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Physiology 1 > Thrombosis- Haemostatis In The Wrong Place > Flashcards

Thrombosis- Haemostatis In The Wrong Place Flashcards

1
Q

What is primary haemostasis?

A

Aggregation of platelets

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2
Q

What is secondary haemostasis?

A

The conversion of fibrinogen into fibrin

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3
Q

What are the three basic steps of fibrinolysis?

A

1- aggregation of platelets
2- fibrinogen -> fibrin mesh by thrombin
3- thrombin is itself converted from prothrombin

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4
Q

What do anticoagulants do?

A

Prevent thrombosis

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5
Q

What does fibrinolysis do?

A

Reverses thrombosis

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6
Q

What are the three main features of arterial thrombosis?

A

Mostly result from atheroma rupture or damage to the endothelium.
Mostly primary, platelet rich ‘white’ thrombosis
May block downstream arteries

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7
Q

What are the main features of venous thrombosis?

A

Often results from stasis or a hypercoagulant state
Mostly secondary, platelet poor ‘red’ thrombus
May move to lungs

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8
Q

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

A

The blood may either coalesce around it and form a clot or von willebrand factors will bind to platelets and start a clot

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9
Q

What does heparin bind to?

A

Antithrombin

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10
Q

What do antithrombin and heperan do?

A

Inhibit clotting prostaglandins, platelets and nitric oxide

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11
Q

What does tissue plasminogen activator cause?

A

Plasminogen to be converted to plasmin, which acts in the clot to give D-dimers

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12
Q

What are d-dimers?

A

Breakdown products of a clot

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13
Q

What are the components of Virchows triad?

A

Stasis, endothelial damage and the hypercoagulant state

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14
Q

How does stasis cause clotting?

A

Static blood lacks kinetic energy and tends to clot

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15
Q

How does endothelial damage lead to clotting?

A

When you have surgery or a cannula you are exposing the subendothelial cells

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16
Q

When may you be in a hypercoagulant state?

A

In infection/ sepsis, drugs or if you have a genetic predisposition

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17
Q

Why is there an increased risk of stasis around venous valves?

A

The blood eddys around them so doesn’t move as efficiently

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18
Q

What happens if venous return is blocked?

A

The affected organ becomes congested with fluid and there is an increased pressure so more filtration

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19
Q

What are the four fates for a thrombus?

A

Resolution, embolism, organised or recanalised and organised

20
Q

What happens when a thrombus is resolved?

A

Thrombolysis

21
Q

What happens when a thrombus embolises?

A

Moves to another location and blocks the vessel

22
Q

What happens when a thrombus is organised?

A

Becomes covered by the endothelium

23
Q

What are the risks with a proximal DVT?

A

Higher risk of pulmonary embolism and post-thrombotic syndrome

24
Q

What are symptoms of proximal DVT?

A

Pain, swelling and maybe even ulcers

25
Q

Where are proximal DVTs found?

A

Upper leg

26
Q

Where are distal DVTs found?

A

Lower leg

27
Q

What are the risks of distal DVT?

A

Not much- they rarely cause PE or post-thrombotic syndrome

28
Q

What is post-thrombotic syndrome?

A

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

29
Q

What causes post thrombotic syndrome?

A

Valvular incompetence combined with a persistent venous obstruction

30
Q

What does post thrombotic syndrome induce?

A

Rupture of small superficial veins, subcutaneous haemorrhage and an increase of tissue permeability

31
Q

What symptoms follow post-thrombotic syndrome?

A

Pain, swelling, discolouration and even ulceration

32
Q

What causes pulmonary embolus?

A

Small venous thrombolus getting through the heart and caught in the lung

33
Q

What happens in platelet adherence?

A
  • von willebrand factors on subendothelial cells activate platelets
  • circulating von willebrand factors may bind to exposed subendothelial cells
  • activated endothelial cells can also express von willebrand factors
34
Q

What happens in platelet activation?

A
  • activated platelets release thromboxane A2 and adenosine disphosphate which induce receptors for fibrinogen
  • bind to receptors and increase expression of GPIIb/IIIa
  • platelets can also be activated by thrombin, collagen and many other mediators
35
Q

What happens in platelet aggregation?

A

Fibrinogen acts as a tether holding platelets together- it is the soluble precursor to fibrin and is in the circulation

36
Q

What happens in platelet substrate for coagulation?

A
  • clumps of platelet form a negatively charged surface

- coagulation involves the conversion of fibrinogen to fibrin and then cross linking the fibrin clot

37
Q

What are the 7 steps in the common coagulation pathway?

A

1- factor IXa activates factor X by proteolysis to create factor Xa
2- factor Xa cleaves prothrombin to form thrombin (IIa)
3- thrombin cleaves fibrinogen into fibrin
4- fibrinogen promotes blood clotting by forming bridges between (and activating) blood platelets through binding to their GPIIb/IIIa surface membrane fibrinogen receptor
5- thrombin cleaves factors V and VIII to give Va and VIIIa
6- Va and VIII together with Ca2+ form a tenase complex and a prothrombinase complex
7- once enough thrombin has been generated, XIII is activated, which cross links the fibrin fibres into a solid clot

38
Q

What do VIIIa and Va amplify?

A

The existing reactions making them hard to overpower

39
Q

What is a GLA domain?

A

10-12 glutamic acids on the N-terminus of the molecule converted to gamma carboxy glutamic acid

40
Q

What is the GLA domain dependant on?

A

Vitamin K

41
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. Then VIIa activated Xa and the common pathway starts

42
Q

What is the extrinsic pathway triggered by?

A

Transcription factors which activates factor VII

43
Q

When is the intrinsic pathway activated?

A

When you put blood onto a charged surface (like glass)

44
Q

What do lab tests distinguish between?

A

Activating the intrinsic or extrinsic pathways in order to assess where a defect may be

45
Q

What is antithrombin expressed by?

A

Endothelial cells

46
Q

What does antithrombin inhibit?

A

A lot of the enzymes in the coagulation cascade

Physiology 1 (65 decks)

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