Haemostasis

Question 1

Define haemostasis

Answer 1

The endogenous process of stopping blood loss from damaged vessels and protecting against haemorrhage.

Question 2

Is it vasoconstriction or vasodilation involved in haemostasis?

Answer 2

Vasoconstriction

Question 3

Which is more solid, a platelet plug or clot?

Answer 3

Clot. Reinforced platelet plug with collagen and fibrin

Question 4

Define thrombosis

Answer 4

Haemostasis in the wrong place. Formation of platelet plug / clot in the absense of vessel damage

Question 5

Compare thrombus and embolus

Answer 5

Thrombus = clot that forms in the vessel and stays there 
Embolus = clot forms elsewhere in the body and travels to a vessel where it then gdts stuck and blocks blood flow

Question 6

Define fibrinolysis

Answer 6

The break down of a clot

Question 7

Compare red and white clots

Answer 7

Red = venous. Made mostly of erythrocytes 
White = arterial, made mostly of platelets

Question 8

Thromboxane A2 is prothrombotic. True or false

Answer 8

True

Question 9

Prothrombotic factors prevent the formation of clots. True or false?

Answer 9

False

Question 10

Prostacyclin and nitric oxide are both ..?

Answer 10

Antithrombotic

Question 11

Vessel injury causes exposed collagen. The collagen then activates platelets. Name 2 molecules that activated platelets release?

Answer 11

ADP and thromboxane A2

Question 12

Do ADP and thromboxane activate platelets or prevent activation?

Answer 12

Activate. They attract more platelets to the site

Question 13

The release of activated platelets is a positive feedback cycle resuLting in the formation of…?

Answer 13

The platelet plug

Question 14

What prevents the platelet plug from continuing to grow and cover the non-injured area of the vessel?

Answer 14

The non-injured endothelium releases nitric oxide and prostacyclin which inhibit further platelet aggregation.

Question 15

Aspirin prevents the platelets from releasing thromboxane by inhibiting which enzyme?

Answer 15

COX 1

Question 16

COX 1 is the enzyme that turns arachidonic acid into PGG2. PGG2 is then turned in to which two molecules?

Answer 16

Thromboxane and prostacyclin

Question 17

P2Y receptors are located where?

Answer 17

On platelets

Question 18

Once activated by ADP, what effect do thr P2Y receptors have?

Answer 18

They release COX and also activate the GPIIb receptors

Question 19

What do the GPIIb receptors do?

Answer 19

Once activated, these receptors join two platelets together via fibrinogen. Therefore, they cause platelet aggregation

Question 20

MOA of clopidrogrel?

Answer 20

Prevents ADP from binding to P2Y receptors which prevents platelet aggregation

Question 21

Abciximab and tirofiban are two drugs with which antiplatelet mechanism?

Answer 21

They prevent GPIIb receptor activation which prevents platelet aggregation

Question 22

Aspirin inhibits the production of both thromboxane and prostacyclin. True or false?

Answer 22

True. However inhibition of prostacyclin is reversible, but thromboxane is not.

Question 23

Name an ADP antagonist

Answer 23

Clopidogrel

Question 24

Can clopidogrel or ticlopidine be used in cojunction with aspirin?

Answer 24

Yes

Question 25

Finrinogen cross-linking occurs at which receptor?

Answer 25

GPIIb

Question 26

Which drug class do abiciximab and tirofiban belong to?

Answer 26

GPIIb inhibitors

Question 27

What reaction does Factor X facilitate?

Answer 27

Turns prothrombin into thrombin

Question 28

What does thrombin do?

Answer 28

Turns fibrinogen (soluble) into fibrin (insoluble)

Question 29

Thrombin activates clotting factor XIII. What role does this factor have?

Answer 29

It stabilises the fibrin network of the clot

Question 30

Name a direct thrombin inhibitor and what action it has

Answer 30

Dabigatran. Stops thrombin from turning fibrinogen into fibrin

Question 31

MOA of rivaroxaban?

Answer 31

Blocks factor Xa (which therefore blocks conversion of prothrombin into thrombin)

Question 32

Anti-thrombin inactivates factor Xa. What drug enhances anti-thrombin?

Answer 32

Heparin

Question 33

How does heparin enhance anti-thrombin’s inhibition of thrombin?

Answer 33

Due to heparin’s large size, it forms a complex with AT amd thrombin

Question 34

Name a low molecular weight heparin

Answer 34

Enoxaparin

Question 35

Antidote to heparin?

Answer 35

Protamine sulphate. Forms a complex with heparin and inactivates it.

Question 36

Explain the role of vitamin K

Answer 36

Promotes the synthesis of vitamin K dependent clotting factors ( II, VII, IX, X)

Question 37

Warfarin MOA?

Answer 37

Vitamin K antagonist. It competes with vitamin K for binding to vitamin K reductase

Question 38

Why does it take around 48 hours for warfarin to reach peak effect?

Answer 38

It immediatelt blocks vitamin K reductase, but the body needs to use up the existing vitamin K for production of clotting factors. Once all the vitamin K stores are used up, then the effects of warfarin are apparent.

Question 39

Why does warfarin have so mant drug interactions?

Answer 39

Because it is heavily bound to albumin. Therefore, competes for binding with other drugs that bind to albumin

Question 40

Storage form of thrombin?

Answer 40

Prothrombin

Question 41

How do fibrinolytic drugs work?

Answer 41

They convert plasminogen into plasmin, which breaks down fibrin, fibrinogen and some of the clotting factors

Question 42

Example of fibrinolytic drugs?

Answer 42

Urokinase, alteplase, anistresplase