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BIOL21361 > Lecture 7/8 - Haemostasis > Flashcards

Lecture 7/8 - Haemostasis Flashcards

1
Q

Haemostasis: what is it and what are the 5 main components of it

A

The ability to minimise blood loss after injury

Blood vessels - vasoconstriction
Platelets
Coagulation factors
Coagulation inhibitors
Fibrinolysis

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2
Q

What is the process of hemostatic plug formation?

A

Vessel injury - collagen exposure - platelet adhesion - platelet activation - platelet aggregation - primary hemostatic plug

Vessel injury + platelet acivation - vasoconstriction - reduced blood flow - primary hemostatic plug

Vessel injury (tissue factor) + platelet phsopholipid (platelet activation) - thrombin - fibrin + primary hemostatic plug - hemostatic plug

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3
Q

Endothelial cells: what do they do, how do they affect hemostasis, and what do they produce

A

Maintain vascular integrity

Have potent anti-hemostatic influence (prostacyclin, nitric oxide, vasodilatory properties, platelet adhesion inhibition)

Von Willebrand factor (vWF), tissue plasminogen activator (fibrinolysis)

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4
Q

Vasoconstriction

A

Immediate (few minutes) smooth muscle cell activation before other mechanisms take over

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5
Q

Platelets

A

Produced in bone marrow as a fragment (2-4µm diameter) of a megakaryocyte (1 ->4000)

Lifespan of 9-10 days, normal platelet count 150-400x10^9/L

Destroyed in spleen and liver by Kupffer cells

700-40-1

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6
Q

Platelet production

A

Endomitotic synchronous nuclear replication
Nuclear lobes increase in multiples of two. Cytoplasmic volume increases and becomes more granular and platelets are produced

Negative feedback - number of platelets circulating

Stimulated by thrombopoietin (TBO) and stimulated by IL-3 and GM-CSF

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7
Q

Platelet structure: what are the components, what do they do, and what do glycoproteins do?

A
  • Glycocalyx (contain glycoproteins (GPIa, GPIb, GPIIb, etc))
  • Glycogen (energy supply), dense tubular system (prostaglandin and thromboxane A2 synthesis)
  • Platelet contractile proteins (make aggregation irreversible)
  • Electron dense (delta) granules (contain Ca²⁺, ADP, ATP, and serotonin)
  • Alpha granules (platelet-derived growth factor, platelet factor 4, fibrinogen, vWF, factors V and VIII)
  • Canalicular system - allow granule release

The glycoproteins allow adhesion to surfaces like collagen

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8
Q

Platelet function

A

Adhesion, secretion (granule release reaction), and aggregation

vWF often binds with GPIIb and GPIIIa

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9
Q

Hemostatic stable plug

A

Secretes ADP - and thromboxane A2 - increasing aggregation

Platelets swell due to the ADP presence

Positive feedback occurs

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10
Q

Coagulation factor I: name and active form

A

Fibrinogen

Fibrin

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11
Q

Coagulation factor II: name and active form

A

Prothrombin

Serine protease

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12
Q

Coagulation factor III: name and active form

A

Tissue factor

Co-factor

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13
Q

Coagulation factor V: name and active form

A

Labile factor

Co-factor

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14
Q

Coagulation factor VII: name and active form

A

Proconvertin

Serine protease

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15
Q

Coagulation factor VIII: name and active form

A

Antihaemophilic factor

Co-factor

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16
Q

Coagulation factor IX: name and active form

A

Christmas factor

Serine protease

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17
Q

Coagulation factor X: name and active form

A

Stuart-Prower factor

Serine protease

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18
Q

Coagulation factor XI: name and active form

A

Plasma thromboplastin antecedent

Serine protease

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19
Q

Coagulation factor XII: name and active form

A

Hageman factor

Serine protease

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20
Q

Coagulation factor XIII: name and active form

A

Fibrin stabilising factor

Serine protease

21
Q

Coagulation cascade initiator

A

TF is the main initiator and binds with coagulation factors (VII-VIIa)

22
Q

The process of fibrin generation

A

Injury -> Factor VII is activated and binds to tissue factor forming factor VIIa TF

VIIa TF -> activates both factor X and IX

IXa and VIIa -> activate factor X

Xa and Va -> convert prothrombin into thrombin

Thrombotic activation -> Va, XIa, and IXa and VIIIa formation

Thrombin converts fibrinogen and fibrin

XIa -> activates more XI and IX

Tissue factor pathway inhibitor (TFPI)

23
Q

Coagulation cascade initiation: what are the steps?

A

Initiation:
* Extrinsic tenase complex
* Generation of trace thrombin
* Down-regulation of initiation by TFPI

Amplification

Propagation:
* Formation of intrinsic tenase complex
* Formation of prothrombinase complex
* Burst of thrombin generation

24
Q

Initiation: Extrinsic tenase complex

A

Involves FVIIa, TF, FX, phospholipids, Ca²⁺

25
Q

Initiation: Generation of trace thrombin

A

Factor IIa is activated, Ca²⁺ is present, and factor Xa activates a small amount of thrombin

26
Q

Initiation: Down-regulation of initiation by TFPI

A

Factor Xa is limited by TFPI

27
Q

Amplification

A

The produced factor IXa and thrombin, although not enough to convert fibrinogen into fibrin, can amplify the process by feedback and activate factor VIII, a co-factor for factor IX, and factor V, a co-factor for factor X

This results in an amplified cascade

28
Q

Propagation: Formation of intrinsic tenase complex

A

FXa and FVIIa activate FIX and the intrinsic tenase complex is formed, consisting of FIXa, FX, FVIIIa, Ca²⁺, and Phospholipids (obviously meaning this is occurring on the membrane, near the site of injury(?))

29
Q

Propagation: Formation of prothrombinase complex

A

The prothrombinase complex is composed of FXa, FVa, FII, Ca²⁺, and phospholipids

Since the process has been amplified, the inhibitor has less of a role in inhibiting FX

This process ends with prothrombin being activated

30
Q

Propagation: Burst of thrombin generation

A

FXa, FVa, FIIa, Ca²⁺

FVa and FXa - convert prothrombin into thrombin

Thrombomodulin, a thrombin co-factor, has procoagulant and anticoagulant properties

The produced thrombin increases the process to be stimulated by positive feedback

The end result of this process is a stable fibrin clot, only degradable by fibrinolysis

31
Q

The core components of the extrinsic tenase, intrinsic tenase, and prothrombinase pathways?

A

Extrinsic tenase: FVIIa, TF, FX, Ca²⁺, and K⁺

Intrinsic tenase: FIXa, FVIIIa, FX, Ca²⁺ and K⁺

Prothrombinase: FXa, FVa and FII, Ca²⁺ and K⁺

32
Q

Fibrin clot: when is it added, what happens to the platelet plug, what is the final form of the hemostatic plug, and what mediates clot retraction?

A

Fibrin is added to the primary hemostatic plug, causing platelet mass and platelet-induced clot retraction/compaction

Fibrin increases as the platelet plug degranulates/autolyses

After a few hours, the entire haemostatic plug is composed of cross-linked fibrin

Clot retraction is medicated by glycoprotein receptors (GpIIb/IIIa)

33
Q

What are the inhibitors present in the activating of the tissue factors?

A

Tissue Factor Pathway Inhibitor (TFPI) – VIIa and Xa

Antithrombin III – Xa and thrombin

Protein C and Protein S – PS inactivate Va and VIIIa, the action of PS is enhanced by PC and PC also enhances fibrinolysis

34
Q

Tissue factor pathway inhibitor: how quickly does it act, where is it found, what causes its accumulation, and what is inhibited?

A

1st inhibitor to act

Found in plasma and platelets

Accumulates due to platelet activation

Inhibits FVIIa and FXa

35
Q

Antithrombin: where is it synthesised and what does it inhibit/inactivate?

A

Synthesized in the liver and endothelium.

Inactivates serine proteases, principally factor Xa and thrombin

36
Q

Protein C: what is it, how is it activated, how is its action enhanced, and what does it do?

A

Vitamin K-dependent protein made in the liver

Activated via a complex which inactivates factors Va and VIIIa

The action of protein C, enhanced by the action of protein S, binds protein C to the platelet surface

Activated Protein C enhances fibrinolysis by inactivating the tissue plasminogen activator (tPA) inhibitor

37
Q

Protein S: what is it, how is it activated, and what does it do?

A

Vitamin K-dependent protein made in the liver

Activated via a complex which inactivates factors Va and VIIIa

Enhances the action of protein C

38
Q

Fibrinolysis: what is it, how does it occur, and what is generated?

A

The degradation of fibrin (clot)

tPA activates plasminogen to plasmin which degrades fibrin

Generates soluble fragments called fibrin degradation products (FDPs)

39
Q

Fibrinolytic systems

A

Plasminogen is activated into plasmin by tissue plasminogen activator (tPA) as well a factor XIIa, and then plasmin breaks fibrinogen down into fibrin

40
Q

Streptokinase: what is it?

A

A drug used to break down clots extremely effectively

41
Q

What inhibits the fibrinolytic system?

A

Plasminogen activator inhibitor (PAI-1) inhibits tPA and factor XII

α2-antiplasmin inhibits the action of plasmin

42
Q

What methods are used to detect haemolytic issues?

A
43
Q

Bleeding time: how is it monitored, how long should bleeding normally last for, and in what conditions is the bleeding time normal/abnormal?

A

Application of pressure to the upper arm (blood pressure cuff) with small incisions made in the forearm surface skin

Bleeding normally stops in 3-8 mins

Prolonged in thrombocytopenia (reduced platelet count) but normal in cases of abnormal vascular bleeding

44
Q

Platelet count and function: how are platelet counts done and how is platelet function monitored?

A
  • Full blood count – platelet count
  • Bone marrow examination - when platelet issues are suspected
  • Platelet aggregometry – most valuable
  • Measure the change in light absorbance as the platelets aggregate
  • Adhesion studies
  • Von Willebrand assay
45
Q

Prothrombin time: what does it do, what is the normal PT, and how is it standardised?

A

Measure factors VII, X, V, prothrombin, and fibrinogen and their integrity

Normal PT is 10-14 seconds

Prolonged in liver disease, oral anticoagulant treatment (OAT), e.g. warfarin

PT standardised as International Normalised Ratio (INR) – used to monitor OAT

46
Q

Activated partial thromboplastin time: what does it do, what is the normal time, and when is it prolonged?

A

APTT measures factors VIII, IX, XI and XII as well as X, V, prothrombin and fibrinogen

Normal 3-40 seconds

Prolonged in haemophilia, heparin therapy

47
Q

Which measuring technique measures which haemolytic pathway?

A

Extrinsic pathway - PT

Intrinsic - APTT

Contains a little overlap when it comes to factors X, V, and prothrombin and fibrinogen

This allows for some diagnosis as if either PT or APTT is fine but the other isn’t then you know there is an issue with the other

48
Q
A

BIOL21361 (13 decks)

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