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Pharmacology (Fall) > Drugs for Antithrombotics & Anticoagulants > Flashcards

Drugs for Antithrombotics & Anticoagulants Flashcards

1
Q

What are the agents for treating coagulants?

A

Anticoagulants: drugs which interfere with coagulation cascade

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2
Q

What are the agents for treating platelets?

A

Antiplatelet agents: drugs which interfere with platelet function

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3
Q

What are the agents for treating clots?

A

Fibrinolytic drugs: clot “busters”

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4
Q

What are the agents for treating arterial thromboembolic disease?

A

antiplatelet agents

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5
Q

What are the agents for treating venous thromboembolic?

A

anticoagulants

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6
Q

What is the list of the Antiplatelet drugs?

A
  • Aspirin
  • Clopidigril
  • Ticagrelor
  • Prasugrel
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7
Q

What is the list of the Anticoagulant drugs?

A
  • Heparin
  • LMW Heparin
  • Warfarin
  • Dabigatran
  • Idarucizumab
  • Rivaroxaban
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8
Q

What is the list of the Clot resolving drugs?

A
  • Tissue Plasminogen Activator
  • Streptokinase
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9
Q

Aspirin’s purpose & site of action:

A

antiplatelet

COX I & II inhibitor

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10
Q

Clopidigril’s purpose & site of action:

A

antiplatelet

ADP receptor antagonist

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11
Q

Ticagrelor’s purpose & site of action:

A

antiplatelet

ADP receptor antagonist

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12
Q

Prasugrel’s purpose & site of action:

A

antiplatelet

ADP receptor antagonist

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13
Q

Heparin’s purpose & site of action:

A

anticoagulant

Antithrombin III activator

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14
Q

LMW Heparin’s purpose & site of action:

A

anticoagulant

Antithrombin III activator

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15
Q

Warfarin’s purpose & site of action:

A

anticoagulant

Vitamin K antagonist

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16
Q

Dabigatran’s purpose & site of action:

A

anticoagulant

Direct thrombin inhibitor

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17
Q

Idarucizumab’s purpose & site of action:

A

anticoagulant

Direct thrombin inhibitor

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18
Q

Rivaroxaban’s purpose & site of action:

A

anticoagulant

Direct Factor Xa inhibitor

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19
Q

Tissue Plasminogen Activator’s purpose & site of action:

A

clot resolving

Activates plasminogen

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20
Q

Streptokinase’s purpose & site of action:

A

clot resolving

Activates plasminogen

21
Q

What is a Thromboembolism?

A

Formation in a blood vessel of a clot (thrombus) that breaks loose and is carried by the blood

22
Q

What are Arterial and venous thrombi composed of?

A

platelet aggregates, fibrin and red blood cells

23
Q

What conditions do Arterial thrombi form under?

A

under high sheer stress conditions: platelets abundant and fibrin sparse

24
Q

What conditions do Venous thrombi form under?

A

low sheer stress conditions: rich in fibrin and trapped red blood cells and contain fewer platelets

25
Q

Hemostasis:

A

cessation of blood loss from a damaged vessel

26
Q

Coagulation:

A

formation of a blood clot

27
Q

Blood clot:

A

also called hemostatic plug, is formed by aggregation of platelets and stabilized by fibrin

28
Q

Thrombosis:

A

a pathologic process in which a platelet aggregate and/or fibrin blot occludes a blood vessel

29
Q

What is Hemostasis & what does it involve?

A

Normal physiological process of terminating blood loss from a vascular wall
Involves:
- platelet activation
- coagulation cascade –> thrombin formation
- clot resolution

30
Q

What is the pathology of thrombosis?

A
  1. Rupture of fibrous cap
  2. Exposure of lipid core (Tissue Factor: procoagulant)
  3. Platelet adherence & activation
  4. Thromboxane A2 release
  5. Membrane glycoprotein IIb/IIIa receptor activation to bind fibrinogen
  6. Complex platelet linkage
  • Process above continues with further fibrin incorporation and inclusion of red blood cells within clot
  • End result is partial or total occlusion of vessel (coronary artery)
31
Q

What is Atherosclerosis (Thrombus)?

A
  • Atherosclerosis (build up of cholesterol) may partially obstruct flow in artery
  • Eventually the plaque damages the endothelium - thrombus forms
  • Blood flow is blocked by the atherosclerosis & the thrombus
  • If thrombus ruptures - emboli lodge in capillary & block flow
32
Q

Thrombus

A

blood clot attached to a blood vessel
- may obstruct flow - harmful
- pieces may break off which then “plug” capillaries

33
Q

Emboli

A

portion of thrombus that breaks away
- clot floating in the blood
- if “mobilized” will get stuck in capillaries
- damage depends on where it lodges (heart, brain, lung)

34
Q

Where doe thrombus/emboli form on?

A

on arterial & venous sides of circulation
- but venous & arterial clots are different
- arterial (platelet rich); venous (RBC rich)

35
Q

Describe Thrombotic disorders in the arteries

A
  • damage ENDOTHELIAL layer stimulates thrombus formation
  • atherosclerosis damage endothelial layer of arteries
  • physical damage caused by:
    – balloon angioplasty
    – stenting
36
Q

What happens if artery perfuses the brain?

A
  • emboli lodge in cerebral capillary
    – acute ischemic stroke
37
Q

What happens if artery perfuses the heart muscle?

A
  • emboli lodge in coronary artery
    – acute MI
38
Q

Describe Thrombotic disorders in the veins

A
  • involves RBC & LESS platelets
    – so antiplatelet drugs are NOT as effective in veins
  • more related to “stagnant flow” in veins &/or atria
  • problem post surgery, long term bed rest or just sitting (long plane rides)
  • clot form & if dislodge (emboli) - flow to capillaries in the lungs
    – known as pulmonary embolism
  • 2 major sites where venous clots form:
    – lower leg veins - deep vein thrombosis (DVT)
    – right atria (if atria not contracting properly)
39
Q

What are the 3 stages of the clot formation/destruction?

A
  1. Formation of platelet plug
  2. Formation of clot
  3. Breakdown of clot
    - if no longer needed
40
Q

Describe platelet binding & activation

A

Platelet adhesion is first step in platelet plug formation: binding to exposed collagen for or von willebrand factor. Granule release

In healthy vasculature, platelets are maintained in an inactive state by nitric oxide and prostacyclin (PCI2) released by endothelial cells and ADPase which degrades ADP

41
Q

Describe signaling pathway

A

Signaling pathways involved in the regulation of platelet activation.Regulation of platelet activation occurs via the interaction of numerous effector molecules with receptors present in the plasma membranes of platelets. Several important receptors are the glycoproteins GPIb-GPIX-GPV and GPIIb-GPIIIa as described above. Numerous G-protein coupled receptors (GPCRs) are also involved in platelet functions. Five different GPCRs, their respective ligands, and brief representations of their signal transduction pathways are shown. The prostacyclin receptor is IP. The represented thrombin receptor is protease-activated receptor-1 (PAR-1). PAR-1 is knoiwn to activate both Gq- and G12/13-type heterotrimeric G-proteins. The platelet serotonin receptor is 5HT2A. The thromboxane (TXA2) receptor is TP. The platelet ADP receptor is P2Y12. Although complex, the complete signaling pathways are not shown for simplicity. Rho represents a typical member of the Rho family of monomeric G-proteins. The β and γ subunits of the Gi-type heterotrimeric G-protein associated with the ADP receptor can activate the kinase, PI3K while the α subunit simultaneously inhibits the activation of adenylate cyclase. NOS is nitric oxide synthase.

Basically:
-receptor binding
-granule release
-amplification
-mediated/mediates other components of the blot clot process

42
Q

What about other NSAIDS?

A

Other NSAIDS (reversible inhibitors of COX-1) have not been shown to have anti-thrombotic efficancy and may even interfere with low-dose aspirin regimes

43
Q

Why does aspirin not promote aggregation given its effect on vascular endothelium production of prostacyclin?

A
  • Aspirin irreversibly blocks COX
  • Platelets lack a nucleus – can’t make new COX
  • Vascular endothelial cells have a nucleus
  • Vascular endothelial cells have ability to continually remake COX and hence maintain prostacyclin production
44
Q

What is Fibrin?

A
  • Fibrinogen converted to fibrin by thrombin
  • Activation involves protease cleavage of fibrinogen to release fibrinopeptides that fit into pre-formed holes in other fibrin monomers to form a fibrin gel
  • Fibrin monomers are initially bound non-covalently
  • Activation of factor XIII by thrombin results in activation of this enzyme that catalyzes interchain covalent cross links
45
Q

What is the INR?

A

International Normalized Ratio (INR)
- Ratio of the patient’s (with Warfarin) pro-thrombin time to that of a control subject (with no Warfarin)
- Pro-thrombin time is a measurement (in sec’s) of the EXTRINSIC pathway
- Target INR is 2.0-3.0
- INR <2 may lead to thrombotic complications
- INR >3 may lead to bleeding

46
Q

What is unique about Fribinolytic drugs - clot blusters?

A
  • these drugs do NOT distinguish b/t fibrin of a beneficial hemostatic plug & unwanted thrombi
  • will decrease thrombi, but may cause bleeding in an unknown lesion (ex: peptic ulcer)
47
Q

What is Fibrinolysis?

A

breaks down clot

Plasminogen activators:
- tPA
- uPA
are syn. in endothelial cells, released in conditions of blood stasis

48
Q

What is tPA?

A
  • tPA plays predominant role in intravascular fibrinolysis
  • tPA is released from endothelial cells in response to stimuli such as stasis
  • tPA activity increases 300-fold in presence of fibrin
  • tPA is rapidly cleared or inhibited by plasminogen activator inhibitor (PAI-1 and/or PAI-2)
  • Plasmin is inhibited by alpha-2-antiplasmin (occurs when plasmin not bound to fibrin)

Pharmacology (Fall) (28 decks)

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