hemostatsis and thrombosis Rx Flashcards
vita k antag
warfarin (po and IV)
warfarin moa
genetics? only effective when?
Inhibits vitamin K epoxide reductase component 1
(VKORC1). Preventing the formation of vitamin K
dependent clotting factors (II, VII, IX, X, protein C, protein S).
The VKORC1 gene is polymorphic resulting in different affinities for warfarin.
Only effective in vivo
warfarin adrs
Bleeding (can be life threatening)- GI bleeding most common
Rash
Skin necrosis
Taste disturbance
“Purple toe” syndrome
warfarin dental
Bleeding- most procedures can be done without
holding medication
Antibiotic use after dental procedure may increase
risk of bleeding
unfractionated heparin
heparin (sq and IV)
heparin moa
works when?
Activation of antithrombin III, thereby inactivating Factor Xa and Thrombin (factor II).
Inhibits coagulation in vivo and in vitro
heparin adrs
Bleeding (can be life threatening)
Thrombosis- both HAT and HIT
Osteoporosis
Aldosterone inhibition-leading to hyperkalemia
Hypersensitivity reaction
heparin dental
Bleeding/bleeding gum
Although unlikely to be on heparin during dental
treatment
Low Molecular Weight Heparin (LMWH names
forms
Enoxaparin
Dalteparin
Tinzaparin
Available: SQ
LMWH moa
in vivo/vitro?
Activation of antithrombin III, thereby inactivating Factor Xa.
Smaller portion of the heparin molecule therefore not large enough to interact with thrombin (factor II).
Inhibits coagulation in vivo and in vitro.
LMWH adrs
Same as UFH
Bleeding (can be life threatening)
Thrombosis- both HAT and HIT- HIT less common with
LMWHs
Osteoporosis
Aldosterone inhibition-leading to hyperkalemia
Hypersensitivity reaction
LMWH dental
Bleeding- most procedures can be done without
holding medication
Coagulation tests (PT/aPTT) are insensitive to anticoagulant effects of LMWHs
Direct Thrombin Inhibitors
forms
Argatroban-Available: IV
Bivalirudin- Available: IV
Dabigatran- Available: PO
direct thrombin inhibitors moa
Binds to the fibrin- binding sites of thrombin preventing the conversion of fibrinogen
direct thrombin inhibitors adrs/ names
Argatroban/Bivalirudin: bleeding (life threatening)
Dabigatran: Bleeding (can be life threatening)- new reversal agent available and Dyspepsia/gastritis with dabigatran due to formulation
direct thrombin inhibitors dental
Bleeding- Although unlikely to be on argatroban or bivalirudin during dental treatment
Bleeding- most procedures can be done without holding dabigatran
factor Xa inhibitors
forms
Apixaban-Available: PO
Edoxaban- Available: PO
Fondaparinux- Available: SQ
Rivaroxaban- Available: PO
factor Xa inhibitors moa
Binds to factor Xa and
prevent the conversion
of prothrombin to
thrombin
factor Xa inhibitors adrs
bleeding
factor Xa inhibitors dental
Bleeding- most procedures
can be done without
holding medications
cox inhibitor
aspirin (PO)
aspirin MOA
Inhibits cyclo-oxygenase 1 (COX 1). Prevents formation of prostaglandin which is subsequently converted to
thromboxane A2
aspirin adrs
Bleeding (GI most common)
Dyspepsia
Rash
Angioedema
Tinnitus
Respiratory distress
aspirin dental
Bleeding- although most procedures can be completed without holding medication
P2Y12 inhibitors and forms
Cangrelor- Available: IV
Clopidogrel- Available: PO
Prasugrel- Available: PO
Ticagrelor- Available: PO
P2Y12 inhibitor moa
Inhibition of ADP binding at the P2Y12 receptor
P2Y12 inhibitors adrs/ names
Cangrelor- Bleeding (major) and Renal insufficiency
Clopidogrel/ Prasugrel/ Ticagrelor-
* Bleeding more common when combined with ASA
* Skin rash (more common with clopidogrel)
* Thrombocytopenia
* Dyspnea and elevated serum creatinine- unique to ticagrelor
P2Y12 inhibitors dental
Bleeding- although it is unlikely patients will be on cangrelor during tx
Clopidogrel/ Prasugrel/ Ticagrelor: Bleeding- it is recommended to continue therapy through dental procedure.
Glycoprotein IIb/IIIa inhibitors
forms
Eptifibatide
Tirofiban
Both Available: IV
Glycoprotein IIb/IIIa inhibitors moa
Bind to GP IIb/IIIa receptor preventing the final
common pathway of platelet aggregation
Glycoprotein IIb/IIIa inhibitors adrs/ names
Bleeding- highest incidence of all antiplatelet medications
Thrombocytopenia
Eptifibatide and Tirofiban
Glycoprotein IIb/IIIa inhibitors dental
Bleeding- although it is unlikely patients will be on
these medications during procedure
PAR-1 antagonist name
form
Vorapaxar
Available: PO
vorapaxar moa
Antagonist of the PAR-1 inhibiting thrombin receptor agonist peptide (TRAP)- induced platelet aggregation
Does not effect the conversion of fibrinogen to fibrin by thrombin
vorapaxar adrs
bleeding
vorapaxar dental
Bleeding-no recommendations made regarding whether or not to hold medication during procedure
Fibrinolytic Therapy (Plasminogen activators)
form
Alteplase
Reteplase
Tenecteplase
Available: IV
Fibrinolytic Therapy (Plasminogen activators) moa
Binds to tissue bound fibrin and plasminogen converting plasminogen to plasmin (fibrin specific)
Fibrinolytic Therapy (Plasminogen activators adr
bleeding (mostly at infusion site)
Fibrinolytic Therapy (Plasminogen activators dental
Bleeding- although it is unlikely that a patient will
be receiving these medications during procedure
Antifibrinolytic Therapy (Hemostatic agents)
forms
Aminocaproic acid
Tranexamic acid
Available: PO and IV
Antifibrinolytic Therapy (Hemostatic agents moa
Competitive inhibition of plasminogen activation by
binding to plasminogen
At higher concentrations non- competitive inhibition of
plasmin
Antifibrinolytic Therapy (Hemostatic agents) adrs
IV vs PO
IV- hypotension and giddiness
PO- headache, abdominal pain, and nasal/sinus
symptoms
Antifibrinolytic Therapy (Hemostatic agents) dental
Used as an off-label indication to prevent or treat dental bleeding
Enoxaparin moa
LMWH:
Activation of antithrombin III, thereby inactivating Factor Xa. Smaller portion of the heparin molecule therefore not large enough to interact with thrombin (factor II).
Inhibits coagulation in vivo and in vitro.
dalteparin moa
LMWH
Activation of antithrombin III, thereby inactivating Factor Xa. Smaller portion of the heparin molecule therefore not large enough to interact with thrombin (factor II).
Inhibits coagulation in vivo and in vitro.
tinzaparin moa
Activation of antithrombin III, thereby inactivating Factor Xa. Smaller portion of the heparin molecule therefore not large enough to interact with thrombin (factor II).
Inhibits coagulation in vivo and in vitro.
Argatroban moa
Binds to the fibrin-
binding sites of thrombin
preventing the
conversion of fibrinogen
bivalirudin moa
Binds to the fibrin-
binding sites of thrombin
preventing the
conversion of fibrinogen
dabigatran moa
Binds to the fibrin-
binding sites of thrombin
preventing the
conversion of fibrinogen
apixaban moa
Binds to factor Xa and
prevent the conversion
of prothrombin to
thrombin
edoxaban moa
Binds to factor Xa and
prevent the conversion
of prothrombin to
thrombin
fondaparinux moa
Binds to factor Xa and
prevent the conversion
of prothrombin to
thrombin
rivarobaxan moa
Binds to factor Xa and
prevent the conversion
of prothrombin to
thrombin
Cangrelor moa
Inhibition of ADP binding
at the P2Y12 receptor
clopidigrel moa
Inhibition of ADP binding
at the P2Y12 receptor
prasugrel moa
Inhibition of ADP binding
at the P2Y12 receptor
ticagrelor moa
Inhibition of ADP binding
at the P2Y12 receptor
Eptifibatide moa
Bind to GP IIb/IIIa receptor
preventing the final
common pathway of
platelet aggregation
tirofiban moa
Bind to GP IIb/IIIa receptor
preventing the final
common pathway of
platelet aggregation
Alteplase moa
Binds to tissue bound fibrin and
plasminogen converting
plasminogen to plasmin
(fibrin specific)
reteplase moa
Binds to tissue bound fibrin and
plasminogen converting
plasminogen to plasmin
(fibrin specific)
tenecteplase moa
Binds to tissue bound fibrin and
plasminogen converting
plasminogen to plasmin
(fibrin specific)
Aminocaproic acid moa
Competitive inhibition of plasminogen activation by
binding to plasminogen
At higher concentrations non-competitive inhibition of plasmin
tranexaminic acid moa
Competitive inhibition of plasminogen activation by
binding to plasminogen
At higher concentrations non-competitive inhibition of plasmin