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Pathological Processes * > S5 Haemostasis > Flashcards

S5 Haemostasis Flashcards

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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
What does prothrombin time (PT) measure?
Measures the extrinsic and common pathway (factors VII, V, X, prothrombin and fibrinogen)
26
What is INR?
International normalised ratio Calculated from PT and is used to measure warfarin
27
What does activated partial thromboplastin time (APTT) measure?
Measures the intrinsic and common pathway (factors VIII, IX, XI, XII, V, X, prothrombin and fibrinogen)
28
What does fibrinogen count measure?
Measures the amount of fibrinogen
29
What does D dimers count measure?
Measures the fibrin degradation product
30
What is TT?
Thrombin time or thrombin clotting time (TCT) Time taken to produce thrombin from prothrombin (time taken to form a clot)
31
What is Von Willebrand Factor (vWF)?
A factor involved in platelet adhesion to the vessel wall, platelet aggregation and it also carries factor VIII
32
What happens to the vessel wall when it is damaged?
* 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
What do natural anticoagulants do?
Stop further coagulation
34
What are the 3 natural anticoagulants?
* protein C * protein S * anti-thrombin
35
What is fibrinolysis?
Break down of the fibrin clot
36
How does fibrinolysis occur?
1. A plasminogen activator catalyses plasminogen to convert to plasmin 2. Plasmin catalyses the break down of the fibrin clot into D-Dimers
37
How do bleeding disorders arise?
Due to abnormalities in the vessel wall, platelets or coagulation factors Can be inherited or acquired
38
What are some congenital coagulation factor disorders?
* haemophilia A (factor VIII) | * haemophilia B (factor IX)
39
What are some acquired coagulation factor disorders?
* liver disease * vitamin K deficiency * anticoagulants inc. warfarin which inhibits vitamin K
40
What signs and symptoms can coagulation factor disorders lead to?
* 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
What is the inheritance of haemophilia A? What is it? What can it cause? How is it treated?
* 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
When is haemophilia A diagnosed? What abnormalities would you expect to see in the blood results?
* diagnosed pre-natally/soon after birth if theres a family history or in infancy if a new spontaneous mutation * prolonged APTT
43
What is haemophilia B?
* has a similar presentation to haemophilia A | * due to a congenital reduction in factor IX
44
What is Von Willebrand’s Disease?
* 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
How does vWD present clinically?
* skin and mucous membrane bleeding (epistaxis - nose bleeding, gum bleeding, bruising) * prolonged bleeding after trauma (heavy periods, post surgery, post dental extraction)
46
How can vessel wall abnormalities present clinically?
* easy bruising * spontaneous bleeding from small vessels * affects skin and mucous membranes
47
What problems can you have with blood vessels?
* 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
What is disseminated intravascular coagulopathy (DIC)?
* 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
What will clotting tests show for someone with DIC?
* raised PT/INR * raised APTT * low fibrinogen * raised D dimers/fibrin degradation products
50
What will a blood film for DIC show?
Schistocytes due to haemolysis
51
How does DIC occur?
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
How do you treat DIC?
* treat the underlying cause | * transfusion of plasma which contains clotting factors (fresh frozen plasma (FFP) or cryoprecipitate)
53
What are thrombophilias?
* 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
What are four types of plasminogen activator?
* tissue plasminogen activator - circulates in the blood * urokinase - found in urine * streptokinase - usually not present in the body * alteplase - recombinant tissue plasminogen activator
55
Why are plasminogen activators used therapeutically?
They dissolve fibrin and so thrombi and thrombolemboli
56
Why should streptokinase only be given once?
As it is antigenic
57
What is a side effect of plasminogen activators?
Bleeding (of gums and nose and more seriously the brain)
58
What is thrombocytopenia? When does spontaneous bleeding occur?
A platelet count of less than 100x10(9)/L When platelet count is less than 20x10(9)/L
59
How will PT, APTT and bleeding time present for someone with thrombocytopenia?
Bleeding time - prolonged PT - normal APTT - normal
60
Where can spontaneous bleeding due to thrombocytopenia occur? What can this present as on the skin?
``` Bleeding from small vessels in: * skin * GI tract * genitourinary trac (* intracerebral) ``` Petechiae
61
What are the 4 possible causes of thrombocytopenia?
* 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
When is warfarin used?
* 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
How does warfarin work?
Prevents formation of vitamin k dependent clotting factors e.g. factors II, VII, IX and X
64
If patient is taking warfarin, what can a high INR suggest?
The dose of warfarin is too high or if a patient is also on antibiotics, the antibiotics are interfering with the warfarin metabolism
65
What treatments can reverse the action fo warfarin?
* give vitamin K (but takes a few days to work) | * give prothrombin complex concentrate (prothrombin and factor VIII) - quicker acting
66
What do rivaroxaban and apixiban inhibit?
Inhibit factor Xa
67
What does dabigatran inhibit?
Inhibits thrombin
68
What are the advantages and disadvantages of these newer anticoagulant drugs?
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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