts fibrinogen into fibrin
  5. Fibrin polymerises
  6. Fibrin is broken down into fragments
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4
Q

How are platelets produced?

A

Produced by megakaryocytes in the bone marrow - platelets bud off from the cytoplasm of megakaryocytes

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5
Q

What is the normal platelet count and oral life span?

A

150-400x10(9)/L

7-10 days

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6
Q

How do platelets adhere to the damaged vessel wall?

A

They adhere to collagen (exposed in the damaged vessel wall) via platelet receptors binding to vWF

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7
Q

How are platelets activated?

A

Platelets secrete ADP, thromboxane and others substances to activate themselves and to activate other platelets

This is part of activating the clotting cascade

  • They also release some coagulation factors buy secretion from internal stored
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8
Q

How do platelets aggregate?

A

They cross-link with other platelets to form a platelet plug

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9
Q

What are some mediating factors of platelet plug formation?

A
  • platelet receptors
  • Von willebrands factor (vWF)
  • fibrinogen
  • collagen
  • ADP
  • thromboxane/arachidonic acid
  • thrombin
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10
Q

What is the clotting cascade?

A

An amplification system that activates precursor proteins to generate thrombin (IIa). Thrombin then converts soluble fibrinogen into insoluble fibrin which entangles with the platelet plug to make a stable clot.

This is a controlled process

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11
Q

What controls the clotting cascade?

A
  • natural anticoagulants inhibit activation

* clot destroying proceedings that are activated by the clotting cascade

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12
Q

Where are coagulation factors made?

A

In the liver

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13
Q

What are the coagulation factors?

A
  • fibrinogen (I)
  • prothrombin (II)
  • factor V
  • factor VII
  • factor VIII
  • factor IX
  • factor X
  • factor XI
  • factor XIII
  • tissue factor
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14
Q

What are the natural anticoagulants?

A
  • protein C
  • protein S
  • antithrombin
  • tissue factor pathway inhibitor
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15
Q

Where does tissue factor pathway inhibitor (TFPI) act to inhibit coagulation?

A

Inhibits activation of factor VII

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16
Q

Where does antithrombin act to inhibit coagulation?

A

Acts to inhibit activation of factor X and action of thrombin (activation of fibrin)

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17
Q

Where does protein C act to inhibit coagulation?

A

Acts to inhibit activation of factor VIII and activation of factor V

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18
Q

How does protein S act to inhibit coagulation?

A

Protein S activates protein C (protein C + thrombomodulin —> activated protein C)

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19
Q

The clotting cascade is an example of positive feedback, how do products of the cascade activate further action of the cascade?

A

Thrombin (IIa) stimulates factor XI and factor VIII, factor V and factor XIII activation but also stimulates protein C + thrombomodulin

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20
Q

What are the three pathways in the clotting cascade? What does each activate?

A
  • extrinsic (endothelial cell injury/trauma) - tissue factor activation
  • intrinsic (damaged surface) - contact activation
  • common
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21
Q

What factors are involved in the extrinsic pathway?

A
  • factor VII
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22
Q

What factors are involved in the intrinsic pathway?

A
  • factor XII
  • factor XI
  • factor IX
  • factor VIII
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23
Q

What factors are involved in the common pathway?

A
  • factor X
  • thrombin (II)
  • fibrin (I)
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24
Q

How can coagulation be measured?

A
  • Using PT, APTT and TT
  • fibrinogen count
  • D dimers
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25
Q

What does prothrombin time (PT) measure?

A

Measures the extrinsic and common pathway (factors VII, V, X, prothrombin and fibrinogen)

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26
Q

What is INR?

A

International normalised ratio

Calculated from PT and is used to measure warfarin

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27
Q

What does activated partial thromboplastin time (APTT) measure?

A

Measures the intrinsic and common pathway (factors VIII, IX, XI, XII, V, X, prothrombin and fibrinogen)

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28
Q

What does fibrinogen count measure?

A

Measures the amount of fibrinogen

29
Q

What does D dimers count measure?

A

Measures the fibrin degradation product

30
Q

What is TT?

A

Thrombin time or thrombin clotting time (TCT)

Time taken to produce thrombin from prothrombin (time taken to form a clot)

31
Q

What is Von Willebrand Factor (vWF)?

A

A factor involved in platelet adhesion to the vessel wall, platelet aggregation and it also carries factor VIII

32
Q

What happens to the vessel wall when it is damaged?

A
  • vasoconstriction
  • production of vWF - platelet adhesion and carrier of factor VIII
  • exposure of collagen and tissue factor - initiates the activation of clotting factors (proteins)
33
Q

What do natural anticoagulants do?

A

Stop further coagulation

34
Q

What are the 3 natural anticoagulants?

A
  • protein C
  • protein S
  • anti-thrombin
35
Q

What is fibrinolysis?

A

Break down of the fibrin clot

36
Q

How does fibrinolysis occur?

A
  1. A plasminogen activator catalyses plasminogen to convert to plasmin
  2. Plasmin catalyses the break down of the fibrin clot into D-Dimers
37
Q

How do bleeding disorders arise?

A

Due to abnormalities in the vessel wall, platelets or coagulation factors

Can be inherited or acquired

38
Q

What are some congenital coagulation factor disorders?

A
  • haemophilia A (factor VIII)

* haemophilia B (factor IX)

39
Q

What are some acquired coagulation factor disorders?

A
  • liver disease
  • vitamin K deficiency
  • anticoagulants inc. warfarin which inhibits vitamin K
40
Q

What signs and symptoms can coagulation factor disorders lead to?

A
  • muscle haematomas
  • recurrent haemarthroses (bleeding into joints)
  • joint pain and deformity
  • prolonged bleeding post dental extraction
  • life threatening post op and post traumatic bleeding
  • intracerebral haemorrhage
41
Q

What is the inheritance of haemophilia A? What is it? What can it cause? How is it treated?

A
  • x-linked recessive
  • a congenital lack of factor VIII (can be mild/moderate/severe dependent on the amount of factor present)
  • bleeding into muscles and joints
  • treated with recombinant factor VIII (or DDAVP)
42
Q

When is haemophilia A diagnosed? What abnormalities would you expect to see in the blood results?

A
  • diagnosed pre-natally/soon after birth if theres a family history or in infancy if a new spontaneous mutation
  • prolonged APTT
43
Q

What is haemophilia B?

A
  • has a similar presentation to haemophilia A

* due to a congenital reduction in factor IX

44
Q

What is Von Willebrand’s Disease?

A
  • a common autosomal dominant disease
  • abnormal platelet adhesion to vessel wall
  • reduced amount/reduced activity of factor VIII
  • main defect is due to a reduction in vWF production
45
Q

How does vWD present clinically?

A
  • skin and mucous membrane bleeding (epistaxis - nose bleeding, gum bleeding, bruising)
  • prolonged bleeding after trauma (heavy periods, post surgery, post dental extraction)
46
Q

How can vessel wall abnormalities present clinically?

A
  • easy bruising
  • spontaneous bleeding from small vessels
  • affects skin and mucous membranes
47
Q

What problems can you have with blood vessels?

A
  • congenital - hereditary haemorrhagic telangiectasia (HHT) - autosomal dominant, dilated micro vascular swellings that increase with time and GI haemorrhage leading to iron deficiency anaemia
  • acquired - senile purpura, steroids, infections, scurvy/vit C deficiency causing defective collagen production
48
Q

What is disseminated intravascular coagulopathy (DIC)?

A
  • type of microangiopathic haemolytic anaemia
  • pathological activation of coagulation
  • many microthrombi form in circulation
  • leads to consumption of clotting factors and platelets and haemolytic anaemia develops
49
Q

What will clotting tests show for someone with DIC?

A
  • raised PT/INR
  • raised APTT
  • low fibrinogen
  • raised D dimers/fibrin degradation products
50
Q

What will a blood film for DIC show?

A

Schistocytes due to haemolysis

51
Q

How does DIC occur?

A

There must be a trigger:

  • malignancy
  • massive tissue injury e.g. burns
  • infections - gram -ve sepsis (bacteria release endotoxins which activate coagulation)
  • massive haemorrhage and transfusion
  • ABO transfusion reaction
  • obstetric cause - placental abruption, pre-eclampsia (high BP and protein in urine), amniotic fluid embolism
52
Q

How do you treat DIC?

A
  • treat the underlying cause

* transfusion of plasma which contains clotting factors (fresh frozen plasma (FFP) or cryoprecipitate)

53
Q

What are thrombophilias?

A
  • acquired or congenital defects of haemostasis that increase patients risk of thrombosis
  • congenital - deficiency of natural anticoagulants or abnormal factor V (factor V Leiden)
  • acquired - antiphospholipid syndrome (immune system disorder)
54
Q

What are four types of plasminogen activator?

A
  • tissue plasminogen activator - circulates in the blood
  • urokinase - found in urine
  • streptokinase - usually not present in the body
  • alteplase - recombinant tissue plasminogen activator
55
Q

Why are plasminogen activators used therapeutically?

A

They dissolve fibrin and so thrombi and thrombolemboli

56
Q

Why should streptokinase only be given once?

A

As it is antigenic

57
Q

What is a side effect of plasminogen activators?

A

Bleeding (of gums and nose and more seriously the brain)

58
Q

What is thrombocytopenia? When does spontaneous bleeding occur?

A

A platelet count of less than 100x10(9)/L

When platelet count is less than 20x10(9)/L

59
Q

How will PT, APTT and bleeding time present for someone with thrombocytopenia?

A

Bleeding time - prolonged
PT - normal
APTT - normal

60
Q

Where can spontaneous bleeding due to thrombocytopenia occur? What can this present as on the skin?

A 
Bleeding from small vessels in:
* skin
* GI tract 
* genitourinary trac 
(* intracerebral)

Petechiae

61
Q

What are the 4 possible causes of thrombocytopenia?

A
  • decreased platelet function - due to bone marrow malignancy, drugs, infections, B12/folate deficiency
  • decreased platelet survival - immunological destruction (immune thrombocytopenic purpura) or non-immunological destruction (DIC)
  • sequestration - hypersplenism
  • dilutional - massive blood transfusions
62
Q

When is warfarin used?

A
  • prophylaxis and treatment for thrombosis
  • atrial fibrillation - risk of clot formation in heart
  • heart surgery - artificial heart valves tend to form clots on surface
63
Q

How does warfarin work?

A

Prevents formation of vitamin k dependent clotting factors e.g. factors II, VII, IX and X

64
Q

If patient is taking warfarin, what can a high INR suggest?

A

The dose of warfarin is too high or if a patient is also on antibiotics, the antibiotics are interfering with the warfarin metabolism

65
Q

What treatments can reverse the action fo warfarin?

A
  • give vitamin K (but takes a few days to work)

* give prothrombin complex concentrate (prothrombin and factor VIII) - quicker acting

66
Q

What do rivaroxaban and apixiban inhibit?

A

Inhibit factor Xa

67
Q

What does dabigatran inhibit?

A

Inhibits thrombin

68
Q

What are the advantages and disadvantages of these newer anticoagulant drugs?

A

Advantage - don’t need to measure INR and can give once a day
Disadvantage - not sure how to reverse the effects

Pathological Processes * (10 decks)

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