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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 - immunological response

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2
Q

What does inflammation activate?

A

Inflammation activates coagulation which promotes inflammation

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3
Q

What is primary haemostasis?

A

Aggregation of platelets

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4
Q

What occurs during secondary haemostasis?

A

the conversion of fibrinogen -> fibrin

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5
Q

Summarise fibrinolysis

A
  1. Aggregation of Platelets
    2a. Fibrinogen -> fibrin mesh via thrombin (protease)

2b. Prothrombrin -> thrombin via a culmination of a
cascade of similar activation steps

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6
Q

When do primary / secondary haemostasis occur?

A

These reactions are continuously occurring in the body

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7
Q

Describe the features of arterial thrombosis

A

Results from mostly atheroma rupture or damage to endothelium (e.g. MI / stroke)
Platelet rich ‘white’ thrombosis - mainly primary
May block arteries downstream

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8
Q

Outline the distinctive features of a venous thrombosis

A

Often results from stasis or a hyper-coagulant state (DVT)
Platelet poor ‘red’ thrombosis - mostly secondary
Can move to lungs

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9
Q

Which process is favoured by endothelial cells when damaged?

A

If damaged / inflamed, endothelial cells they may favour coagulation

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10
Q

What is released from the subendothelial cells during coagulation?

A

Subendothelial cells release Von Willebrand Factor or Tissue factor if disturbed

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11
Q

How does the blood ensure clotting doesn’t occur?

A

Many mechanisms are in place to prevent clotting
e.g.
- Binding of Heparan and antithrombin to their
receptors inhibits clotting
- Release of NO inhibits platelet activation

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12
Q

What is the role of tissue plasminogen activator?

A

Tissue plasminogen activator causes:
plasminogen -> plasmin
which lyses on clot forming D dimers

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13
Q

What is Virchow’s Triad?

A

Describes the 3 broad categories of factors that are thought to contribute to thrombosis:

  • stasis
  • hypercoagulant state
  • endothelial damage
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14
Q

How does stasis cause thrombosis?

A

Static blood lacks kinetic energy and tends to clot

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15
Q

What causes a hypercoagulant state to occur?

A 
Infection 
Hereditary drugs (HRT)
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16
Q

What can cause endothelial damage?

A

surgery or canula

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17
Q

What is the role of valves in veins?

A

One way valves prevent backflow of blood

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18
Q

How do veins transport blood back to the heart?

A

Contraction of nearby muscles squashes veins, acting as a pump to return blood to the heart
- low venous pressure aids this mechanism

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19
Q

How is risk of stasis increased around valves?

A

Blood tends to eddy around valves increasing the risk of stasis around the valves

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20
Q

What effect do varicose veins have on valves?

A

Varicose veins compromise valves, causing blood to pool leading to DVT

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21
Q

How does DVT occur?

A

Blocked venous return congests the affected organ with fluid - Pressure increases
More hydrostatic pressure pushes fluid out causing oedema and swelling

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22
Q

What is a major risk of DVT?

A

The thrombosis might become dislodged and make its way back to the heart

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23
Q

What is the fate of a thrombus?

A
  • Resolution: resolves completely
  • Embolism: usually lodges in smaller vessels blocking
    blood flow
  • Organised: endothelium can grow over thrombus;
    reducing stretchiness of vessel
  • Recanalised & Organised
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24
Q

Which vessels does a proximal DVT affect?

A 
Common femoral v.
Femoral V.
Great saphenous V.
External Iliac V.
Deep femoral v.
popliteal v.
  • Higher risk of pulmonary embolism and post- thrombotic syndrome
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25
Q

Which vessels does a distal DVT potentially affect?

A

small saphenous v.

posterior & anterior tibial veins

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26
Q

What is post-thrombotic syndrome?

A

when a thrombus remains and continuously blocks blood flow for a longer duration

27
Q

What are the consequences of post-thrombotic syndrome?

A

Inflammation along with damage to the venous valves from the thrombus itself

Valvular incompetence combined with persistence venous obstruction inducing:

  • rupture of small superficial veins
  • subcutaneous haemorrhage
  • increased tissue permeability
28
Q

What is a pulmonary embolism?

A

When an embolism returns to the lung via the right side of the heart

29
Q

Describe the route taken by a pulmonary embolism

A

RA -> RV -> PA -> Lungs

30
Q

Describe the pathology of a distal DVT

A
  • rarely causes pulmonary embolism
  • rarely causes post-thrombotic syndrome
  • Not as serious as the thrombus is moving from area of
    small vessels to larger vessel so has smaller effect
31
Q

What is the fate of a venous thrombus in the lungs?

A
  • Asymptomatic

- Can cause sudden death

32
Q

Describe what occurs when a thrombolus may be asymptomatic

A
  • small venous thrombolus
  • slight V/Q mismatch
  • or slight Infarct zone
33
Q

What reasons could cause a venous thrombolus to cause sudden death ?

A
  • large venous thrombolus

- saddle embolism blocks pulmonary arteries

34
Q

What causes a saddle embolism?

A

Thrombus from femoral artery can cause saddle embolism

35
Q

How are Platelets are activated ?

A
  1. Von Willebrand factor on subendothelial cells (or
    activated endothelial cells) activates platelets
  2. Activated platelets release TxA2 - thromboxane & ADP
    • inducing receptors for fibrinogen
  3. TxA2 & ADP bind to receptors on adjacent platelets
    increasing GpIIb/IIIa expression
  4. Collagen, thrombin & many other mediators activate
    platelets
36
Q

What causes platelet adherence?

A

Fibrinogen acts as a tether, holding platelets together

37
Q

What is fibrinogen?

A

The soluble precursor to Fibrin present in circulation

38
Q

What is required for successful coagulation?

A

A negatively charged platelets surface

39
Q

What provides a negative platelet surface for coagulation to occur?

A

The clump of activated platelets provides the negative surface

40
Q

What is coagulation?

A

Coagulation involves:

  1. conversion of fibrinogen -> fibrin
  2. cross-linking the clot
41
Q

What are the pathways involved in coagulation?

A

Intrinsic Pathway
Extrinsic Pathway
Common Pathway

42
Q

Explain how the 3 coagulation pathways come together

A

Extrinsic pathway is the most significant in vivo
Intrinsic pathway forms the basis of lab tests of coagulation and has some interaction with the extrinsic pathway
- come together to common pathway (activating Fx)

43
Q

Describe the features of the coagulation pathways

A
  • Amplification of signals at each step
  • Process can be inhibited at multiple steps
  • Small amounts of activated factors cause big effects
  • Factors constantly circulate blood
44
Q

Outline the steps of Intrinsic & Extrinsic pathways leading to the Common Pathway

A
  1. Factor iXa activates Factor X by proteolysis -> FXa
  2. FXa cleaves prothrombin -> thrombin (FIIa)
  3. Thrombin (FIIa) cleaves fibrinogen -> fibrin
45
Q

How does fibrinogen promote blood clotting?

A

Is converted to fibrin
Also forms bridges between and activating blood platelets by binding to their GPIIb/IIIa surface membrane fibrinogen receptor

46
Q

Outline the stages of the final Common Pathway

A
  1. Thrombin cleaves Factors V and VIII -> FVa + FVIIIa
  2. FVa + FVIIa with plasma Ca2+ form:

Tenase Complex:
- FVIIIa + FIXa -> FXa

Prothrombinase Complex
- FVa + FXa -> thrombin

  1. Once enough thrombin produced, FXIIIa cross-links
    fibrin fibres into solid clots
  2. Once activated FVIIIa activates FXa => inhibiting
    common pathway
47
Q

What is tissue factor?

A

Receptor for FVIIIa also bound to a negatively charged surface of a platelet phospholipids, along with Ca2+

48
Q

Where is tissue factor found?

A

TF is present on most subendothelial cells and is exposed if the endothelium is inhibited - ready for FVIIIa to bind

49
Q

What is the role of Tissue factors?

A

Assemble on the charged phospholipid surfaces of the activated platelets. FVIIIa and FVa amplify existing reactions making them harder to overcome

50
Q

What is the function of warfarin?

A

an anticoagulant that inhibits the production of carboxyglutamic residues

51
Q

Describe the features of the prothrombinase complex

A

Factor Xa is bound to negatively charged platelet via GLA

52
Q

What is GLA?

A

GLA domain is 10 - 12 glutamic acids in the N-terminus of the molecule converted to ɣ-carboxyglutamic acid
-> Vitamin K dependent process

53
Q

What is the significance of coagulation pathways in the laboratory?

A

The common pathway is the bulk of the coagulation pathway - traditionally activated in the lab; still reflected in the way initiation pathways are described

Intrinsic & Extrinsic pathways represent laboratory tests still carried out today to assess coagulation

54
Q

Describe what occurs in the extrinsic pathway

A

TF: receptor for VIIa, also bound to negatively charged platelet phospholipids surface along with calcium.

Once activated, VIIa activates Xa and the common pathway is initiated.
TF present in subendothelial cells;
exposed if endothelium is damaged, ready for VIIa to bind to & initiate coagulation.

Major one happening in vivo
triggered by tissue factor which activates factor VII and feeds into the common pathway.

55
Q

Summarise the intrinsic Pathway

A

Activated when blood placed onto a charged surface such as glass.

56
Q

Explain the consequence of defects in the pathways

A

Defects in the factors of the extrinsic pathway have far larger physiological effects than mutations in the enzymes of the intrinsic pathway.

57
Q

How would we detect where a defect is present in the pathways?

A

Laboratory tests distinguish between activating the intrinsic or extrinsic pathways in order to assess where a defect may be.

58
Q

Explain the use of thrombolytic agents

A

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

59
Q

What is the role of tissue plasminogen activator?

A

Converts plasminogen -> Plasmin

60
Q

What is the function of antithrombin?

A

Inhibits a lot of the enzymes in the coagulation cascade but thrombin and Factor VII in particular

61
Q

Where is antithrombin found?

A

Expressed by endothelial cells

62
Q

What is the role of Heparan?

A

Heparan binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation

63
Q

What does activated AT do?

A

The activated AT then inactivates thrombin, factor Xa and other proteases

Cardiovascular System (16 decks)

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