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Cardiovascular system > Thrombosis: haemostasis in the wrong place > Flashcards

Thrombosis: haemostasis in the wrong place Flashcards

1
Q

What does coagulation prevent?

A

Coagulation prevents blood loss

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2
Q

What does inflammation activate?

A

Inflammation activates coagulation which promotes inflammation

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3
Q

What type of response is coagulation?

A

Coagulation is an inflammatory response

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4
Q

What can Ischemia’s of the brain be caused by?

A

Embolic stroke either from the carotids or heart

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5
Q

What is primary haemostasis?

A

Aggregation of platelets

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6
Q

What is secondary haemostasis?

A

The conversion of fibrinogen into fibrin

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7
Q

Briefly describe what occurs in response to tissue damage

A

Primary platelets become activated –> Activated platelets clump together with RBCs

At the same time:

Secondary fibrinogen –> Fibrin –> Secondary blood clot –> The fibrin is cross-linked to form a solid blood clot

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8
Q

What is important in coagulation?

A

The surface of platelets

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9
Q

What do anticoagulants prevent?

A

Thrombosis

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10
Q

What does fibrinolysis reverse?

A

Thrombosis

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11
Q

Examples of anticoagulants

A
  • Heperin
  • Warfarin
  • EDTA
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12
Q

Describe the reactions that occur in thrombosis

A
  1. Aggregation of platelets
  2. Fibrinogen is converted into Fibrin mesh by Thrombin (a protease)
  3. Thrombin converted from Prothrombin
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13
Q

What two reactions constantly occur in the body to maintain a balance?

A

Thrombosis and Fibrinolysis

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14
Q

Where do different types of thrombosis form?

A

In different kinds of vessels: arterial thrombosis forms in arteries and venous thrombosis forms in veins

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15
Q

Where does arterial thrombosis result from?

A

Mostly result from atheroma rupture or damage to the endothelium (e.g. MI, stroke)

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16
Q

What type of thrombosis is arterial thrombosis?

A
  • Platelet-rich ‘white’ thrombosis

- Mostly primary

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17
Q

What damage can arterial thrombosis cause?

A

May block downstream arteries

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18
Q

What does venous thrombosis result from?

A
  • Often results from stasis or a hyper-coagulant state (DVT)
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19
Q

What type of thrombosis is venous thrombosis?

A
  • Platelet-poor ‘red’ thrombus

- Mostly secondary

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20
Q

What damage can venous thrombosis cause?

A

May move to lungs

  • Very hypercoagulant state
  • Can lead to immobilization of the legs
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21
Q

What mechanisms are balanced?

A

Balance of:

  • mechanisms for clotting
  • mechanism for resistance to clotting
  • mechanism for undoing clotting
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22
Q

Describe the conflicting events that occur in the coagulation vs fibrinolysis balance

A
  • The endothelial cells are the cells lining the lumen of the vessel
  • Damage to the endothelium means that the sub-endothelial cells will be exposed
  • The coagulation response will activate clotting/Von Willebrand factors and platelets will bind to it: CLOTS form
  • Clots can be inhibited by: Antithrombin, Heparan (which binds to Antithrombin)
  • Prostaglandin & Nitric Oxide: inhibits platelets causing vasodilation
  • When the clot does form, Tissue Plasminogen Activator works on the Plasminogen gives D-dimers
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23
Q

What is coagulation inhibited by?

A
  • Prostaglandins
  • Antithrombin and Heparan
  • Nitric Oxide
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24
Q

What is the role of tissue plasminogen activator?

A
  • Converts plasminogen into plasmin

- Cleaves plasmin into D dimer (a fibrin degradation product)

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25
Q

What is the role of tissue factors?

A

Initiates clotting

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26
Q

What do Von Willebrand factors activate?

A

Activates platelets

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27
Q

Role of Anti-thrombin

A

inhibits clotting

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28
Q

Role of Nitric Oxide

A

Inhibits platelets

29
Q

Role of Prostaglandin I2

A

Inhibits platelets

30
Q

What are the three factors that make up Virchow’s triad (things that will lead to clots)?

A
  1. Stasis: static blood lacks kinetic energy and tends to clot
  2. Hyper-coagulant state: eg. infection/sepsis; genetic predisposition; drugs (e.g. HRT)
  3. Endothelial damage: e.g. surgery or cannula
31
Q

What is the role of valves in veins?

A

Valves prevent the backflow of blood

32
Q

What is the role of muscles in veins?

A

Contraction of nearby muscles squash the veins, acting as a pump and returning the blood back to the heart

33
Q

What can increase the risk of stasis?

A

Blood tends to eddy around valves, increasing the risk

34
Q

How does Deep Vein Thrombosis occur?

A
  • If venous return is blocked, the affected organ becomes congested with fluid
  • Increased hydrostatic pressure, so more filtration: which pushes fluid out
  • The risk is that the thrombosis might be dislodged and make its way back to the heart
35
Q

What are the four possible fates of a thrombus?

A
  1. Resolution: i.e. thrombolysis (breakdown of the thrombus)
  2. Embolism: i.e. thrombus moves to another location and blocks the vessel, usually a smaller vessel preventing blood flow
  3. Organised: i.e. becomes covered by endothelium, in this case you won’t even know if you have one because the vessel just becomes a bit narrower
  4. Recanalized and organized: new vessel, just with more holes
36
Q

What is there a higher risk of in proximal DVT and what are the symptoms?

A
  • There is a higher risk of pulmonary embolism and post-thrombotic syndrome (pain, swelling, maybe even ulcers)
  • these don’t break off
37
Q

What does distal DVT rarely cause?

A
  • rarely cause pulmonary embolism
  • rarely cause post-thrombotic syndrome
  • if it occurs in the lower legs, not as serious because the vessels here are very small
38
Q

What can a small venous thrombolus cause?

A
  • Slight VQ mismatch or small infarct zone

- May be asymptomatic

39
Q

What can a large venous thrombolus cause?

A
  • Saddle embolism blocking both pulmonary arteries

- Can cause rapid death

40
Q

What activates platelets?

A

von Willebrand factors on subendothelial cells

41
Q

What do circulating VWF bind to?

A

exposed subendothelial cells

42
Q

What can also express VWF?

A

Activated subendothelial cells

43
Q

What do activated platelets release?

A
  • Thromboxane A2 (TxA2)
  • Adenosine diphosphate (ADP)
    These induce receptors for fibrinogen
    They behave in a paracrine/autocrine way
44
Q

What does TxA2 and ADP bind to?

A

Bind to receptors on adjacent platelets and increase expression of the glycoprotein complex GPIIb/IIIa

45
Q

How else can platelets be activated?

A

Can also be activated by thrombin, collagen and many other mediators

46
Q

What is the role of fibrinogen?

A

Acts as a tether, holding platelets together (this is platelet aggregation, not blood coagulation)

47
Q

What is fibrinogen and where does it remain?

A

Fibrinogen is the solid precursor to fibrin and is in the circulation

48
Q

What occurs after platelet aggregation?

A

Once you have a clump of platelets, they form a negatively charged surface which is required for coagulation.

  • Charged phospholipids
  • Fibrinogen tethers
49
Q

What is coagulation?

A

Coagulation is the conversion of fibrinogen tethers to fibrin and then the cross-linking of the fibrin clot

50
Q

When is the extrinsic pathway most important?

A

In vivo

51
Q

When is the intrinsic pathway most important?

A

It forms the basis of laboratory tests of coagulation, not so important in vivo, there is some interaction with the extrinsic

52
Q

What occurs at each step during the coagulation pathway?

A
  • Amplification of the signal at each step
  • Multiple steps at which you can inhibit the process
  • Small amounts of activated factors can have a big effect
53
Q

What are the three coagulation pathways?

A
  1. Intrinsic
  2. Extrinsic
  3. Common
54
Q

Describe the common pathway of coagulation

A
  1. Factor IXa activates Factor X by proteolysis to create Factor Xa
  2. Factor Xa cleaves prothrombin to form thrombin (IIa)
  3. Thrombin (IIa) is a protease that cleaves fibrinogen into fibrin. Fibrinogen is a large molecule present in plasma- once cleaved it becomes insoluble fibrin
  4. Fibrinogen promotes blood clotting by forming bridges between, and activating blood platelets through binding to their GpIIb/IIIa surface membrane fibrinogen receptor

TENASE & PROTHROMBINASE

  1. Thrombin cleaves factors V and VII to give Va and VIIIa
  2. Va and VIIIa together with plasma C2+ form:
    • Tenase complex: VIIIa + IXa -> Xa
    • Prothrombinase complex: Va + Xa -> Thrombin
    • These assemble n the charged phospholipid surfaces of the activated platelets

CROSS-LINKING FIBRIN CLOT

  1. Once enough thrombin has been generated, XIII is activated, which cross links the fibrin fibres into a solid clot
55
Q

What is the GLA domain?

A

GLA domain is 10-12 glutamic acids in the N-terminus of the molecule converted to gamma-carboxyglutamic acid (GIa)

56
Q

What is the formation of gamma-carboxyglutamic acid dependent on?

A

It is a vitamin K dependent process

57
Q

What inhibits the production of carboxygutamic residues?

A

Warfarin inhibits the production of carboxygutamic residues

58
Q

What is the significance of the common pathway?

A

It is the bulk of the coagulation pathway

59
Q

What are the common pathway reactions easily overpowered by?

A

Inhibitors

60
Q

Describe the extrinsic pathway

A
  • Tissue factor is a receptor for VIIa, also bound to a negatively charged surface of platelet phospholipids, along with calcium
  • Once activated, the VIIa activates Xa and the common pathway is initiated
  • TF present on most subendothelial cells; exposed if the endothelium is damaged, ready for VIIa to bind to and initiate coagulation
  • Major one happening in vivo and is triggered by tissue factor which activates factor VII and feeds into the common pathway
61
Q

What is the intrinsic pathway activated by?

A

Activates when you put blood into a charged surface such as glass

62
Q

Defects in extrinsic vs intrinsic pathway

A
  • Defects in the factors of the extrinsic pathway have far larger physiological effects than mutations in the enzymes of the intrinsic pathway
  • Laboratory tests distinguish between activating the intrinsic or extrinsic pathways in order to assess where the defect might be
63
Q

What can thrombolytic agents such as tissue plasminogen activator be used for?

A

Some of these thrombolytic agents such as tissue plasminogen activator and related
compounds are used to treat strokes and myocardial infarctions

64
Q

What can inhibit clotting?

A

Antithrombin

65
Q

What is a clot broken down by?

A

Clot is broken down by plasmin which is activated from plasminogen by tPA

66
Q

Where is antithrombin expressed?

A

antithrombin is expressed by endothelial cells

67
Q

What does antithrombin inhibit?

A

antithrombin inhibits a lot of the enzymes in the coagulation cascade, but thrombin and Factor VII in particular

68
Q

What does Heparan bind to and what does this cause?

A

Heparan binds to the enzyme inhibitor antithrombin III (AT) causing a confromational change that results in its activation
- The activated AT then inactivates thrombin, factor Xa and other proteases

Cardiovascular system (16 decks)

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