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Clinical Therapeutics > Anticoags > Flashcards

Anticoags Flashcards

1
Q

Knee surgery, SOB, heart palpitations. What would a diagnosis be?

A

PE

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2
Q

What is the best diagnostic tool for a PE?

A

CTA

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3
Q

Well’s criteria

A

Clinical si/sx of DVT, HR>100, immobilization atleast 3 days or surgery previous 4 weeks, previous PE or DVT, hemoptysis, malignancy with recent or palliative treatment

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4
Q

What are some considerations regarding anticoags for PE treatment?

A

Risk of bleeding, which drug is most appropriate, what’s the best dose, how should it be monitored, what complications can happen, how long should pt be treated

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5
Q

What are some risk factors for bleeding complaints with anticoags?

A

> 65, previous episodes of significant bleeding, thrombocytopenia, concurrent antiplatelet therapy, issues with admin or monitoring, recent surgery, frequent falls, liver failure

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6
Q

What would be the most appropriate initial treatment for someone with PE?

A

Parenteral anticoags or oral factor Xa inhibitors

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7
Q

What are the factor Xa inhibitors?

A

Rivaroxaban (Xarelto) and Apixaban (Eliquis)

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8
Q

What are the advantages of factors Xa inhibitors?

A

Avoid injections such as with LMWH, avoid frequent lab draws for monitoring like Warfarin

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9
Q

Direct factor Xa inhibitors

A

No risk of HIT, only oral, expensive, no antidote if bleeding

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10
Q

What is Rivaroxaban (Xarelto) used to treat?

A

DVT, PE, AFib

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11
Q

What does Apixaban (Eliquis) treat?

A

DVT, PE, AFib

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12
Q

How should Rivaroxaban (Xarelto) be dosed for VTE?

A

15mg PO BID x 21 days, followed by 20mg PO Daily

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13
Q

What are the 3 functions of thrombin in coagulation?

A
  1. Converts fibrinogen to loose fibrin
  2. Converts factor 13 to 13a which converts loose fibrin to stable fibrin
  3. Activates many proteins and platelets in a + feedback loop within clotting cascade
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14
Q

What are the 2 clotting pathways?

A

Intrinsic and extrinsic

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15
Q

What is the intrinsic pathway?

A

Everything necessary for it is in the blood

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16
Q

What is the extrinsic pathway?

A

Requires cellular elements outside the blood

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17
Q

How does the intrinsic pathway work?

A

Exposed collagen-> 12 to 12a, 11 to 11a, 9 to 9a, 10 to 10a, prothrombin to thrombin, fibrinogen to fibrin

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18
Q

How does the extrinsic pathway work?

A

Subendothelial tissue is exposed to blood-> tissue factor binds factor 7, 9 to 9a, 10 to 10a, prothrombin to thrombin, fibrinogen to fibrin

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19
Q

What is antithrombin 3?

A

Naturally occurring anticoagulant that inactivates thrombin and several other clotting factors (including factor 10a)

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20
Q

What must be bound to heparin in order for activation?

A

Antithrombin 3

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21
Q

Heparin is naturally occurring and present on what?

A

Endothelial cells

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22
Q

What are some advantages of LMWH over UFH?

A

Greater bioavailability when given SUBQ, duration of effect is greater with less frequent injections, response is correlated with body weight (can use fixed dose), no monitoring, low risk HIT, less bleeding, less recurrent VTE events

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23
Q

Fondaparinux (Arixtra)

A

Similar to LMWH in structure and function, similar safety and efficacy as it, no difference in mortality, VTE disease or major bleeding

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24
Q

Binds to antithrombin and catalyzes reaction of factor Xa inactivation

A

Fondaparinux (Arixtra)

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25
Q

Synthetic pentasaccharide

A

Fondaparinux (Arixtra)

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26
Q

Used for DVT PPX for patients with a history of HIT

A

Fondaparinux (Arixtra)

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27
Q

What are the types of LMWH?

A
  1. Enoxaparin sodium (Lovenox)
  2. Dalteparin sodium (Fragmin)
  3. Tinzaparin sodium (Innohep)
  4. Nadroparin
28
Q

What type of LMWH is most commonly used?

A

Enoxparin

29
Q

Which type of LMWH can cause renal failure?

A

Tinzaparin Sodium (Innohep)

30
Q

Which drug is preferred in patient who cannot take oral meds?

A

LMWH

31
Q

LMWH is also preferred in who?

A

Patients if Factor Xa inhibitors are unavailable or unaffordable

32
Q

What is the appropriate dose of Enoxaparin to treat PE in a patient with normal renal function?

A

1mg/kg q12hr
OR
1.5mg/kg q24hr

33
Q

What are the indications for IV UFH in an acute PE?

A

Persistent hypotension (massive PE), increased risk of bleeding, concern about SUBQ absorption (morbid obesity), CrCl<30mL/min, anticipate imminent surgical procedure

34
Q

What is the most appropriate diagnosis chest to order for DVT?

A

LE venous Doppler ultrasound (NIVS)

35
Q

What is the Well’s criteria for DVT?

A

Active cancer, bedridden, unilateral calf swelling >3cm, entire leg swollen, localized tenderness, pitting edema, recent lower extremity immobilization, alternative diagnosis at least as likely

36
Q

Your patient with acute DVT has CrCl 25mL/min, what is the best initial treatment?

A

Unfractionated heparin (gtt)

37
Q

Anticoagulation in severe renal failure (CrCl <30)

A

Lovenox -> dont use
Rivaroxaban -> dont use
Eliquis -> was not studied
UFH -> safe

38
Q

What is the dose of Enoxparin used for DVT PPX in a hospitalized patient?

A

40mg SC Daily

39
Q

What is the dose of Enoxparain used to prevent DVT in a hospitalized pt with CrCl <30mL/min?

A

30mg SC daily

40
Q

What is the loading dose of heparin for acute PE?

A

80 units/kg

41
Q

What rate do you order the heparin drip to run?

A

18 units/kg/hr

42
Q

How do yo monitor the effect of a heparin drip?

A

Check interval PTT levels, check interval Factor Xa activity

43
Q

After being on heparin gtt x 5 days, there is a significant drop in PLT level. What condition should you be most concerned for?

A

HIT (heparin induced thrombocytopenia)

44
Q

What is type 1 HIT?

A

Within first 2 days of exposure and platelet count normalized with continued heparin therapy

45
Q

What is type 1 HIT a result of?

A

Form direct effect of heparin on the platelet activation

46
Q

What is type 2 HIT?

A

Occurs 4-10 days after exposure and has life and limb threatening thrombotic complications

47
Q

How is type 2 HIT mediated?

A

Autoimmune mediated

48
Q

When should you suspect HIT if the pt has had no previous heparin exposure?

A

Decreased in platelets by >50%, 5-10 days after initiation of heparin, evidence of thrombosis

49
Q

When should you suspect HIT for someone with a previous heparin exposure?

A

Decrease in platelets >50%, 1-10 days after re-exposure to heparin, evidence of thrombosis

50
Q

What is the best next step for someone who develops HIT?

A

D/C heparin, start a direct thrombin inhibitor

51
Q

What is the MOA of direct thrombin inhibitors?

A

Bind to thrombin directly and inhibit its activity

52
Q

DTIs

A

No risk of HIT, used for treatment of HIT

53
Q

What are the parenteral DTIs?

A

Bivalirudin (IV)
Argatroban (IV)
Desirudin (SC)

54
Q

What is an oral DTI?

A

Dabigatran (Pradaxa) used to treat VTE and AFib

55
Q

What is used to treat HIT?

A

DTIs, direct thrombin inhibitors

56
Q

How long should someone with antiphospholipid ab syndrome remain on anticoagulation?

A

Indefinitely

57
Q

Provoked VTE therapy duration

A

3 months

58
Q

Unprovoked VTE duration of therapy

A

Atleast 3 months, after 3 months assess the risks/benefits of continued therapy
If low-mod bleeding risk -> indefinite
If high-> stop at 3 months

59
Q

What is the INR goal?

A

2-3

60
Q

How many days after starting Warfarin is it reasonable to adjust the dose based on the INR?

A

3 days

61
Q

What dose of Warfarin is most commonly used to start?

A

5mg

62
Q

Initial therapy for VTE is typically what?

A

LMWH, UFG, or DOA

63
Q

HIT is a potential complication of what?

A

UFH

64
Q

Txt of PE for a pt with HIT usually involves what?

A

DTIs

65
Q

Warfarin is commonly prescribed as the long term agent for what?

A

VTE, 3 months indefinite, INR 2-3

66
Q

Bridge the heparin product with warfarin due to what?

A

Delayed Warfarin activity

67
Q

Cancer patients do better on what?

A

Long term LMWH or VTE

Clinical Therapeutics (8 decks)

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