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SGUL - Physiology 1 > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

Why does coagulation occur?

A

Immunological response
- Prevents blood loss

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2
Q

Describe arterial thrombosis.

A
  • Mostly result from an atheroma rupture or damage to the endothelium (eg. MI, stroke)
  • Platelet-rich thrombosis - mostly primary haemostasis
  • May block downstream arteries - since they become narrower and more likely to be obstructed
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3
Q

Describe venous thrombosis

A
  • Often results from stasis or a hyper-coagulant state (eg. DVT)
  • Platelet-poor thrombus - mostly secondary haemostasis
  • May move to the lungs
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4
Q

List some factors/substances that affect the coagulation-fibrinolysis balance. PART 1

A
  • Tissue plasminogen activator: initiates fibrinolysis
  • von Willebrand factor: activates platelets - in coagulation
  • Tissue factor: initiates clotting - in coagulation
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5
Q

List some factors/substances that affect the coagulation-fibrinolysis balance. PART 2

A
  • Antithrombin: inhibits clotting
  • Prostaglandin I2: inhibits platelets
  • Nitric oxide: inhibits platelets
    INVOLVED IN FIBRINOLYSIS
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6
Q

What is Virchow’s Triad?

A

Describes the three categories that are thought to contribute to thrombosis

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7
Q

What are the components of Virchow’s Triad?

A
  • STASIS: static blood lacks kinetic energy and tends to clot
  • HYPER-COAGULANT STATE: eg. infection e.g sepsis, hereditary, drugs (eg. HRT)
  • ENDOTHELIAL DAMAGE: eg. surgery or cannula
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8
Q

How are the valves involves in stasis?

A

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

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9
Q

What are the four possible fates of a thrombus?

A
  • RESOLUTION
  • EMBOLISM
  • ORGANISED
  • RECALANISED AND ORGANISED
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10
Q

What occurs during resolution?

A

Fibrinolytic system destroys the whole clot over time

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11
Q

What occurs during embolism?

A
  • Thrombus dislodges and goes to the heart/lungs
  • This is life threatening
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12
Q

What occurs during organisation?

A
  • Endothelial cells grow over the clot
  • Person more prone to having another clot due to the narrower vein
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13
Q

What occurs during recalanisation?

A
  • Thrombus is so big that it can’t be grown over
  • Can be grown through
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14
Q

What is the difference between a proximal DVT and a distal DVT?

A

With a proximal DVT, there is a higher risk of a pulmonary embolism and post-thrombotic syndrome.
- Rare in distal DVT

MINOR DIFFERENCE: Proximal affects upper leg. Distal affects lower leg.

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15
Q

What does a platelet release when it has been activated?

A

Releases thromboxane A2 and adenosine diphosphate (ADP)
- Both induce receptors for fibrinogen.

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16
Q

Describe the common pathway. PART 1

A
  • Factor IXa activates Factor X by proteolysis to create Factor Xa.
  • Factor Xa (FXa) cleaves prothrombin to form thrombin (FIIa).
  • Thrombin (FIIa) is a protease that cleaves fibrinogen into fibrin.
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17
Q

Describe the common pathway. PART 2

A
  • Thrombin cleaves Factors V and VIII to give FVa and FVIIIa. This is known as amplification. It can also activate platelets.
  • FVa and FVIIIa together with Ca2+ form the tenase complex and prothrombinase complex
  • These complexes assemble on the negatively charged phospholipid surfaces in the activated platelets.
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18
Q

What does fibrinogen promote?

A
  • Blood clotting by activating, blood platelets through binding to their GpIIb/IIIa surface membrane fibrinogen receptor
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19
Q

Describe the prothrombinase complex.

A
  • Negative surface of the activated platelet causes calcium, prothrombin and Factor Xa and Va to bind.
  • Components all bind by a particular domain of glutamic acids (GLA); they stabilise the complex. Synthesis is Vitamin K dependent.
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20
Q

What can formation of the GLA domain be inhibited by?

A

Warfarin

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21
Q

What is fibrinolysis?

A

The breakdown of fibrin into fibrinogen
- Reverse of coagulation

22
Q

How does coagulation occur?

A
  • When endothelial cells become damaged/inflamed they favour coagulation
  • Subendothelial cells release Von Willebrand factors
  • Von Willebrand factors activate platelets and tissue factors initiate clotting
23
Q

How is coagulation inhibited?

A
  • Endothelial cells release nitric oxide which inhibit platelets
  • Also produce prostaglandin 12 which inhibits platelet activation
  • Endothelial cells express heparan and when bound to antithrombin, inhibits clotting
24
Q

What can happen as a result of thrombosis in the leg?

A
  • Blocks venous return causing the leg to become congested with fluid
  • Increases capillary pressure so filtration increases. Causes oedema
  • Hypoxia may occur as some cells are not supplied with oxygen
  • Thrombosis might become dislodged and make its way to the heart
25
Q

What happens during post-thrombotic syndrome? PART 1

A
  • Occurs when a big vein is blocked by a clot
  • Causes inflammation along with damage to valves from the thrombus
  • Causes valvular incompetence which combines with persistent venous obstruction to cause small superficial veins to haemorrhage
26
Q

What happens during post-thrombotic syndrome? PART 2

A
  • Increase in tissue permeability leading to oedema (swelling) due to release of inflammation factors
  • Pain, swelling and ulceration follows
27
Q

What happens when a small venous thrombus reaches the heart? PART 1

A
  • Highly unlikely to be lodged in the heart
  • Will pass through the right atrium and ventricle into the pulmonary artery and reach the lungs
  • Pass down the arterioles and may get lodged blocking these arterioles.
28
Q

What happens when a small venous thrombus reaches the heart? PART 1

A
  • Leads to the formation of a slight VQ mismatch - area of the lung that is not perfused but is well ventilated
  • Cause hypoxia and in severe cases will eventually leads to necrosis or oedema
29
Q

What happens when a large venous thrombus reaches the heart?

A
  • Pass through the right atria and the right ventricle
  • Enters the pulmonary artery and becomes lodged
  • Causes embolism that can block both pulmonary arteries
30
Q

How are blood clots formed? PART 1

A
  • Von Willebrand factors bind to and activate platelets.
  • Activated platelets release Thromboxane A2 and Adenosine Diphosphate (ADP)
  • Bind to receptors on adjacent platelets and increases expression of the fibrinogen receptor (a glycoprotein complex)
31
Q

How are blood clots formed? PART 2

A
  • Fibrinogen binds to its receptor and hold the platelets together (called aggregation)
  • Once a few platelets aggregate they form a negatively charged clump where the fibrinogen is converted to fibrin and the fibrin clot is crosslinked (called coagulation)
32
Q

How can subendothelial cells be exposed?

A
  • Tissue damage
  • Release of inflammatory factors
33
Q

What is the purpose of having different pathways leading to the common pathway in blood clotting?

A
  • Allows for the amplification of proteases found
  • One protease can cleave many molecules which can form many proteases
34
Q

Which is more important, the extrinsic or intrinsic pathway?

A

The extrinsic pathway is more important
- It is shown that mutations in the extrinsic pathway have a much bigger effect than mutations of the intrinsic pathway

35
Q

What is the role of tissue plasminogen activator?

A
  • Serine protease found on endothelial cells which catalyses the activation of plasminogen (in circulation) to plasmin.
    -Plasmin then catalyses the breakdown of the cross linked fibrin cloth into fragments called D-dimers
36
Q

What is the role of antithrombin?

A
  • A small protein molecule made by the liver which circulates in the plasma.
  • Binds to heparan, found on endothelial cells, to form active antithrombin which inhibits clotting by inactivating thrombin and other components
37
Q

How are stroke and myocardial infarctions treated?

A

Using thrombolytic agents such as tissue plasminogen activator

38
Q

What is primary haemostasis?

A

Aggregation of platelets

39
Q

What is secondary haemostasis?

A

Conversion of fibrinogen into fibrin

40
Q

What are the three basic steps of fibrinolysis?

A
  • Aggregation of platelets
  • Conversion of fibrinogen to fibrin
  • Thrombin converted from prothrombin
41
Q

What do anticoagulants do?

A

Prevent thrombosis

42
Q

What happens if the endothelial cells get damaged and the subendothelial cells get exposed?

A

von Willebrand factors will bind to platelets and start a clot

43
Q

What do antithrombin and hepsrin do?

A

Inhibit clotting prostaglandins, platelets and nitric oxide

44
Q

What is the extrinsic pathway?

A
  • Tissue factor is a receptor for VIIa which is bound to negatively charged platelet phospholipid surface along with calcium.
  • VIIa activates Xa and the common pathway starts
45
Q

What is the extrinsic pathway triggered by?

A

Transcription factors which activates factor VII

46
Q

RECAP: Why do the veins need valves?

A

Prevent backflow of blood

47
Q

RECAP: What would happen if the veins were to contract?

A

Venous return occurs

48
Q

Describe the process of platelet adherence.

A
  • Von Willebrand factor on subendothelial cells activates platelets.
  • Circulating Von Willebrand factor may bind to exposed subendothelial cells
  • Activated endothelial cells can also express von Willebrand factor
49
Q

Describe the intrinsic pathway.

A
  • Begins in the blood stream. It is basically activated when blood is exposed to collagen (or other damaged surfaces).
  • Activated when you put blood onto a charged surface such as glass.
50
Q

Why are D-dimers measured clinically?

A
  • Measured to see the level of thrombolysis
  • Degradation products of thrombuses are D dimers

SGUL - Physiology 1 (68 decks)

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