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Cardio Week 3 > TBL 1: Anticoagulants > Flashcards

TBL 1: Anticoagulants Flashcards

1
Q

what are anticoagulants?

A

a class of drugs that work on factors of the coagulation cascade to fight unwanted clot formation in the body

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2
Q

what type of anticoagulants are used to treat acute cases?

A

parenteral anticoagulants –> they are used in acute settings because they become readily available in the blood

you can then transition these acute cases for long-term management with slower acting oral anticoagulants.

ex. DVT

this means not by the mouth/enteric system so things like intravenous, intramuscular, or subcutaneous injection especially

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3
Q

what type of anticoagulants are used to treat chronic cases?

A

oral anticoagulants

used for long=term prophylaxis against clot formation in conditions like atrial fibrillation

during A-fib, the atria does not effectively push blood into the ventricles and thus causes stasis of blood in atria. Clots can form in the left atrial appendage, which can embolize into the systemic vasculature, clog an artery feeding the brain, and cause a stroke

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4
Q

when we do we use parenteral anticoagulants versus use oral anticoagulants?

A

we use parenteral anticoagulants for the management of acute, life-threatening diseases like venous thromboembolism (VTE) due to their more rapid onset compared to oral agents

we then transition to oral anticoagulants for long-term management after the acute phase and for prophylaxis in recurrent VTE or chronic A-fib

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5
Q

what is a common cause of a-fib?

A

hyperthyroidism

so always check lab T4 levels to check thyroid function!

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6
Q

what are the 4 anticoagulant classes?

A
  1. clotting factor synthesis inhibitor
  2. antithrombin activators
  3. direct factor Xa inhibitors
  4. direct thrombin inhibitors
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7
Q

what are clotting factor synthesis inhibitors? what is the delivery method, adverse effects and antidotes?

A

ex. warfarin

oral

adverse effects: hemorrhage

antidote: FFP, vitamin K

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8
Q

what are antithrombin activators? what is the delivery method, adverse effects and antidotes?

A

ex. heparin, enoxaprin, dalteparin, fondaparinux

parenteral

adverse effects: hemorrhage, HITT

antidotes: protamine sulfate

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9
Q

what are direct factor Xa inhibitors? what is the delivery method, adverse effects and antidotes?

A

ex. apixaban, rivaroxaban, edoxaban

oral

side effects: hemorrhage

antidote: activated prothrombin complex concentrate (aPCC)

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10
Q

what are direct thrombin inhibitors? what is the delivery method, adverse effects and antidotes?

A

ex. dabigatran, agratroban, bivalirudin, lepirudin

dabigatran is oral then rest are parenteral

adverse effects: hemorrhage

antidote: aPCC and idarucizumab specifically for dabigatran

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11
Q

what is the coagulation cascade pathway?

A

draw it out!!!

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12
Q

what are the vitamin K-dependent clotting factors?

A

vitamins 2, 7, 9, 10 C and S

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13
Q

what is the MOA of warfarin?

A

warfarin interferes with the γ-carboxylation of vitamin K-dependent clotting factors by inhibiting epoxide reductase

vitamin K dependent clotting factors = 2, 7, 9, 10, C and S

so it indirectly acts on coagulation cascade factors by acting as a clotting factor synthesis inhibitor

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14
Q

how do we monitor warfarin?

A

PT aka the extrinsic pathway even though it effects all vitamin K dependent clotting factors which involves both intrinsic and extrinsic pathways, we still just use PT mainly to monitor

we do so because factor VII has the shortest half-life of all the factors, so the PT/INR will become abnormal before the PTT –> this way we can monitor the patient’s coagulation status early in the process, before all of the vitamin-K-dependent factors are all knocked out

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15
Q

what is the antidote to warfarin?

A

vitamin K

warfarin inhibits the synthesis of vitamin K-dependent factors

but this takes a while to kick in so if you want rapid reversal, we give fresh frozen plasma (FFP), which replenishes the patient’s coagulation factors

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16
Q

what is warfarin-induced skin necrosis?

A

warfarin blocks vitamin K dependent coagulation factors of which, proteins C and S have the shortest half life and are natural anticoagulants

so they get knocked out first which leaves the coagulation cascade free to go rampant and you have a temporary hyper coagulable state where the anticoagulant concentration is lower than usual and the clotting factors can just wreak havoc

this leads to small vessels clotting which causes the skin to die

17
Q

how do you avoid warfarin-induced skin necrosis?

A

give a heparin bridge!

when we administer warfarin to a patient, we also provide heparin to activate antithrombin which is an anticoagulant

18
Q

what are the common drug interactions associated with warfarin?

A

warfarin is metabolized by the liver P450 enzymes

so drugs that mess with the P450 system can alter warfarin metabolism…

liver enzyme inhibitors = ↓liver enzymes = ↓warfarin metabolism = ↑[warfarin] = ↑risk of bleeding.

liver enzyme inducers = ↑ liver enzymes = ↑warfarin metabolism = ↓[warfarin] = ↑risk of thrombosis

19
Q

which outcome, clot or bleed, is more likely when warfarin is combined with a liver enzyme inhibitor?

A

bleeding

because warfarin is metabolized by P450 so if you inhibit it, warfarin levels will remain higher for longer and continue to block the vitamin K dependent clotting factors

20
Q

what is the MOA of heparin?

A

it acts indirectly on coagulation factors by activating the anticoagulant antithrombin

antithrombin acts on IIa, VIIa, IXa, Xa, XIa and XIIa = 2, 7, 9, 10, 11, 12

low molecular weight heparins like enoxaparin, dalteparin, and fondaparinux work mainly on Xa and IIa

21
Q

which anticoagulant is safe for use during pregnancy?

A

warfarin is a teratogen

heparin derivatives are safe for use during pregnancy

22
Q

what is the antidote for heparin?

A

protamine sulfate

it’s a positively charged molecule that binds to negatively charged heparin

23
Q

what is the hallmark side effect of heparin?

A

heparin-induced thrombocytopenia and thrombosis = HITT

heparin binds to platelet factor 4 (PF4) and some individuals form IgG antibodies against the heparin-PF4 complex –> the triad of heparin-PF4-Ig antibody activates platelets, simultaneously causing platelets consumption combined with thrombosis

even though there’s low platelets, to combat the thrombotic effect of HITT, use a direct thrombin inhibitor like argatroban, dabigatran, lepirudin, or bivalirudin

24
Q

what is the MOA of direct factor Xa inhibitors?

A

they bind to and directly inhibit coagulation factor Xa

ban on factor Xa = apiXaBAN, rivaroXaBAN, edoXaBAN

25
Q

what is the antidote for of direct factor Xa inhibitors?

A

activated prothrombin complex concentrate (aPCC)

26
Q

what is the MOA of direct thrombin inhibitors?

A

they inhibit thrombin directly

direct ThRombin inhibitors include argaTRoban, dabigaTRan and the “rudins” – bivalirudin and lepirudin.

27
Q

what is the main indication for argatroban?

A

it’s a direct thrombin inhibitor

it’s an alternative to heparin for anticoagulating patients with HITT

28
Q

what is the antidote for direct thrombin inhibitors?

A

dabigatran = idarucizumab

the rest can be reversed with aPCC

29
Q

which drugs are clotting factor synthesis inhibitors?

A

warfarin

30
Q

which drugs are activators of antithrombin?

A
  1. heparin
  2. enoxaparin
  3. dalteparin
  4. fondaparinux
31
Q

which drugs are direct factor Xa inhibitors?

A
  1. apixaban
  2. rivaroxaban
  3. edoxaban
32
Q

which drugs are direct thrombin inhibitors?

A
  1. argatroban
  2. dabigatran
  3. bivalirudin
  4. lepirudin
33
Q

A patient on chronic warfarin is newly prescribed with a known liver P450 enzyme inhibitor. Which of the following risks is increased in this patient?

A. Budd-Chiari syndrome

B. DVT

C. hemorrhagic stroke

D. PE

E. thrombocytopenia

A

C. hemorrhagic stroke

warfarin is metabolized by liver enzymes, and if we happen to inhibit these liver enzymes, warfarin’s metabolism is decreased, ultimately increasing warfarin concentration in the blood and increasing the risk of a bleed

Cardio Week 3 (13 decks)

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