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Cardiology > Antiplatets/Anticoagulants > Flashcards

Antiplatets/Anticoagulants Flashcards

1
Q

What are some thrombus disorders?

A

Arterial:
Atrial fibrillation –> left atrial appendage
Acute coronary syndrome
Myocardial infarction
Stroke
Critical Limb Ischemia (peripheral vascular disease)
Gut ischemia

Vein:
DVT/PE

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2
Q

What is required for a thrombus?

A

Fibrin + activated platelets + trapped RBC

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3
Q

What is the target for anticoagulants?

A

Fibrin formation

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4
Q

What are some anticoagulants?

A

Heparin
Warfarin
Direct Thrombin Inhibitors (ie. Dabigatran)
Factor Xa inhibitors (ie. apixaban)

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5
Q

What are some antiplatelets?

A

Aspirin
ADP blockers
Phosphodiesterase inhibitors

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6
Q

What are a thrombolytic agent?

A

tPA

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7
Q

Which agents would be used for acute MI?

A

ASA, heparin, tPA (ie. all three categories)

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8
Q

Which agents would be used for acute and chronic atrial fibrillation?

A

Acute –> heparin

Chronic –> warfarin

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9
Q

Which agents would be used for stroke event?

A

ASA, heparin, tPA (same as MI)

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10
Q

What agents would be used for acute DVT/PE or limb ischemia?

A

heparin, tPA

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11
Q

What are some Factor X related drugs?

A 
Unfractionated heparin 
low-MW heparin
Fondaparinux
Rivaroxaban (oral) -  Xa inhib.
Apixaban (oral) - Xa inhib.
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12
Q

What does heparin activate?

A

Antithrombin 3 –> inhibits activation of fac 10, inactivates the formation of thrombin from pro-thrombin

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13
Q

T or F: UF heparin given to acute onset situations

A

T

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14
Q

Why is there a highly variable response to UF heparin and how to get around it?

A

Because lots binding to plasma proteins and cells

- dose is dependent on reaching a target PTT

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15
Q

How to reverse UF heparin?

A

protamine

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16
Q

Which drug is for prophylaxis for DVT?

A

UF heparin

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17
Q

UF heparin is used in which acute events?

A

DVT/PE, MI, stroke

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18
Q

What are side effects of UF hep?

A

bleeding and thrombocytopenia
Osteoporosis with LT use
Elevated AST

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19
Q

What is heparin-induced thrombocytepnia

A

immune mediated where immune complexes bind to platelet factor 4 –> cause decrease in platelet and formation of arterial/venous thrombosis

–> must use direct thrombin inhibitors

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20
Q

Whats the difference in effect of LMWH and UFH?

A

LMWH does not block the change of prothrombin to thrombin and it is IRREVERSIBLE

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21
Q

T or F: LMWH need to be titrated

A

F:

Dosage is based on weight (not PTT measurements)

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22
Q

How is LmWH administered?

A

SubQ

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23
Q

How does warfarin lower all Vit K factors (2, 7, 9, 10)?

A

Antagonizes Vit K

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24
Q

T or F: Warfarin effect takes several days and dose need to be titrated

A

T:

Needs to titrated based on PT/INR

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25
Q

What a CI for warfarin?

A

Pregnancy

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26
Q

What are side effects of warfarin ?

A

bleeding

skin necrosis

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27
Q

What are indications for warfarin?

A

Stroke and atrial fib (esp. chronic)
Mechanical valve
Prior DVT/PE

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28
Q

Why does skin necrosis happen due to warfarin?

A

Warfarin inactivates Protein C, which a anti-clotting factor. High doses of warfarin creates the initial lack of protein C and leave blood as pro-thrombotic.

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29
Q

What drugs are preferred over warfarin for chronic disease and why?

A

Factor Xa inhibitors:

  1. rivaroxaban
  2. apixaban

Direct Thrombin Inhibitors
Dabigatran

WHY–> no InR checks required (as in warfarin needs to be titrated)

30
Q

How to reverse Warfarin?

A

VitK (oral bc IV –> allergies) when INR is 5-9

31
Q

What are some thrombolytics and do they work?

A

tPA
Streptokinase
Urokinase

MOA –> they increase plasmin levels which is a clot buster
(degrades fibrin)

32
Q

When is fresh frozen plasma administered?

A

When INR is greater than 9 (IV Vit K may be used instead)

33
Q

What is the difference between arterial and venous thrombi?

A

Arterial thrombi:
Rich in platelets
Appear white

Venous thrombi:
Rich in fibrin and trapped platelets
Appear red.

34
Q

What is the endothelium’s natural antiplatelet activity mediated by?

A

Antiplatelet activity because of synthesis and release of prostacyclin and nitric oxide (NO) and expression of CD39, a membrane-associated ectoADPase

35
Q

What is the endothelium’s natural anticoagulant activity mediated by?

A

Anticoagulant activity because of heparan sulfate proteoglycan-mediated activation of antithrombin and expression of thrombomodulin (TM) and endothelial protein C receptor (EPCR), which are involved in protein C activation, and surface-bound tissue factor pathway inhibitor (TFPI).

36
Q

What is the endothelium’s natural profibrinolytic activity mediated by?

A

Profibrinolytic activity because of release of tissue and urokinase-type plasminogen activator (t-PA and u-PA, respectively)

37
Q

What are the three steps to a platelet-plug formation?

A
  1. Adhesion
  2. Activation
  3. Aggregation
38
Q

What happens in activation?

A
  • Platelets adhere via glycoproteins to exposed collagen with von Willebrand factor (vWF).
  • Adhered platelets have a change in shape and leads to activation.
39
Q

What happens in activation?

A
  • Release of substances that leads to further recruitment of additional platelets, further activation and thrombin formation.
  • Adenosine diphosphate (ADP) released from dense granules.
  • -> ADP binds to P2Y12 receptor
  • Activation of protein kinases leads to formation of thromboxane A2 (TXA2) from arachidonic acid with COX-1.
  • Increased intracellular Calcium release leads to conformational change of GP IIb/IIIa to active form.
40
Q

What happens in aggregation?

A
  • Activated GP IIb/IIIa allows for crosslinking on platelets forming a platelet plug,
  • This plug will be further stabilized by fibrin mesh of the coagulation pathway.
41
Q

How does aspirin work?

A

Irreversibly blocks cyclooxygenase-1 (COX-1)

ie. formation of TXA2 from arachidonic acid

42
Q

What is ASA used for?

A

Used in the secondary prevention of established coronary, cerebrovascular and peripheral vasc. disease.

43
Q

T or F: Ticagrelor compared to clopidogrel has increased benefit in patients with acute coronary syndromes

A

T

44
Q

What kind of antagonist is Ticagrelor?

A

Reversible inhibitor (P2Y12 antagonist) at the ADP receptor at platelet

45
Q

What are some Thienopyridiens?

A

Ticlopidine
Clopidogrel
Plasugrel

46
Q

How do Thienopyridiens work?

A

Irreversibly bind to P2Y12 receptor therefore decreasing the activation process.

47
Q

Who are prescribed Thienopyridiens?

A

In patients with acute coronary syndrome (combined with ASA have improved outcomes)
OR
Substituted for ASA allergy

48
Q

T or F: Thienopyridiens are prodrugs

A

T

49
Q

What are some parentral anticoagulants?

A

Heparin
LMWH
Fondaparinaux
Direct thrombin inhibitors (Dabigatran)

50
Q

What are some oral anticoagulants?

A

-Vitamin K inhibitor (warfarin)
-Noacs/DOACS:
Direct thrombin inhibitors (dabigatran)
Factor Xa inhibitors (rivaroxaban, apixaban, endoxaban)

51
Q

How does heparin work?

A

Heparin binds to antithrombin III via its pentasaccharide sequence. This induces a conformational change in the reactive center loop of antithrombin that accelerates its interaction with factor Xa.
–> both Xa and thrombin inhibition

52
Q

What is a common issue with prolongued heparin use?

A

Treatment with therapeutic doses of heparin for over 1 month can cause a reduction in bone density (ie. osteoporosis)

53
Q

How it HIT/HITT induced?

HIT: Heparin induced thrombocytopenia.
HITT: Heparin induced thrombocytopenia and thrombosis.

A

Heparin binds to PF4 [platelet factor 4] forming heparin-PF4 complex. This binds to antibody that is stimulated by the complex.

This Ab-complex binds to platelets, causing the formation of microparticles. The microparticles are prothrombotic

Overall effect decreased platelets and prothrombotic state.
*can also happen with LMWH

54
Q

What should and should not be done in HIT/HITT?

A

Stop all heparin
Give an alternative anticoagulant, such as lepirudin, argatroban, bivalirudin, danaparoid, or fondaparinux.
Do not give platelet transfusions.
Do not give warfarin until the platelet count returns to its baseline level. If warfarin is administered, give vitamin K to restore the INR to normal.
Evaluate for thrombosis, particularly deep vein thrombosis.

55
Q

When do you suspect HIT/HITT?

A

Suspect if platelets count drops >50% within 5-10 days after starting heparin

56
Q

T or F: Heparin is more potent than LMWH to inhibit Xa

A

F:
Low-molecular-weight heparin (LMWH) has greater capacity to potentiate factor Xa inhibition by antithrombin than thrombin does because, with a mean molecular weight of 4500 to 5000, at least half of the LMWH chains are too short to bridge antithrombin to thrombin (ie. Xa inhibition > thrombin inhibition)

57
Q

How does fondapariux?

A

The pentasaccharide accelerates only factor Xa inhibition by antithrombin because the pentasaccharide is too short to bridge antithrombin to thrombin.

Only activity is against Factor Xa inhibition, no thrombin inhibition.

No concerns with HIT/HITT

58
Q

What are vitamin K dependent coagulant agents?

A

Vit K dependent factors: Factor II, VII, IX, X
–> Also required for anticoagulant Protein C, S
Vit K is required for the final stages of the synthesis of coagulation proteins.

59
Q

How does coumadin (ie. warfarin) work?

A

Coumadin inhibits vit K epoxide and therefore oxidised Vit K cannot be converted back to its activated state.

Coumadin decreases all vitamin K dependent factors, both procoagulant (II, VII, IX, X) and anticoagulant (protein C & S). Proteins C/S have shortest t1/2, therefore patients are hypercoagulable for first few days on coumadin (cover with heparin) –> skin necrosis

60
Q

T or F: there is a delay of effect onset of coumadin

A

T:
Works on newly synthesized factors and therefore there is a delay until action, 6 hrs for factor VII and 72 hours for factor II.
–> May need to keep on other agents until therapeutic.

61
Q

What are some side effects of coumadin?

A

Bleeding
Crosses placenta and can cause fetal abnormalities (especially in the first trimester)
Skin necrosis. Microvascular thrombi caused by coumadin’s effect on Protein C and S.

62
Q

What are the NOACS/DOACS?

A

Dabigatran (direct thrombin inhibitor)

Rivaroxaban (factor Xa inhibitor)

Apixaban (factor Xa inhibitor)

All not to be used for mechanical heart valves

63
Q

What are some antidotes for anticoagulants?

A

4 factor PCC: Prothrombin complex concentrate. Contains factors II, VII, IX, X, as well as protein C and S.
–> used for Xa inhibitors

FFP: fresh frozen plasma, also contains factors II, VII, IX, X to above but less concentrated.
–> used for extreme INR with warfarin

Idarucizumab: antibody that directly neutralizes dabigatran

Protamine: combines with heparin to form an inactive salt.

64
Q

What actions should be taken if blood has INR of greater than 4.5 and on warfarin?

A
  • hold off on coumadin

- give vitamin K

65
Q

What is the antidote for heparin and LMWH?

A

protamine but

100% neutralization with heparin and not LMWH

66
Q

What is the antidote for dabigatran?

A

moderate - activated charcoal

life threatening - idarucizumab

67
Q

What is the antidote for oral Xa inhibitors (ie. (rivaroxaban, apixaban, endoxaban)?

A

4 factor PCC (prothrombin plasma concentrate)

68
Q

What are some natural plasmin activator inhibitors?

A

The most important isendothelial cell-derived type 1 plasminogen activator inhibitor(PAI-1), which blocks the action of tPA.

Another inhibitor,α2-antiplasmin,rapidly complexes with and inactivatesfreeplasmin. Fibrin-bound plasmin is relatively protected from inactivation so that fibrinolysis can occur despite physiological plasma concentrations of this inhibitor.

An enzyme, known asthrombin-activatable fibrinolysis inhibitor(TAFI), attenuates fibrinolysis by cleaving carboxyl-terminal lysine residues from fibrin, the removal of which decreases plasminogen and plasmin binding to fibrin, retarding the lytic process. TAFI thus serves as a link between coagulation and fibrinolysis.

69
Q

How does streptokinase work?

A

Binds to Plasminogen, leading to a conformational change and therefore exposes its active sites. This allows for easier conversion to plasminogen to plasmin.

70
Q

What are issues with streptokinase?

A

Non specific plasminogen activators, and can cause systemic lytic state.

Patients can also develop Abs to streptokinase, similar Abs can form with previous streptococcal infections. This can lead to decreased effectiveness.

71
Q

What is alteplase?

A

Single recombinant t-PA
Usually for continuous infusion for ACS or ischemic strokes
IV bolus for pulmonary embolism
Fibrin specific

72
Q

What is Tenecteplase?

A

Genetically engineered variant of tissue type plasminogen activator (t-PA).
Most fibrin specific.
Given as a single bolus for ACS

Cardiology (29 decks)

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