Antithrombotics Flashcards

1
Q

The exposure of circulating blood elements to thrombogenic material, activation and aggregation of platelets, and triggering of the coagulation cascade are all elements to the formation of what?

A

A clot

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2
Q

After platelets adhere to the site of injury, how do they trigger aggregation?

A

Release reaction (secretion of platelet products)

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3
Q

Do collagen, thrombin, ADP, serotonin, fibrinogen, growth factor, procoagulants, and TXA2 activate or inactivate platelet aggregation?

A

Activate

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4
Q

What receptors allow binding of the platelets to fibringoen molecules?

A

IIb/IIIa

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5
Q

Which 4 drugs inhibit IIb/IIIa receptors, so platelets can’t aggregate?

A

ASA, thienophyridines, GP IIb/IIIa antagonists, and dipyridamole

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6
Q

ASA irreversibly acetylates and inactivates COX, which reduces which pro-aggrevating factor?

A

TXA2

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7
Q

Thienopyridines inhibit activation of the platelets by blocking the activation by which molecule?

A

ADP

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8
Q

When activated by the liver, which enzyme does theinopyridines block?

A

P2Y12

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9
Q

What are the 3 thienopyridines that are used currently?

A

clopidogrel, ticlopidine, and prasugrel

….that ADP is “-gel”ly….

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10
Q

Which is the most potent antiplatelet agents because they reversibly inhibit the aggregation by inhibitng the binding of activated platelet GP IIb/IIIa recepotors to fibrinogen and vWF?

A

GP IIb/IIIa receptor antagonists

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11
Q

So say your pt has an ASA intolerance, which drug can u give which increases platelet cAMP levels, which decreases Ca++ levels?

A

Dipyridamole

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12
Q

This si the class of drugs that interfered with the coagulation cascade and impair secondary hemostasis (formation fo the fibrin clot).

A

Anticoagulant drugs

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13
Q

What molcule is the main target for inactivation for heparin?

A

inhibits thrombin activation by factor Xa

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14
Q

So given the strengths, put the following in order from strongest to weakest:

dipryidamole
thienopyridines
ASA
GP IIa/IIa antagonists
pedal pump
A

GP IIb/IIIa antagonists&raquo_space; Thienopyridines > Aspirin > pedal-pump&raquo_space;> dipyridamole

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15
Q

This form of heparin is a mixture of glycosainoglycans, that, when assocated with antithrombin in the circulation, reduces thrombin ability to generate fibrin from fibrinogen.

A

Unfractionated hepatin

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16
Q

This form of heparin is more predictable and has a longer 1/2 life, smaller than UFH, and when associated with antithrombin, preferntially inhibits Xa rather than thrombin.

A

Low Molecular Weight Heparin

17
Q

This is the main complication of heparin therapy, where there can be direct heparin-induced platelet aggregation or immune-mediated problems.

A

Heparin-induced thrombocytopenia (HIT)

18
Q

In HIT, if there is direct hepatin-induced platelet aggregation, do you need to stop therapy?

A

Nah. It’s not too bad.

19
Q

What are the crazy complications of immune-mediated form of HIT?

A

life-threatening bleeding and thrombosis

20
Q

Do u need to stop heparin therapy if the pt develops immune-mediated HIT?

A

YES. YOULL KILL THEM YOU DICK.

21
Q

Long term use of UFH can cause what other medical condition?

A

Osteoporosis

22
Q

Say u give too much heparin and the pt starts to bleed a shit ton. What drug can u give to combat this?

A

protamine sulfate

23
Q

This is the period of time where u overlap heparin and warfarin when treating thrombosis.

A

Anticoagulant bridging

24
Q

Under what condition do u do anticoagulant bridging?

A

only when immediate anticoagulation is necessary

25
Q

What is the delay of onset for warfarin?

A

2-7 days

26
Q

Which vitamin can be given in case ur pt starts to have massive bleeding due to warfarin use?

A

Vit K