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Topics in medical biosciences > Platelets, clotting, and thrombosis > Flashcards

Platelets, clotting, and thrombosis Flashcards

1
Q

What is haemostasis?

A

The stopping of bleeding

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2
Q

What is thrombosis

A

Unwanted blood clotting

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3
Q

What are the 4 stages of haemostasis

A

Vasoconstriction
Platelet activation
Coagulation cascade and plug formation
Fibrinolysis

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4
Q

Which factors promote vasoconstriction

A

Serotonin and thromboxin a2

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5
Q

Which coagulation component further promotes vasoconstriction

A

Fibrinopeptides

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6
Q

What is the development pathway of a platelet

A

Myeloid stem cell
Megakaryocyte
Proplatelet
Platelet

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7
Q

How many platelets does each megakaryocyte give rise to

A

~1000

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8
Q

What are megakaryocytes

A

Precursor to platelets
Undergone multiple replications where they do not replicate
Can reach 128n

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9
Q

Where do megakaryocytes reside

A

Bone marrow

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10
Q

Where do platelets reside

A

Blood

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11
Q

How does megakaryocyte release platelets into blood

A

Megakaryocyte sticks to sinusoidal endothelial cell
Proplatelet structures elongate off the megakaryocyte and are pushed into the blood vessel
Platelets bud off into flowing blood

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12
Q

What is the role of membrane proteins on platelets

A

Dictate how they respond to environment
Triggers activation

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13
Q

What is the role of open membrane on platelets

A

Canicular membrane created by invaginations of the plasma membrane provides large sa for coagulation proteins to be absorbed

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14
Q

What are the storage proteins in paltelets

A

Alpha granules store big proteins e.g. fibrinogen, factor V, vWF
Dense granules store smaller molecules e.g. calcium ions and serotonin
Storage granules are discharged on activation

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15
Q

What makes up the platelet phospholipid

A

Plasma membrane and open canalicular system

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16
Q

How do non-active platelets reside in blood vessels

A

Platelets are pushed to the side of blood vessel
Endothelial cells release platelet inhibitors PG12, NO, and CD39

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17
Q

How do platelets become activated

A

Damage exposes subendothelial proteins
Platelets cell surface receptors recognise these proteins
Recognition triggers platelet activation

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18
Q

What proteins trigger platelet activation

A

Subendothelial proteins collagen and laminins

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19
Q

How does platelets morphology change as they become activated

A

Filopodia protrusions allow them to stick to site of damage
Sheets of lamellipodia membrane fill in the gaps

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20
Q

Which proteins mediate platelet tethering

A

GP1b on platelet tethers to vWF on collagen
Fast on-off binding rate allows rolling

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21
Q

Which protein is responsible for platelet activation

A

GPVI on platelet binding to collagen

22
Q

What happens when the platelet is activated

A

Degranulation of alpha granules
Release of ADP, thromboxane, and A2 act as positive feedback mediators
Coagulation cascade
Integrins become activated

23
Q

What mediates adhesion of platelets and thrombus growth

A

Integrin

24
Q

What is the role of chemokines

A

Attract wbc - required for phagocytosis

25
Q

What is the role of cytokines

A

Activate wbc - increase immune response

26
Q

What is the role of growth factors

A

Stimulate surrounding cells e.g. endothelial to grow and repair

27
Q

How does lipid flipping aid in repair

A

On inactive platelets, phosphatidylserine is on inside of lipid bilayer
Activated platelets have phosphatidylserine flip, making the surface of the platelet negatively charged
Coagulation factors are positively charged so they are attracted to platelet plug

28
Q

6 steps of coagulation

A

Vessel injury
Activation of coagulation factors on TF, collagen, and platelet
Amplification cascade
Thrombin generation
Fibrinogen –> fibrin
Clot stabilisation

29
Q

What is the role of thrombin

A

Activate platelets and fibrin

30
Q

What is the role of TF

A

Transmembrane protein that is on surface of smooth muscle
Exposed to blood when there is damage
leads to thrombin production by extrinsic pathway

31
Q

What is responsible for clot retraction

A

Platelet integrin alphaIIbeta3
This links fibrin to platelet actin cytoskeleton

32
Q

What process does plug autodigest by

A

Fibrinolysis

33
Q

What are physical limitations of coagulation

A

Coagulation factor inhibitors
Protein C and S - inhibit clot formation process
Blood flow - too rapid and clot will be washed away
Fibrinolysis - correct fibrinolysis prevents excessive bleeding or prolonged clot presence

34
Q

What is the role of TFPI

A

Inhibits TF, FVIIa, FXa
Negative regulation to prevent excessive clotting

35
Q

What is the role of protein C and S in coagulation cascade

A

Protein C is a serine protease released by endothelial cells and platelets
Protein C is activated by thrombin and enhanced by protein S
It negatively regulates FVIII and FV

36
Q

What is the role of antithrombin in coagulation cascade

A

Inhibits thrombin to prevent excess clot formation

37
Q

What is the key enzyme for clot degradation

A

Plasmin from inactive plasminogen
Tissue plasminogen activator released by injured endothelial cells activates plasminogen

38
Q

What is arterial thrombosis

A

Formation of a blood clot within an artery
Often caused by platelet aggregation at site of atherosclerotic plaque rupture
Build up of fatty deposits and immune cells -chronic inflammatory rection underneath endothelial cells

39
Q

What is atherosclerosis

A

Build up of plaque in arteries that forms over time
Fat is in form of LDL

40
Q

4 stages of atherosclerosis progression

A

Fatty streak
Intermediate lesion
Lesion vulnerable to rupture
Advanced obstruction lesion

41
Q

Risk factors for arterial thrombosis

A

Environmental: high cholesterol, physical inactivity, smoking, high blood pressure, obesity
Inherited: familial tendency, gene susceptibility

42
Q

What is venous thrombosis

A

Formation of blood clots
DVT - usually in legs
Superficial - closer to skins surface
Endothelium remains intact

43
Q

Inherited risk factors for venous thrombosis

A

FV Leiden
Deficiency in protein C, S, or antithrombin
Prothrombin polymorphism (high levels)

44
Q

Acquired risk factors for venous thrombosis

A

Prolonged immobility - slow blood flow and pooling
Postoperative
Cancer - hyper-coagulable state or tumor pushes on vessels
Contraceptive pill - oestrogen is associated with high levels of coagulation factors
Heart failure
Varicose veins

45
Q

Treatments of venous thrombosis

A

Warfarin - Vitamin k antagonist so prevents FXa, FVIIa, FIXa, and thrombin
Heparin - activates antithrombin to inhibit thrombin and FX

46
Q

Limitations of warfarin and heparin

A

Genetic polymorphisms and drug-drug/food interactions cause varying anti-coagulation ability
Dose varies between patients
Coagulation monitoring required

47
Q

What oral anticoagulants can be used for venous thrombosis

A

Apixaban
Edoxaban
Rivaroxaban
Dabigatran

48
Q

Benefits of other oral anticoagulants than warfarin and heparin

A

Less intercranial bleeding
Predictable anticoagulant effect, less monitoring
Quick onset and offset
Fewer drug-food interactions
Used for deep vein thrombosis, pulmonary embolism, post-operative for hip and knee replacements, stroke prevention in atrial fibrillation

49
Q

What is atrial fibrillation

A

Abnormal heart rhythm caused by atria not beating properly
Causing abnormal blood flow, increasing risk of ischaemic stroke and dementia

50
Q

How can ischaemic stroke be treated

A

Clot busters
Streptokinase binds to plasminogen
Activated plasminogen will activate plasmin
Plasmin degrades fibrin meshwork
Streptokinase is only effective within 3 hours of event

51
Q
A

Topics in medical biosciences (3 decks)

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