Antiplatelets, Anticoagulants, And Thrombolytics

Front 1

What is the main risk of therapy with these classes of drugs?

Back 1

Bleeding!

Front 2

What are some common risk factors for bleeding?

Back 2

Severe, uncontrolled hypertension
Aneurysm
Recent surgery
Recent trauma
Hepatic disease
Renal disease
Bone marrow suppression

Front 3

What does the Bleeding Time (BT) test tell us?

Back 3

Platelet function as well as platelet count

Front 4

What is the Prothrombin Time (PT) test used for?

Back 4

To evaluate Vitamin K dependent factors (2,7,9,10) when patient is on Warfarin

Normal is 10-13 seconds; goal is 15-26 seconds

Front 5

What is the International Normalized Ratio (INR)?

Back 5

Test that replaces PT test for patients on Warfarin

Normal is 1.0 ; goal is 2.0 - 3.0
*Goal is 2.5 - 3.5 for patients with mechanical heart valves and patients who threw a clot while on warfarin and within the 2 - 3 range

Front 6

What is the Activated Partial Thromboplastin Time (aPTTT) test?

Back 6

Evaluates serine protease factors (2, 9, 10, 11, and 12) for patients on Heparin

Normal is 30-50 seconds; goal is 50-75 seconds

Front 7

What is the Anti-Xa assay?

Back 7

Used in place of aPTTT for patients on Heparin to avoid the variability of the aPTTT test.

Normal 0.3 - 0.7 units/mL

Front 8

What is Activated Clotting Time (ACT)?

Back 8

Used for patients on high dose unfractionated Heparin during percutaneous coronary intervention and coronary arter bypass grafts.

Normal 70 - 180 seconds; goal 250 - 350 seconds

Front 9

What is the only antiplatelet COX inhibitor and its MOA?

Back 9

Aspirin (Acetyl Salicylic Acid)

MOA: Irreversible inhibition of COX, preferentially TxA2 vs PGI2. Effects last life of platelet (7-10 days)

Front 10

What are the side effects of aspirin?

Back 10

GI related

Use caution in asthmatics due to potential cause of bronchospasm

Front 11

What drugs are included in the ADP Antagonist group?

Back 11

Antiplatelet drugs:

Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor

Front 12

What is the MOA of the ADP Antagonists?

Back 12

Inhibition of ADP binding to the P2Y12 surface receptor.

Irreversible inhibition of platelets (except Ticagrelor), inhibiting activation of GP 2b/3a receptor and downstream binding to other platelets, vWF, and fibrinogen.

Front 13

What are some differing indications of ADP antagonists vs ASA?

Back 13

Use for ASA hypersensitivity or allergy
In combo with ASA and anticoagulants

Front 14

T or F: All of the ADP antagonists are pro drugs

Back 14

False; Ticagrelor does NOT require hepatic activation

Front 15

What are the side effects of the ADP antagonists?

Back 15

Similar to ASA; clopidogrel less GI and Ticlopidine more GI than aspirin

Prasugrel increased bleeding compared to Clopidogrel

Ticagrelor increases serum creatinine

Front 16

What should be monitored for a patient who is taking ADP antagonists?

Back 16

CBC count for platelets
Liver function test (for the pro drugs)
Serum creatinine (Ticagrelor)

Front 17

What is the most potent receptor for platelet activation?

Back 17

GP 2b/3a Receptor

Front 18

What drugs are found in the GP 2b/3a receptor antagonist group?

Back 18

Antiplatelets drugs:

Abciximab
Eptifibatide
Tirofiban

Front 19

What is the MOA of the GP 2b/3a receptor antagonists?

Back 19

Inhibits GP 2b/3a receptor activation and binding with fibrinogen, vWF, platelets

Front 20

Which GP 2b/3a antagonist is a monoclonal antibody?

Back 20

Abciximab (ends in MAB)

Front 21

Which GP 2b/3a antagonist is used as a prophylaxis of thromboembolic events in percutaneous coronary intervention?

Back 21

Abciximab, Eptifibatide, and Tirofiban

Abcix used in acute coronary syndrome as well.

Front 22

What GP 2b/3a antagonists are used to treat unstable angina and non Q wave MI's?

Back 22

Eptifibatide and Tirofiban

Front 23

T or F: All GP 2b/3a antagonists are administered IV?

Back 23

True

Front 24

What side effects are seen in patients on GP 2b/3a antagonists?

Back 24

Hypotension - all 3
GI/Myalgia with abciximab
Thrombocytopenia with abciximab and tirofiban (rare)

Front 25

What should be monitored for a patient on GP 2b/3a antagonists?

Back 25

Platelet count, Serum creatinine, BUN

Front 26

What are the PDE3 inhibitors?

Back 26

Antiplatelet drugs:

Anagrelide
Cilostazol
Dipyridamole

Front 27

What is the MOA of the PDE3 inhibitors?

Back 27

Inhibits PDE3 which causes an increase in cAMP levels which causes vasodilation and decreases platelet aggregation

Front 28

Which PDE3 inhibitor at high dose is indicated for thrombocythemia (high platelet count)?

Back 28

Anagrelide

Front 29

Which PDE3 inhibitor is used for intermittent claudication (pain due to little blood flow during exercise) associated with PVD?

Back 29

Cilostazol

Contraindicated with CHF

Front 30

Which PDE3 inhibitor is used with other antiplatelets for prophylaxis of thromboembolism?

Back 30

Dipyridamole

Not often prescribed

Front 31

T or F: PDE3 inhibitors cause hypotension.

Back 31

True, all three drugs can cause hypotension as a side effect.

Front 32

Which PDE3 inhibitor can cause GI problems as well as tachy- arrhythmias?

Back 32

Cilostazol

Front 33

Which PDE3 inhibitor can cause dizziness?

Back 33

Dipyridamole

Front 34

What should be monitored on a patient on PDE3 inhibitors?

Back 34

AST/ALT for liver toxicity
SCr and BUN for dosing

Front 35

What drugs belong to the Anti Thrombin 3 Enhancers (Heparins), specifically the Low Molecular Weight Heparins (LMWHs)?

Back 35

Unfractionated Heparin (UFH) is full molecule

LMWHs: Anticoagulants that end in -parin

Dalteparin
Enoxaparin
Tinzaparin

Front 36

What is the MOA of the Heparins?

Back 36

Bind to AT-3 and induces a conformational change enhancing binding to serine protease clotting factors (active forms of 2, 9, 10, 11, 12, and plasmin/kallikrein)

Front 37

Factor _______ requires a tri-bond to inactivate and can only be inactivated by the ___________ complex

Back 37

2a ; UFH-AT 3

Front 38

T or F: Factor 10a has no tri-bond requirement to inactivate and can be inactivated by both the LMWH-AT 3 and UFH-AT 3 complexes.

Back 38

True

Front 39

What drugs are indicated for prophylaxis and treatment of thrombotic events?

Back 39

Both UHF and the LMWHs

Front 40

How are UHF and LMWHs administered?

Back 40

UHF: Administered SQ for prophylaxis and IV for treatment

LMWHs: Always SQ

Front 41

What are the side effects of the AT 3 enhancers?

Back 41

Heparin induced thrombocytopenia (less with LMWHs)
Osteoporosis w/ long term treatment
Hyperkalemia

Front 42

What are the treatment options for a patient on heparin who begins to bleed?

Back 42

Protamine sulfate
Whole blood or fresh frozen plasma (for the activated clotting factors)

Front 43

What drug belongs to the Vitamin K inhibitors and what is its MOA?

Back 43

Anticoagulant: Warfarin

MOA: Inhibits Vit. K dependent factors (2, 7, 9, 10) as well as protein C and S
**Does not inhibit activated factors**

Front 44

How does Vitamin K activate an inactive clotting factor?

Back 44

Reduced Vitamin K is the active form that carboxylates a K dependent factor, thus activating it.

Front 45

T or F: Warfarin has many drug interactions.

Back 45

True

Need to know patients med list before prescribing warfarin

Front 46

How long does it take for warfarin to reach steady state?

Back 46

5-7 days, mostly because the factors have long half lives

Front 47

What are the side effects of warfarin?

Back 47

Skin necrosis and gangrene

Contraindicated in pregnancy

Front 48

What is the antidote if a patient develops warfarin toxicity?

Back 48

Vitamin K and whole blood/fresh frozen plasma

Front 49

What drugs belong to the class of 2a inhibitors?

Back 49

Anticoagulants:

Argatroban
Bivalirudin
Desirudin
Dabigatran
Lepirudin
*All of the -rudins are from leech spit*

Front 50

What is the MOA of the 2a inhibitors?

Back 50

Reversibly inhibit thrombin (2a) **lepirudin irreversibly** which in turn inhibits platelets, factors 5, 8, 13, protein C and fibrin

Front 51

What are the side effects of the 2a inhibitors?

Back 51

1. Dermal/systemic reactions - lepirudin/desirudin
2. Hirudin antibodies/anaphylaxis - unseen w/ argatroban
3. Hypotension/arrhythmias/GI upset - argatroban/bivalirudin
4. Gi upset/anaphylaxis - dabigatran

Front 52

What is the "antidote" for 2a inhibitor toxicity?

Back 52

No antidote, but they all have short half lives!

Front 53

What should be monitored in a patient on 2a inhibitors?

Back 53

Hemoglobin and hematocrit (H/H)
SCr and BUN
aPTT/PT/INR/ACT/TT/BT may be affected as well

Front 54

What drugs belong to the class of 10a inhibitors?

Back 54

Anticoagulants:

Fondaparinux
Rivaroxaban

Front 55

What is the MOA of the 10a inhibitors?

Back 55

Selective inhibition of the AT-3 mediated inhibiiton of factor 10a

*No action on factor 2a or platelets*

Front 56

What are the side effects of the 10a inhibitors?

Back 56

Thrombocytopenia
AST/ALT increase

Front 57

What is the possible antidote for rivaroxaban?

Back 57

Prothrombin Complex Concentrate (PCC)

**Not useful for fondaparinux*

Front 58

What should be monitored in a patient on 10a inhibitors?

Back 58

SCr and BUN
Platelet count - for toxicity
Anti-Xa serum test

Front 59

What are the thrombolytic drugs?

Back 59

All end in -ase

Alteplase
Reteplase
Streptokinase
Tenecteplase
Urokinase

Front 60

What is the MOA of the thrombolytics?

Back 60

Aids in the conversion of plasminogen to plasmin which initiates local fibrinolysis (clot busting)

Front 61

What are the contraindications for thrombolytics?

Back 61

Active/recent bleeding
Uncontrolled hypertension
Cerebral tumors

Front 62

What should be done if a patient is over-treated with a thrombolytic agent?

Back 62

Stop infusion immediately, give fresh frozen plasma or whole blood

Front 63

What are the side effects related to thrombolytic use?

Back 63

Hemorrhagic CVA (cerebrovascular accident or "stroke")
Reperfusion arrhythmias
Hypotension
Hypersensitivity reactions
Antibody resistance (thrombolytics are made from recombinant DNA)