Anti-coags Flashcards

1
Q

What are the 4 oral anti-platelet drugs?

A

Aspirin, clopidogrel, Ticgrelor, dipyridamole + ASA

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2
Q

ASA MOA?

A

Irreversibly acetylates COX, preventing platelet syn of TXA2 and thus platelet aggregation

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3
Q

3 non-cardio uses of ASA?

A

anti-pyretic, analgesic, anti-inflamm

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4
Q

PK of ASA?

A

half = 2-3 hours; Tx effect = 7-10 days (life of platelet)

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5
Q

MOA of clopidogrel and ticagrelor? Difference?

A

Antagonist of ADP receptor P2Y12 on platelets - prevents ADP induced cAMP decrease and subsequent aggregation
C is irreversible, T is reversible

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6
Q

Half life and metabolism of clopidogrel?

A
  • t1/2 = 7-10 days (irreversible)

- CYP2C19 pro-drug metal (some are ‘slow’ metabolizers, inhibited by omeprazole)

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7
Q

Half life and metab of ticagrelor?

A
  • active drug
  • 7 hours (9 for active metabolite)
  • CYP3A metabolism (watch for inducers, inhibitors)
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8
Q

MOA of dipyridamole? Why combine with ASA?

A
  • blocks adenine uptake, inhibits phoshodiesterase (increased cAMP, decreased aggregation, vasodilation)
  • not very effective alone
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9
Q

What anti-platelet drug is parenteral?

A

Abciximab

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10
Q

Dual f(x)/MOA of Abciximab?

A
  • antagonist of GP IIb/IIIa – prevents fibrinogen and vWF from binding platelets
  • prevents PT binding to platelets, decreasing thrombin formed = ANTI-COAG
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11
Q

Half life of abciximab?

A
free drug = 30 min
bound drug = 18-24 hours
platelet f(x) returns in 48 hours
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12
Q

What are the parenteral anti-coagulants?

A

Heparin, enoxaparin, fondaparinux, bivalirudin

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13
Q

How does UFH work?

A

Complexes with AT, increasing its activity – inactivation of IIa, IXa, Xa

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14
Q

How is UFH administered?

A

IV or SC - large molecules

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15
Q

Half life of heparin? Monitoring?

A

DOSE DEPENDENT - 30-150 min

Must monitor using aPTT

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16
Q

Three AE’s of heparin?

A
  • HI thrombocytopenia
  • heparin hypersensitivity
  • osteoporosis
17
Q

Heparin antidote?

A

protamine sulfate

18
Q

What kind of drug is enoxaparin?

A
  • LMWH

- complexes AT increasing its activity – inactivates Xa ONLY

19
Q

How do LMWH’s compare to UFH pharmacokinetically?

A
  • longer t1/2 = 3-6 hours
  • equally efficacious
  • greater SC bioavailability (fewer doses)
  • more predictable levels/PK - Xa monitoring not required
20
Q

What is fondaparniux? Administration? Metabolism?

A
  • synthetic heparin-like pentasaccharide
  • SC
  • t1/2 = 17 HOURS 1x day injection
21
Q

aPTT therapeutic goal in heparin Tx?

A

2-3x patient’s normal aPTT

22
Q

Bivalirudin MOA and metabolism?

A

direct irreversible inhibition of circulating and clot-bound thrombin

IV infusion t1/2 = 25 MINUTES

23
Q

When is bivalirudin indicated?

A

Pt’s who require hep but have had HIT; microvascular surgery to re-attach digits

24
Q

Which coag factors depend on Vitamin K?

A

2, 7, 9, 10, C, S

25
Q

Warfarin MOA and onset?

A
  • inhibits Vit K epoxide reductase

- onset observed in 8-12 hours; full effect in 3 days

26
Q

Warfarin administration and metabolism?

A
  • PO

- long plasma half-life, highly plasma protein bound, hepatic metab via VARIOUS CYPS (many interactions)

27
Q

Four AE’s of warfarin?

A
  • bleeding
  • skin necrosis due to early imbalance of pro/anti coag factors
  • purple toe syndrome (cholesterol microemboli)
  • teratogen cat X
28
Q

Warfarin antidotes?

A
  • Vit K, FFP, PT complex or recombinant VIIa
29
Q

Advantages of Dabigatran over Warfarin?

A

direct action on II, no CYP450 interactions, more effective with fewer interactions

30
Q

Dabigatran MOA?

A

competitive inhibitor of thrombin activity on both fibrinogen and platelets decreasing both coag and platelet activity; PO

31
Q

Dabigatrain metabolism? Half life? Special dosing considerations?

A
  • prodrug cleaved by esterases and glucuroniated without CYP450 activity
  • 14 HOURS = LONG
  • dose adjustment needed in RENAL DISEASE
32
Q

How does Rivaroxaban work? Administration?

A

DIRECTLY inhibits Xa; oral 1x day t1/2 = 9 hours LONG

33
Q

Metabolism and administration of Alteplase tPA?

A

IV ONLY; t 1/2 = 5-10 minutes

34
Q

How does tPA work?

A

binds fibrin and converts plasminogen to plasmin permitting clot degradation

35
Q

Fibrinolytic antidote?

A

Epsilon aminocaproic acid, PO, IV tranxenamic acid – inhibits plasminogen activation