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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
What are the 4 things that can happen to a thrombus?
RESOLUTION → thrombolysis EMBOLISM → moves to another location + blocks vessel ORGANIZED → becomes covered by endothelium RECANALISED AND ORGANISED
26
What happens with a small venous thrombolus?
→ Slight VQ mismatch or small infarct zone
27
What happens with a large venous thrombolus?
→ Saddle embolism blocks both arteries | → can cause rapid death
28
How does platelet adherence happen?
→ VWF on subendothelial cells activates/binds platelets → Circulating VWFs may bind to exposed subendothelial cells → Activated endothelial cells can express VWF
29
How does platelet activation happen?
→ Platelets release thromboxane A2 and ADP → Thromboxane A2 and ADP induce receptors for fibrinogen →Platelets can also be activated by thrombin and collagen
30
What holds platelets together?
→ Fibrinogen acts as a tether holding platelets together
31
What is required platelet wise for successful coagulation?
→Negatively charged platelet surfaces | → Charged phospholipids are required
32
How does the common pathway happen?
→ 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
What is the tenase complex?
→ 8A + 9A = 10 A
34
What is the prothrombinase complex?
→ 5A + 10A = Thrombin
35
How does fibrinogen promote blood clotting ?
→ Forms bridges between and activates platelets through binding to GPIIB fibrinogen receptors
36
What does warfarin inhibit?
→ production of carboxyglutamic residues | → by inhibiting vitamin K
37
How does a solid clot form?
→ Once enough thrombin has been generated | → Factor 13 is activated which cross-links the fibrin fibres into a solid clot
38
What is the common pathway?
→ The bulk of the coagulation pathway
39
How is the common pathway initiated via the extrinsic?
→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
Where is TF present?
→ Present on most sub-endothelial cells
41
When is TF exposed?
→ When the endothelium is damaged
42
How does anti thrombin work?
→ 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
Why are d dimers measured clinically?
→ measured to see the level of thrombolysis | → Degradation products of thrombuses are D dimers
44
Describe Tissue Plasminogen Activator and its' function:
→ 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
What exactly does the Plasmin break down during lysis of the clot?
→ It breaks down the fibrin cross linkages between the platelets.
46
What do ADP and Thromboxane A2 do?
→ Induce receptors for fibrinogen GP2B and GP3A
47
What is endocrine?
→ hormone released and moves somewhere else in the body
48
What is paracrine?
→A cell releases a hormone and it goes to the adjacent cell
49
What is autocrine?
→ releases a hormone that activates itself
50
Why is it called the coagulation cascade?
→ 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
How is factor 10 bound to the -vely charged phospholipids and what is needed for this?
→ 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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