Step 1 - Pharm - Bleeding

Front 1

MOA of heparin

Back 1

Activates antithrombin III, resulting in decreased thrombin and factor Xa

Front 2

This anticoagulant can be used during pregnancy because it doesn't cross the placenta

Back 2

Heparin

Front 3

This is given to induce rapid reversal of heparinization

Back 3

Protamine sulfate (positive molecule that binds negatively charged heparin)

Front 4

This anticoagulant may cause osteoporosis

Back 4

Heparin

Front 5

This anticoagulant may cause thrombocytopenia

Back 5

Heparin

Front 6

Half lives of heparin and warfarin

Back 6

Heparin has a short halflife, warfarin has a long halflife

Front 7

This anticoagulant acts more on factor Xa than on ATIII

Back 7

Enoxaparin

Front 8

This anticoagulant is not easily reversible, unlike its cousin heparin

Back 8

Enoxaparin

Front 9

This anticoagulant can be administered subcutaneously, and does not require monitoring

Back 9

Enoxaparin

Front 10

How does heparin cause thrombocytopenia?

Back 10

Autoantibodies to heparin-bound platelets; platelets are destroyed, and remaining plateletes become overactivated

Front 11

MOA of lepirudin

Back 11

Directly inhibits thrombin. Derived from hirudin

Front 12

MOA of bivalirudin

Back 12

Directly inhibits thrombin. Derived from hirudin

Front 13

These anticoagulants can be used as an alternative to heparin in patients with HIT (heparin-induced thrombocytopenia)

Back 13

Lepirudin, bivalirudin

Front 14

MOA of warfarin (coumadin)

Back 14

Blocks epoxide reductase (activator of vitamin K). Interferes with synthesis and gamma-carboxylation of vit K-dependent factors II, VII, IX, X and proteins C and S.

Front 15

This anticoagulant is metabolized by the CYP450 pathway

Back 15

Warfarin (Coumadin)

Front 16

This anticoagulant can cross the placenta and is therefore contraindicated in pregnancy

Back 16

Warfarin (Coumadin)

Front 17

Does warfarin affect PT or PTT?

Back 17

Both. Causes increased PT (factor VII, and therefore the extrinsic pathway, is affected)

Front 18

This anticoagulant can cause skin and tissue necrosis

Back 18

Warfarin (Coumadin)

Front 19

This anticoagulant is teratogenic

Back 19

Warfarin (Coumadin)

Front 20

Compare the structures of heparin and warfarin

Back 20

Heparin is polymer (large) that is anionic and acidic. Warfarin is a small, lipid-soluble molecule (that therefore can cross the placenta)

Front 21

Route of administration of heparin vs warfarin

Back 21

Heparin is given parenterally (IV, SC); warfarin is po

Front 22

Site of action of warfarin

Back 22

Liver

Front 23

Site of action of heparin

Back 23

Blood

Front 24

Onset of heparin vs warfarin

Back 24

Heparin has a rapid onset (seconds), whereas warfarin has a slow onset, limited by the half-lives of normal clotting factors. Protein C has the longest half-life

Front 25

This anticoagulant is a vitamin K antagonist

Back 25

Warfarin (Coumadin)

Front 26

Duration of action of heparin vs wafarin

Back 26

Heparin lasts for hours, warfarin lasts for days

Front 27

Treatment of acute overdose of warfarin

Back 27

IV vitamin K and fresh frozen plasma

Front 28

Monitoring of heparin

Back 28

Check PTT (intrinsic pathway)

Front 29

Monitoring of warfarin (coumadin)

Back 29

Check PT (extrinsic pathway; the vitamin K dependent factors are all included)

Front 30

These are the thrombolytics (5)

Back 30

tPA (alteplase), APSAC (anistreplase), streptokinase, urokinase

Front 31

MOA of thrombolytics

Back 31

Directly or indirectly aid conversion of plasminogen to plasmin. Plasmin cleaves thrombin and fibrin clots.

Front 32

What are the laboratory changes seen in thrombolytic therapty: PT, PTT, platelets

Back 32

PT and PTT both increase; platelet counts don't change

Front 33

Clinical uses of thrombolytic therapy

Back 33

Early MI, early ischemic stroke

Front 34

These drugs are contraindicated in patients with active bleeding history

Back 34

Thrombolytics (streptokinase, urokinase, tPA, APSAC)

Front 35

These drugs are contraindicated in patients with history of intracranial bleeding

Back 35

Thrombolytics (streptokinase, urokinase, tPA, APSAC)

Front 36

These drugs are contraindicated in patients with active bleeding

Back 36

Thrombolytics (streptokinase, urokinase, tPA, APSAC)

Front 37

These drugs are contraindicated in patients with severe hypertension, recent surgery, or known bleeding diatheses

Back 37

Thrombolytics (streptokinase, urokinase, tPA, APSAC)

Front 38

Treatment of acute overdose of thrombolytics

Back 38

Aminocaproic acid (inhibits fibrinolysis)

Front 39

MOA of tPA

Back 39

Directly converts plasminogen to plasmin

Front 40

MOA of urokinase

Back 40

Directly converts plasminogen to plasmin

Front 41

MOA of streptokinase

Back 41

Indirectly converts plasminogen to plasmin by activating an endogenous activator

Front 42

MOA of anistreplase

Back 42

Indirectly converts plasminogen to plasmin by activating an endogenous activator and proactivator

Front 43

MOA of aminocaproic acid

Back 43

Directly inhibits conversion of plasminogen to plasmin

Front 44

MOA of aspirin

Back 44

Acetylates COX-1,2 (irreversibly) in platelets only (leaves leukocytes alone); prevents TXA2 formation by inhibiting glycoprotein expression in activated platelets

Front 45

Laboratory findings in aspirin therapy (PT, PTT, bleeding time)

Back 45

No effect on PT, PTT. Increased bleeding time. (Platelet plug formation, or primary coagulation, is being impeded, NOT the coagulation cascade)

Front 46

Side effects of aspirin

Back 46

Gastric ulcers, hyperventilation, Reye's syndrome (hepatoencephalopathy in kids), tinnitus (CN VIII toxicity)

Front 47

MOA of clopidogrel

Back 47

Irreversibly blocks ADP receptors on platelets. IIb and IIIa receptors cannot be expressed (fibrinogen binders; Ia binds collagen and Ib binds vWF).

Front 48

MOA of ticlopidine

Back 48

Same as clopidogrel. Irreversibly blocks ADP receptors, preventing fibrinogen binding and therefore preventing aggregation.

Front 49

These drugs are shown to reduce incidence of incidence or recurrence of thrombotic stroke

Back 49

Clopidogrel, ticlopidine

Front 50

Side effects of ticlopidine

Back 50

Neutropenia

Front 51

MOA of abciximab

Back 51

Binds IIb/IIIa on activated platelets, preventing aggregation. (Clopidogrel and ticlopidine prevent expression of these same receptors)

Front 52

This drug is given for percutaneous transluminal coronary angioplasty

Back 52

Abciximab

Front 53

Side effects of abciximab

Back 53

Bleeding, thrombocytopenia

Front 54

These drugs are given in the setting of coronary stenting

Back 54

Clopidogrel, ticlopidine

Front 55

These drugs are given in the setting of acute coronary syndromes

Back 55

Clopidogrel, ticlopidine, abciximab