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Blood and Lymph > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

what subedothelial substances are exposed after vascular injury?

A

collagen and vWF

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2
Q

what mediators are released after platelet activation that further activate other platelets?

A

ADP/5-HT

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3
Q

What does GPIIb/IIIa do?

A

binds to circulating fibrinogen and cause platelet aggregation

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4
Q

What occurs after Tissue Factor complexes with Factor VII?

A

further activates the cascade to convert Factor II (prothrombin) to factor IIa (thrombin)

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5
Q

What does Thrombin do?

A

further stimulates XIII to cross link the fibrin and stabilize the clot, in addiction thrombin amplifies generation of thrombin by activating V, VIII, XI

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6
Q

What class of drug is Unfractionated Heparin?

A

Indirect Thrombin Inhibitors

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7
Q

Describe the mechanism and advantage of LMWH

A

too short to bridge ATIII to thrombin, metabolized in liver by heparinase. Advantages are less bleeding, longer t1/2, SC, no lab monitoring

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8
Q

What are some common LMWH

A

Enoxaparin, Dalteparin, FONDAPARINUX

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9
Q

What are the major SE of Heparins

A

BBW: can cause spinal/epidural hematomas

Hemorrhage, HAT, HIT

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10
Q

What is the antidote for Hemorrhage and how does it work

A

Protamine, which is positively charged to neutralize the negative charge on Heparin

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11
Q

Describe the mechanism of HAT (Type 1)

A

(non-immune mediated Heparin) direct interaction between heparin and platelets -> platelet aggregation

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12
Q

Describe the mechanism of HIT

A

(Immune-mediated) rare, fatal; IgG Abs vs heparin- platelet factor 4 complexes. Complex bind to Fc(g)IIa receptors -> platelet aggregation and release of more platelet factor 4 and thrombin

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13
Q

List the Direct Thrombin Inhibitors

A

Lepirudin, Desirudin, Bivalirudin, Argatroban, Dabigatran

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14
Q

What is the MOA of Lepirudin, Desirudin, Bivalirudin

A

Directly binds to thrombin to prevent thombin-mediated activation of fribrinogen and factor XIII

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15
Q

What makes Lepirudin highly effective?

A

a) inhibits free and fibrin bound thrombin

b) binding to thrombin is irreversible

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16
Q

What potential disadvantages are there to Lepirudin?

A

prolonged t1/2 in renally compromised pts- caution for dose adjustments

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17
Q

Describe the MOA for Argatroban and Dabigatran;

A

binds only to the active site of thrombin

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18
Q

Describe Argatroban

A

used for tx of pts with HIT, safe to be give in renal insufficiency b/c excreted via biliary route: CYP3A4 dependent metabolism

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19
Q

Describe Dabigatran

A

oral produrg, advantages; no need to monitor blood levels

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20
Q

What is the Oral Anticoagulant?

A

Warfarin (Coumadin)

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21
Q

Why does warfarin have an onset delay

A

Onset parallels t1/2 of the coagulation factors

Affected factors are 2,7,9,10 but factor 7 has the shortest t1/2(6 hrs)

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22
Q

How long until you see the effect of Warfarin?

A

18-24 hours

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23
Q

What gene provides Warfarin resistance?

A

VKORC1 gene

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24
Q

What are the adverse effects of Warfarin?

A

skin necrosis- widespread microvasculature necrosis

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25
Q

What drug is under the category of Antiplatelet Agents?

A

Aspirin

26
Q

What is the MOA of Aspirin?

A

inhibits COX-1

27
Q

what would you expect with a high does of aspirin and how would you prevent it?

A

inhibit COX-1 in endothelial cells which would prevent formation of PGI2 (vasodilator) use Baby aspirin

28
Q

What is the MOA of the Thienopyridine ADP Inhibitors

A

irreversible inhibitors of platelet ADP receptrs that covalently modify and inactivate P2Y(ADP) recpetors (aka P2Y12)

29
Q

What is the BBW for Thienopyridine ADP Inhibitors

A

bleeding risk, contraindicated in conditions like active pathological bleeding or a Hx of transient ischemic attacks or stroke

30
Q

Name the ADP Inhibitors: Thienopyridines

A

1) Ticlopidine- 1st gen
2) Clopidogrel- 2nd gen.
3) Prasugrel- 3rd gen.
4) Ticagelor- oral

31
Q

Describe Ticlopidine

A

8-11 days for max effect b/c converts to thiol metabolites that accumulate->delay in action, shorten delay onset with aspirin or loading does

BBW: life threatening hematological rxns like neutropenia thrombotic thrombocytopenic purpura and aplastic anemia

32
Q

Describe Clopidogrel

A

metabolized via CYP219, may show rates of higher CV SE, screening pts for CYP2C19 used to determining therapeutic strategy

BBW: diminished effectiveness in poor metabolizers

33
Q

Describe Prasugrel

A

more effectively metabolized than Clopidogrel, higher levels of active metabolite, greater P2Y ADP antagonism, metabolized via CYP3A4, more prone to bleeding

BBW: bleeding risk, contraindicated in conditions like active pathological bleeding, Hx of transient ischemic attacks or stroke

34
Q

Describe Ticagelor

A

parent drug and major metabolite reversibly interact with P2Y12 ADP receptor, both parent and metabolite- equipotenet(equally powerful), metabolized by CYP3A4

BBW: bleeding risk, contraindicated in conditions like active pathological bleeding, Hx of transient ischemic attacks or stroke

35
Q

how does expression of GP IIb/IIIa occur

A

activation of platelets from stimulating thrombin, ADP, collagen, and TxA2

36
Q

What are the Platelet Glycoprotein IIb/IIIa receptor blockers

A

Abciximab, Eptifibatide, Trifiban

37
Q

what is the MOA for GP IIb/IIIa receptor blockers

A

bind to GP IIb/IIIa and prevent interaction with fibrinogen (all are given IV)

38
Q

Which GP IIb/IIIa recptor blocker is a chimeric mouse-human monoclongal Ab that irreversibly binds

A

Abciximab

39
Q

What are the 2 Phosphodiesterase Inhibitors

A

1) Dipyridamole

2) Cilostazol

40
Q

Describe the MOA of Phosphodiesterase Inhibitors

A

increase in [intreacellular cAMP] leads to a decrease in platelet aggregation

41
Q

Describe Dipyridamole

A

vasodialtor, has weak antiplatelet effects, so is given with warfarin or aspirin
SE: may paradoxically induce angina in pts with CAD

42
Q

What can Dipyridamole + warfarin be used for

A

prevent thrombus on prosthetic heart valves

43
Q

what can Dipyridamole + aspirin be used for

A

decrease incidence of thombotic diathesis in pts.

44
Q

Descirbe Cilostazol

A

inhibitor of phosphodiesterase III, and is contraindicated in pts with congestive heart failure

45
Q

What are the 3 Thrombolytic Drugs

A

1) Alteplase (t-PA)
2) Reteplase
3) Tenecteplase

46
Q

what is Firbrinolysis

A

breakdown of fibrin by protease plasmin

47
Q

Describe tPA

A

free tPA has low activity for circulating plasminogen and is inhibited by PAI-1 and 2

48
Q

how do thormbolytic agents work

A

by converting the inactive zymogen plasminogen to the active protease plasmin

49
Q

Descirbe Alteplase

A

t-PA is a serine protease produced by human endothelial cells, therefore, t-PA is NOT antigenic; t-PA binds to fibrin in fresh thrombi with high affinity, causing conversion of plasminogen to plasmin

50
Q

Describe Reteplase and Tenecteplase

A

genetic variant of t-PA; more resistant to PAI-1 (increase fibrin specificity)

51
Q

What does the mneumoni TEA NECK IS REAL mean

A

TENECtelepase REtepase ALteplase

52
Q

What is an example of a Hemostatic Agent

A

Vit K

53
Q

What is the MOA for Vit K

A

essential cofactor required in (gamma)-carboxylation of multiple glutamate residues of several clotting factors (2,7,9,10)

54
Q

What is the caution of Vit K administration

A

fast IV infusion can lead to dyspnea, chest pain and even death

55
Q

What are the 2 Fibrinolytic Inhibitors

A

1) Aminocaproic

2) Tranexamic acid

56
Q

What is the MOA of Fibrinolytic Inhibitors

A

Lysine analog that competes for lysine binding sites on fibrinogen and plasmin->blocking plasmin fibrin interaction

57
Q

What is the problem with Aminocaproic acid

A

thrombi that form during drug Tx do not get lysed

58
Q

When would you use Aminocaproic acid

A

reduce bleeding in hemophiliacs after prostatic surgery or tooth extractions

59
Q

When would you use Tranexamic acid

A

used to control heavy menstrual bleeding

60
Q

What is one other Anticoagulating Agents

A

Rivaroxaban; which is a direct inhibitor of factor Xa and inhibits free and clot bound factor Xa, used to prevent DVT

Blood and Lymph (3 decks)

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