Blood (HLB) Flashcards

1
Q

What is haemostasis?

A

Process of stopping bleeding

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2
Q

What are the stages of haemostasis?

A

1) Vasoconstriction
2). Primary haemostasis = formation of platelet plug
3). Secondary haemostasis = reinforcement of platelet plug

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3
Q

What is the name of the process which produces platelets?

What is the receptor involved in this?

What cell do platelets originate from?

A

Thrombopoiesis

TPO

Megakaryocytes

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4
Q

What is the name of the process which produces RBCs?

Which receptor is involved in this?

A

Erythropoeisis

EPO

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5
Q

What causes vasoconstriction when blood vessels are injured?

A

Endothelial cells produces endothelin - this causes regional arterioles to constrict.

Endothelial cells that are injured also produce thromboxane A2 and 5HT - these cause nearby smooth muscle to contact, also increasing vasoconstriction.

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6
Q

What are the three steps of platelet plug formation?

A

Platelets adhere to a BV wall
Platelets are activated
Platelets aggregate

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7
Q

How to platelets bind to an injured blood vessel wall?

A

Beneath the wall lies collagen which has been exposed. VWF can bind to this collagen - and then it attaches to platelets via the GP1b receptor

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8
Q

When platelets are activated, what do they release?

A

Granules of ADP, thromboxane A2 and 5HT

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9
Q

How does platelet aggregation occur in an injury?

A

ADP & Thromboxane A2 are released from bound, activated platelets. These attract other passing platelets to the site of injury.

Platelets can then bind to each other via GP2b3a receptors - fibrinogen binds them together.

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10
Q

Which disease can cause a defect in the receptor GP1b on platelets - causing haemophilia.

A

Bernard-Soulier syndrome

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11
Q

Which disease can cause a decrease in levels of VWF?

A

VW disease

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12
Q

What is thrombocytopenia?

A

A decreased amount of platelets in the blood - can cause inability to clot properly.

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13
Q

Which disease can affect the platelet receptor GP2b3a - thereby reducing coagulation?

A

Glanzmann’s thrombasthenia

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14
Q

What are the three pathways of the coagulation cascade?

A

Intrinsic
Extrinsic
Common

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15
Q

Which factors are involved in the intrinsic pathway?

A

12, 11, 9, & 8

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16
Q

Which factors are involved in the extrinsic pathway?

A

7 & 3

17
Q

What is the result of both of the intrinsic and extrinsic pathways?

A

They convert Factor X to Xa

Factor Xa + Va + Platelet Factor 3 + Ca convert Prothrombin to Thrombin (FII)

Thrombin converts Fibrinogen –> Fibrin (F I). Fibrin jellies the blood and forms a mesh over the clot.

Thrombin + FXIII + Ca = F XIIIa = cross links fibrin strands making the mesh stronger.

18
Q

Which factors require Vitamin K?

A

7, 9 & 10

19
Q

Which drug is a vitamin K inhibitor?

A

Warfarin

20
Q

How affect does liver disease have on Vitamin K?

A

Decreases its absorption

21
Q

How is excessive clot formation controlled by the body?

A

Plasminogen activator is also secreted from damaged cells.

This converts Plasminogen to plasmin.

Plasmin degrades fibrin fibres and limits growth of thrombi.

22
Q

What is naturally secreted by endothelial cells of blood vessels to prevent unnecessary blood clotting?

What other mechanisms do these cells have to stop blood clotting?

A

PGI2 and NO

They also have heparin sulphate - which binds to Anti-thrombin and activates it - in turn this inactivates 2, 9 & 10

Finally they have thrombomodulin - binds thrombin and activates Protein C. Protein C degrades 5 & 8.

23
Q

Which deficiency would you have with
- Haemophilia A
- Haemophilia B

A

A - F8 deficiency
B - F9 deficiency

24
Q

What are the natural anticoagulants in the body?

A

Protein C

Protein S

Anti-Thrombin

25
Q

How does anti-thrombin work as a natural anticoagulant?

A

It inhibits 2 + 7 = 9… 10, 11,12

26
Q

How does heparin work?

A

It enhances the effect of anti-thrombin - heparin binds and activates it.

The APTTR is derived from the activated partial thromboplastin time (APTT) of the patient and the midpoint of the APTT reference range.