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Pharmacology I > Hemostasis and Thrombosis > Flashcards

Hemostasis and Thrombosis Flashcards

1
Q

define hemostasis

A

the arrest of blood loss from damaged blood vessles

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2
Q

hemostasis is caused by

A
  • platelet adhesion and activation
  • fibrin formation
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3
Q

define thrombosis

A
  • pathological formation of a hemostatis plug within the vasculature in the absence of bleeding
  • hemostasis in the wrong place
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4
Q

what makes up Virchow’s triad in thrombosis

A
  • stasis
  • vessel wall injury
  • hypercoagulability
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5
Q

describe white thrombus

A
  • arterial clot
  • primarily platelets and some fibrin mesh
  • associated with atherosclerosis
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6
Q

describe red thrombus

A
  • venous clot
  • mostly fibrin and small amount of platelets
  • higher risk of embolus
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7
Q

what does antithrombin III do

A

prevents coagulation by lying factor Xa and thrombin

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8
Q

what does thrombin (factor IIa) do

A

causes platelet activation

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9
Q

describe the intrinsic pathway

A
  • 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)
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10
Q

describe the extrinsic pathway

A
  • some components come from outside blood: tissue factor
  • starts when tissue damage releases tissue factor
  • monitored by prothrombin time and INR
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11
Q

describe vitamin K and how it is obtained

A
  • fat soluble vitamin with little stored in the body
  • most vitamin K obtained from diet or produced by bacteria in the gut
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12
Q

vitamin K is a cofactor in the formation of which clotting factors:

A
  • factor I
  • factor 7
  • factor 9
  • factor 10
  • protein C
  • protein S
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13
Q

warfarin works by inhibiting the action of:

A

vitamin K

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14
Q

what is the platelet role in thrombus formation

A
  • platelet adhesion: following vascular damage, VWF
  • platelet activation: mediators are ADP, TXA2, collagen, thrombin -> shape change
  • platelet aggregation: final common pathway, GP IIb/IIIa receptor
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15
Q

what is the key mediator in fibrinolysis

A

plasmin

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16
Q

what makes plasmin

A

tissue plasminogen activator and plasminogen

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17
Q

what does plasmin do

A

fibrin -> clot fragmentation

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18
Q

what are the types of anticoagulant medications

A
  • vitamin K antagonist
  • unfractionated heparin
  • low molecular weight heparins
  • direct thrombin inhibitors
  • factor Xa inhibitors
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19
Q

what is an example of a vitamin K antagonist and its MOA

A
  • warfarin
  • acts only in vivo
  • inhibits vitamin K epoxide reductase component 1
  • this gene is polymorphic resulting in different affinities for warfarin
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20
Q

what are the pharmacokinetics of wafarin

A
  • rapidly absorbed after oral administration
  • highly bound to plasma proteins
  • hepatically metabolized
  • onset of action 5-7 days
  • half life is about 40 hours
  • requires new steady state of clotting factors to be achieved
  • effects of dose change require 2-3 days to present
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21
Q

what are the effects of coagulation parameters from warfarin

A
  • INR increases
  • PT increases
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22
Q

warfarin exerts an ______ effect on aPTT

A

inconsistent

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23
Q

warfarin is monitored using ____ and the goal is ____

A

INR; 2-3

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24
Q

what are the adverse drug reactions for warfarin

A
  • bleeding- can be life threatening
  • GI bleeding most common
  • rash
  • skin necrosis
  • taste disturbance
  • purple toe syndrome
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25
Q

what are the drug-drug interactions with warfarin

A
  • drugs that change hepatic metabolism of warfarin
  • drugs that displace warfarin from protein binding sites
  • drugs that change vitamin K levels
  • drugs that increase the risk of bleeding
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26
Q

what are the effects of drugs that change hepatic metabolism of warfarin

A
  • inhibition -> more effect of warfarin -> elevated INR
  • induction -> less effect of warfarin -> decreased INR
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27
Q

what are the effects of drugs that displace warfarin from protein binding sites

A
  • more free drug -> more effect of warfarin -> elevated INR
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28
Q

what are the effects of drugs that change vitamin K levels

A
  • 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
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29
Q

what is the use and main interactions with warfarin

A
  • atrial fibrillation, DVT/PE tx and prevention
  • interactions: acetominophen
  • narrow therapeutic index medication
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30
Q

what are the dental implications for warfarin

A
  • 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 dental surgical procedure
  • AB use after dental procedure may increase the risk of bleeding
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31
Q

what is the MOA of heparin

A
  • inhibits coagulation in vivo and in vitro
  • activation of antithrombin III
  • increases antithrombin III affinity for factor Xa and thrombin
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32
Q

what are the pharmacokinetics of heparin

A
  • not absorbed from the GI tract
  • administered IV or SQ
  • fast onset: immediately after IV, 60 minutes after SQ
  • half life is about 40-90 minutes
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33
Q

what is heparins effect on coagulation paramaters

A

aPTT increases

34
Q

heparin is monitored using ____ and the goal is _____

A

aPTT; 1.5-2.5 times control

35
Q

what are the adverse drug reactions for heparin

A
  • bleeding
  • thrombosis: heparin associated thrombocytopenia (HAT) and heparin induced thrombocytopenia (HIT)
  • osteoporosis with long term treatment
  • aldosterone inhibition -> hyperkalemia
  • hypersensitivity reaction
36
Q

what can reverse the bleeding effects of heparin and how

A

protamine - binds heparin

37
Q

what is the use, drug interactions and dental implications of heparin

A
  • use: many including ACS, DVT/PE, atrial fibrillation
  • drug interactions: none significant to dentistry
  • dental implications: none besides bleeding
38
Q

what is the MOA of low molecular weight heparin

A
  • 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
39
Q

what are the pharmacokinetics of low molecular weight heparin

A
  • not absorbed from the GI tract
  • administered SQ
    = fast onset and predictable response
  • cleared by the kidneys
  • half life is 4.5-7 hoursw
40
Q

what is LMWH effect on coagulation parameters

A

LMWH do not require monitoring of coagulation parameters

41
Q

what is the use, ADRs and drug interactions of LMWH

A
  • use: many including ACS, DVT/PE, atrial fib
  • ADRs: bleeding, thrombosis, osteoporosis, hyperkalemia, hypersensitivity
  • lower incidence of HIT than unfractionated heparin
  • drug interactions: increased risk of bleeding with NSAIDs and aspirin
42
Q

what are the dental implications of LMWH

A
  • determine why pt is taking medication
    = delay proceudre until tx complete
  • do not discontinue therapy
  • consider local hemostasis to prevent excessive bleeding
43
Q

what is the MOA for direct thrombin inhibitors

A
  • derived for the saliva of medicinal leeches
  • binds to the fibrin binding sites of thrombin preventing the conversion of fibrinogen to fibrin
44
Q

what are the pharmacokinetics of direct thrombin inhibitors

A
  • IV agents: argatroban and bivalirudin
  • oral agent: dabigatran
45
Q

what are the direct thrombin inhibitors effect on coagulation parameters

A
  • argatroban has a drug-lab interaction resulting in falsely elevated INR
  • dabigatran does not require monitoring of coagulation tests
  • argatroban and bivalirudin may be monitored by aPTT depending on indication
46
Q

what is the brand name, use, ADRs, drug inreactions, dental implications of direct thrombin inhibitors

A
  • pradaxa
  • use: atrial fibrillation, DVT/PE treatment and prevention
  • ADRs: bleeding, dyspepsia/gastrisis (25-35%)
  • drug interactions: incresed risk of bleeding with NSAIDs and aspirin
  • dental implications: high risk of bleeding, high risk of thrombosis if stopped- short half life
47
Q

what drug reverses direct thrombin inhibitors for bleeding issues and what is the downside of it

A
  • idarucizumab
  • reversal costs $5,000
48
Q

what is the MOA of factor Xa inhibitors

A
  • binds to factor Xa and prevents the conversion of prothrombin to thrombin
49
Q

what are the pharmacokinetics of factor Xa inhibitors

A
  • parenteral agent: fondaparinux (SQ)
  • oral agents: apixaban, edoxaban, rivaroxaban
50
Q

what are the factor Xa inhibitor effects on coagulation parameters

A
  • factor Xa inhibitors have an inconsistent effect on coagulation tests
  • factor Xa inhibitors do not require monitoring, do require renal dosing
51
Q

what is the brand name, use, ADRs, drug interactions and dental implications of factor Xa inhibitors

A
  • eliquis
  • use: atrial fibrillation and DVT/PE treatment and prevention
  • ADRs: bleeding
  • drug interactions: increases risk of bleeding with NSAIDs and aspirin
  • dental implications: high risk of bleeding, high risk of thrombosis if stopped - short half life
52
Q

what is the reversal agent for factor Xa inhibitors and what is the downside of it

A
  • andexanet alfa
  • $25,000-$30,000
53
Q

non vitamin K oral anticoagulants is an overarching term referring to:

A
  • apixaban
  • dabigatran
  • edoxaban
  • rivaroxaban
54
Q

NOACs are recommended over warfarin for:

A

prevention of stroke and systemic embolism AF and DVT/PE treatment due to ease of use

55
Q

what is another name for NOACs

A

direct acting oral anticoagulants

56
Q

what is the coagulation cascade of the intrinsic pathway

A
  • factor 12 -> factor 11 -> factor 10 -> factor Xa
57
Q

what is the extrinsic pathway coagualtion cascade

A

factor 7 + tissue factor -> factor 7a -> factor Xa

58
Q

what are the antiplatelet medications

A
  • COX inhibitor
  • P2Y12 inhibitors
  • glycoprotein IIb/IIa inhibitors
  • PAR-1 antagonist
59
Q

what is the MOA of aspirin

A
  • inhibits cyclo oxygenase 1
  • prevents formation of prostaglandin which is converted to thromboxane A2
  • low dose ASA (81mg) inhibits more than 95% of platelet TXA2 formation
  • platelets can not make new COX-1 ASA effects last for life of platelet 7-10 days
60
Q

what are the more common and less common adverse reactions from aspirin

A
  • more common: bleeding (GI), GI distress, rash
  • less common: angioedema, tinnitus, respiratory distress
61
Q

what is the use, and drug interactions of aspirin

A
  • use: many including secondary prevention of coronary disease, arthritis, anti-inflammatory
  • drug interactions: increased risk of bleeding with NSAIDS and other anticoagulants. may lower the effectiveness of anti hypertensive agents
62
Q

what are the dental implictions of aspirin

A
  • determine why it is being taken
  • most procedures can be done without holding aspirin
  • increased risk of bleeding
  • consider local hemostatis mesure to prevent excessive bleeding
63
Q

what is the MOA of P2Y12 inhibitors

A

inhibition of ADP binding to the P2Y12 receptor

64
Q

what is the metabolism of P2Y12 inhibitors

A
  • clopidogrel: CYP 2C19
  • prasugrel: CYP 2C19
65
Q

what are the ADRs of P2Y12 inhibitors

A
  • bleeding: less occurence than aspirin when used as a monotherapy, increased ocurrence when used with aspriin
  • skin rash (10%)
  • thrombocytopenia (rare)
  • ADRs unique to tricagrelor: dyspnea and elevated serum creatinine
66
Q

what are the drug interactions of P2Y12 inhibtors

A
  • mainly due to CYP 450 inhibition
  • prodrugs require activation by CYP 450 therefore have less activity resulting in increased risk of thrombotic event
  • tricagrelor active upon administered therefore inhibition results in increased levels and activity leading to increased risk of bleeding
  • all P2Y12 inhibitors interact with other medciations that increase risk of bleeding
67
Q

what is the use of P2Y12 inhibitors

A

treatment of acute coronary syndrome

68
Q

what are the dental implications of P2Y12 inhibitos

A
  • plan for increased bleeding
  • do not stop without consulting prescribing physician
  • do not alter aspirin prescribed dose
  • ticagrelor specific
69
Q

what is the mechanism of action of glycoprotein IIb/IIIa inhibitors

A
  • bind to GP IIa/IIIa receptor preventing platelet aggregation
  • only available IV
  • eptifibatide and tirofiban
70
Q

what is the example, use, ADRs, drug interactions and dental implications of glycoprotein IIb/IIIa inhibitors

A
  • eptifibatide
  • use: treatment of acute coronary syndrome
  • ADRs: bleeding (highest of all antiplatelet agents), thrombocytopenia
  • drug interactions: none significant to dentistry
  • dental implications: none
71
Q

what is the MOA of PAR-1 antagonist

A
  • 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
72
Q

what is the brand name, use, ADRs, drug interactions and dental implications of PAR-1 antagonist

A
  • brand name: Zontivity
  • use: secondary prevention of coronary artery disease
  • ADRs; bleeding (25%)
  • drug interactions: other drugs that increase bleeding
  • dental implications: high bleeding risk
73
Q

should warfarin or antiplatelet medications be alterred before dental procedures

A

no

74
Q

in patients with comorbid medical conditions that can increase the risk of prolonged bleeding after dental treatment:

A

consult with patients physician

75
Q

what are the fibrinolytic and antifibrinolytic medications

A
  • fibrinolytic therapy: plasminogen activators
  • antifribinolytic therapy: hemostatic agents
76
Q

what is the MOA of plasminogen activators

A
  • binds to tissue bound fibrin and plasminogen converting plasminogen to plasmin
  • recombinant form of tissue plasminogen activator (TPA)
77
Q

what is the example, use, ADRs, drug interactions and dental implications of plasminogen activators

A
  • tenecteplase
  • use: STEMI, stroke
  • ADRs; bleeding from any site
  • drug interactions: none significant to dentisry
  • other drugs that increase bleeding
  • dental implications: none
78
Q

what is the MOA of hemostatic agents

A
  • competitve inhibition of plasmin activation by binding to plasminogen
  • at higher concentrations non competitive inhibition of plasmin
79
Q

what is the example, use, ADRs, drug interactions of hemostatic agents

A
  • tranexamic acid
  • use: prohylaxis of bleeding in patients at high risk of bleeding during dental procedures of surgery
  • ADRs: IV- hypotension and giddiness; PO- headache, abdominal pain and nasal/sinus symptoms
  • drug interactions: reduced the effectiveness of anticoagulants, increased risk of thrombosis
80
Q

what are the dental implications of hemostatic agents

A
  • used as an antifibrinolytic mouthwash following dental surgery to prevent hemorrhage in patients taking oral anticoagulants
  • topical administration should have limited systemic effects. if sysemic adminsitration considered consult with physician prescribing anticoagulant
81
Q
A

Pharmacology I (12 decks)

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