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1 STEP Uworld coagulation > Oral anticoagulants (p/o) Amboss mainly > Flashcards

Oral anticoagulants (p/o) Amboss mainly Flashcards

1
Q

What are p/o anticoagulants?

A

vit.K antagonists: warfarin
direct thrombin inhib: dabigatran
direct Xa inhib: apixaban, rivaroxaban, edoxaban

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2
Q

What is direct thrombin p/o inhibitor?

A

dabigatran

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3
Q

What is direct Xa p/o inhibitors?

A

apixaban, rivaroxaban, edoxaban

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4
Q

Dabigatran antidote?

A

Idarucizumab (monoclonal antibody)

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5
Q

Apixaban and rivaroxaban antidote?

A

andexanet alfa

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6
Q

Management/screening of direct inhibitors p/o?

A

Regular monitoring of coagulation parameters is not required → improved patient compliance!

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7
Q

Management/screening of warfarin p/o?

A

Regular monitoring of the PT/INR required (as vitamin K antagonists affect the extrinsic coagulation pathway)
THEREFORE WORSE PATIENT COMPLIANCE

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8
Q

If before procedure is consumed warfarin, what to do?

A

requires periprocedural bridging anticoagulation

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9
Q

cost of warfarins compared to direct anticoagulants p/o?

A

wafarin - low cost;

p/o direct - costly

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10
Q

Fibrillation arising from mitral stenosis with a significantly increased risk of thromboembolism (aka valvular AF); Treatment?

A

coumarins are the only approved treatment

p/o direct (dagibatran; rivarox, apix) - NOT SUITABLE

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11
Q

Indications for all oral anticoagulants?

A

Prophylaxis of thromboembolism following:
DVT and/or pulmonary embolism
Prolonged immobilization after surgery (e.g., especially in knee or hip surgery)
Nonvalvular atrial fibrillation (for valvular AF - only coumarins)

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12
Q

Expected laboratory changes of warfarin?

A

Increased PT/INR, no change to PTT or TT (routinely monitored)

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13
Q

Expected laboratory changes of direct thrombin inhib (dabigatran)?

A

prolonged thrombin time (TT), no change to PTT or PT (not routinely monitored)

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14
Q

Expected laboratory changes of direct factor Xa inhibitors?

A

prolonged PT and PTT, unchanged thrombin time (not routinely monitored)

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15
Q

The most important side effect of all oral anticoagulants is?

A

is a dose-dependent increase in bleeding risk

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16
Q

WARsaw is an EXTRaordinary Place To check out: abbreviation?

A

WARfarin affects the EXTRinsic pathway; therefore, PT should be regularly checked.

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17
Q

WEPT abbreviation?

A

WEPT: Warfarin Extrinsic pathway PT

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18
Q

warfarin site of action?

A

liver

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19
Q

warfarin onset of action?

A

slow

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20
Q

warfarin half time?

A

longer than heparin

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21
Q

warfarin duration of action?

A

days

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22
Q

warfarin monitoring?

A

PT or INR (affects extrinsic pathway)

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23
Q

Heparin route of administration?

A

i/v; subcutaneous

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24
Q

Heparin site of action?

A

blood

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25
Q

Heparin onset of action?

A

rapid

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26
Q

Heparin half time?

A

shorter than heparin

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27
Q

heparin duration of action?

A

hours

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28
Q

Heparin mechanism of action?

A

Activates antithrombin → ↓ action of factors IIa and Xa

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29
Q

heparin monitoring?

A

PTT (affects intrinsic pathway)

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30
Q

warfarin reversal?

A

Vitamin K

FFP, PCC (for rapid reversal)

31
Q

heparin reversal?

A

Protamine sulfate

32
Q

Coumarins adverse? two groups of effects

A
  1. DOSE DEPENDENT increased risk of bleeding

2. Warfarin induced skin necrosis

33
Q

Coumarins adverse. DOSE DEPENDENT increased risk of bleeding.
What to do if bleeding from small wound?

A

nothing, it ceases spontaneously, no additional measured recquired

34
Q

Coumarins adverse. DOSE DEPENDENT increased risk of bleeding.
Where is bleeding in severe cases of hemorrhage?

A

Severe cases of hemorrhage are usually retroperitoneal, intracranial, or gastrointestinal.

35
Q

Countermeasures for extensive or life-threatening bleeding when used warfarin include: 3

A

STOP USE COUMARINS;
Antidotes: Vit K for delayed
FFP and PCC for rapid reversal

36
Q

Warfarin-induced skin necrosis. Onset time?

A

few days after initiation of warfarin.

37
Q

Depletion of which K dependent substances occurs more rapid?

A

anticoagulants protein C and protein S have a relatively short half-life and are depleted more quickly than procoagulants factors II, IX, and X –> increased factor V and VIII activity.

38
Q

In warfarin skin necrosis. Lack of C and S increase V and VII action? how?

A

Protein C and S normally inactivate factor Va and VIIIa.

39
Q

What is result os decr. C and S –> increased V and VII activity?

A

initial hypercoagulable state → formation of microthrombi → vascular occlusion, tissue infarction, and blood extravasation

40
Q

What patients have increased risk in warfarin induced skin necrosis?

A

Increased risk in patients with underlying hereditary protein C deficiency

41
Q

Warfarin-induced skin necrosis. PRESENTATION?

A

PAINFUL purpura, hemorrhagic blisters, and large areas of necrosis; mostly affects subcutaneous adipose tissue

42
Q

Warfarin-induced skin necrosis. What part of skin is affected?

A

subcutaneous adipose tissue

43
Q

Warfarin-induced skin necrosis. Management?

A

Immediate management: discontinue warfarin, administer IV vitamin K, unfractionated heparin, and source of protein C (protein C concentrate, FFP); surgical debridement and grafting in therapy-refractory cases

44
Q

Warfarin-induced skin necrosis. Prevention?

A

Prevention: temporary bridging anticoagulation with heparin until warfarin has started to act and the initial hypercoagulable state has been bridged

45
Q

Direct factor Xa inhibitors and direct thrombin inhibitors: adverse according to amboss? 1

A

Dose-dependent increased risk of bleeding

46
Q

Direct factor Xa inhibitors and direct thrombin inhibitors. What management if life-threatening bleeding occurs?

A

ADMINISTER PCC

Only to be administered in case of imminent risk of death because PCC use involves an increased thrombotic risk. FFP is not indicated, since the amount of FFP needed to counteract the effects of thrombin and factor Xa would most likely lead to volume overload and further complicate emergency situations.

47
Q

Direct factor Xa inhibitors and direct thrombin inhibitors. General management and specific medication antidotes?

A 
Antifibrinolytic agents (e.g., tranexamic acid)
Oral activated charcoal reduces absorption if anticoagulants were ingested in the past couple of hours.
Apixaban and rivaroxaban: andexanet alfa (recombinant modified factor Xa protein) 
Dabigatran: idarucizumab (monoclonal antibody)
48
Q

valvular and non-valvular AF. What anticoagulants?

A

For both - coumarins (warfarin)
for non-valvular AF - direct p/o thrombin and Xa
direct p/o thrombin and Xa cannot bet used for valvular AF!

49
Q

heart Indications of direct factor Xa inhibitors and direct thrombin inhibitors?

A

non-valvular AF

50
Q

Indications for coumarins?

A

Prophylaxis of thromboembolism (e.g., stroke) in patients with the following:

a) Valvular AF and nonvalvular AF
b) Heart valve replacement
c) Heart failure

Myocardial ischemia

Standard target INR: 2.0–3.0 (higher in mechanical heart valves or in special high-risk circumstances; usually 2.0–3.5)

51
Q

Coumarins target INR?

A

2.0–3.0

52
Q

ALL p/o anticoagulants indications. Prophylaxis

A

Therapy and secondary prophylaxis of:
Deep vein thrombosis
Pulmonary embolism

Prophylaxis of thromboembolism following:
Total knee or hip replacement, hip fracture surgery

53
Q

Contraindications. Which one cross placenta and may cause fetal bleeding

A

Warfarin crosses the placenta, causing teratogenicity and fetal bleeding

54
Q

Direct oral anticoag affect on pregnancy and breastfeeding?

A

Side effects of NOACs during pregnancy and breastfeeding are unknown. Therefore, they are currently not recommended.

55
Q

General contraindication for oral anticoagulations?

A

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

Acute bleeding

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy); TENDENCY TO FALL

Severe renal insufficiency

Concurrent administration of several anticoagulants

56
Q

Specific contraindications for Dabigatran?

A

concurrent administration of ketoconazole, itraconazole, ciclosporin, tacrolimus, or dronedarone

57
Q

Warfarin is metabolized by ….

A

CYP450 enzymes

58
Q

Why warfarins effects can be significantly impacted by a variety of interactions? How to monitor?

A

Because warfarin is metabolized by CYP450. Its effects can be significantly impacted by a variety of interactions; for this reason, warfarin serum levels should be monitored regularly.

59
Q

NO CARDS FOR WARFARIN CYP450 interactions. NO from amboss no from UW

A

.

60
Q

What is bridging anticoagulation?

A

Bridging anticoagulation: the administration of heparin for the duration of the transient hypercoagulable state caused by warfarin therapy.

61
Q

bridging anticoagulation. How heparin works?

A

Heparin prevents coagulation by activating antithrombin.

62
Q

bridging anticoagulation effect/use?

A

Reduces risk of venous thromboembolism and skin necrosis

May also be used during interruptions of warfarin therapy (e.g., surgery)

63
Q

Periprocedural bridging anticoagulation.

A

A method of reducing the risk of both periprocedural thromboembolism and bleeding in patients on VKAs.

VKAs are discontinued a few days prior to an elective procedure and, when the INR is no longer in the therapeutic range, a parenteral anticoagulant such as low molecular weight heparin (LMWH) or unfractionated heparin (UFH) is administered. After the procedure, VKAs are reinitiated, and the parenteral agent is continued until the INR is in the therapeutic range again

64
Q

Periprocedural bridging anticoagulation. Steps to do?4

A
  1. Interrupt VKAs as needed (e.g., patients with high periprocedural bleeding risk) a few days before the procedure.
  2. Initiate bridging anticoagulation once the INR is in the SUBtherapeutic range,
  3. Administer the last dose of LMWH 24 hours before the procedure (4–6 hours before the procedure for UFH).
  4. Resume VKA after surgery ; consider postprocedural bridging anticoagulation as needed (e.g., patients with high periprocedural thrombotic risk.
65
Q

Indications for coumarins?

Prophylaxis of thromboembolism (e.g., stroke) in patients with the following:

a) ………
b) Heart valve replacement
c) Heart failure

Myocardial ischemia

A

Valvular AF and nonvalvular AF

66
Q

Indications for coumarins?

Prophylaxis of thromboembolism (e.g., stroke) in patients with the following:

a) Valvular AF and nonvalvular AF
b) ……….
c) Heart failure

Myocardial ischemia

A

Heart valve replacement

67
Q

Indications for coumarins?

Prophylaxis of thromboembolism (e.g., stroke) in patients with the following:

a) Valvular AF and nonvalvular AF
b) Heart valve replacement
c) ………….

Myocardial ischemia

A

Heart failure

68
Q

Indications for coumarins?

Prophylaxis of thromboembolism (e.g., stroke) in patients with the following:

a) Valvular AF and nonvalvular AF
b) Heart valve replacement
c) Heart failure

…………

A

Myocardial ischemia

69
Q

General contraindication for oral anticoagulations?

……………

Acute bleeding

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy); TENDENCY TO FALL

Severe renal insufficiency

Concurrent administration of several anticoagulants

A

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

70
Q

General contraindication for oral anticoagulations?

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

………………

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy);

TENDENCY TO FALL

Severe renal insufficiency

Concurrent administration of several anticoagulants

A

Acute bleeding

71
Q

General contraindication for oral anticoagulations?

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

Acute bleeding

…………

TENDENCY TO FALL

Severe renal insufficiency

Concurrent administration of several anticoagulants

A

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy);

72
Q

General contraindication for oral anticoagulations?

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

Acute bleeding

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy);

………..

Severe renal insufficiency

Concurrent administration of several anticoagulants

A

TENDENCY TO FALL

73
Q

General contraindication for oral anticoagulations?

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

Acute bleeding

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy);

TENDENCY TO FALL

……………

Concurrent administration of several anticoagulants

A

Severe renal insufficiency

74
Q

General contraindication for oral anticoagulations?

Coagulopathies; hepatic dysfunction with impaired hepatic production of coagulation factors

Acute bleeding

Suspected vascular lesions, increased risk of severe bleeding: Severe arterial hypertension, aneurysm; Endocarditis; Recent cardiovascular events (e.g., cerebral ischemia); Gastrointestinal bleeding; Surgery or interventional procedures (e.g., biopsy); TENDENCY TO FALL

Severe renal insufficiency

……………..

A

Concurrent administration of several anticoagulants

1 STEP Uworld coagulation (6 decks)

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