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Physiology 1 : cardiovascular > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

What does coagulation prevent?

A

→Blood loss

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2
Q

What is coagulation?

A

→An immunological response

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3
Q

What do anticoagulants prevent?

A

→ Thrombosis

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4
Q

What are the steps for the contact activation pathway?

A

Factor 12 → activated factor 12
activated factor 12 → Activated factor 11
Activated factor 11 → Activated factor 9
Activated factor 9 → Activated factor 10
Pro thrombin → Thrombin

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5
Q

What is the intrinsic pathway activated by?

A

→ Damaged surfaces

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6
Q

What are the steps for the extrinsic pathway?

A

Factor 7 → activated factor 7
Tissue factor → activated factor 10
Prothrombin → Thrombin

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7
Q

What is the extrinsic pathway activated by?

A

→ trauma

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8
Q

What is reverse thrombosis?

A

→ Fibrinolysis

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9
Q

What happens when tissue is damaged/inflammation?

A

→ Platelets become activated

→ Fibrinogen turns into fibrin

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10
Q

What does arterial thrombosis result from?

A

→ Atheroma rupture or damage to the endothelium

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11
Q

What is arterial thrombosis described as?

A

→ Platelet rich ‘white’ thrombosis

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12
Q

What can arterial thrombosis do to arteries downstream?

A

→ May block arteries downstream

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13
Q

What does venous thrombosis result from?

A

→ From stasis or a hypercoagulant state DVT

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14
Q

What is venous thrombosis described as?

A

→ Platelet poor ‘red’ thrombosis

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15
Q

What can venous thrombosis do?

A

→ move to the lungs

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16
Q

What do endothelial cells express?

A

→ Factors inhibiting coagulation

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17
Q

What does tissue plasminogen activator do?

A

→ Activates Plasminogen to Plasmin

→ Plasmin carries out lysis of the clot to D Dimers.

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18
Q

What do subendothelial cells release if they are disturbed?

A

→ Tissue factor

→ Von Willebrand Factor

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19
Q

What is Virchow’s triad?

A

STASIS
→ Static blood lacks kinetic energy and tends to clot

HYPER-COAGULANT STATE
→ Infection, hereditary or drugs (HRT)

ENDOTHELIAL DAMAGE
→Surgery or cannula

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20
Q

What do valves do?

A

→ Prevent backflow of blood

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21
Q

How is blood returned to the heart in veins?

A

→ Contraction of nearby muscles squash veins

22
Q

What does blood do around valves?

A

→ Tends to eddy around valves which increases the risk of stasis

23
Q

What is DVT?

A

→ If a venous return in blocked the affected organ becomes congested with fluid

24
Q

What is the difference between distal DVT and proximal DVT?

A

→ Distal rarely causes pulmonary embolism

→ Proximal has a higher risk of pulmonary embolism

25
Q

What are the 4 things that can happen to a thrombus?

A

RESOLUTION
→ thrombolysis

EMBOLISM
→ moves to another location + blocks vessel

ORGANIZED
→ becomes covered by endothelium

RECANALISED AND ORGANISED

26
Q

What happens with a small venous thrombolus?

A

→ Slight VQ mismatch or small infarct zone

27
Q

What happens with a large venous thrombolus?

A

→ Saddle embolism blocks both arteries

→ can cause rapid death

28
Q

How does platelet adherence happen?

A

→ VWF on subendothelial cells activates/binds platelets
→ Circulating VWFs may bind to exposed subendothelial cells
→ Activated endothelial cells can express VWF

29
Q

How does platelet activation happen?

A

→ Platelets release thromboxane A2 and ADP
→ Thromboxane A2 and ADP induce receptors for fibrinogen
→Platelets can also be activated by thrombin and collagen

30
Q

What holds platelets together?

A

→ Fibrinogen acts as a tether holding platelets together

31
Q

What is required platelet wise for successful coagulation?

A

→Negatively charged platelet surfaces

→ Charged phospholipids are required

32
Q

How does the common pathway happen?

A

→ Factor 9A activates factor 10 by proteolysis to make factor 10A
→ factor 10A cleaves prothrombin to form thrombin
→thrombin (protease) cleaves fibrinogen into fibrin
→ Fibrinogen becomes insoluble fibrin
→ Thrombin cleaves factor 5 and 8 to give 5A and 8A

33
Q

What is the tenase complex?

A

→ 8A + 9A = 10 A

34
Q

What is the prothrombinase complex?

A

→ 5A + 10A = Thrombin

35
Q

How does fibrinogen promote blood clotting ?

A

→ Forms bridges between and activates platelets through binding to GPIIB fibrinogen receptors

36
Q

What does warfarin inhibit?

A

→ production of carboxyglutamic residues

→ by inhibiting vitamin K

37
Q

How does a solid clot form?

A

→ Once enough thrombin has been generated

→ Factor 13 is activated which cross-links the fibrin fibres into a solid clot

38
Q

What is the common pathway?

A

→ The bulk of the coagulation pathway

39
Q

How is the common pathway initiated via the extrinsic?

A

→TF is a receptor for Factor 7A
→ Bound to a -vely charged surface of platelet phospholipids along with calcium
→Once activated Factor 7A activates Factor 10A and the common pathway starts

40
Q

Where is TF present?

A

→ Present on most sub-endothelial cells

41
Q

When is TF exposed?

A

→ When the endothelium is damaged

42
Q

How does anti thrombin work?

A

→ Inhibits clotting in the first place.
→ Inhibits many enzymes in coagulation cascade.
→ Particulary inhibits Thrombin and Factor 7.
→ Heparan binds to and activates anti thrombin.

43
Q

Why are d dimers measured clinically?

A

→ measured to see the level of thrombolysis

→ Degradation products of thrombuses are D dimers

44
Q

Describe Tissue Plasminogen Activator and its’ function:

A

→ Tissue Plasminogen activator activates Plasminogen into Plasmin.
→ Plasmin causes Fibrinolysis of the Fibrin Clot into D - Dimers.
→ tPA can be used therapeutically in the treatement of clots.
→ tPA is an inherent anti thrombolytic

45
Q

What exactly does the Plasmin break down during lysis of the clot?

A

→ It breaks down the fibrin cross linkages between the platelets.

46
Q

What do ADP and Thromboxane A2 do?

A

→ Induce receptors for fibrinogen GP2B and GP3A

47
Q

What is endocrine?

A

→ hormone released and moves somewhere else in the body

48
Q

What is paracrine?

A

→A cell releases a hormone and it goes to the adjacent cell

49
Q

What is autocrine?

A

→ releases a hormone that activates itself

50
Q

Why is it called the coagulation cascade?

A

→ Amplification of the signal at each step
→Multiple steps where you can inhibit the process
→Small amounts of activated factors can have a big effect

51
Q

How is factor 10 bound to the -vely charged phospholipids and what is needed for this?

A

→ Factor 10 is bound to the -vely charged phospholipid by the GLA domain
→ To make the GLA domain vitamin K is needed

Physiology 1 : cardiovascular (18 decks)

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