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Topics in Medical Biosciences > Platelets and clotting > Flashcards

Platelets and clotting Flashcards

1
Q

What are the 4 components of Haemostasis?

A
  1. Blood vessel vasoconstriction
  2. Platelets
  3. Coagulation
  4. Fibrinolysis
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2
Q

What happens during step 1 of haemostasis?

A
  1. Blood vessel injury induces vasoconstriction
    - nervous reflex
    - releases serotonin, thromboxane A2 from activated platelets and fibrinopeptides
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3
Q

Describe platelet structure?

A
  • surface glycoproteins
    (important for activation)
  • an open membrane system
    (provides large surface to which coagulation proteins are absorbed)
  • storage granules
    (discharged on activation)
  • rich in signalling and cytoskeletal proteins
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4
Q

What do platelets do in the body?

A
  1. platelets monitor blood vessel integrity
    - damage exposes the sub-endothelial layer in vessels and the site of injury is exposed
    - platelets then plug hole at site of injury forming a platelet clot or thrombus
    - activated platelets fight infection and promote repair (release of chemokines, cytokines and growth factors)
    - activated platelets also promote coagulation by using a negatively charged phospholipid surface to recruit coagulation factors
    (using phosphatidylserine that flips from inner membrane to the outer of the plasma membrane)
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5
Q

What morphology change is seen during platelet activation?

A

Circular to star shaped to egg shapes (from resting to activated)

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6
Q

What is the mechanism by which platelets undergo adhesion and aggregation?

A
  1. A break in the endothelial lining allows initial adherence of platelets to exposed connective tissue. It adheres to the connective tissue either directly through Glp1a, or more importantly, the platelet uses Glp1b to adhere to Von Willebrand Factor (vWF) already adhered to the connective tissue.
  2. Collagen & thrombin at site of injury cause platelets to release granules: ADP, serotonin, fibrinogen, lysosomal enzymes and heparin-neutralising factor. Binding to collagen also activates platelet prostaglandin synthesis leading to the formation and release of thromboxane A2.
    - causing a positive feedback cycle
  3. Thromboxane A2 potentiates platelet release reactions, platelet aggregation & vasoconstriction. Platelets aggregate and attach onto each other through glycoproteins IIb/IIIa.
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7
Q

What does GPIb-IX-V bind to?

A

vWF

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8
Q

What does GPVI bind to?

A

Collagen

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9
Q

What happens during coagulation?

A
  1. activation of coagulation factors on tissue factor, collagen and platelet surface
  2. Dramatic amplification cascade
  3. Thrombin generation
  4. Converts soluble plasma fibrinogen into fibrin
  5. Fibrin enmeshes the platelet aggregate, stabilising the clot
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10
Q

Name 3 coagulation factors?

A

serine proteases, cofactors and calcium

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11
Q

What is blood coagulation initiated by?

A

Tissue Factor (FT) which is a transmembrane protein.

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12
Q

Where is tissue factor usually expressed?

A

Smooth muscle cells
fibroblasts
activated endothelial cells

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13
Q

What is the extrinsic pathway?

A

Generates small amount of thrombin after factor 7a is activated. Starts due to the damage.
Factor 7a cleaves the serine protease factor X (10). Bind to factor Va (5a) which cleaves prothrombin to thrombin.

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14
Q

Which pathway generates the most thrombin?

A

the Intrinsic pathway

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15
Q

What is the intrinsic pathway?

A

Generates lots of thrombin. Positive feed back occurs. Thrombin generates Factor VIII (8). Factor VIII activates more Factor X. Thrombin also activates Factor X1 (11) Factor V that feeds into Factor Xa.

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16
Q

What does Thrombin do?

A

Thrombin will cut fibrinogen. Cause fibrin to polymerase. Factor XIII (13) covalently crosslinks fibrin - to create mesh work for the platelet plug. Making the platelet plug resistant to being pulled away by the blood.

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17
Q

How does clot retraction work?

A

It is mediated by the integrin ALPHAIIbBETA3 which links fibrin to the platelet actin cytoskeleton. Plug then begins to auto digest by the process of fibrinolysis.

18
Q

What can limit coagulation to the site of injury?

A

coagulation inhibitors - tissue factor pathway inhibitor (TFPI)
protein C and S inhibit the intrinsic pathway - activated by thrombin
antithrombin in plasma inhibits thrombin

19
Q

What is fibrinolysis?

A

Plasmin degradation of fibrin to fibrin degradation products. Plasmin comes from Plasminogen (which is usually present in the blood) by being activated by a Tissue plasminogen activator (a serine protease).

20
Q

What are common coagulation disorders?

A

Haemophilia A - factor VIII deficiency
Haemophilia B - factor IX deficiency
von Willebrand disease - vWF deficiency

21
Q

What is Haemophilia A?

A

Disorder where factor VIII is defective or missing and so does not activate factor X. Affects males. Bleeding tendencies.

22
Q

What treatment is used for Haemophilia A?

A

Treatment with recombinant factor VIII

23
Q

What is Haemophilia B?

A

Deficiency of factor IX - mutations. Fails to generate fibrin meshwork. X-linked so affects males.

24
Q

What treatment is used for Haemophilia B?

A

Treatment with recombinant factor IX

25
Q

What is von Willebrand disease?

A

Common disorder due to mutation that lowers vWF or no vWF is present. Bleeding tendencies. Affects factor VIII - affects coagulation and tethering.

26
Q

What treatment is used for von Willebrand disease?

A

Treatment to increase vWF production, vWF, anti-fibrinolytics

27
Q

What is thrombosis?

A

unwanted formation of a blood clot in the vessels (can block the vessels)

28
Q

What is arterial thrombosis caused by?

A

Typically caused by vessel disease leading to atherosclerotic plaque rupture (platelets)

29
Q

What is venous thrombosis due to?

A

Slow blood flow, endothelial dysfunction or altered blood properties (coagulation)

30
Q

What is the initiation and progression of atherosclerosis?

A
  1. There are fatty deposits/ cholesterol LDL’s
  2. An intermediate Lesion occurs
    - lesion is very vulnerable to rupture
    - immune cells try to clear the deposits which forms an inflammatory immune response (T cells come in)
    - Smooth muscle cells form a cap
  3. Advanced obstructive lesion occurs
    - rupture of the cap
    - endothelial cells undergo apoptosis
    - necrotic core occurs
31
Q

How can atherosclerosis cause a heart attack?

A

Atherosclerosis build up with a blood clot, causing a heart attack

32
Q

What is deep vein thrombosis?

A

A blood clot that develops within a deep vein in the body, usually in the leg.

33
Q

How can atherosclerosis cause a stroke?

A

Blood clot stops the flow of blood to an area of the brain.

34
Q

What are the causes of arterial thrombosis?

A
  • environment/ lifestyle
    (high blood cholesterol, physical inactivity, smoking, high blood pressure)
  • inherited
    (strong familial tendency, multiple gene responsible)
35
Q

What are statins used for?

A

Cholesterol lowering drugs used to treat atherosclerosis

36
Q

What is used as treatment of arterial thrombosis?

A

standard treatment is aspirin and clopidogrel.
Voropaxar has recently been approved as a thrombin receptor.
Integrin inhibitors have high bleeding risk in long term use

37
Q

Name some percutaneous coronary interventions.

A

Angioplasty (stenting). Stent with un-inflated balloon. Stent on inflated ballon. Remove balloon and expanded stent is in place.

38
Q

What are the aims of anti-platelet therapy?

A
  • to not completely inhibit the platelet response

- effectiveness balanced with acceptable bleeding risk

39
Q

What are the main inherited risk factors for venous thrombosis?

A
  • Factor V Leiden (activated protein C resistance)
  • Protein C, protein S or antithrombin deficiency
  • Prothrombin polymorphism (increased levels)
40
Q

What are the main acquired risk factors for venous thrombosis?

A
  • prolonged immobility (happens post op - during bed rest)
  • cancer
  • contraceptive pill and hormone replacement therapy
  • heart failure
  • varicose veins
41
Q

How does a pulmonary embolism happen?

A

If pieces of the clot from a deep vein thrombosis break off (embolisation) and lodge in the lungs - causes death

42
Q

What treatment is available for venous thrombosis?

A

Warfarin
- vitamin K antagonist
Heparin
- activated anti-thrombin

Topics in Medical Biosciences (12 decks)

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