Haemostasis Flashcards

1
Q

Describe a venous thrombosis

A

Red- because high fibrin content

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2
Q

Describe an arterial thrombosis

A

White- because high platelet content

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3
Q

What are the three components of Virchow’s triad?

A

Rate of blood flow, consistency of blood and blood vessel wall integrity

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4
Q

Describe the cell based theory and which drugs target which part.

A

Initiation (small scale production of thrombin)-ANTICOAGULANTS, amplification (large scale thrombin production on the surface of platelets)- ANTIPLATELETS and propagation (throbin mediated generation of fibrin strands)-THROMBOLYTICS.

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5
Q

Describe the 3 steps of initaition

A

5a and 10a are activated by a TF bearing cell. This is a prohombinase complex that actiavtes thrombin (IIa). Antithrombin inactivates 2a, 9, 10a, 11.

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6
Q

What is Dabigatran and Rivaroxaban. Why is Rivaroxaban better than Dabigatran? Why are either easier to use than heparin?

A

Dabaigtran and Rivaroxiban are both anticoagulants. Dabigatran inhibits 2a and Rivaroxiban inhibits 10a (part of the promthrombinase complex). Lit suggests Rivaroxiban is less likely to cause GI bleeds tha Dabigatran. They are orally administered, so easier than heparin to administer (only SC).

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7
Q

What is dalteparin? What would you treat with it?

A

A LMW heparin, so a AT-III activator. This decreases conc of Factor 10a (not thrombin itself). Number one treatment for PE.

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8
Q

Name 3 problems with warfarin. Which coagulation factors does it affect?

A

Narrow therepeutic window, takes 5-6 days for biocehmical effect, has many drug interactions. It is a vit K anatgonist, so inhibits actiavtion of factors 2,7,9, 10.

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9
Q

DEscribe the sequence of events in amplification (large scale production of thrombin)

A

Thrombins binds to PAR on platelet surface, This has two effects. Firstly , the PAR stimulation increases intracellular calcium, which leads to the exocytosis of ADP from dense granules. The ADP binds to P2Y12 receptors and stimulates platelet activation and aggregation. Secondly, the PAR stimulation liberates Arachidonic Acid, which is converted to TXA2 by COX enzymes. The TXA2 stimulates expression of Glp2b/3a receptors on platelet surface, hence enhancing platelet aggregation.

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10
Q

What is clopidogrel?

A

A P2Y12 receptor anatagonist (so an antiplatelet). Orally admisnistered

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11
Q

What is aspirin?

A

An irreversible COX1 inhibitor, so it inhibits the production of TXA2 (inhibits expression of Glp2b/3a).

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12
Q

What is abciximab?

A

A Glp2b/3z inhibitor. Only can admisnitered SC or IV, usually done by specialists.

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13
Q

Give three indications for antiplatelets

A

Arterial thrombosis, actue coronary syndrome or atrial fib (as stroke prophylaxis)

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14
Q

What is alteplase? Give 2 indications.

A

Alteplase is a thrombolytic. It is a recombinant tissue type plasminogen activator. Give 1st line for stroke and also for an ST-elevated MI.

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