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Pharmacology > Hemostasis and thrombosis > Flashcards

Hemostasis and thrombosis Flashcards

1
Q
  • “the arrest of blood loss from damaged blood vessels”
  • Essential to life
  • Caused by:
  • Platelet adhesion and activation
  • Fibrin formation
A

Hemostasis

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2
Q

• “pathological formation of a ‘hemostatic plug’ within the
vasculature in the absence of bleeding”
• Hemostasis in the wrong place
• Virchow’s triad

A

Thrombosis

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3
Q

What are the 3 components of Virchow’s triad?

A

Stasis
Endothelial injury
Hypercoaguability

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4
Q 
\_\_\_\_ Thrombus
• Arterial clot
• Primarily platelets and some 
fibrin mesh
• Associated with atherosclerosis
A

White thrombus

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5
Q 
\_\_\_ Thrombus
• Venous clot
• Mostly fibrin and small amount 
of platelets
• Higher risk of embolus
A

Red thrombus

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6
Q

Prevents coagulation
by lysing
Factor Xa and Thrombin

A

Antithrombin III

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7
Q

______ also

causes platelet activation

A

Thrombin (Factor IIa)

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8
Q

What are the 4 vitamin K dependent clotting factors?

A

2, 7, 9, 10

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9
Q 
\_\_\_\_\_\_ Pathway of coagulation cascade
• All components present in the 
blood
• Starts when blood comes in 
contact with foreign object or 
damaged endothelium
• Monitored by Activated Partial 
Thromboplastin time (aPTT)
A

Intrinsic

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10
Q

______ Pathway of coagulation cascade

• Some components come from 
outside blood
• Tissue factor
• Starts when tissue damage 
releases tissue factor
• Monitored by Prothrombin time 
(PT) and INR
A

Extrinsic Pathway

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11
Q
  • Fat soluble vitamin with little stored in the body
  • Mostly obtained from diet or produced by bacteria in the gut
  • iT is a cofactor in the formation of several clotting factors
A

Vitamin K

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12
Q

What factor is involved in platelet adhesion?

A

von Willebrand factor

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13
Q

What are the 4 mediators of platelet activation?

A

ADP
TXA2
Collagen
Thrombin

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14
Q

Which factor of platelet activation does not have a pharmacological inhibitor at this time?

A

Collagen

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15
Q

What is the receptor involved in platelet aggregation?

A

GP IIb/IIIa

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16
Q

What is the key mediator of fibrinolysis?

A

Plasmin

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17
Q 
• Acts only in vivo
• Inhibits vitamin K epoxide 
reductase component 1 
(VKORC1)
• The VKORC1 gene is 
polymorphic resulting in 
different affinities for it
• Genetic testing is available for this 
polymorphism
A

Warfarin

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18
Q
  • Rapidly absorbed after oral administration
  • Highly bound to plasma proteins (i.e. albumin)
  • Hepatically metabolized (CYP 450 2C9 and 3A4)
  • Polymorphism of CYP 450 2C9
  • Onset of action 5-7 days
  • Half-life is ~ 40 hours
  • Requires new steady-state of clotting factors to be achieved
  • Vitamin K dependent clotting factors: II, VII, IX, X, protein C, protein S
  • Effects of dose change require 2-3 days to present
A

Warfarin

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19
Q

How does Warfarin affect coagulation parameters?

A

Increases INR

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20
Q 
Adverse Drug Reactions
• Bleeding (can be life threatening)
• Gastrointestinal bleeding most common
• Rash
• Skin necrosis 
• Taste disturbance
• “Purple toe” syndrome
A

Warfarin

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21
Q

DDI for what drug?
• Drugs that change hepatic metabolism of warfarin
• Inhibition  more effect of warfarin  elevated INR
• Induction  less effect of warfarin  decreased INR
• Drugs that displace warfarin from protein binding sites
• More free drug  more effect of warfarin  elevated INR
• Drugs that change vitamin K levels
• Broad spectrum antibiotics reduce GI flora  less vitamin K and more effect
of warfarin  elevated INR
• Intake of vitamin K decreases effect of warfarin  decreased INR
• Drugs that increase risk of bleeding
• ASA and NSAIDS inhibit platelet function  increased risk of bleeding

A

Warfarin

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22
Q
  • MOA: Inhibit vitamin K epoxide reductase component 1 (VKORC1)
  • Use: Many including Atrial fibrillation, DVT/PE treatment and prevention
  • ADRs: bleeding, taste disturbances, skin necrosis
  • Narrow therapeutic index medication
  • Drug-Drug interactions:• Increased effect with NSAIDs, antibiotics, acetaminophen?
  • Decreased effects with barbiturates
A

Warfarin (Vitamin K Antagonist)

• Brand name: Coumadin®, Jantoven®

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23
Q

Dental Implications
• Most procedures can be done without holding
• For dental procedure that may result in
excessive bleeding consult prescribing physician
to adjust dose or hold if possible
• Consider local hemostasis measures to prevent
excessive bleeding
• Check INR level prior to performing a dental surgical
procedure
• Antibiotic use after dental procedure may increase risk of
bleeding

A

Warfarin

24
Q 
Mechanism of Action
• Inhibits coagulation in vivo and 
in vitro
• Activation of antithrombin III
• Increases antithrombin III affinity 
for Factor Xa and Thrombin
A

Heparin

25
Q
  • Not absorbed from the gastrointestinal (GI) tract
  • Administered intravenously (IV) or subcutaneously (SQ)
  • Fast onset: immediate after IV, 60 minutes after SQ
  • Half-life is ~ 40-90 minutes
A

Heparin

26
Q

What is the Effect on coagulation parameters of heparin?

A

Increased aPTT

27
Q

Adverse Drug Reactions
• Bleeding (can be life threatening)
• Protamine can reverse effects (binds heparin)
• Thrombosis
• Heparin associated thrombocytopenia (HAT)
• Heparin induced thrombocytopenia (HIT)
• Osteoporosis- with long-term treatment, mechanism unclear
• Aldosterone inhibition hyperkalemia
• Hypersensitivity reaction

A

Heparin

28
Q
  • MOA: Activation of antithrombin III leading to inhibition of thrombin and factor Xa
  • Use: Many including ACS, DVT/PE, Atrial fibrillation, etc..
  • ADRs: bleeding, thrombosis, osteoporosis, hyperkalemia, hypersensitivity
  • Drug-Drug interactions: none of significance to dentistry
  • Dental implications: none beyond bleeding
A

Heparin

29
Q 
Mechanism of Action
• Inhibits coagulation in vivo and 
in vitro
• Smaller portion of the heparin 
molecule
• Not large enough to interact with 
thrombin
• Activation of antithrombin III
• Increases antithrombin III affinity 
for Factor Xa but NOT thrombin
A

Low Molecular Weight Heparin (LMWH)

30
Q
  • Not absorbed from the GI tract
  • Administered subcutaneously (SQ)
  • Fast onset and predictable response
  • Cleared by the kidneys
  • Half-life is 4.5-7 hours
A

Low Molecular Weight Heparin (LMWH)

31
Q

• MOA: Activation of antithrombin III leading to
inhibition factor Xa but NOT thrombin
• Use: Many including ACS, DVT/PE, Atrial fibrillation, etc..
• ADRs: bleeding, thrombosis, osteoporosis, hyperkalemia,
hypersensitivity
• Lower incidence of HIT than unfractionated heparin
• Drug-Drug interactions
• Increased risk of bleeding with NSAIDs and Aspirin
Dental Implications
• Determine why patient is taking medication
• Delay procedure until treatment complete
• Do not discontinue therapy
• Consider local hemostasis measures to prevent
excessive bleeding

A

enoxaparin

• Brand name: Lovenox®

32
Q 
Mechanism of Action
• Derived for the saliva of 
medicinal leeches 
• Binds to the fibrin-binding sites 
of thrombin preventing the 
conversion of fibrinogen to fibrin
A

Direct Thrombin Inhibitors

33
Q
  • Intravenous agents: Argatroban and Bivalirudin
  • Oral agent: Dabigatran (pro-drug)
  • Effect on coagulation parameters:
  • Dabigatran does not require monitoring of coagulation tests
  • Argatroban and bivalirudin may be monitored by aPTT depending in indication
A

Direct thrombin inhibitors

34
Q

• MOA: Binds to thrombin preventing conversion of fibrinogen to fibrin
• Use: Atrial fibrillation and DVT/PE treatment and prevention
• ADRs: bleeding (reversal agent available- idarucizumab),
dyspepsia/gastritis (25%-35%)- due to formulation • Drug-Drug interactions
• Increased risk of bleeding with NSAIDs and Aspirin
• Dental Implications:
• High risk of bleeding
• High risk of thrombosis if stopped (short half-life)

A

Dabigatran

• Brand name: Pradaxa®

35
Q

Mechanism of Action
• Binds to factor Xa and prevent
the conversion of prothrombin
to thrombin

A

Factor Xa inhibitors

36
Q

Pharmacokinetics
• Parenteral agent: Fondaparinux (SQ)
• Oral agents: Apixaban, Edoxaban, Rivaroxaban
• Effect on coagulation parameters:
• Factor Xa inhibitors have an inconsistent effect on coagulation tests
• Factor Xa inhibitors do NOT require routine monitoring- do require renal dosing

A

Factor Xa Inhibitors

37
Q

• MOA: Binds to factor Xa and prevents conversion of prothrombin to
thrombin
• Use: Atrial fibrillation and DVT/PE treatment and prevention
• ADRs: bleeding (reversal agent available- andexanet alfa)
• Drug-Drug interactions
• Increased risk of bleeding with NSAIDs and Aspirin
• Dental Implications:
• High risk of bleeding
• High risk of thrombosis if stopped (short half-life)

A

Apixaban

• Brand name: Eliquis®

38
Q 
• Overarching term referring to:
• Apixaban
• Dabigatran
• Edoxaban
• Rivaroxaban
• Generally NOACs are recommended in guidelines over 
warfarin for prevention of stroke and systemic embolism AF 
and DVT/PE treatment due to ease of use
• Also called DOACs
• Direct-acting Oral Anticoagulants
A

NOACsNon-Vitamin K Oral Anticoagulants

39
Q 
Mechanism of Action
• Inhibits cyclo-oxygenase 1 (COX 1)
• Prevents formation of 
prostaglandin which is 
subsequently converted to 
thromboxane A2
• Low dose ASA (81mg) inhibits > 95% 
of platelet TXA2 formation 
• Platelets can not make new COX-1, 
ASA effects last for life of platelet 7-
10 days
A

Aspirin

40
Q 
Adverse Reactions
More Common:
• Bleeding- gastrointestinal
• Gastrointestinal distress
• Rash
Less common 
• Angioedema
• Tinnitus 
• Respiratory distress
A

Aspirin

41
Q

• MOA: Inhibition of COX-1 preventing the formation of TXA2
• Use: Many including secondary prevention of coronary
disease, arthritis, anti-inflammatory
• ADRs: bleeding, rash, GI distress, angioedema, tinnitus,
respiratory distress
• Drug-Drug interactions
• Increased risk of bleeding with NSAIDs and other anticoagulants
• May lower the effectiveness of anti-hypertensive agents
Dental Implications
• Determine why ASA is being taken- most
procedures can be done without holding ASA
• Increased risk of bleeding
• Consider local hemostasis measures to prevent excessive bleeding

A

Aspirin

• Brand name: Bayer® and many others

42
Q

Mechanism of Action

Inhibition of ADP binding to the P2Y12 receptor

A

P2Y12 inhibitors

43
Q 
The following drugs are what type of drug?
Cangrelor
Clopidogrel
Prasugrel
Ticagrelor
A

P2Y12 inhibitors

44
Q

Adverse Drug Reactions
• Bleeding
• Less occurrence than aspirin when used as monotherapy
• Increased occurrence when combined with aspirin (DAPT)
• Skin rash (~ 10%)
• Thrombocytopenia (rare)
• ADRs unique to ticagrelor:
• Dyspnea- due to off-target adenosine effects
• Elevated serum creatinine- unknown mechanism usually clinically insignificant

A

P2Y12 inhibitors

45
Q

Drug-Drug interactions
• Mainly due to CYP 450 inhibition
• Ticagrelor 3A4, Clopidogrel & Prasugrel 2C19
• Prodrugs (Clopidogrel & Prasugrel) require activation by CYP 450 therefore have
less activity resulting in increased risk of thrombotic event
• Proton Pump Inhibitor resulting in a significant drug-drug interaction
• Ticagrelor active upon administered therefore inhibition results in
increased levels and activity leading to increased risk of bleeding
• All P2Y12 inhibitors interact with other medications that increase risk of
bleeding (i.e. anticoagulants, NSAIDs, etc..)

A

P2Y12 inhibitors

46
Q

• MOA: Inhibition of ADP binding to the P2Y12 receptor
• Use: Treatment of Acute Coronary Syndrome
• ADRs: bleeding, rash, dyspnea, elevated serum creatinine
• Drug-Drug interactions
• Increased risk of bleeding with NSAIDs, aspirin, and other
anticoagulants
• CYP 3A4 inhibitors (i.e. macrolide antibiotics and azoles) may
increase effect
Dental Implications
• Plan for increased bleeding
• Consider local hemostasis measures to prevent
excessive bleeding
• Do not stop/hold without consulting prescribing
physician
• Do not alter aspirin dose prescribed
• Ticagrelor specific- potential shortness of breath

A

ticagrelor

• Brand name: Brilinta®

47
Q 
Mechanism of Action
• Bind to GP IIb/IIIa receptor 
preventing platelet 
aggregation  
• Only available intravenously 
• Abciximab (no longer available)
• monoclonal antibody
• Eptifibatide and tirofiban
• small molecules
A

Glycoprotein IIb/IIIa inhibitors

48
Q
  • MOA: Bind to GP IIb/IIIa receptor preventing platelet aggregation
  • Use: Treatment of Acute Coronary Syndrome
  • ADRs: bleeding (highest of all antiplatelet agents), thrombocytopenia
  • Drug-Drug interactions:
  • none of significance to dentistry
  • other drugs that increase bleeding
  • Dental Implications: none
A

Eptifibatide

• Brand name: Integrilin®

49
Q 
Mechanism of Action
• Antagonist of the protease 
activated receptor-1 inhibiting 
thrombin receptor agonist  
peptide (TRAP)- induced 
platelet aggregation
• Does NOT effect the 
conversion of fibrinogen to 
fibrin by thrombin
A

PAR-1 antagonist (Vorapaxar)

50
Q

• MOA: Antagonist of the protease activated receptor-1 inhibiting thrombin
receptor agonist peptide (TRAP)- induced platelet aggregation
• Use: secondary prevention of coronary artery disease
• ADRs: bleeding (~25%)
• Drug-Drug interactions:
• Other drugs that increase bleeding (i.e. aspirin, NSAIDs, anticoagulants)
• Dental Implications:
• High bleeding risk medication

A

Vorapaxar

• Brand name: Zontivity®- approved late 2014

51
Q

Does the ADA recommend routinely stopping anticoag and antiplatelet meds for dental tx?

A

No; will under certain circumstances following a med consult

52
Q 
Mechanism of Action 
Binds to tissue bound 
fibrin and plasminogen  
converting plasminogen 
to plasmin 
(fibrin specific)
Recombinant form of 
tissue plasminogen 
activator (TPA)
A

Plasminogen activators

53
Q 
• MOA: Binds to tissue bound fibrin and plasminogen  converting plasminogen to plasmin 
• Use: STEMI, Stroke (alteplase only) 
• ADRs: bleeding from virtually any site
• Drug-Drug interactions: 
• None of significance to dentistry
• Other drugs that increase bleeding (i.e. heparin, aspirin, and 
clopidogrel)
• Dental Implications: none
A

Tenecteplase

• Brand name: TNKase®

54
Q 
Mechanism of Action 
Competitive inhibition of 
plasminogen activation 
by binding to 
plasminogen
At higher concentrations 
non-competitive 
inhibition of plasmin
A

Hemostatic Agents

55
Q

• MOA: Competitive inhibition of plasminogen activation by binding to
plasminogen; at higher concentrations non-competitive inhibition of plasmin
• Use: Prophylaxis of bleeding in patients at high risk of bleeding during
dental procedures or surgery
• ADRs: IV- hypotension and giddiness; PO- headache, abdominal pain, and
nasal/sinus symptoms
• Drug-Drug interactions:
• Reduces the effectiveness of anticoagulants
• Increased risk of thrombosis
Dental Implications
• Used as an antifibrinolytic mouthwash following
dental surgery to prevent hemorrhage in
patients taking oral anticoagulants.
• Topical administration should have limited
systemic effects. If systemic administration
considered consult with physician prescribing
anticoagulant.

A

Tranexamic acid

• Brand name: Lysteda®

Pharmacology (12 decks)

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