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Anticoagulants Flashcards

(60 cards)

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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
What drug is under the category of Antiplatelet Agents?
Aspirin
26
What is the MOA of Aspirin?
inhibits COX-1
27
what would you expect with a high does of aspirin and how would you prevent it?
inhibit COX-1 in endothelial cells which would prevent formation of PGI2 (vasodilator) use Baby aspirin
28
What is the MOA of the Thienopyridine ADP Inhibitors
irreversible inhibitors of platelet ADP receptrs that covalently modify and inactivate P2Y(ADP) recpetors (aka P2Y12)
29
What is the BBW for Thienopyridine ADP Inhibitors
bleeding risk, contraindicated in conditions like active pathological bleeding or a Hx of transient ischemic attacks or stroke
30
Name the ADP Inhibitors: Thienopyridines
1) Ticlopidine- 1st gen 2) Clopidogrel- 2nd gen. 3) Prasugrel- 3rd gen. 4) Ticagelor- oral
31
Describe Ticlopidine
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
Describe Clopidogrel
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
Describe Prasugrel
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
Describe Ticagelor
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
how does expression of GP IIb/IIIa occur
activation of platelets from stimulating thrombin, ADP, collagen, and TxA2
36
What are the Platelet Glycoprotein IIb/IIIa receptor blockers
Abciximab, Eptifibatide, Trifiban
37
what is the MOA for GP IIb/IIIa receptor blockers
bind to GP IIb/IIIa and prevent interaction with fibrinogen (all are given IV)
38
Which GP IIb/IIIa recptor blocker is a chimeric mouse-human monoclongal Ab that irreversibly binds
Abciximab
39
What are the 2 Phosphodiesterase Inhibitors
1) Dipyridamole | 2) Cilostazol
40
Describe the MOA of Phosphodiesterase Inhibitors
increase in [intreacellular cAMP] leads to a decrease in platelet aggregation
41
Describe Dipyridamole
vasodialtor, has weak antiplatelet effects, so is given with warfarin or aspirin SE: may paradoxically induce angina in pts with CAD
42
What can Dipyridamole + warfarin be used for
prevent thrombus on prosthetic heart valves
43
what can Dipyridamole + aspirin be used for
decrease incidence of thombotic diathesis in pts.
44
Descirbe Cilostazol
inhibitor of phosphodiesterase III, and is contraindicated in pts with congestive heart failure
45
What are the 3 Thrombolytic Drugs
1) Alteplase (t-PA) 2) Reteplase 3) Tenecteplase
46
what is Firbrinolysis
breakdown of fibrin by protease plasmin
47
Describe tPA
free tPA has low activity for circulating plasminogen and is inhibited by PAI-1 and 2
48
how do thormbolytic agents work
by converting the inactive zymogen plasminogen to the active protease plasmin
49
Descirbe Alteplase
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
Describe Reteplase and Tenecteplase
genetic variant of t-PA; more resistant to PAI-1 (increase fibrin specificity)
51
What does the mneumoni TEA NECK IS REAL mean
TENECtelepase REtepase ALteplase
52
What is an example of a Hemostatic Agent
Vit K
53
What is the MOA for Vit K
essential cofactor required in (gamma)-carboxylation of multiple glutamate residues of several clotting factors (2,7,9,10)
54
What is the caution of Vit K administration
fast IV infusion can lead to dyspnea, chest pain and even death
55
What are the 2 Fibrinolytic Inhibitors
1) Aminocaproic | 2) Tranexamic acid
56
What is the MOA of Fibrinolytic Inhibitors
Lysine analog that competes for lysine binding sites on fibrinogen and plasmin->blocking plasmin fibrin interaction
57
What is the problem with Aminocaproic acid
thrombi that form during drug Tx do not get lysed
58
When would you use Aminocaproic acid
reduce bleeding in hemophiliacs after prostatic surgery or tooth extractions
59
When would you use Tranexamic acid
used to control heavy menstrual bleeding
60
What is one other Anticoagulating Agents
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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