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OU Module Cardio Spring 2018 > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

TxA2

A

a platelet activator & vasoconstrictor synthesized from arachidonic acid

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2
Q

ADP

A

induces platelet aggregation; makes platelets sticky

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3
Q

5HT

A

stimulates platelet aggregation and vasoconstriction

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4
Q

What are the granules released from platelets?

A
  • TxA2
  • ADP
  • 5HT
  • PAF
  • thrombin
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5
Q

How does increase in intracell. Ca induce platelet aggregation?

A

Increase in intracellular Ca -> granule release -> TxA2 synthesis & activation of GPIIb/IIIa receptors -> expressed on surface of platelets which bind to circulating fibrinogen in blood -> further platelet aggregation

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6
Q

GPIIb/IIIa receptors

A
  • activated by intracell. Ca and reduced cAMP
  • expressed on surface of platelets to activate other platelets
  • activated GPIIb/IIIa receptors bind to circulating fibrinogen in blood to cause further platelet aggregation
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7
Q

What are the 3 categories that regulate platelet function?

A
  • Agents generated outside the platelet that interact with platelet membrane receptors
  • Agents generated within the platelet that interact with membrane receptors
  • Agents generated within the platelet that act within the platelet
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8
Q

Agents generated outside the platelet that interact with platelet membrane receptors

A
  • catecholamines
  • collagen
  • thrombin
  • prostacyclin
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9
Q

Agents generated within the platelet that interact with membrane receptors

A
  • ADP
  • prostaglandin D2
  • prostaglandin E2
  • serotonin
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10
Q

Agents generated within the platelet that act within the platelet

A
  • prostaglandin endoperoxidases
  • thromboxane A2
  • cyclic nusleotides cAMP and cGMP
  • calcium ion
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11
Q

What are the 5 mechanisms of action of antiplatelets?

A
  • Inhibition of PG (TxA2 precursor) synthesis
  • Inhibition of ADP-induced platelet aggregation
  • Protease activated receptor -1 inhibitor
  • Blockade of glycoprotein IIb/IIIa receptors
  • Phosphodiesterase inhibitors / vasodilators
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12
Q

ASA

A

irreversible acetylation of the COX1 enzyme

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13
Q

Inhibition of ADP-induced platelet aggregation

A

Irreversibly block ADP receptors -> decreased intracellular Ca and increased intracellular cAMP

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14
Q

Glanzmann’s thrombasthenia

A

when pts do not have the glycoprotein IIb/IIIa receptors complex and cannot aggregate

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15
Q

Clopidogrel

A
  • Inhibition of ADP-induced platelet aggregation

- thrombotic thrombocytopenic purpura

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16
Q

Cangrelor

A
  • Kengreal
  • Inhibition of ADP-induced platelet aggregation
  • acts on allosteric site (doesn’t compete with ADP for binding) -> reversible in its action
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17
Q

Vorapaxar

A
  • Zontivity
  • Protease activated receptor -1 inhibitor
  • Inhibits thrombin receptor on platelets
  • leads to decreased Ca and increased cAMP -> reduced platelet activation and aggregation
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18
Q

Abciximab

A
  • Reopro
  • inhibit GP IIb/IIIa complex -> decreased platelet aggregation
  • Can bind to fibrinogen receptor or the vitronectin receptor
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19
Q

Dipyridamole

A
  • Persantine
  • Phosphodiesterase inhibitors / vasodilators
  • decreases Ca -> decreased muscle contraction | also inhibits phosphodiesterase enzyme (PDE) -> increased cAMP -> decrease TxA2 synthesis -> decreased platelet aggregation
  • Not very useful alone -> Given in combination with aspirin to prevent cerebrovascular ischemia
20
Q

mechanisms of action for anticoagulants

A
  • Indirect thrombin inhibitors
  • Direct thrombin inhibitors
  • Direct inhibitors of Factor Xa
  • Vitamin K antagonists
21
Q

Indirect thrombin inhibitors

A
  • UFH

- LMWH

22
Q

UFH

A
  • works with antithrombin to prevent activation of coagulation factors; helps AT work much faster
  • Is allergenic, impure (only 1/3 have potential activity), binds to a lot of proteins which pts can develop resistance and unpredictable PK
  • Can develop Heparin-induced thrombocytopenia and thrombosis (HITT) in which they become hyper-coagulable; body develops antibodies that attacks the body’s platelets and makes the body more prone to having clots (mainly veins)
  • Heparin is acidic and negative; if overdose, administer protamine which is basic and positive charge but excess protamine can cause anticoagulation
23
Q

LMWH

A
  • made from unfractionated heparin by various methods of depolymerization: works with thrombin in the activation of factor X to Xa
  • Enoxaparin, Dalteparin, Tinzaparin
24
Q

Direct thrombin inhibitors

A
  • Desirudin
  • Bivalirudin
  • Dabigatran etexilate mesylate
25
Q

Desirudin

A
  • Iprivask
  • irreversible thrombin inhibitor
  • Binds to catalytic sites of thrombin as well as the substrate recognition site
  • Excreted by kidney; careful with renal patients
  • Pts can develop antibody against the complex that forms when this drug binds to thrombin -> anaphylaxis
26
Q

Bivalirudin

A
  • Angiomax
  • Reversible bivalent inhibitor of free & clot-bound thrombin
  • Inhibits platelet activation
  • Bivalirudin ↑ protein C activity vs Lepirudin ↓activity
27
Q

Dabigatran etexilate mesylate

A
  • Pradaxa
  • Prodrug
  • Bioavailability: 6-7%
  • Prodrug requires acidic environment for absorption (do not take PPI while on this drug)
28
Q

Direct inhibitors of Factor Xa

A
  • Fondaparinux
  • Rivoraxaban
  • Apixaban
  • Edoxaban
29
Q

Fondaparinux

A
  • Arixtra
  • allows Xa to bind to AT by binding to Xa
  • More predictable PK -> less monitoring
  • Does not cross react with pathologic HIT antibodies
30
Q

Rivoraxaban

A
  • Xarelto
  • Drug-Drug interactions: Interactions with CYP3A4 and for P-glycoprotein
  • No antidote for overdose
31
Q

Apixaban

A
  • Eliquis
  • Drug-Drug interactions: Interactions with CYP3A4 and for P-glycoprotein
  • No antidote for overdose
32
Q

Warfarin

A
  • Coumadin
  • Can cross placental barrier; could cause hemorrhage in fetus and/or abortion; teratogenic, birth defects; contraindicated in pregnancy; give LMWH instead
33
Q

SNPs’ impact on warfarin

A
  • Genetic polymorphisms (SNPs) in VKOR complex subunit (VKORC1)  higher risk of bleeding due to reduced Vitamin K dependent coagulation factors.
  • Because of this SNP, there is 30% patient variability
34
Q

Differentiate between the mechanisms of unfractionated heparin and low molecular weight heparins

A
  • Unfractionated heparin: works on both AT and thrombin

- Low molecular weight heparins: only works on thrombin

35
Q

tPA

A
  • Alteplase, Reteplase, Tenecteplase
  • prefer plasminogen bound to fibrin -> fibrinolysis will only occur in the formed thrombus and avoids activation in the systemic flow
  • converts plasminogen to plasmin; plasmin works on fibrin to break down the clot
36
Q

hemostatic agents

A
  • Aminocaproic acid
  • tranexamic acid
  • Protamine sulfate
  • Vitamin K
37
Q

Aminocaproic acid

A
  • inhibitor of fibrinolysis

- competitively inhibits plasminogen activation

38
Q

tranexamic acid

A
  • analog of aminocaproic acid

- same properties; 10 times more potent

39
Q

Protamine sulfate

A
  • antagonizes effect of heparin

- positive charge of protamine interacts with negative charge of heparin and forms a sable complex that has no activity

40
Q

Positive regulators of the fibrinolytic process

A
  • Damaged endothelium releases tissue Plasminogen Activator (tPA)
  • tPA binds plasminogen bound to fibrin rather than circulating plasminogen
  • tPA cleaves (activates) plasminogen into plasmin
41
Q

Negative regulators of the fibrinolytic process

A
  • tPA inhibitors (PAI-1, PAI-2) inhibit tPA
  • Circulating antiplasmin (AP) inhibits plasmin that is not bound to a clot
  • AP is also found covalently bound to clot, protects the clot from premature lysis
42
Q

Alteplase

A
  • Activase
  • fibrin selective; will only work on fibrin in those clots
  • more efficient in dissolving older clots (than streptokinase)
  • glycosylated human tPA
  • efficient in dissolving older clots
43
Q

Reteplase

A
  • Retavase
  • non-glycosylated recombinant human tPA
  • Longer half life
  • lower affinity for fibrin vs. alteplase
  • improved ability to penetrate into clots
44
Q

Tenecteplase

A
  • TNKase
  • recombinant protein with substitutions of amino acids
  • Binds to the fibrin component of the thrombus and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus
  • Higher fibrin specificity and greater resistance to inactivation
45
Q

risks of tPA

A

Increased chance to cause local thrombi as clot dissolves and parts come loose -> used in conjunction with aspirin (antiplatelet agent) or heparin (antithrombotic agent)

OU Module Cardio Spring 2018 (16 decks)

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