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Pharm Exam 1 > Antithrombotic Drugs > Flashcards

Antithrombotic Drugs Flashcards

1
Q

Which drug is an angiotensin receptor blocker?

A

losartan

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2
Q

Describe the process of clot formation, including the actions of platelets and clotting factors

A
  1. Clot formation begins with subendothelial matrix exposure due to damaged vessel wall that exposes underlying endothelial proteins that are not normally exposed (ie. collagen and TF)
  2. Platelet adhesion and activation
    • forms a platelet plug
    • platelets start to make ADP and TxA2 (thromboxane)
    • now a feedforward action starts where more platelets come in and form clot
  3. Coagulation cascade
    • receptors on the cell membrane that grab onto fibrinogen that ultimately form the clot and go from fibrinogen precursor to fibrin that forms the clot
  4. Thrombin will then take fibrinogen to fibrin which is the active form. It will form the mesh and contain the platelet plug
  5. T-PA = tissue plasminogen activator. Plasminogen will come in later and break down fibrin to dissolve the clot away
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3
Q
  • Binding of platelets to collagen causes activation of what?
A

Binding of platelets to collagen causes activation:

  • Release of chemical mediators: ADP and TXA2
  • Change in surface receptor expression: grabs onto fibrinogen
  • Become more sticky: sticks to each other and the wall

Activated platelets aggregate: stick to each other; forming a plug

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4
Q

What do ADP and thromboxane A2 cause?

A

ADP and thromboxane A2 cause further platelet activation and trigger vasoconstriction

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5
Q

What is the function of aspirin and how does it inhibit clot formation?

A

aspirin inhibits cyclooxygenase which makes TXA2 (thromboxane A2)

Therefore aspirin is an antithrombin drug

Recall: ADP and thromboxane A2 cause further platelet activation and trigger vasoconstriction

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6
Q

How does actin and myosin play a role in clot formation?

A

Platelets have actin and myosin - contract to close damaged vessels

Once platelets get activated they will pull the actin and myosin to create the plug

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7
Q

Explain coagulation

A

coagulation

enzymatic steps converge on thrombin, which converts fibrinogen to fibrin (leads to stable clot)

Factor X = prothrombin to Factor Xa = thrombin (active form)

Factor XIII: makes the fibrin mesh = Crosslinked fibrin is broken down by the enzyme plasmin in order to dissolve a stable clot

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8
Q

T/F RBCs are not required to make a clot?

A

TRUE

Clots in slower moving blood cause them to trap RBC BUT RBC ARE NOT REQUIRED to make a clot!!!!

only platelets are necessary to form a clot

White clot: artery clots

  • faster blood flow = platelet-rich
  • coronary vessels then an antiplatelet drug is a good choice because they are mainly the activation of platelet clots

Red clot: venous clot

  • Sitting for a long time you can get DVT with stasis of blood that involves platelet and clotting factors where there are higher level of clotting factors vs. platelets
    • therefore drugs that target the clotting factors are the better drug
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9
Q

What is an embolus vs. embolism

A

Embolus: a clot moving through to body

Embolism: when the embolus gets lodged in a vessel (ie. lungs)

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10
Q

What are the reasons for taking antithrombin drugs for clot prevention when vascular endothelial cells are disrupted?

A
  • clot prevention when vascular endothelial cells are disrupted
    • Atherosclerosis - plaque forming in the arteries that can rupture and cause clot formation
    • Stents - the stent in the area causes disruption of the endothelium
    • Bypass surgery - working with the BV directly
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11
Q

What are the reasons for taking antithrombin drugs for clot prevention when other risk factors are present

A
  • previous stroke, MI or deep vein thrombosis
  • atrial fibrillation (disorganized atrial contraction)
  • cardiomyopathy (disease of the heart muscle)
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12
Q

What are antithrombin drug targets for antiplatelet drugs

A

Antithrombic drug targets

  • Antiplatelet drugs: decrease platelt activation/plug formation
    • ADP receptor antagonist: clopidogrel (Plavix)
    • TXA2 synthesis inhibitor: aspirin
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13
Q

What are antithrombin drug targets for anticoagulants

A

Antithrombotic drug targets

Anticoagulants: decrease clotting factor activity

  • Decrease synthesis of clotting factors: Warfarin (coumadin)
  • inhibit factor Xa (thrombin): apixaban
  • Inhibit thrombin: dabigatran
  • inhibit the action of multiple clotting factors: heparin
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14
Q

inhibit thrombin

A

dabigatran

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15
Q

inhibit factor Xa

A

apixaban

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16
Q

inhibit action of multiple clotting factors

A

heparin

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17
Q

ADP receptor antagonist

A

clopidogrel (plavix)

antiplatelet drug

18
Q

decrease synthesis of clotting factors

A

warfarin (coumadin)

anticoagulant

19
Q

TXA2 synthesis inhibitor

A

aspirin

antiplatelet drug

20
Q

Explain the action of aspirin

what are the adverse effects of aspirin?

A

inhibits cyclooxygenase - 1 (COX-1), which is required in the pathway to synthesize TXA2 from arachidonic acid

  • COX-I is ubiquitous but low doses (baby aspirin) are more selective for platelets
    • due to aspirin has an irreversible quality to it and therefore aspirin is the best antiplatelet medication vs. other anti-inflammatory medications that also target the same receptors but are doing it in a reversible way
  • GI symptoms (heartburn, ulcers) are most common adverse effect
  • Must weigh risks/benefits with regard to daily prophylactic use (mainly only for those who have already had stroke or heart attack)
21
Q

Explain the action of Clopidogrel

A

aka Plavix

  • Irreversibly blocks the P2Y12 (ADP) receptor expression by platelets
    • ADP is a signaling molecule that is produced during platelet activation and therefore it is used for a signaling molecule during platelet aggregation
      • the platelets cannot restore the function after the receptor has been inhibited
  • Synergistic effects when taken with aspirin
    • = EXTREME INHIBITION OF CLOTTING
  • Bruising, bleeding most common side effect
22
Q

Factor IIa = ?

A

Factor IIa = thrombin (activated form)

vs. Factor II = prothrombin

which is activated by Xa

23
Q

Explain the Warfarin mechanism

A
  • Vitamin K-dependent carboxylase produces active clotting factors
  • Vit. K is a cofactor* that gets *oxidized* in this reaction and *must be reduced in order to be used again
  • This step is performed by vitamin K reductase, which is blocked by warfarin
24
Q

What is prothrombin time?

A

most related with warfarin

Common lab test to measure ability of blood to clot

  • Tissue factor added to* *patient* *sample,* *timed* *until a clot forms
    • often expressed as international normalized ratio (INR), which is a ratio of patient’s clotting time to normal reference value
      • INR = 1 = normal
      • INR = 2 = longer to clot (2x longer)
  • Higher INR means decreased ability to clot - patients with high likelihood of clotting are purposely kept at elevated INR
    • this is how warfarin is titrated for the dose and you want to frequently ccheck the dose
25
Q

Explain warfarin therapy

A
  • INR (measure of coagulability) must be closely monitored and dose titrated
  • sensitivity to dietary intake of vitamin K, liver function, drug interaction
    • important to have a steady diet if you are on warfarin
  • Effects are long-lasting - can be resolved with
    • vitamin K (~24 hours)
    • Kcentra (a mixture of clotting factor proteins) or fresh frozen plasma (these rapidly lower INR) = ANTIDOTE
      • must be monitored with frequent blood tests
        • if you have too much warfarin in their diet then they have an increased risk of bleeding - Kcentra = antidote
26
Q

What is the antidote to warfarin?

A

Kcentra

A mixture of clotting factor proteins or frozen plasma (rapidly lower INR)

27
Q

What are alternates to warfarin that may replace warfarin in the future?

A

Direct oral anticoagulants (DOACs)

or

Non-vitamin K oral anticoagulants (NOACs)

Rivaroxaban (Xarelto): factor Xa inhibitor

Dabigatran (Pradaxa): thrombin inhibitor

both have xa in their name :)

28
Q

what DOAC or NOAC is a factor Xa inhibitor?

A

Rivaroxaban (Xarelto)

29
Q

What DOACs and NOACs is a thrombin inhibitor?

A

Dabigatran (Pradaxa)

30
Q

What are advantages of Direct oral anticoagulants (DOACs) and Non-vitamin K oral anticoagulants (NOACs)

A

Advantages

  • Monitoring of coagulation and dose titration generally not needed
    • standardized dose based on blood tests is very predictable
  • Rapid onset/offset of action - easy to get on and off instead of waiting for clotting factors to be depleted
  • Few drug/diet interactions
31
Q

What are disadvantages of Direct oral anticoagulants (DOACs) and Non-vitamin K oral anticoagulants (NOACs)

A

Disadvantages

  • less clinical experience
  • higher cost
  • antidotes just now becoming available and very expensive
    • Andexxa: a replacement factor Xa that reverses rivaroxaban (recombinant protein you can inject to reverse)
    • Praxbind: an antibody that binds to dabigatran (inactivates via antibody-antigen binding process)
32
Q

What is the antidote to rivaroxaban?

A

Andexxa

replacement factor Xa that reverses rivaroxaban

33
Q

what is the antidote for Dabigatran?

A

Praxbind

antibody that binds to dabigatran
inactivates antibody-antigen binding process

34
Q

Explain Heparin

A

Inhibits clotting factors within the cascade, including thrombin

  • A polysaccharide that binds and activates antithrombin
  • Antithrombin inhibits thrombin and other clotting factors
  • immediate effect, useful when there is acute clotting risk
35
Q

T/F: routine dental work, including single tooth extractions, can usually be performed without altering anticoagulant

A

True

consult patient physician if questions

however: multiple extractions or more complex surgery may require dose adjustment

36
Q

What are the several topical options available when excessive bleeding occurs?

A
  • Tranexamic acid = mouth rinse - inhibits plasmin (therefore preventing the dissolving of the clot)
  • Collagen
  • thrombin
  • fibrin
37
Q

tranexamic acid

A

plasmin inhibitor (enhances clotting)

38
Q

name the anticoagulants and what their mode of action is

A

Anticoagulants: decrease clotting factor activity

  • Decrease synthesis: warfarin
  • inhibit factor Xa: apixaban
  • inhibit thrombin: dabigatran
  • inhibit action of multiple factors: heparin
39
Q

name the antiplatelet drugs and what their mode of action is

A

antiplatelet drugs: decrease platelet activation/plug formation

  • ADP receptor antagonist: clopidogrel
  • TXA2 synthesis inhibitor: aspirin
40
Q

name the antidotes for antithrombin drug lectures

A

Antidotes:

  • warfarin: Kcentra
  • Dabigatran: Praxbind
  • Rivaroxaban: Andexxa

Pharm Exam 1 (5 decks)

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