Thrombosis Flashcards

1
Q

What does coagulation prevent?

A

Prevents blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does inflammation activate?

A

Inflammation activates coagulation and coagulation promotes inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of response is coagulation?

A

Coagulation is an immunological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is primary haemostasis?

A

Primary haemostasis is the aggregation of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is secondary haemostasis?

A

Secondary haemostasis is the conversion of fibrinogen into fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Surface of what is an important component in coagulation?

A

The surface of platelets is an important component in the process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do anticoagulants prevent?

A

Prevent thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does fibrinolysis reverse?

A

Reverses thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is fibrinogen converted into and by what?

A

Fibrinogen is converted into a fibrin mesh by thrombin which is a protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is thrombin converted from?

A

Prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does arterial thrombosis most result from?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of thrombosis is arterial thrombosis?

A

Platelet-rich “white” thrombosis

o Mostly primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can arterial thrombosis do?

A

May block downstream arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does venous thrombosis often result from?

A

Often results from stasis or a hyper-coagulant state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of thrombosis is venous thrombosis?

A

Platelet-poor “red” thrombus

o Mostly secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where can venous thrombosis move to?

A

May move to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is usually being inhibited?

A

Usually coagulation is being inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is coagulation inhibited by?

A

o Prostaglandins
o Antithrombin and Heparan
o Nitric Oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the tissue plasminogen activator cleave?

A

Cleaves plasmin into D dimer (a fibrin degradation product)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does vonWillebrand factors activate?

A

activates platelets and makes them clump together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does tissue factor initiate?

A

Initiates clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Virchow’s triad?

A

Stasis-Static blood lacks kinetic energy and tends to clot
Endothelial damage-Surgery
Hyper-coagulant state-Infection/sepsis

23
Q

What do valves do in veins?

A

Valves in veins prevent backflow of blood

24
Q

what do nearby muscles of the veins do?

A

Contraction of nearby muscles squashes veins, acting as a pump to return blood to
the heart

25
Q

What does blood do around valves?

A

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

26
Q

Why does DVT occur?

A

If venous return is blocked, the affected organ becomes congested with fluid

27
Q

What happens to pressure in DVT?

A

There is increased pressure so there is more filtration

28
Q

What risk is there in DVT?

A

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

29
Q

What is the fate of thrombus?

A
  • Resolution
  • Embolism
  • Organised
  • Recalled and organised
30
Q

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

A

Higher risk of pulmonary embolism and post-thrombotic
syndrome
- Pain, swelling, maybe even ulcers

31
Q

What does distal DVT rarely cause?

A
  • Rarely cause pulmonary embolism

- Rarely causes post-thrombotic syndrome

32
Q

What can a small venous thrombus cause?

A

A slight VQ(ventilation perfusion) mismatch or small infarct zone

33
Q

what can a large venous thrombus cause?

A

A saddle embolism blocking both pulmonary arteries

34
Q

What activates platelets?

A

Von Willebrand factor on subendothelial cells activates platelets

35
Q

What do circulating VWF bind to?

A

Circulating VWF may bind to exposed subendothelial cells

36
Q

What can also express VWF?

A

Activated endothelial cells can also express VWF

37
Q

What do activated platelets release and what do these bind to?

A

The activated platelets release Thromboxane A 2 (TxA 2 ) & Adenosine diphosphate
(ADP) which induce receptors for fibrinogen
- These bind to receptors on adjacent platelets and increase the expression of the
glycoprotein complex GPIIb/IIIa

38
Q

What else can platelets be activated by?

A

Platelets can also be activated by thrombin, collagen and many other mediators

39
Q

What does fibrinogen act as?

A

Fibrinogen acts as a tether holding the platelets together (this is not blood
coagulation)

40
Q

What is fibrinogen?

A

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

41
Q

What do a clump of platelets form?

A

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

42
Q

Coagulation pathway process

A

See notes

43
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 (Gla)

44
Q

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

A

Vitamin K dependent process

45
Q

What inhibits the production of carboxygutamic residues?

A

warfarin inhibits production of carboxygutamic

residues

46
Q

Extrinsic pathway

A

See notes

47
Q

What is the intrinsic pathway activated by?

A

Activated when you put blood onto a charged surface such as glass

48
Q

Defects in extrinsic vs inttinsic pathway

A

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

49
Q

What can inhibit clotting?

A

Antithrombin inhibits clotting in the first place

50
Q

What is the clot broken down by?

A

The clot is broken down by plasmin which is activated from plasminogen by tPA

51
Q

What are some thrombolytic agents used for?

A

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

52
Q

How its anti-thrombin activated?

A

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

53
Q

What does activated AT do?

A

activated AT then inactivates thrombin, factor Xa and other proteases

54
Q

What is AT expressed by and what does it do?

A

AT is expressed by the endothelial cells and inhibits a lot of the enzymes in the
coagulation cascade but thrombin and FVII in particular