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Pharmacology II > Antiplatelets/coagulants (exam 2) > Flashcards

Antiplatelets/coagulants (exam 2) Flashcards

1
Q

When does endothelium injury occur?

A

Single layer of cells lining blood vessels is damaged

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2
Q

Injured vessel wall exposes blood to ___ and ____.

A

collagen

von Willebrand’s Factor

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3
Q

Neutrophils and macrophages in response to endothelium injury release

A

Platelet Activating Factor (PAF)

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4
Q

Activated platelets secrete

A

ADP, serotonin, and TxA2

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5
Q

Endothelium injury leads to

A

vasoconstriction then eventually a platelet plug which forms a clot

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6
Q

Consequences of endothelium injury

A

inflammation
vascular changes
thrombosis
leukocyte adhesion

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7
Q

Hemostasis

A
  1. Vessel constriction
  2. Primary hemostasis (formation of platelet plug)
  3. Secondary hemostasis (formation of clot)
  4. Stable clot formed
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8
Q

Formation of platelet plug

A

Platelet adhesion –> platelet activation –> platelet aggregation

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9
Q

Activation of a clotting cascade results in a _____

A

fibrin-containing clot

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10
Q

Platelets

A

blood cells that help form clots to stop bleeding

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11
Q

Adhesion

A

Process of spreading across surface of damaged blood vessel to stop bleeding

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12
Q

No injury present, platelet aggregation is prevented by

A

separating blood from collagen
secreting NO and PGI2
enzyme CD39 breaks down ADP in blood

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13
Q

platelet adhesion

A

circulating platelets attach to exposed vWF and collagen via glycoprotein receptors

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14
Q

platelet activation

A

irreversible change in shape to increase surface area and secrete granules

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15
Q

during platelet activation, ADP binds to _________ which increases _______________

A

P2Y12 receptors

platelet activation

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16
Q

platelet aggregation

A

fibrinogen binds to GP IIb/IIIa receptors on platelets –> crosslinks them to form a platelet plug

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17
Q

extrinsic pathway and factors involved

A

external trauma that causes blood to leave the circulatory system
factors 7 and 10

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18
Q

intrinsic pathway and factors involved

A

activated by trauma inside the vascular system
factors 8-12

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19
Q

the intrinsic and extrinsic pathways converge at _____________ which is also known as the _____________

A

factor X

common pathway

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20
Q

factor V is a __________ for Factor X because it ________-

A

cofactor

fits into the notch on X

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21
Q

activated factor X converts

A

prothrombin to thrombin

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22
Q

thrombin cuts

A

fibrinogen into fibrin

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23
Q

fibrin fibers form

A

clots

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24
Q

fibrinolysis pathway

A

plasminogen activator (tPA) –> plasminogen to plasmin –> breaks down fibrin and dissolves the clot

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25
Q

arterial thrombus are formed under ___________ and is ___________. Also called a _____________

A

high pressure

platelet rich

white thrombi

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26
Q

venous thrombus are formed under ___________ and is ___________. Also called a _____________

A

low pressure

fibrin rich

red thrombi

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27
Q

antithrombin primarily inactivates

A

factors II and Xa

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28
Q

Protein S is a cofactor of

A

Protein C

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29
Q

Protein C inactivates

A

factors Va and VIIIa

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30
Q

tissue factor pathway inhibitor

A

inhibits the tissue factor to factor VIIa complex and inhibits factor Xa

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31
Q

Virchow’s triad

A

endothelial injury
abnormal blood flow
hypercoagulability

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32
Q

endothelial injury

A

main influence on thrombus formation in the heart and the arterial circulation

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33
Q

endothelial injury is caused by

A

hypertension
hyperlipidemia
elevated blood glucose in DM
traumatic vascular injury

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34
Q

abnormal blood flow

A

state of turbulence and/or stasis

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35
Q

abnormal blood flow is caused by

A

hyperlipidemia
aneurysm
MI
cardiac arrythmia
immobility or paralysis

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36
Q

inherited (primary) hypercoaguability

A

Factor V lieden (resistence to anticoagulant effects of protein C)
Protein C or S deficiency

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37
Q

acquired (secondary) hyper coagulability

A

cancer
smoking
pregnancy
some medications (estrogen, heparin)

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38
Q

tissue plasminogen activators (tPAs) examples

A

altepase (activase)
reteplase (retavase)
tenecteplase (TNKase)

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39
Q

tissue plasminogen activators MOA

A

used to break down a clot that’s already formed by increasing the conversion of plasminogen to plasmin

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40
Q

uses for fibrinolytics

A

STEMI
acute ischemic use (most common)
severe cases of VTE, PE, DVT

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41
Q

tissue plasminogen activator binds to ____________ and converts __________________________

A

fibrin

plasminogen to plasmin

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42
Q

fibrinolytics are given

A

intravenously

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43
Q

MW and half life of alteplase

A

5-10 min

70 kd

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44
Q

MW and half life of reteplase

A

15 mins

39 kd

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45
Q

MW and half life of tenecteplase

A

20 mins

75 kd

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46
Q

ADRs of fibrolytics

A

high risk of bleeding

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47
Q

older clots have more ________ cross linking and are harder to ____________

A

fibrin

break down

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48
Q

do not give fibrinolytics to patients who

A

have an increased risk of bleeding

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49
Q

fibrinolytics must be given ____________ for benefit to outweigh bleeding risk

A

soon after thrombotic event

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50
Q

antiplatelet medication examples

A

COX1 inhibitors
P2Y12 receptor antagonists
PDE inhibitors
GP IIa/IIIa receptor antagonists

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51
Q

COX1 inhibitor example

A

aspirin

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52
Q

P2Y12 receptor antagonists examples

A

Clopidogrel (Plavix)
Prasurgel (Effient)
Ticagrelor (Brilinta)
Cangrelor (Kengreal)

53
Q

PDE inhibitors examples

A

Dipyridamole (Persantine)
Cilostazol (Pletal)

54
Q

GP IIa/IIIa receptor antagonists examples

A

Abciximab (Reopro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)

55
Q

anti platelet medications are used for

A

prevention of heart attack/stroke
ACS, especially when a stent (PCI) is used

56
Q

_____________ is recommended after stent therapy

A

Dual anti platelet therapy (aspirin and P2Y12 receptor antagonist)

57
Q

which type of drugs are used more frequently in arterial thrombosis?

A

anti platelet drugs

58
Q

aspirin decreases the synthesis of ______________ which decreases ___________ and causes __________

A

thromboxane 2

platelet activation

vasodilation

59
Q

ADRs of aspirin

A

gastric bleeding
tinnitus and hearing lose (high doses)
Reye’s syndrome in children

60
Q

Aspirin should not be given in anyone ______________ during fever causing illness

A

under 19 years old

61
Q

In ACS, it is recommended to chew __________________ for immediate effects

A

non-enteric coated aspirin

62
Q

Emax for inactivation of platelet COX1 is achieved with ______________

higher doses of aspirin do not seem to __________________________

A

a daily aspirin dose of about 75mg

improve efficacy for platelet effects but increase risk of bleeding

63
Q

what is given in the case of aspirin overdose?

A

sodium bicarbonate

64
Q

clopidogrel and prasurgel are ________________

ticagrejor and cangrelor are _________________

A

irreversible inhibitors and prodrugs

reversible inhibitors

65
Q

______________ is important in bio activation of clopidogrel

66
Q

ADRs of P2Y12 receptor antagonists

A

bleeding
ticagrejor can cause dyspnea

67
Q

which P2Y12 receptor antagonist is available as IV only?

68
Q

some _________________ inhibit CYP2C19 and may reduce the effectiveness of clopidogrel

69
Q

which P2Y12 receptor antagonist should not be used in patients with high bleeding risk due to higher rates of life threatening bleeding?

70
Q

PDE inhibitors inhibit the PDE enzyme which increases _________________ which does what?

A

increases cAMP and cGMP

reduces platelet activation and causes vasodilation

71
Q

ADRs of PDE inhibitors

A

bleed risk
headache
dizziness
diarrhea

72
Q

Cilostazol is _________________ and is primarily used in ______________

A

selective for PDE3

PAD

73
Q

Dipyridamole inhibits __________________ and is combined with aspirin for treatment of _______________

A

PDE3 and PDE5

secondary stroke prevention

74
Q

GP IIa/IIIa receptor antagonists are all given by

75
Q

ADRs of GP IIa/IIIa receptor antagonists

A

risk of bleeding
thrombocytopenia

76
Q

GP IIa/IIIa receptor antagonists are used during

A

PCI in ACS

77
Q

half life of GP IIa/IIIa receptor antagonists

A

eptifibatide (2.5 hrs) > tirofiban (2 hrs) > abciximab (mins)

78
Q

PDE inhibitors examples

A

dipyridamole (persantine)
cilostazol (pletal)

79
Q

GP IIa/IIIa receptor antagonists examples

A

Abciximab (reopro)
eptifibatide (integrilin)
tirofiban (aggrastat)

80
Q

abciximab is a

A

monoclonal antibody drug

81
Q

eptifibatide is a

A

peptide derived from rattlesnake venom

82
Q

tirofiban is a

A

non peptide small molecule inhibitor

83
Q

which drugs are used more frequently in venous thrombosis?

A

anticoagulants

84
Q

what are anticoagulants used to treat?

A

treatment and prevention of VTE
prevent cardioembolic stroke in patients with atrial fibrillation

85
Q

anti platelet medications target ______________ while anticoagulants target ___________

A

primary hemostasis (platelet plug)

secondary hemostasis (clotting cascade)

86
Q

which anticoagulants are also known as direct oral anticoagulants?

A

dabigatran
all direct factor Xa inhibitors

87
Q

vitamin K antagonist MOA

A

inhibits the enzyme vitamin K epoxide reductase which prevents the conversion if inactive vitamin K to active vitamin K

88
Q

vitamin K is required for the

A

synthesis of clotting factors VII, IX, X and II

89
Q

vitamin K epoxide reductase converts

A

vitamin K epoxide to vitamin K hydroquinone

90
Q

onset of action of warfarin is _______ due to _______

A

slow

long half life of clotting factors

91
Q

full anticoagulant effect of warfarin takes

92
Q

ADRs of warfarin

A

risk of bleeding
increased risk of clotting during initial days of therapy
purple toe syndrome

93
Q

what to monitor when taking a vitamin K antagonist

A

prothrombin time
INR (international normalized ratio)

94
Q

prothrombin time is used to calculate

95
Q

drug interactions with vitamin K antagonists

A

2C9 inducers and inhibitors
1A2 and 3A4 inducers/inhibitors

96
Q

“Fab Four” that inhibit warfarin metabolism and increase bleed risk

A

fluconazole
metronidazole
amiodarone
bactrim

97
Q

metabolism of warfarin

A

2C9, 2C19, 1A2, 3A4

98
Q

bioavailability of vitamin K antagonists is

A

almost 100%

99
Q

reversal agent of warfarin

100
Q

vitamin K antagonists requires intensive ___________ monitoring.
how to monitor?

A

INR

every 2-3 days to start, then every 3-4 weeks when stable

101
Q

MOA of indirect inhibitors

A

bind to antithrombin and make antithrombin more efficient
inhibits activated factors Xa and thrombin (IIa)

102
Q

heparin is a mix of

A

polysaccarhides

103
Q

heparin is an endogenous substance found in

A

mast cells

104
Q

how are indirect inhibitors given? why?

A

parenteral route (IV or SQ)

they would be digested if given orally

105
Q

mean size of saccharide chains of heparin

A

various lengths – 45 saccharide units

106
Q

mean size of saccharide chains of LMW heparin

A

15 saccharide units

107
Q

mean size of saccharide chains of fondaparinux

A

5 saccharide units

108
Q

heparin inhibits ____________

LMWH inhibits ____________

fondaparinux inhibits _________

A

Xa and IIa equally

Xa» IIa

Xa only

109
Q

the shorter the molecules, the _________________ at enhancing binding of antithrombin to IIa

A

less efficient

110
Q

ADRs of indirect inhibitors

A

risk of bleeding
heparin induced thrombocytopenia
hyperkalemia
increased risk of osteoporosis

111
Q

heparin can bind to _______________ creating a complex that is recognized by the body’s immune system as foreign

A

platelet-factor-4

112
Q

reversal agent for heparin and LMWH

A

protamine sulfate

113
Q

is there a reversal agent for fondaparinux?

114
Q

heparin is monitored by

A

measuring the aPTT (activated partial thromboplastin time

115
Q

is monitoring required for LMWH or fondaparinux?

116
Q

Heparin is given _______ because it has a __________

A

IV

quick onset and short duration

117
Q

what indirect inhibitors are drugs of choice in pregnancy and why?

A

heparin and LMWH

do not cross the placental barrier

118
Q

direct thrombin inhibitors MOA

A

binds thrombin and inactivates it directly

119
Q

oral direct thrombin inhibitors

A

dabigatran (Pradaxa)

120
Q

parenteral direct thrombin inhibitors

A

argatroban (Acova)
bivalirudin (Angiomax)

121
Q

dabigatran is given as a _______ which is converted to the active form by _________________

A

prodrug

plasma esterase enzymes

122
Q

reversal agent for dabigatran

A

idarucizumab (Praxbind) - monoclonal antibody

123
Q

direct factor Xa inhibitors examples

A

Rivaroxaban (Xarelto)
apixaban (eliquis)
edoxaban (savaysa)
betrixaban (Bevyxxa)

124
Q

direct factor Xa inhibitors MOA

A

reversibly bind to factor Xa and directly inactivates it

125
Q

do direct factor Xa inhibitors require monitoring?

126
Q

direct factor Xa inhibitors are increasingly used in place of

127
Q

reversal agent for factor Xa inhibitors

A

andexanet alfa (AndexCa)

128
Q

ADRs of direct factor Xa inhibitors

A

increased risk of bleeding

Pharmacology II (17 decks)

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