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POM Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

(55 cards)

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1
Q

What is thrombosis

A

Formation of a blood clot in an intact blood vessel

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2
Q

What is primary Haemostasis

A

Formation of an unstable platelet plug at the site of vessel wall damage

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3
Q

What is secondary Haemostasis

A

Formation of a stable fibrin clot aka coagulation

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4
Q

What 3 processes follow blood vessel trauma

A
  1. Vasoconstriction
  2. Primary Haemostasis
  3. Secondary haemostasis / coagulation
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5
Q

What 2 actions are involved in primary haemostasis

A

Platelet adhesion

Platelet aggregation

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6
Q

What is the last step in response to injury

A

Fibrinolysis

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7
Q

Where do platelets originate from

A

Fragmentation of megakaryocyte cytoplasm in bone marrow

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8
Q

What is the circulating life span of a platelet

A

10 days

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9
Q

How do platelets stick to damaged endothelium

A

Either:
Directly to collagen via the platelet GPIa receptor

Or:
Indirectly via Von Willebrand factor which binds to GPIb receptor

This causes them to be activated

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10
Q

Why do platelets change from disk shaped to rounded with spicules

A

To encourage platelet-platelet interaction

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11
Q

When activated, what do platelets release from their storage granules

A

ADP
Fibrinogen
Von Willebrand Factor

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12
Q

How do platelets release the contents of their granules

A

Platelet membrane is invaginated (turned inside out to form cavity) to form surface-connected cannalicular system

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13
Q

What is the prostaglandin thromboxane A2 synthesised from

A

Arachiodonic acid from cell membrane of activated platelet

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14
Q

What are the roles of thromboxane A2

A

Platelet aggregation
Vasoconstriction
Important during tissue injury and inflammation

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15
Q

Why is aspirin classed as an anti platelet drug

A

Irreversibly Inhibits COX (cyclooxygenase), an enzyme involved in TXA2 synthesis, reducing platelet aggregation

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16
Q

What follows the granular release of ADP and thromboxane A2

A

Positive feedback effect; further platelet recruitment activation and aggregation

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17
Q

What receptors do ADP and TXA2 bind to on platelet membrane

A

P2Y12 and thromboxane A2 receptor respectively

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18
Q

Platelet activation causes a) what kind ofconformational change and b) in which receptor and c) for what purpose

A

a) ‘Inside out’ or ‘flip flopping’
b) GPIIb/IIIa
c) provide binding sites for fibrinogen

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19
Q

How does fibrinogen link platelets together to form the platelet plug?

A

Binds to GPIIb/IIIa receptor

Also causes ‘outside in’ signalling which further activates platelets

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20
Q

What 2 things counterbalance the effect of platelet aggregation

A

Active flow of blood

Prostacyclin (PGI2) released from endothelial cells

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21
Q

What are the roles of prostacyclin

A

Powerful vasodilator
Suppresses platelet activation
Thus prevents inappropriate platelet aggregation

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22
Q

How long do the anti-platelet effects of aspirin and clopidogrel last

A

7 days, until new platelets have been produced

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23
Q

What is clopidogrel and how does it work

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A

Anti platelet drug
Irreversibly blocks ADP receptor P2Y12
Prevents further activation of platelets

24
Q

What is Von Willebrand Factor (VWF) and what is its function

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A

Glycoprotein synthesised by endothelial cells and megakaryocytes.

Circulates in plasma as multimers

Mediates adhesion of platelets to site of injury and promotes platelet platelet aggregation

Specific carrier for factor 8

25
Where are most clotting factors synthesised and what are the exceptions
Liver Factor 8 synthesised in endothelial cells VWF synthesised in endothelial cells and megakaryocytes, incorporated into platelet granules
26
What do blood coagulation pathways centre on
Generation of thrombin, which cleaves fibrinogen to generate fibrin clot which stabilises platelet plug
27
What vitamin are factors 2 (prothrombin), 7, 9 and 10 dependent on and why
vitamin k, for carboxylation their glutamic acid residues, essential for the function of these clotting factors
28
How are inactive zymogens (proemzymes) converted into active clotting factors
Splitting of 1+ peptide bonds to expose active site
29
Which clotting factors are cofactors
5 and 8
30
Where do many clotting factors work on
Exposed phospholipid surface of platelets, localising and accelerating reactions
31
What role do calcium ions play in coagulation
Binding of active clotting factors to phospholipid surfaces of platelets Factor 4 is calcium
32
What triggers initiation of coagulation at site of injury
Tissue factor (TF) exposed on surface of endothelial cells and leukocytes and on most extravascular cells at site of damage Therefore, blood only encounters TF at sites of vascular injury
33
Describe the initiation phase of coagulation
TF binds to factor 7a This activates factors 4 to 4a and 10 to 10a This activates activation of prothrombin (factor 2) to generate small initial amount of thrombin (factor 2a)
34
Describe the amplification phase of coagulation
Small amount of thrombin from amp phase mediates activation of co factors 5 and 8, the zymogen factor 6 and platelets
35
Describe the propagation phase of coagulation
Factor 6 converts more factor 4 to 4a Factor 4a and 8a amplifies conversion of factor 10 to 10a Consequent rapid burst in thrombin generation Cleaves circulating fibrinogen to form insoluble fibrin clot
36
Which three substances are part of the natural anticoagulant pathway and how
Protein C, protein S and antithrombin Thrombin binds to thrombomodulin on endothelial cell surface, activating protein C to APC which inactivates factors 5a and 8a in the presence of cofactor protein S Thrombin and factor Xa are inactivated by circulating inhibitor antithrombin
37
Name three anticoagulant drugs and their mode of action
Heparin - indirect; potentiates action of antithrombin, administered intravenously or by subcutaneous injection Warfarin - indirect; vitamin k antagonist which interferes with protein carboxylation, reduced synthesis of factors 2,7,9,10. Oral tablet, takes several days to take effect Direct Oral Anticoagulants - directly inhibit thrombin or factor 10a, do not require monitoring like warfarin
38
What is the role of plasmin
Fibrinolysis (activated from plasminogen to plasmin by t-PA when bound to lysine residues on fibrin together) Breaks down other protein plasma components eg fibrinogen and factors 5a and 8a
39
What is thrombolytic therapy
Generate plasmin to lyse clots, given to patients presenting ischaemic stroke and pulmonary embolism, needs to be administered quickly, eg recombinant t-PA
40
What is tranexamic acid
Antifibrinolytic drug Synthetic derivative of lysine, competitively inhibits plasminogen
41
What is PT and why would it be prolonged
Prothrombin time Blood sample is citrated (chelates Ca) and spun to produce platelet poor plasma TF and Ca added, time taken for mixture to clot recorded Prolonged if there is a reduction in activity of factors 7, 10, 5, 2 (prothrombin) or fibrinogen
42
What is APTT and why would it be prolonged
Activated partial thromboplastin time Isolated prolonged APPT (normal PT) seen in patients with haemophilia A (factor 8 def), haemophilia B (factor 9 def) and factor 11 def (Could also be factor 12 def which doesn’t cause bleeding)
43
What may cause thrombocytopenia
Failure of platelet production; drugs, viruses, megaloblastic anaemia, hereditary, bone marrow infiltration
44
Name 3 congenital causes of reduced cofactors
Von Willebrand disease (VWD) - most common, autosomal Haemophilia A (factor 8 def, X linked) Haemophilia B (factor 9 def, X linked)
45
Name three acquired causes of reduced coagulation factors
Liver disease Anticoagulant drugs Disseminated intravascular coagulation (DIC)
46
What is DIC
Disseminated intravascular coagulation generalised and uncontrolled activation of coagulation followed by activation of fibrinolytic system due to TF in circulation. Causes thrombocytopenia, depletion of thrombin, depleted clotting factors, thrombi in micro circulation which cause shearing of RBCs (schistocytes on blood film) Caused by bacterial sepsis, advanced cancer, obstetric emergencies
47
What 3 factors contribute to thrombosis (Virchow’s triad)
Blood (venous thrombosis) Vessel wall (arterial thrombosis) Blood flow (complex, contributes to both)
48
What 3 conditions may increase the risk of venous thrombosis
Inherited antithrombin deficiency Factor V Leiden
49
What is APTT and why would it be prolonged
Activated partial thromboplastin time Isolated prolonged APPT (normal PT) seen in patients with haemophilia A (factor 8 def), haemophilia B (factor 9 def) and factor 11 def (Could also be factor 12 def which doesn’t cause bleeding)
50
What may cause thrombocytopenia
Failure of platelet production; drugs, viruses, megaloblastic anaemia, hereditary, bone marrow infiltration
51
Name 3 congenital causes of reduced cofactors
Von Willebrand disease (VWD) - most common, autosomal Haemophilia A (factor 8 def, X linked) Haemophilia B (factor 9 def, X linked)
52
Name three acquired causes of reduced coagulation factors
Liver disease Anticoagulant drugs Disseminated intravascular coagulation (DIC)
53
What is DIC
Disseminated intravascular coagulation generalised and uncontrolled activation of coagulation followed by activation of fibrinolytic system due to TF in circulation. Causes thrombocytopenia, depletion of thrombin, depleted clotting factors, thrombi in micro circulation which cause shearing of RBCs (schistocytes on blood film) Caused by bacterial sepsis, advanced cancer, obstetric emergencies
54
What 3 factors contribute to thrombosis (Virchow’s triad)
Blood (venous thrombosis) Vessel wall (arterial thrombosis) Blood flow (complex, contributes to both)
55
What 3 conditions may increase the risk of venous thrombosis
Inherited antithrombin deficiency Factor V Leiden

POM Haematology (1 decks)

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