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POM 2 G: HAEMATOLOGY > 2.7 Haemostasis And Thrombosis > Flashcards

2.7 Haemostasis And Thrombosis Flashcards

(66 cards)

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1
Q

What is Haemostasis

A

Halting of blood following trauma to blood vessels

A state of equilibrium

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2
Q

Functions of Haemostasis

A

Prevention of blood loss from intact vessels
Arrest of bleeding from injured vessels

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3
Q

Balance model

A

Fibrinolytic factors, anticoagulant proteins vs. Coagulation factors, platelets

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4
Q

Why is the balance important

A

Coagulation, thrombosis, fibrinolysis

Allows stimulation of blood clotting processes following injury
Limits extent of response to prevent excessive or generalised blood clotting
Starts the process leading to the breakdown of the clot as part of the healing process

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5
Q

First stage o Haemostasis

A

Vessel constriction

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6
Q

Stage 2 of Haemostasis

A

Primary Haemostasis
Formation of unstable platelet plug

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7
Q

Stage 3 of Haemostasis

A

Secondary Haemostasis
Stabilisation of the plug with fibrin

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8
Q

4th stage of Haemostasis

A

Fibrinolysis

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9
Q

Brief vessel constriction

A

Vascular smooth muscle cells contract locally
Limits blood flow to injured vessel

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10
Q

Brief formation of unstable platelet plug

A

Platelet adhesion
Platelet aggregation

Limits blood loss and provides surface for coagulation

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11
Q

Brief stabilisation of the plug with fibrin

A

Blood coagulation
Stops blood loss

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12
Q

Brief vessel repair and dissolution of clot (fibrinolysis)

A

Cell migration/ proliferation and fibrinolysis
Restores vessel integrity

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13
Q

Why is it important to understand Haemostatic mechanisms

A

Diagnose and treat bleeding disorders
Control bleeding
Identify and treat thrombotic disorders
Monitor drugs used in treatment

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14
Q

What are platelets differentiated from

A

Megakaryocytes

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15
Q

How long do platelets circulate

A

10 days

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16
Q

Haemostatic 0latelet plug formation overview

A

Vessel constriction

Primary Haemostasis (formation of unstable platelet plug)

Secondary Haemostasis (stabilisation of plug with fibrin)

Fibrinolysis (dissolution of clot and vessel repair)

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17
Q

Platelet adhesion

A

Primary

Vwf forms a bridge for platelet to bind to via Glp1b

Or platelets bind directly to exposed collagen by Glp1a

Changes shape from discoid to rounded with spicules for platelet platelet interactions

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18
Q

What’s released following platelet adhesion

A

ADP and prostaglandins

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19
Q

Which components are used in binding sites between platelets in platelet aggregation

A

Fibrinogen and Ca2+

Glp2b/3a

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20
Q

How is the prostaglandins thromboxane a2 produced

A

From arachidonic acid in the cell membrane

Catalysed by cyclo oxygenate (cox) to cyclic endoperoxides

Thromboxane synthesise in platelets then produces TXA2

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21
Q

Arachidonic acid in endothelial cells

A

Catalysed by cox to cyclic endoperoxides

Prostacyclin synthetase then catalyses to prostacyclin PGI2 in endothelial cells

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22
Q

Prostacyclin function

A

Inhibits platelet aggregation

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23
Q

Aspirin and clopidogrel are

A

Antiplatelet drugs

Irreversibly bind to. Cox

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24
Q

Clopidogrel function

A

Irreversibly blocks ADP receptor p2y12 on platelets

Last 7-10 days due to platelet life span

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25
Why can endothelial cells still produce prostacyclins even with aspirin
Can synthesise it’s own cox
26
Where are clotting factors produced
Mostly in the liver Vwf in endothelial cells and platelets Factor 5 in platelets
27
Which factors are reliant on vit k
1972 - 10, 9, 7 and 2 (prothrombin)
28
Initiation stage
Tissue factor binds to factor 7a Triggers activation of 9 and 10 to a Results in generation of small amount of thrombin (2a) from prothrombin (2)
29
Amplification propagation phase
Thrombin activates factor 11 and cofactors 5 and 8 to a and platelets to their activated form 11a amplifies factor 9 to 9a Factors 9a and 8a cause amplification of conversion of 10 to 10a 10a causes a rapid burst in the generation of thrombin 2a which cleaves the soluble fibrinogen to insoluble fibrin clot
30
What is calcium needed for in coagulation
Binding clotting factors to the platelet surface
31
Direct coagulation inhibition
Antithrombin - inhibitor of thrombin and other clotting proteinases
32
Indirect coagulation inhibition
Inhibition of thrombin generation by pathways (e.g. protein c and s antiocoagulant oathways)
33
What does antithrombin bind to
Heparin
34
What are protein c and protein s involved in
Thrombin generation
35
What does antithrombin have its affect on
10a and thrombin (2a)
36
What does protein c have its affect on
8a
37
What does protein s have its affect on
5a
38
Therapeutic anti coagulation approaches
Reduce procoagulant factors (vit k antagonist) Inhibit procoagulant factors (direct oral anticoagulant) Enhance natural anticoagulant pathways (heparins and derivatives)
39
Anticoagulant drugs
Heparin Warfarin DOACs (direct oral antiocoagulant drugs)
40
Heparin works by
Indirectly by potentiating acting of antithrombin causing inactivation of factors 10a and 2a (thrombin) Long chains of heparin wrap around both antithrombin and thrombin
41
How is heparin administered
Intravenously or subcutaneous injection
42
What is heparin derived from
Mixture of glycosaminylglycan chains extracted from porcine mucosa
43
What is warfarin derived from
Coumarin
44
How does warfarin work
Vit k antagonist which works by interfering with protein carboxylation (factors 1972) Competes with vit k to stop its recycling
45
How is warfarin administered
Oral tablet
46
Why does warfarin take several days to take effect
Because it reduces synthesis of coagulation factors rather than inhibiting existing factor molecules
47
DOACs
Orally available drugs which directly inhibit 10a or 2a (thrombin) without antithrombin Don’t need monitoring predictable
48
Why is there usually no fibrinolytic reaction
Plasminogen and tPA need to be brought together
49
Fibrinolysis
Plasminogen binds to the lysine residues of fibrin, activated by tissue plasminogen activator to plasminogen causing degradation of the clot
50
Plasmin breaks down
Fibrin (1a) 5a and 8a
51
What inhibits plasmin
Antiplasmin Alpha 2 macroglobulin
52
Tranexamic acid in fibrinolysis
Competitive inhibitor of of plasminogen to lysine residues of fibrin Used to treat bleeding in trauma patients surgical patients and those with inherited bleeding disorders
53
Haemophilia
Failure to generate fibrin to stabilise platelet plug
54
What is a prolonged aptt without prolonged pt seen in
Haemophilia A (factor 8 deficiency) Haemophilia b (facto r9 deficiency) Factor 12 deficiency(no bleeding)
55
What is a prolonged aptt seen in
Reduction in single or multiple clotting factors If multiple may also be prolonged pt
56
Aptt
Activated partial thromboplastin time Measure Intrinsic (and common) pathways Performed by the contact activation of factor 12 by glass silica or kaolin Added with phospholipid to citrated plasma followed by calcium Time taken for mixture to clot is measured
57
Prothrombin time
Measures integrity of extrinsic (and common pathway) Blood added to sodium citrate which doesn’t contain calcium to prevent clotting Spun to produce platelet poor plasma TF and phospholipid added to citrated plasma sample with calcium to start the reaction Time taken for mixture to clot is recorded
58
What does pt estimate
Activity of factors 7,10,5 and 2 and fibrinogen
59
What is often used as a source of TF and phospholipid in pt
Thromboplastin
60
What are results of pt expressed as in the control of vit k antagonist anticoagulant therapy
INR international normalises ratio
61
What could loss of Haemostatic equilibrium balance result in
Bleeding
62
What can cause bleeding in regards to the Haemostatic balance
Reduction in platelet number or function (primary Haemostasis) Reduction in coagulation factors (secondary haemostasis) Increased fibrinolysis
63
Thrombocytopenia
Reduction in platelet number
64
Thrombosis describes
Formation of blood clot where you don’t need it - within an intact vessel
65
Virchow’s triad
Three contributory factors to pathological clotting (thrombosis) Blood Blood flow Vessel wall
66
Changes in blood constituents is important in regard to which thrombosis
Venous thrombosis

POM 2 G: HAEMATOLOGY (8 decks)

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