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haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

The arrest of bleeding and maintenance of vascular patency

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2
Q

Outline the 4 main requirements of haemostasis.

A
  • Permanent state of readiness
  • Prompt response
  • Localised response
  • Protection against unwanted thrombosis
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3
Q

Outline the 4 components of the normal haemostasis system.

A
  • Formation of platelet plug – primary haemostasis – platelets that are circulating in the blood come together and stick to form a plug
  • Formation of fibrin clot - secondary haemostasis
  • Fibrinolysis – this starts as soon as the clot is formed as the body knows that the clot cannot occlude the lumen and blood flow must continue
  • Anticoagulant Defences
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4
Q

What is primary haemostasis?

A

Formation of the platelet plug

Platelets that are circulating in the blood come together and stick to form a plug

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5
Q

What is secondary haemostasis?

A

Formation of the fibrin clot

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6
Q

When does fibrinolysis start? Why?

A

As soon as the clot has formed

The body knows that the clot cannot occlude the lumen and blood flow must continue so it starts to break down the clot as soon as it has been made

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7
Q

If someone has a very minor injury e.g a paper cut, what is needed?

A

Just primary haemostasis as the platelet plug is strong enough here

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8
Q

Describe a platelet.

A

Small + anucleate (no nucleus) discs

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9
Q

What is the lifespan of a platelet?

A

7-10 days

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10
Q

How are platelet formed?

A

Formed in the bone marrow from budding of megakaryocytes

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11
Q

Where are megakaryocytic seen?

A

Megakaryocytes aren’t seen in the blood (only the bone marrow) as they are so big

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12
Q

How long does the effects of aspirin on a platelet last?

A

The entire lifespan of the platelet

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13
Q

What is primary haemostasis/platelets activated by?

A

Endothelial (vessel wall) damage exposes collagen and releases Von Willebrand Factor (VWF), and other proteins to which platelets have receptors

  • Platelet adhesion at the site of injury
  • Secretion of various chemicals from the platelets leads to aggregation of the platelets at the site of injury
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14
Q

What does VWF do?

A

This lets platelets know where they need to come and adhere to

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15
Q

Where releases VWF?

A

Platelets and endothelial cells

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16
Q

Outline the 3 main causes of failure of the platelet plug formation.

A
  • Vascular – older people have weak vessels, HSP in young children
  • Platelets – reduced number or reduced function
  • VWF – commonest inherited bleeding disorder
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17
Q

Most common causes is someone with low platelets from being put on Aspirin or Clopidogrel

A

T

18
Q

How does purpura come about?

A

Due to the effects of gravity, the platelets leak out of vessel walls and this leaves the skin with a purple discolouration

19
Q

Outline some of the consequences of failure of the platelet plug to form.

A
  • Spontaneous bruising and purpura
  • Mucosal bleeding – epistaxis, GI, conjunctival, menorrhagia
  • Intracranial haemorrhage
  • Retinal haemorrhages
20
Q

What causes senile purpura?

A

Lack of collagen in the vessel walls

21
Q

What is the main screening tool for primary haemostasis?

A

Platelet count

There usb really a screening test - it is more a diagnosis of exclusion

22
Q

What is secondary haemostasis?

A

Formation of the fibrin clot

It occurs on the surface of platelets

23
Q

Outline the events that occur during secondary haemostasis.

A
  1. Platelets are full of phospholipid which is negatively charged
  2. They are also full of Ca2+ which is positively charged
  3. Calcium on surface makes the surface of platelets positively charged
  4. Clotting factors have a negative charge, so are attracted to surface of platelets.
  5. Clotting factors start off inactivated, but become activated
24
Q

Outline the process of fibrin clot formation.

A
  1. Initiation
  • Tissue factor (TF) is released from endothelial cell, and activates clotting factor VII
  • TF/VIIa then go on to activate factors V/Xa
  1. Propagation
  • V/Xa break down prothrombin to thrombin
  • Thrombin then cleaves fibrinogen to form fibrin
  1. Amplification
  • Thrombin activates factors VIII/IX
  • VIII/IXa then activated factors V/X which produces more thrombin  amplification
25
Q

Outline some of the potential causes for failure of fibrin clot to form.

A
  • Single clotting factor deficiency – usually hereditary e.g haemophilia
  • Multiple clotting factor deficiencies – usually acquired e.g DIC
  • Increased fibrinolysis – usually part of complex coagulopathy
26
Q

What are the most common factor deficiencies which lead to failure of the fibrin clot to form?

A

Factor 8 and 9

  • Haemophilia A - 8
  • Haemophilia B – 9
27
Q

Blood clotting factors are produced in the liver, if someone has liver disease then this means they cannot form clotting factors

A

T

28
Q

What is DIC?

A

Patient gets clots everywhere, then get so much activation that all of the clotting factors are used up, resulting in a severe bleeding tendency

29
Q

What are the 2 reactions which occur leading to fibrinolysis?

A
  • Plasminogen is converted to plasmin by tissue plasminogen activator (tPA)
  • Plasmin then converts fibrin to FDPs (fibrin degradation products)
30
Q

What are d-dimers?

A

Fibrinogen breakdown products

31
Q

How can measuring d-dimers help you to decide if someone has a clot?

A

As soon as a clot (e.g. in the leg) forms, fibrinolysis will begin to occur

Therefore, if have no d-dimer in blood, there’s no clot there

32
Q

As soon as you start forming a clot, you start breaking it down as your body knows that the clot cannot occlude the lumen

A

T

33
Q

What are the 2 main screening tests to check for fibrin clot formation?

A
  • Prothrombin time

* Activated partial thromboplastin time

34
Q

What does prothrombin time measure?

A

How long it takes for a sample to clot

35
Q

When measuring prothrombin time, what is added to the sample to see how long it takes for clotting to occur?

A

Add tissue factor, and see how long it takes for the sample to clot

36
Q

If a prothrombin sample result is normal, what does this tell us?

A

There is no abnormality of factors VII, V, X prothrombin or fibrinogen

37
Q

If activated partial prothrombin time is elevated, what should you be worried about?

A

If prolonged, be particularly concerned about VIII/IX deficiency

38
Q

Outline the clinical approach to bleeding disorders.

A
  • History – bleeding, bruising, duration, previous surgery/dental extractions
  • Drug History e.g aspirin
  • Family History
  • Examination
39
Q

What are the 2 main groups of naturally occurring anticoagulants?

A
  • Serine protease inhibitors

* Protein C and protein S

40
Q

What are serine protease inhibitors?

A

Antithrombin

Switches off clotting factors

41
Q

Explain how protein C and protein S act as naturally occurring anticoagulants.

A

Thrombin binds to thrombomodulin, which gives thrombin a new function whereby it activates proteins C and S to switch off blood clotting – by switching off V/Xa and VIII/IXa

42
Q

What is a thrombophilia?

A

Deficiency of naturally occuring anticoagulants may be hereditary

Increased tendency to develop venous thrombosis (deep vein thrombosis/pulmonary embolism)

haematology (26 decks)

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