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Pharmacology 2 > Antithrombotics > Flashcards

Antithrombotics Flashcards

1
Q

Thrombus

A

A clot that adheres to the wall of a blood vessel

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2
Q

Embolus

A

A clot that has dislodged from the vessel wall and is freely moving in the blood stream

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3
Q

What is the difference between an arterial and venous thrombus

A

Arterial is usually due to a collection of platelets. Where as a venous clot usually forms because of inappropriate activation of the coagulation cascade (rich in fibrin)

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4
Q

What is the MOA of anti-platelet therapies

A

Prevents platelets from aggregating by inhibiting the COX-1 enzyme (cox-1 is cyclooxgenase)

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5
Q

Which NSAID is the only one that irreversibly exhibits antithrombotic efficacy

A

Aspirin (also has a 7-10 half life)

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6
Q

What are anti platelet drugs used for

A

Treatment of MI and stroke (arterial clot prevention)

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7
Q

What is the MOA of anticoagulation

A

Either inhibits the action of the coagulation factors (thrombin inhibitors) or inhibits the synthesis of coagulation factors (vitamin K antagonists)

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8
Q

What is the extrinsic clotting system triggered by

A

Factor VII

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9
Q

What is the intrinsic clotting system triggered by

A

Factor XII

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10
Q

What are the steps of blood clot (clotting cascade - basic end pathyway)

A

Factor Xa initiates the conversion of prothrombin to thrombin. Thrombin then activates fibrinogen to fibrin formation which becomes the blood clot

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11
Q

Which pathway can you test PTT for

A

Intrinsic

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12
Q

Which pathway can you test pT for

A

Extrinsic

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13
Q

What drug works on the intrinsic pathway (pTT)

A

Heparin

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14
Q

What drug works on the extrinsic pathway

A

Warfarin

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15
Q

Which drug is a thrombin inhibitor

A

heparin

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16
Q

Which drug is a vitamin K antagonist

A

warfarin

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17
Q

What is the MOA of the antithrombin drugs

A

Blocks the prothrombin/thrombin interaction in the clotting cascade (interferes with formation of thrombi)

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18
Q

What is the MOA of the Vitamin K antagonists

A

Protein coagulation factors need vitamin K as a cofactor. By blocking vitamin K, it results in clotting factors with diminished activity (prevents clot from getting bigger)

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19
Q

What is a major difference of heparin and warfarin

A

Takes a lot longer for warfarin to work 8-12 hours, but peak effects may be even as late as 72 hrs.

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20
Q

How to you reverse the effects of coumadin

A

give vitamin K

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21
Q

What are anticoagulation drugs used for

A

prevention of venous thromboembolism, DVT, PE

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22
Q

What is the MOA of thrombolytic agents

A

Act directly or indirectly to cover plasminogen to plasmin, which cleaves fibrin (lyses clot = fibrinolysis)

23
Q

What are the adverse effects of coumadin

A
  1. Hemorrhage

2. Numerous drug drug interactions due to liver metabolism (aspirin, alcohol, metronidazole)

24
Q

How do you monitor coumadin

A

INR 2-3 is therapeutic window, or pT test

25
Q

What additional clinical uses does heparin have

A
  1. surgical prophylaxis

2. Pregnant women with prosthetic heart valves or DVT/PE, do not cross placenta

26
Q

Administration of heparin

A

Must be given parenterally - IV (1-2 hours) - NO IM INJECTIONS. Due to potential hemorrhagic issues

27
Q

Administration of warfarin

A

Given orally. 99% bound which prevents diffusion into CSF, urine or breast milk. Crosses the placenta.

28
Q

What is the absorption of LMWH

A

Subcutaneous injection that takes 4 hours to get max effect.

29
Q

What are the adverse effects of heparin

A
  1. Bleeding
    2 Hypersensitivity
  2. Thrombocytopenia
  3. abnormal LFT
30
Q

MOA of dabigatran (Pradaxa)

A

Antithrombotic (anticoagulant)

31
Q

What is the use of dabigatran

A

Prodrug that is a direct thrombin inhibitor used for prevention of stroke and systemic embolism with atrial fibrillation.

32
Q

How is dabigatran administered

A

Orally, very few side effects, does not need to be monitored

33
Q

MOA of rivaroxaban (xarelto)

A

Antithrombotic (anticoagulant)

34
Q

What is the use of rivaroxaban

A

DVT, afib in nonvalvular patients

35
Q

What is the MOA of aspirin

A

it is an anti platelet drug. Which means that it inhibits platelet aggregation factors (COX 1). And more specifically in aspirin thromboxane A2 is inhibited

36
Q

What is aspirin used for

A

MI, stoke (transient cerebral ischemia)

37
Q

Adverse effects of aspirin

A
  1. Bleeding
  2. Increased risk for hemorrhagic stroke
  3. GI bleeding
38
Q

MOA of ticlopidine (ticlid)

A

Anti platelet aggregation but different mechanism than aspirin. Blocks ADP from binding to receptors which then inhibits platelets to bind to fibrinogen and to each other

39
Q

What is ticlopidine used for

A

Prevention of transient ischemic attacks and strokes for patients with prior cerebral thrombotic events. Also used during coronary stent placement to decrease risk of clot forming on the stent.

40
Q

Adverse effects of ticlopidine

A
  1. Neutropenia/agranulocytosis
  2. Thrombotic thrombocytopenia purpura *TTP
  3. Aplastic anemia
41
Q

MOA of copidogrel (plavix)

A

Anti platelet, same mechanism as ticlopidine

42
Q

What is the use of clopidogrel

A

Prevention of atherosclerotic events following recent MI, stroke, or established peripheral arterial disease. Also used for with coronary stent procedures (used more in heart patients than in ticlopidine)

43
Q

Adverse effects of clopidogrel

A

Better adverse effects than ticlopidine. Still can cause TTP.

44
Q

MOA of dipyridamole (persantine)

A

Antiplatelet mechanism. Increases cellular levels of cAMP which results in decreased thromboxane A2 synthesis

45
Q

What is thromboxane A2 responsible for

A

Promotes clumping process of platelets

46
Q

What is dipyridamole (persantine) used for

A
  1. Coronary vasodilator - given to patients with artificial heart valves
  2. Usually given in combo with aspirin/or warfarin
47
Q

Adverse effects of dipyridamole

A
  1. GI bleeding
  2. should not be used in elderly
  3. Orthostasis problems
48
Q

MOA of alteplase (tPA, activate)

A

Low affinity for free plasminogen but rapidly activates plasminogen that is bound to fibrin in a clot or hemostatic plug. “fibrin selective”

49
Q

Use of alteplase

A

MI, massive PE, acute ischemic strokes

50
Q

Adverse effects of alteplase

A
  1. Major bleeding complications
  2. GI bleeding
  3. Cerebral hemorrhage
51
Q

MOA of Urokinase (abbokinase)

A

Directly cleaves arganine-valine bond of plasminogen to yield active plasmin

52
Q

Use of urokinase

A

Only approved for lysis of PE.

off label use - acute MI, arterial thromboembolism, coronary thrombosis and DVT

53
Q

Adverse effects of urokinase

A

Bleeding

Pharmacology 2 (8 decks)

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