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Haematology Sem 1 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

A process that changes blood from fluid to solid state

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2
Q

Why is haemostasis important?

A

minimise blood flow during injury
maintain blood in fluid state in absence of injury
maintain balance between bleeding too much and clotting too much

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3
Q

What are the three stages of haemostasis?

A

Primary haemostasis (vascular components), secondary haemostasis (biochemical reactions) and fibrinolysis

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4
Q

What is primary haemostasis? What are the three main components of primary haemostasis?

A

Initial response to vessel injury
Interactions between vessel and circulating platelets begin the formation of clot.
3 main components of haemostasis: platelets, vessel wall and von willebran factor

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5
Q

Whats the first response to blood loss? What is its restrictors?

A

Vasoconstriction: mediated by vasocontrictors (ADH, adrenaline) that are derived from platelets.

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6
Q

What are the main source of vWB factor?

A

Endothelial cells is the main source of vWB, along with thrombomodulin and TFPI (tissue factor pathway inhibitor)

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7
Q

Where does prostaglangulin metabolism occur? What do its metabolites enable?

A

Prostaglandulin metabolism occurs in endothelial cells of vessel. It produces prostacyclin (PGI2) which is a powerful vasocontriction inhibitor; causes vasodilation

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8
Q

What do adventitia cells release?

A

Tissue factor for coagulation

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9
Q

What happens when the vascular endothelium is breached?

A

Vascular subendothelial layer provides surface for platelet activation, aggregation and adhesion. Coagulation cascade activated.

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10
Q

How does blood flow contribute to the effectiveness of haemostasis.

A

Blood vessels constrict at site of injury. Blood flow slower at vessel walls due to friction. (so if breach in blood there will be less blood). Platelets flow at the centre of blood vessel so that they can be ready for action if there is a breach.

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11
Q

Is vWF an enzyme?

A

No

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12
Q

What does vWF bind to when there is a breach in vessel wall?

A

Subendothelial collagen at vessel wall
To receptor surface of unactivated platelets (GB1b complex)
To receptor surface of activated platelets (GB11b111a complex)
To coagulation factor VIII to protect it from degredation

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13
Q

What are platelets?

A

Anuclear fragments from megakaryoctye cytoplasm

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14
Q

Tell me about platelets:

A

Circulate in doormant state.
Rapid response to injury
Platform for haemostatic mechanisms

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15
Q

How does a primary haemostatic plug form?

A

Platelets contain vWB factor which allows platelets to adhere to the subethothelial collagen wall. The vWB factor also adheres to the activated platlets to bind them together platlet to platelet. Secondary haemostasis is activated. Platelets combine with RBC and WBC and fibrin to form a stable clot.

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16
Q

What is the main function of a platelet

A

Interacts with vWF to form initial barrier to blood loss via thrombus (vWF allows platelet-platelet interactions to strengthen blockage)
Platelets provide negatively charged lipid surface for secondary coagulation.
Promotes vasoconstriction and vessel repair.

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17
Q

What is another name of a platelet surface membrane and how does it result in a negative charge

A

Called a glycolax: has high concentration of proteins and sailic acid residues. Responsible for adhesion and aggregation. Both cause negatively charged surface.

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18
Q

What is the name of the channels that invaginate the plasma membrane?

A

surface-connected canalicular system.

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19
Q

What is the structure of the surface-connected canalicular system?

A

Continuous with extrnal membrane of plasma molecule (plasma externa). Extends throughout the cytoplasm

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20
Q

What is the purpose of the surface-connected canalicular system?

A

Increases cell surface area. Allows for substances from within the cell to be removed (like granular contents) and allows molecules to enter deep inside the plasma cell

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21
Q

What does the dense tubular membrane do?

A

It is a seperate internal membrane (that does not interact with plasma externa) that is present throughout the cell. It releases calcium and regulated platelet activation. It is derived from endoplasmic reticulum from parent megakayrocyte

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22
Q

What are contained within dense granules?

A

ATP, ADP, serotonin and Ca2+

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23
Q

What are contained within alpha granules

A 
platelet factor 4
plasminogen activor inhibitor
platelet-derived growth factor
vWF
Coagulation factor V
Fibrinogen
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24
Q

What maintains the discoid shape of the plasma cells?

A

Cytoskeleton

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25
Q

How are platelets transformed from inactive platelets to active platelets?

A

Adhesion, activation, aggregation

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26
Q

Describe what happens during adhesion of platelets?

A

Platelets adhere to collagen component of vascular subendothelium. This is mediated by the glycoprotiens from platelet surface membrane binding to glycoprotien receptors.
Interactions with vWF causes fusion between platelets (GB1b to GB11b111a)
Adhesion generates monolayer
Initiates plug platelet formation
Insufficient to stop bleeding

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27
Q

Describe what happens during the activation stage of platelets?

A

Damage to endothelial layer of vessel activates release of collagen, tissue factors and von willebrand factor into the blood stream.
This causes the platelets to activate and change shape
Platelet activation releases tromboxane which activates more platelets
Platelets also activated by thrombin and the negativelt charged lipid sruface (caused by glycoprotiens and sailic acid on plasma surface)
Once activated platelets can change shape

28
Q

What is the name of the substance that activates more platelets once some have already been activated?

A

Thormboxane

29
Q

Why do platelets change shape once activated?

A

Increases surface area of the cell, allows closer interaction with each other and forces granules into centre of plasma cells (so more vasoconstriction from dense granules ADH and vWF from apla granules for more platlet-platelet interactions)

30
Q

Describe the degranulation of platelets

A

Alpha and dense granules move to platelet surface. Activated platelets release granules into surface-connected canalicular system and then into the blood

31
Q

Why do dense granule and alpha granules release their content?

A

In order to amplify platelet aggregation and trigger more adhesion

32
Q

Describe platelet aggregation

A

Platelets express surface receptors for agonists
Platelets activate agonists as they arrive at the plug point (ADP, thrombin, thromxane)
activated platelets accumulate on monolayer
Cross linking of platelets through GB11b111a complex (vWF platelet-platelet) which allows thrombus to grow
This is a platform for secondary haemostasis

33
Q

What is secondary haemostasis?

A

Usually platelet plug formation is enough to stop but large vessels may need more reinforcement.
Biochemical coagulation converts soluble fibrinogen to mesh of insoluble fibrin
This forms a thrombus

34
Q

What is the classical blood coagulation cascade?

A

Described what happens in vitro (outside of body)

35
Q

What is the modern coagulation cascade?

A

Describes what happens in vivo (in body)

36
Q

What are coagulation factors?

A

Serine proteases circulating as zymogens (proenzymes)
Some are cofactors so catalyse reactions
Two cannot be classified as more than one thing

37
Q

Where are coagulation factors sythesised?

A

In the liver

38
Q

Von Willebran factor is a coagulation factor. Where is produced?

A

In vascular subendothelial cells, in alpha granules of platelets

39
Q

What other coagualtion factors do platelets contain?

A

FV, FXIII and fibrinogen (fI)

40
Q

What is the role of vitamin K?

A

Some coagulation factors are vit K dependant: II, VII, IX, X.
Dietry vit K found in leafy green veg.

41
Q

What is the role of protein C and S in coagulation?

A

Natural inhibitors of coagulation

42
Q

What is the main role of the classical pathways?

A

activation of Factor X so it can act as a biological activation system

43
Q

What activates the intrinsic pathway?

A

Contact with blood on either physiological (collagen) or non physiological (glass)
Activated with contact with: FXII, prekallikrein and high molecular weight kinonogen
There are all plasma proteins on a negatively charge surface

44
Q

Describe the intrinsic pathway

A

The interaction between FXII, prekallikrein and high molecular weight kinonogen activates FXI to FXIa
(XI must bond to the activation surface before it itself is activated)
FXIa activates FIX to FIXa
FIXa forms complex with FVIIIa, FX, Calcium ions and phospholipid (tenase complex)
This complex activates FX to FXa

45
Q

Describe the extrinsic pathway

A

Tissue factors (TF, thromboplastin) forms complex with VII and VIIa.
Calcium ions required
Once complexed, FVII rapidly activated to FVIIa
FVIIa activates IX to IXa
IXa activates X to Xa
FVIIa can activate X by itself too

46
Q

Describe the common pathway

A

FXa formed by either pathway.
Factors Xa,V, II(prothombin), Calcium ions and phospolopid become complex called prothrombinase complex.
Prothrominase complex activates FII (prothrombin) to FIIa (thrombin)

47
Q

What is the main function of thrombin?

A

To convert fibrinogen (FI) to fibrin

48
Q

What is the final stage of coagulation?

A

Stabilisation: fibrin clot using FXIII

49
Q

Describe the stabilisation of fibrin via FXIII

A

FXIII stimulated by thrombin. FXIII catalyses formation of stable cross links between adjacent fibrin molecules

50
Q

What is the modern/cell-based coagulation theory?

A

In vivo generation of thrombin via amplification and negative feedback. There is only one pathway. The biochemical details are the same but the factor order is different

51
Q

What is the main physiological activator of blood coagulation in the modern theory

A

Tissue factor thromboplastin

52
Q

What are the two stages of moden based theory?

A

Initiation and amplificaion

53
Q

Describe the initiation phase of modern coagulation theory

A

Tissue factor (thromboplastin) released after vascular injury.
Tissue factor reacts with VIIa - VIIa cannot display proeolytic activities unless bound to tissue factor
Tissue factor initiiates thrombin formation and fibrin formation.
FVIIa/TF complex activates:
FIX to IXa and therefore FX to FXa
Xa can produce small amounts of thrombin (FIIa) from prothrombin (FII) but not enough
amplification required.

54
Q

Describe the amplification phase of the modern coagulation theory

A

Trace amount of thrombin (FIIa) activate FV to FVa
FVa acts as a cofactor for FX to FXa

Thrombin activates FIII to FIIIa
FIIIa acts as a cofactor for IX to IXa (and therefore more X to Xa)

Thrombin activates platelets - more exposure of lipid surface for modern pathway to occur

Large scale of thrombin produced which is known as thrombin burst.

55
Q

What is the role of thrombin in coagulation?

A

Thrombin acts as a regulator of haemostasis:

FVIII and FV which are required for links between fibrin are not structurally changed when activated. They are cofactors of coagualtion.

Thrombin enhances FVIII and FV through positive feedback

If too much thrombin in the blood blood then FVIII and FV is supressed via negative feedback

56
Q

What is fibrinolysis?

A

Prevention of excess firbin formation. Its activity is always present in plasma as it controls low levels of coagulation

57
Q

How does fibrinolysis occur?

A

Removal of fibrin as part of new tissue production. It is multi-component like coagulation cascade where inactive precursors become active.

58
Q

What is the key component in fibrinolysis?

A

Plasmin

59
Q

What is a coagulant?

A

Agent that stops blood from clotting

60
Q

What are the three main natual coagulants?

A

Antithrombin, Protien S and C

61
Q

What does antithrombin inhibit?

A

IIa Xa XIa TF-VIIa

62
Q

What do protein S and C inhibit?

A

Cofactors FVa and VIIIa

63
Q

What could cause a deficiency of a coagulant?

A

Mutations so there is only low level of functioning protein

mutation altering the function of proteins

64
Q

What do deficiencies of coagulants cause?

A

Increased risk of blood clots. - Venous thrombo embolsim (VTE) is 10 x more likely if antithrombin not available

65
Q

How would you clot a sample in the lab?

A

Remove calcium as most steps require calcium - use citrate anticogagulant
Add controlled calcium at each step to check pathway
Platelets removed via centrifusion so phospholipid surface is the same for all samples.

Haematology Sem 1 (8 decks)

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