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YEAR 5: Haematology > Haem: Coagulation Pt.2 > Flashcards

Haem: Coagulation Pt.2 Flashcards

1
Q

How is the common final pathway monitored?

A

Thrombin time (TT)
Assesses the activity of fibrinogen

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2
Q

Why is the prothrombinase complex important?

A

It allows activation of prothombin at a much faster rate

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3
Q

What is required for adequate production/absorption of vitamin K?

A
  • Bacteria in the gut produce Vitamin K
  • It is fat-soluble so bile is needed for viatmin K to be absorbed
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4
Q

What is the most common cause of vitamin K deficiency?

A

Warfarin

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5
Q

Name two factors that convert plasminogen to plasmin.

A
  • Tissue plasminogen activator
  • Urokinase
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6
Q

Name a factor that inhibits the tissue plasminogen activator and urokinase.

A

Plasmingoen activtor inhibitor 1 and 2

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7
Q

Name two factors that directly inhibit plasmin.

A
  • Alpha-2 antiplasmin
  • Alpha-2 macroglobulin
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8
Q

What is the role of thrombin-activatable fibrinolysis inhibitor (TAFI)?

A

Inhibitor of fibrin breakdown

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9
Q

Describe the action of antithrombins.

A

Bind to thrombin in a 1:1 ratio and this complex is excreted in the urine

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10
Q

How many types of antithrombin are there?

A

Five (antithrombin-III is the most active)

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11
Q

What is the most thrombogenic hereditary condition?

A

Antithrombin deficiency

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12
Q

Outline the role of protein C and protein S.

A
  • Trace amounts of thrombin generated at the start of the clotting cascade activate thrombomodulin
  • This allows protein C to bind to thrombomodulin through the endothelial protein C receptor
  • Protein C is then fully activated in the presence of protein S
  • Fully activated protein C will inactivate factors 5a and 8a
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13
Q

Why does Factor V Leiden cause a prothrombotic state?

A

The factor 5a will be resistant to breakdown by protein C.

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14
Q

State two causes of activated protein C resistance.

A
  • Mutated factor 5 (e.g. factor V Leiden)
  • High levels of factor 8
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15
Q

What is the role of tissue factor pathway inhibitor?

A
  • TFPI neutralises the tissue factor-factor 7a complex once it has initiated the clotting cascade
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16
Q

List some categories of genetic defects that cause excessive bleeding.

A
  • Platelet abnormalities
  • Vessel wall abnormalities
  • Clotting factor deficiencies
  • Excess clot breakdown
17
Q

List some acquired defects that cause excessive bleeding.

A
  • Liver disease
  • Vitamin K deficiency
  • Autoimmune diseases (platelet destruction)
  • Trauma
  • Anti-coagulants/anti-platelets
18
Q

List some genetic defects that cause excessive thrombosis.

A
  • Clotting factor inhibitor deficiencies
  • Decreased fibrinolysis
19
Q

List the types of disorders of haemostasis.

A
  • Vascular disorders (e.g. scurvy)
  • Platelet disorders
  • Coagulation disorders
  • Mixed disorders (e.g. DIC)
20
Q

What is the difference between immediate and delayed bleeding with regards to the underlying pathological process?

A
  • Immediate - issue with the primary haemostatic plug (platelets, endothelium, vWF)
  • Delayed - issue with the coagulation cascade
21
Q

Describe the key clinical differences between platelet disorders and coagulation factor disorders.

A

Platelet disorders:

  • Bleeding from skin and mucous membranes
  • Petechiae
  • Small, superficial ecchymoses
  • Bleeding after cuts and scratches
  • Bleeding immediately after surgery/trauma
  • Usually mild

Coagulation factor disorders:

  • Bleeding into soft tissues, joints and muscles
  • No Petechiae
  • Large, deep ecchymoses
  • Haemarthroses
  • No bleeding from cuts and scratches
  • Delayed bleeding from surgery or taruma
  • Often SEVERE
22
Q

When is treatment for platelet disorders required?

A

Platelet count <30x109/L (this is associated with spontaneous haemorrhage)

23
Q

Why is it important to look at platelets under the microscope in thrombocytopaenia?

A
  • To check whether it is pseudothrombocytopaenia (platelets clump together giving an erroneously low result)
  • Also allows identification of other abnormalities (e.g. Grey platelet syndrome - large platelets)
24
Q

What can cause a decrease in platelet number?

A
  • Decreased producton
  • Decreased survival (TTP)
  • Increased consumption (DIC)
  • Dilution
25
Q

What can cause defective platelet function?

A
  • Acquired (e.g. aspirin)
  • Congenital (e.g. thrombasthenia)
  • Cardiopulmonary bypass

YEAR 5: Haematology (37 decks)

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