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Pathological Processes > 5. Haemostasis > Flashcards

5. Haemostasis Flashcards

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1
Q

Define haemostasis.

A

The process of preventing or stopping bleeding in cases of trauma or disease while maintaining blood in its fluid state.

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2
Q

What are the 3 major steps in haemostasis?

A
  1. Vasoconstriction
  2. Primary haemostatic plug - friable platelet plug
  3. Secondary haemostatic plug - stable fibrin clot
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3
Q

What cell are platelets derived from?

A

Megakaryocytes

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4
Q

What blood components are essential for haemostasis?

A

Platelets
Coagulation factors - clotting proteins
Anticoagulation factors

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5
Q

What is the first step of formation of a platelet plug following vessel damage?

A

Exposure of underlying tissue containing collagen with vWF. Platelets bind to the exposed collagen via vWF.

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6
Q

Once bound to vWF, what happens to the platelets in order to form a plug?

A

They secrete ADP, thromboxane and other substances to become activated and change shape. They then cross-link to form a platelet plug.

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7
Q

Other than the formation of the platelet plug, what else do platelets do in response to vessel injury?

A

Activate the clotting cascade

Provide some coagulation factors (V) by secreting from internal stores.

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8
Q

What properties does the primary haemostatic clot have?

A

Weak, friable

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9
Q

What are the benefits of the primary haemostatic plug?

A

Forms very quickly - seconds to minutes and may control bleeding.

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10
Q

What is the key action of thrombin in coagulation?

A

Converts soluble fibrinogen to insoluble fibrin which enmeshed the platelet plug to form a stable clot

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11
Q

What factors contribute to the control of the clotting cascade?

A

Clot destroying proteins are activated by the clotting cascade
Natural anticoagulants inhibit unnecessary activation

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12
Q

What are some examples of natural anticoagulants?

A

Protein C
Protein S
Antithrombin
Tissue factor

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13
Q

What coagulation factors are synthesised in the liver?

A

Fibrinogen
Prothrombin
Factors 5,7,8,9,10,11,13
Tissue factor

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14
Q

What pathway does prothrombin time measure?

A

Extrinsic pathway

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15
Q

What pathway does APPT measure?

A

Intrinsic pathway

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16
Q

If a patient has a deficiency in factor VIII,IX,XI or XII will APPT or PT be prolonged?

A

APPT

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17
Q

If a patient has a deficiency in factor VII, will APPT or PT be prolonged?

A

PT

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18
Q

If a patient has a deficiency in factor V, which test will be prolonged?

A

Both APPT and PT

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19
Q

What is the thrombin burst?

A

When thrombin comes into contact with exposed tissue factor, it initiates the coagulation cascade and has a positive feedback loop to produce more thrombin. Extrinsic pathway.

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20
Q

What are the roles of vWF?

A
  • platelet adhesion and aggregation

- carrier and ‘protector’ of factor VIII, preventing it from premature destruction

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21
Q

Explain fibrinolysis.

A

Plasminogen is converted to plasmin by plasminogen activator. Plasmin breaks down fibrin into fragments called D-dimers.

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22
Q

Other than plasmin, what else contributes to preventing further clot formation?

A

Natural anticoagulants: Protein C, Protein S, Anti-thrombin

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23
Q

What will does deficiency in natural anticoagulants lead to?

A

Thrombophilia

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24
Q

What could lead to an aquired coagulation disorder?

A

Vitamin K deficiency
Liver disease
Anticoagulant medication - warfarin

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25
What are some congenital causes of coagulation factor disorders?
Haemophilia A and B
26
What is the difference between haemophilia A and B?
Haemophilia A is more common- deficiency in factor VIII | B- factor IX
27
What inheritance pattern does haemophilia A demonstrate?
X-linked recessive
28
How is haemophilia A treated?
Recombinant factor VIII
29
What symptoms and signs would you expect in haemophilia A?
Bleeding into muscles and joints (haematomas and haemarthroses) Post operative bleeding
30
How is Von Willebrands disease inherited?
Autosomal dominant
31
How does VWD affect clotting?
Abnormal platelet adhesion to the vessel wall | Reduced factor VIII activity
32
How would the presentation of vWD differ to haemophilia?
Platelet-associated bleeding in VWF- skin and mucous membranes, epistaxis, gum bleeding, heavy periods Spontaneous muscle bleeds are rare Haemophilia - muscle haematomas and haemarthroses
33
What symptoms would you expect in patients with vessel wall abnormalities?
Easy bruising - mainly skin
34
What is a congenital vessel wall abnormality?
Hereditary haemorrhagic telangiestasia (HTT) | CT disorders - Ehlers-danlos
35
How is HTT inherited?
Autosomal dominant
36
How would a bone marrow biopsy help to determine the cause of thrombocytopenia?
If lots of megakaryocytes present then it suggests that production is normal and cause is increased removal.
37
What disease is characterised by immune destruction of platelets?
Immune thrombocytopenic purpura (ITP) - antibodies against glycoproteins on surface of platelets
38
How is ITP treated?
Immunosuppression
39
Why would a blood transfusion be inappropriate in patients with ITP?
Autoimmune disease, so transfused platelets will be destroyed too.
40
Suggest some reasons for non-immune destruction of platelets.
Miceoangiopathic haemolytic states - TTP, DIC, HUS | Cardiopulmonary bypass surgery can consume platelets
41
What could cause decreased platelet production?
B12 or folate deficiency Infiltration of bone marrow by cancer cells or fibrosis Drugs- chemotherapy, antibiotics Viruses - HIV, EBV, CMV
42
Why does the artery contract in haemostasis?
Decrease the pressure downstream (arteries only), isn't enough to stop the bleeding.
43
Which coagulation factors require vitamin K for their synthesis?
II, VII, IX and X | Anticoagulants - protein C and protein S
44
What properties of coagulation factors enables control of the coagulation cascade?
They are pro-enzymes which have to become activated, and then act as endopeptidases to active other proenzymes in signal amplification
45
What co-factor is required for clotting?
Calcium - allows negative exposed membrane to bind to negative gla residues on thrombin.
46
How is this intrinsic pathway triggered?
By a negatively charged surface, e.g subendothelium | The vessel does not need to be broken for it to occur
47
How is the extrinsic pathway activated?
It needs a 'tissue factor' which is present outside of the blood. This is triggered by thromboplastin released from damaged cells adjacent to haemorrhage.
48
Which factors are secreted by the endothelium to oppose clotting?
Plasminogen activator | Thrombomodulin
49
Plasmin activates as an inactive precursor. How is it activated?
Tissue plasminogen activator Urokinase Streptokinase (from streptococci)
50
How does the clotting cascade initiate fibrinolysis?
Fibrin increases the activity of tissue plasminogen activator which activated plasmin to break down fibrin.
51
What happens after resolution of a clot?
Fibrous repair, granulation tissue and a tiny scar
52
Why do people with haemophilia suffer from bleeding?
They cannot produce an adequate amount of fibrin as they have impaired clotting
53
Are petechiae a symptom of haemophilia?
No, they are caused by blood leaking from capillaries, which is the result of platelet abnormalities.
54
What would the PT of a patient with haemophilia show?
No change - factor VIII is not a part of the extrinsic pathway
55
What affect does haemophilia have on APPT?
Prolongs APPT as this measures the intrinsic pathway which involves factor VIII.
56
What is the cause of vWD?
Deficiency or abnormality in von Willebrand factor
57
In vWD, what changes would you see in bleeding time and APTT?
Raised because it affects platelet adhesion and factor VIII which is involved in the intrinsic pathway.
58
What changes to bleeding time,PT and APPT would you see in thrombocytopenia?
Prolonged bleeding time but normal AP and APPT as these assess the clotting cascade and not platelet function
59
Would you expect to see petechiae in patients with thrombocytopenia?
Yes
60
What is the pathophysiology of DIC?
Microthrombi are formed throughout the circulation, which consumes platelets, fibrin and coagulation factors and activates fibrinolysis. The patient may then experience haemorrhage.
61
How is DIC usually caused?
Never occurs as a disease in itself but is always a complication of another condition - sepsis (gram negative endotoxin activates clotting) - severe trauma - extensive burns - malignancy
62
How can you measure the fibrinolytic systems activity in the blood?
Presence of D-dimers
63
What is factor V Leiden an example of?
Thrombophilia
64
What clotting tests will be affected by DIC?
Raised PT Raised APPT Low fibrinogen Raised D-dimers
65
What is a thrombophilia?
Thrombophilias are inherited or acquired defects of haemostasis resulting in a predisposition to thrombosis
66
What is the function of thrombomodulin?
Thrombin binding to thrombomodulin (endothelial receptor) activates protein C

Pathological Processes (12 decks)

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