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3/ IIH > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

What does the normal haemostatic response involve?

A
  • the process that results in the stopping of bleeding following blood vessel injury
  • complex interactions between activated clotting factors and platelets at the site of blood vessel injury
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2
Q

What is the sequence of events following blood vessel injury?

A
  • Localised vasoconstriction at the sit of injury
    1. Platelet adhesion to sub endothelium of damaged blood vessel
    Platelet aggregation and activation
    2. Activation of coagulation cascade
    Fibrin formation
  • Thrombus Formation
  • Fibrinolytic degradation of clot / blood vessel repair
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3
Q

What are the two glycoprotein receptors incorporated into the lipid bilayer of platelets?

A

GPIb and GPIIb/IIIa

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4
Q

What allows platelets to change shape?

A

actin and myosin fibrils which interact upon platelet activation

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5
Q

What are the 3 types of storage granules found in platelets? What are their purposes?

A

dense - mediators of activation including serotonin, ADP, catecholamines and calcium
alpha - contain clotting factors V, VIII, fibrinogen, VWF and other substances including platelet factor 4 and platelet-derived growth factor
glycogen - provide the energy source for platelet reactions

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6
Q

Draw the coagulation cascade

A

see booklet

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7
Q

Describe the role of platelets in the haemostatic response

A
  • transient localised vasoconstricción –> platelets form a mechanical plug
  • platelets adhere to exposed sub-endothelial collagen
  • vWF adheres GP1b
  • GPIIb/IIIa upgraded to membrane, binds to vWF and allows aggregation
  • ADP is released from damaged blood vessel endothelial cells
  • ADP and exposed collagen and thrombin activates platelets and they release aloha and dense granules
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8
Q

What are the bleeding tendency disorders and what causes them?

A
  • Bernard-Soulier sundrome = deficiency of GPIb
  • Glanzmann;s Thrombasthenia = deficiency of GPIIb/IIIa
  • Haemophilia A - factor 8
  • Haemophilia B - factor 9
  • vWF deficiency
  • autoimmune acquired thrombocytopenia
  • vitamin K deficient
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9
Q

What factors are synthesised from vitamin K?

A
  • 7, 9, 10
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10
Q

Describe the fibronolytic response and blood vessel repair

A
  • tPa released from intact endothelial cells
  • attaches to fibrin clot
  • enables binding of plasminogen
  • converted to plasmin
  • proteolytic dissolution of clot
  • degradation products removed by reticulo-endothelial system
  • blood vessel repair occurs simultaneously
  • smooth muscle of blood vessels and endothelial cells undergo mitosis - under control of PDGF
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11
Q

What are the 3 anticoagulant mechanisms?

A
  • antithrombin
  • protein C
  • natural heparins
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12
Q

What does antithrombin do?

A
  • inactivated thrombin and factor 9. 10, 11
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13
Q
  • Where in the circulation is the protein C system most important?
  • What does protein C do?
A
  • venous side
  • in the vicinity of clot formation, free thrombin binds to thrombomodulin
  • enables binding of Protein C and thrombin activates it
  • activates protein C complexes with protein S and inactive FV, and enzymatically degrades factor 5 and 8
  • suppression of coagulation factors and restricts the thrombus to the site of injury
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14
Q

What do natural heparins do?

A
  • operate at the level of the blood vessel endothelium
  • present on endothelial surface which bind to and enhance the anticoagulant activity of anti-thrombin and the synthesis and relays of platelet inhibitory prostaglandin called prostacyclin
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15
Q

Give examples of causes of acquired thrombophilia states

A
  • myeloproliferative disorders
  • malignancy
  • lupus anticoagulant
  • surgery
  • long haul flights
  • prolonged periods of immobility
  • pregnancy
  • smoking
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16
Q

Give examples of hereditary thrombophilia states

A
  • Factor V leiden mutation, factor V has impaired protein C cofactor activist and is resistant to neutralisation
  • protein C, S and AT deficiencies
  • mutation of prothrombin gene –> increased prothrombin levels
  • hyperhomocysteinaemia
17
Q

What routine tests are used to investigate the clotting cascade?

A
  • platelet count
  • prothrombin time
  • activate partial thromboplastin time (APTT)
  • fibrinogen level
  • von Willebrand Factor levels
  • platelet aggregation studies
18
Q

What are the two most common test requested?

A
  • prothrombin time (PT)

- activated partial thromboplastin time (APTT)

19
Q

What does an prolonged prothrombin time indicate?

What are the possible causes?

A 
- factor 7 deficiency 
Causes:
- hereditary factor 7 deficiency 
- mild liver disease 
- mild VitK deficiency
20
Q

What does an prolonged APTT indicate?

A
  • requires further testing
  • repeat, with mixing test
  • if clotting time return to normal –> 8, 9, 11, 12 deficiency
  • if clotting time fails to correct –> inhibitor present such as lupus anticoagulant or F8 antibodies
21
Q

What does a prolonged prothrombin and APTT indicate?

A
  • a single factor deficiency in the ‘common pathway’
    e. g. 10, 5, prothrombin, or fibrinogen
  • of multiple factor deficiencies due to liver disease, VitK deficiency, warfarin therapy, DIC, dilutional coagulopathy

3/ IIH (28 decks)

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