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Cardiovascular > Anticoagulant & Antiplatelet Drugs > Flashcards

Anticoagulant & Antiplatelet Drugs Flashcards

1
Q

What are venous thrombi primarily composed of?

A

Fibrin and trapped RBCs with relatively few platelets

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2
Q

What are arterial thrombi primarily composed of?

A

Platelet aggregates held together by small amounts of fibrin

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3
Q

True or false: Venous thrombi are fibrin rich

A

True

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4
Q

True or false: Arterial thrombi are platelet rich

A

True

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5
Q

Venous thrombosis is primarily treated with ________.

A

Anticoagulation

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6
Q

Arterial thrombosis is primarily treated with _______.

A

Anti platelet therapy

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7
Q

Do you use anticoagulation or anti platelet therapy for atrial fibrillation?

A

Anticoagulation

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8
Q

When using anticoagulation, you need to assess if the benefit of preventing coagulation worth the risk of ______ of the patient.

A

Bleeding

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9
Q

What medications do you give to treat stable angina? (4 things)

A
  1. Anti-anginal agents (nitrates, beta blockers)
  2. Anti-HTN
  3. Lipid-lowering medication (statins)
  4. Anti-platelet therapy (aspirin)
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10
Q

True or false: You should use anticoagulation to treat stable angina.

A

False, Use anti-platelet therapy (aspirin)

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11
Q

What medications do you give to treat coronary artery disease? (4 things)

A
  1. Anti-anginal agents (nitrates, beta blockers)
  2. Anti-HTN
  3. Lipid-lowering medication (statins)
  4. Anti-platelet therapy (aspirin)
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12
Q

Do you use anti platelets or anticoagulation for unstable angina?

A

Both

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13
Q

Immediate aspirin is given for treatment of ____.

A

Acute myocardial infarction with ST elevation

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14
Q

What is the “clot buster” used for thrombolytic therapy?

A

Plasmin. Fibrinolytic medications are tissue plasminogen activators which makes plasminogen into plasmin.

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15
Q

What is dual anti platelet therapy?

A

Aspirin + choice of P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor)

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16
Q

What is the suffix for P2Y12 inhibitors?

A

-grel (or -grelor)

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17
Q

Name 3 P2Y12 inhibitors

A
  1. clopidogrel
  2. prasugrel
  3. ticagrelor
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18
Q

If the patient is proceeding to the catheterization lab or is high risk, what kind of inhibitor do you add in addition to the dual anti platelet therapy?

A

G2b/3a inhibitors. Eptifibatide, tirofiban, abciximab

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19
Q

Name 3 G2b/3a inhibitors

A
  1. Eptifibatide
  2. Tirofiban
  3. Abciximab
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20
Q

For anticoagulation, what medications do you use?

A

Unfractionated heparin or enoxaparin/fondaparinux. Enoxaparin and fondaparinux are both low molecular weight heparin.

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21
Q

Name 3 low molecular weight heparins (LMWH).

A
  1. Enoxaparin
  2. Fondaparinux
  3. Dalteparin
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22
Q

If the patient is proceeding to catheterization, what anticoagulant should you consider?

A

Bivalirudin

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23
Q

Rivaroxaban is an oral drug that directly inhibits what factor? What does this do?

A

Factor Xa, this inhibits the conversion from prothrombin to thrombin.

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24
Q

Is Rivaroxaban delivered orally or IV?

A

oral

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25
Q

Dabigatran is an oral drug that directly inhibits what?

A

Thrombin

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26
Q

Is Dabigatran delivered orally or IV?

A

oral

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27
Q

How can you remember that rivaroxaban is a direct Factor Xa inhibitor?

A

rivaroXAban. Xa is in the name.

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28
Q

How can you remember that Dabigatran is the direct Thrombin inhibitor?

A

Da-Big-atran. “da big” can help you remember that it inhibits Thrombin directly which is the big player in the cascade.

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29
Q

What two molecules are released from platelets to activate neighboring platelets?

A

ADP, TXA2

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30
Q

What does the activation of platelets do?

A

It moves GP2b/3a to the surface of the platelet which allows circulating fibrinogen to bind platelets together

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31
Q

What does thrombin do?

A

Converts fibrinogen to fibrin which creates the fibrin reinforcement of the platelet clot

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32
Q

In the platelet and coagulation cascades, which sites do anti platelet therapies target?

A

They target the GP2b/3a sites to inhibit aggregation. They also target ADP/TXA2 receptors to prevent activation of platelets

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33
Q

In the platelet and coagulation cascades, which sites do anticoagulation agents target?

A

They target thrombin, which prevents the conversion of fibrinogen into fibrin (prevents the final steps of the coagulation cascade from happening on the surfaces of platelets). And they target factor Xa which prevents the creation of thrombin from prothrombin.

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34
Q

Anti platelet and anticoagulation agents prevent clots. But what if clots are already present? Tissue plasminogen activators are used to break existing clots. What do tissue plasminogen activators do?

A

They turn plasminogen into plasmin which degrades fibrin.

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35
Q

For lab monitoring of anticoagulant drugs, which 3 tests do you use?

A

aPTT, PT/INR, and dTT

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36
Q

What does the aPTT monitor?

A

Intrinsic pathway

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37
Q

What does PT/INR monitor?

A

Extrinsic pathway

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38
Q

What does dTT monitor?

A

Directly monitors thrombin (hence, direct thrombin time = dTT)

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39
Q

Which test is used to monitor management of patients taking warfarin?

A

PT/INR

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40
Q

Name the 3 parenteral administered indirect thrombin-Xa inhibitors

A

Heparin (UFH), Enoxaparin (LMWH), Fondaparinux (LMWH)

Notice the “-parin(-)” in each of the drug names

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41
Q

Name the 2 parenteral administered direct thrombin inhibitors

A

Lepirudin, Bivalirudin

Notice the “-rudin” suffix

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42
Q

Name 3 oral anticoagulant agents.

A

Warfarin, Dabigatran, Rivaroxaban

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43
Q

Out of Warfarin, Dabigatran, and Rivaroxaban, which of these oral anticoagulants are direct-acting? And where do they directly act?

A

Dabigatran (thrombin) and Rivaroxaban (factor Xa)

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44
Q

Are Heparin (UFH) and LMWH’s direct or indirect inhibitors of thrombin and Xa?

A

Indirect, they work by complexing with antithrombin (ATIII) which increases its anticoagulation action by 1000X.

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45
Q

Heparin is an indirect inhibitor of thrombin. What must occur for this to happen?

A

Heparin binds to ATIII and thrombin. It is large enough to bind to both at once

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46
Q

LMWH (e.g. Fondaparinux) is an indirect inhibitor of Xa. What must occur for this to happen?

A

Binds to ATIII.

LMWH’s are small heparins and they aren’t big enough to bind more than just the ATIII. However, this is fine, because that’s all it needs to inactivate Xa

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47
Q

What molecule must Heparin bind to exert its anticoagulant effect?

A

ATIII (antithrombin III)

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48
Q

What is the most commonly used vitamin K antagonist?

A

Warfarin

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49
Q

Why is UFH and LMWH used for anticoagulation in pregnancies?

A

Because, UFH and LMWH are large, negatively charged molecules that cannot cross the placenta and are not absorbed from GI tract (given IV).

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50
Q

Why is vitamin K antagonist not given in pregnancies?

A

Because, it can cross into the placenta. It has almost 100% oral absorption. This is why Warfarin is orally administered. (UFH and LMWH are IV administered)

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51
Q

Between LMWH and UFH, which is dose-dependent and needs monitoring?

A

Heparin (UFH) is dose-dependent (zero order elimination kinetics) and needs monitoring!

Zero order elimination kinetics means that the drug elimination is independent of concentration in the body. This means that you can saturate the elimination process which can result in toxicity.

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52
Q

Does LMWH need monitoring?

A

Not generally, because it has first-order renal elimination kinetics.

53
Q

What is the difference between first order and zero order elimination kinetics? What is alcohol an example of?

A

Zero order kinetics are independent of concentration in the body. So, same amount is eliminated regardless of the concentration. Alcohol is an example of this.

First order kinetics are dependent on concentration in the body. When there is more in the body, more is eliminated.

This is important clinically because zero order kinetics can saturate elimination processes while first order kinetics cannot (the body can adapt to needs bc more drugs present means more drugs eliminated)

54
Q

What is the main adverse side effect of UFH and LMWH?

A

Hemorrhage

55
Q

How do you treat overdose of UFH/LMWH?

A

Protamine. UFH and LMWH are large negatively charged molecules and you give a large positively charged molecule to counter it. Protamine is large and positively charged.

56
Q

What is a paradoxical adverse reaction that can happen when giving UFH and LMWH?

A

There can be mild (30%) to severe (1-2% of patients) platelet activation and sequestration effect (thought to be an immune-mediated reaction). In severe cases of this adverse reaction, it can be potentially life-threatening and cause thromboembolic sequelae.

57
Q

What is an adverse effect of giving heparin for longer than 6 months?

A

Osteoporosis. Reduction in bone mineralization

58
Q

What is Bivalirudin? What is interesting about the “-rudin” suffix?

A

It is the parenterally administered direct thrombin inhibitor. “-rudin” comes from the word “Hirudin” which is what leeches use for anticoagulation so they can drink your blood!

59
Q

UFH and LMWH can be used as prophylactic treatment of _____ and ______.

A

DVT pulmonary embolism and cerebral thrombosis in evolving stroke

60
Q

Heparin complexes with ATIII and inactivates ____ and ____

A

Thrombin (IIa) and Xa

61
Q

LMWH complexes with ATIII and inactivates ____.

A

Xa

62
Q

Can LMWH overdose be treated with protamine?

A

Yes, but it’s less effective.

63
Q

Which coagulation lab test do you use to monitor for Heparin?

A

aPTT

64
Q

What coagulation lab test do you use to monitor LMWH?

A

None. Dosed mg/kg

65
Q

How are UFH and LMWH administered?

A

Parenteral (IV/SC)

66
Q

What is parenteral?

A

Administration is not through GI. Parenteral is IV/SC

67
Q

Why does Warfarin have a delay in onset of action?

A

Because, it inhibits the factors that haven’t been activated yet. (e.g. prothrombin and X)

68
Q

Are Rivaroxaban and Dabigatran slow or fast acting?

A

They are fast acting because they target active factors (Thrombin a.k.a. IIa and Xa).

This is different form Warfarin which is slow acting because it targets X and Prothrombin (inactivated factors)

69
Q

Where does Warfarin act and which factors does it prevent synthesis of?

A

Liver, factors 2, 7, 9, 10

70
Q

Where do Dabigatran and Rivaroxaban act? and what do they inhibit?

A

They act in the plasma to directly inhibit Thrombin and Xa

71
Q

Warfarin is a _____ antagonist.

A

Vitamin K

72
Q

Since Warfarin is a Vitamin K antagonist, what is also a concern, in addition to DDIs?

A

Dietary Vitamin K

73
Q

How does dietary vitamin K change the effects of warfarin?

A

If you increase dietary vitamin k, the effects of warfarin are decreased.

If you decrease dietary vitamin k, the effects of warfarin are increased.

74
Q

Vitamin K is involved in bone formation. Long-term use of which drug would cause osteoporosis?

A

Warfarin

75
Q

What enzyme metabolizes Warfarin into inactive metabolites?

A

CYP2C9

76
Q

What is important to understand about the way Warfarin is metabolized?

A

Warfarin is metabolized by the CYP2C9 enzyme which can be a potential reason for DDIs. Also, genetic polymorphisms of the CYP2C9 enzyme can affect dosing and bleeding reactions during induction of therapy.

77
Q

Name a CYP450 inducer that would decrease the effect of Warfarin

A

Barbiturates

78
Q

Name the drug that can bind to warfarin and cause a decrease in the effect of warfarin.

A

Cholestyramine (a drug that binds bile acids in the GI but also Warfarin)

79
Q

True or False: Dabigatran is a Prodrug

A

True. Dabigatran is a prodrug which means that it needs to be metabolized to become active. Dabigatran is activated by esterases when it is rapidly absorbed from the GI tract.

80
Q

How is Dabigatran eliminated?

A

Primarily by renal excretion (80%) - requires dose adjustment of CrCl

81
Q

How is Rivaroxaban eliminated?

A

Rivaroxaban is metabolized in the liver (CYP3A4) and also renal excretion (so you have to be cautious in patients with renal impairment)

82
Q

What is the main adverse side effect of Warfarin?

A

Hemorrhage

83
Q

In addition to hemorrhage, what are other side effects of Warfarin?

A

Necrosis of fatty soft tissue (especially in females during the first 10 days of therapy), GI problems (nausea, vomiting, diarrhea, and cramping), and osteoporosis

84
Q

How do you treat overdose of Warfarin?

A

Vitamin K is given orally if INR > 10 or through IV if there is major bleeding

85
Q

What can FFP (fresh frozen plasma) be given for?

A

During emergencies of major bleeding from overdose of anticoagulants, you can give FFP to help treat the overdose.

86
Q

What is a recently available overdose treatment for Dabigatran?

A

Idarucizumab (monoclonal antibody)

87
Q

WTF is a DOAC?

A

Direct Oral Anti-Coagulant

88
Q

Are DOAC (dabigatran/rivaroxaban) generally preferred or Warfarin?

A

DOAC is generally preferred. It is at least as effective as warfarin but appears to be safer. Warfarin has issues with variability in dosage due to the enzyme that metabolizes it and also the vitamin K dietary consideration. With warfarin, there needs to be close monitoring with INR.

89
Q

Are DOAC (dabigatran/rivaroxaban) typically monitored when given?

A

No

90
Q

Should Warfarin or DOAC be used for A Fib?

A

For A fib that is nonvalvular, DOAC is preferred. For A fib with a mechanical or bioprosthetic valve or prior mitral repair or mitral valve stenosis, Warfarin should be used.

91
Q

What are 4 things that make Warfarin a reasonable choice over DOAC?

A
  1. Patients already on warfarin who are comfortable with INR monitoring and who are easily maintained in the therapeutic range
  2. Patients that are unlikely to comply with BID dosing of DOACs. (Once daily DOAC are not a thing)
  3. Patients with chronic kidney disease (GFR less than 25-30)
  4. Patients for whom cost is a concern ($80 per month [including monitoring] vs $290)

(5. also, Warfarin should be used for A Fib over DOACs when the patient has valvular a fib)

92
Q

Should Warfarin or DOAC be used in patients with renal problems?

A

Warfarin. Warfarin is hepatic metabolism while both DOAC have renal elimination even though rivaroxaban is metabolized in the liver before being eliminated renally.

93
Q

What is the dosing schedule for apixaban and dabigatran? (DOAC drugs)

A

BID

94
Q

Are DOAC drugs okay for pregnancy use?

A

Category C - not studied

95
Q

What is the onset of action for warfarin?

A

Hrs-days

96
Q

What is the onset of action for dabigatran?

A

1-2h

97
Q

What is the onset of action for apixaban and rivaroxaban?

A

2.5-4h

98
Q

Aspirin in low doses produces an anti-clotting effect because of its action on ____.

A

Irreversible inhibition of COX-1 which typically converts AA to TXA2. This decreases levels of TXA2 (thromboxane A2)

99
Q

How do ticagrlor, clopidogrel, and prasugrel cause their anti-platelet therapy effects?

A

They inhibit the ADP (P2Y12) receptor

100
Q

Of the P2Y12 drugs, which two are prodrugs?

A

Clopidogrel and Prasugrel are prodrugs. They are activated by CYP450 to cause irreversible inhibition of the P2Y12 receptor.

101
Q

Of the P2Y12 drugs, which is reversible?

A

Ticagrelor is a reversible inhibitor of the P2Y12 receptor and it does NOT need activation (unlike the other 2 drugs in this class which are prodrugs)

102
Q

How are P2Y12 inhibitor drugs administered?

A

Orally. Clopidogrel/prasugrel are dosed once daily orally. Ticagrelor is given orally BID with meals.

103
Q

How are G2b/3a inhibitors administered?

A

IV. Basically, the ones you use in acute settings are parenteral.

104
Q

Are the P2Y12 drugs slow or fast onset?

A

Slow onset so often given with loading dose.

105
Q

The risk of bleeding in patients receiving heparin is increased by aspirin because aspirin _____

A

inhibits platelet function

106
Q

What are adverse reactions of low-dose aspirin?

A

Generally none. Sometimes GI problems.

107
Q

What are adverse reactions for P2Y12 and G2b/3a inhibitors?

A

Bleeding

108
Q

How do you treat Acute MI (NSTEMI/STEMI)

A

Dual platelet therapy (aspirin plus a P2Y12)

109
Q

How do you treat unstable angina?

A

Dual platelet therapy (aspirin plus a P2Y12)

110
Q

How do you treat PCI (percutaneous

A

Dual platelet therapy (aspirin plus a P2Y12) and +/- G2b/3a inhibitors

111
Q

What do you use for secondary prevention of MI?

A

Aspirin

112
Q

What do you use for secondary prevention of ischemic stroke?

A

Aspirin

113
Q

What is DDI for aspirin?

A

Increased bleeding with anticoagulants, also all other NSAIDS

114
Q

What is DDI for clopidogrel?

A

PPI (Proton pump inhibitors) can block clopidogrel from being activated by P450. This results in decrease of clopidogrel effect which can result in an unsuspected clotting event

115
Q

What is the suffix for fibrinolytic agents?

A

-teplase

116
Q

Name 3 fibrinolytic agents

A

Alteplase, Reteplase, Tenecteplase

117
Q

What is a good way to remember the -teplase suffix for fibrinolytic agents?

A

-teplase stands for tPA (tissue Plasminogen Activator)

118
Q

When treating ACS–STEMI, why would you give beta blockers or nitrates?

A

To reduce myocardial oxygen demand

119
Q

When would you use fibrinolytic for treatment of STEMI?

A

If you can’t open the artery within 90 minutes (no cath lab available). So, you would give fibrinolytics and transfer them to somewhere with a cath lab.

120
Q

What is a major concern when giving fibrinolytic treatment?

A

Intracranial hemorrhage

121
Q

Why is fibrin specificity important for fibrinolytic agents?

A

Fibrinolytic agents target plasminogen to activate into plasmin which is the clot buster. However, if you bind to circulating plasminogen, you will end up clot busting systemically which causes bleeding complications. The fibrin specificity is a measure of how specific these fibrinolytic agents only target fibrin-bound plasminogen.

122
Q

Which fibrinolytic agent has the highest fibrin specificity?

A

Tenecteplase (TNK-tPA)

123
Q

Which fibrinolytic agent has the lowest fibrin specificity?

A

Streptokinase (no longer used in USA), but next lowest is Reteplase (rPA)

124
Q

Which fibrinolytic agent has second-to-highest fibrin specificity?

A

Alteplase (rtPA)

125
Q

Which fibrinolytic agent is easiest to administer?

A

Tenecteplase (TNK-tPA). It is single bolus dose. Reteplase is 2 bolus dose and Alteplase is bolus followed by infusions over 90 minutes.

126
Q

Which fibrinolytic agent seems to be best (fibrin specific and easy to administer?)

A

Tenecteplase (TNK-tPA)

127
Q

What are 4 limitations of fibrinolytics compared to Primary PCI (percutaneous coronary intervention)?

A
  1. Failure to obtain TIMI grade 3 flow in high % of patients
  2. Vessel reocclusion
  3. Significant risk of intracerebral hemorrhage
  4. contraindications in about 30% of candidates including active peptic ulcer disease, underlying bleeding disorders, recent stroke, or recent surgery
128
Q

What are 4 contraindications for fibrinolytics (~30% not suitable candidates)?

A
  1. Active peptic ulcer disease
  2. Underlying bleeding disorders
  3. Recent stroke
  4. Recovering from recent surgery

Cardiovascular (22 decks)

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