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Pharm II exam 2 > Antithrombotics > Flashcards

Antithrombotics Flashcards

1
Q

What are the 3 categories of antithrombotics?

A

Anticoagulants
Fibrinolytics
Antiplatelets

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2
Q

What do anticoagulants do?

A

stop clot formation and extension (won’t break up an existing clot)

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3
Q

What do Fibrinolytics do?

A

Break up existing clots

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4
Q

What do antiplatelets do?

A

stop platelets

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5
Q

What are the two types of thrombi?

A

White thrombus

Red Thrombus

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6
Q

What are white thrombi made up of?

A

Rich in platelets

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7
Q

Where do white thrombi form?

A

in the arteries

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8
Q

What are red thrombi made up of?

A

Fibrin and RBC rich

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9
Q

Where do red thrombi form?

A

Veins

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10
Q

What are the mediators of platelet aggregation?

A

TXA2:
ADP
5-HT

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11
Q

What does TXA2 do?

A

Platelet activation and vasoconstriction

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12
Q

What is ADP’s role in platelet aggregation?

A

Platelet activation and aggregation

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13
Q

What is 5-HT’s role in platelet aggregation?

A

Platelet aggregation and vasoconstriction

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14
Q

What activates platelets (7 step process)

A
  1. Injury
  2. Collagen and vWF exposed
  3. Platelet adherence and activation
  4. Vasoconstrictors platelet recruiters and platelet activators
  5. Conformational change to IIb/IIIa receptor
  6. Binding of fibrinogen
  7. Aggregation and platelet plug formation
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15
Q

Where in the 7 step process do anti platelets work?

A

4-vasocontrictors, platelet recruiters, and platelet activators
5-IIb/IIIa receptors

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16
Q

What are the three pathways of the coagulation cascade?

A

Intrinsic pathway
Extrinsic pathway
Common pathway

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17
Q

What is the intrinsic pathway activated by?

A

Exposed endothelium

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18
Q

What is the extrinsic pathway activated by?

A

Tissue damage

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19
Q

What contributes to the common pathway?

A

merging of the intrinsic and extrinsic pathway

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20
Q

What is the final step in both extrinsic and intrinsic pathways?

A

conversion of factor X to factor Xa(activated)

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21
Q

What does factor Xa do in the common pathway?

A

Converts prothrombin (Factor II) to Thrombin (with the help of other contributors)

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22
Q

What does Thrombin do in the common pathway?

A

Converts Fibrinogen to fibrin

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23
Q

What does fibrin form in the common pathway?

A

fibrin clot

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24
Q

So if we don’t have factor ____ or factor ____ we can’t have a clot-any anticoag we have will most likely effect these two factors?

A

X and II

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25
Q

What factors does Warfarin target?

A 
SNOT
Seven (7)
Nine (9)
Ten (10)
Two (2)
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26
Q

What tests can be used to measure clotting ability of different pathways of the cascade?

A 
PT
INR
PTT
aPTT
ACT
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27
Q

What does PT measure?

A

activity of factors II, VII, IX, X (test varies per hospital)

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28
Q

What does INR measure

A

Same as PT II, VII, IX, X but standardized worldwide

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29
Q

What does PTT measure?

A

activity of factors II, V, VII, IX, X, XI, XII

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30
Q

What does ACT measure

A

same as PTT II, V, VII, IX, X, XI, XII but used in invasive/operative procedures

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31
Q

How do indirect thrombin inhibitors act?

A

by helping antithrombin de-activate clotting factors

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32
Q

What indirect thrombin inhibitors exist?

A

Unfractionated Heparin
LMWH-Enoxaparin
Fondaparinux

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33
Q

What is the normal active of antithrombin in the body?

A

Binds to factors IIa, IXa, XIa, and XIIa to inactivate them

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34
Q

What factors does unfractionated heparin bind to?

A

Xa and IIa (increases antithrombin by several 1,000 fold)

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35
Q

How is unfractionated heparin used?

A

continuous infusion for ACS and warfarin bridging (acute VTE tx)
Subcutaneous injection for VTE prophylaxis

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36
Q

How do you monitor heparin? (what is goal?)

A

aPTT - 2-2.5 x control approx 60-80sec

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37
Q

ADE of Unfractionated heparin

A

Bleeding
HIT
Osteoporosis (long term)

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38
Q

Define HIT

A

Antibody mediated adverse effect of heparin

strongly associated with thrombosis

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39
Q

What are the parameters for HIT?

A
  1. Platelets fall greater that 50% baseline with nadir greater than 20,000
  2. Platelets start to fall on day 5-10 of therapy
  3. Thrombosis occurs wile on heparin!!
  4. Rule out other causes of thrombocytopenia (chemo,abx, critically ill)
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40
Q

What is tx for HIT?

A
  1. Stope heparin and tx with a IV direct thrombin
  2. DO NOT ADMINISTER PLATELETS
  3. DO NOT give warfarin to a pt with HIT until platelets return to normal
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41
Q

Why is there a decreased platelet count with HIT?

A

when heparin attaches to the lately it causes the platelet to clump up and activate. This results in a lower platelet count because there appear to be less platelets.

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42
Q

Name the 1 LMWH we are supposed to know.

A

Enoxaparin

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43
Q

What is the MOA of Enoxaparin

A

Inhibits factor Xa and a little IIa

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44
Q

How is enoxaparin given?

A

Subcutaneously

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45
Q

What is enoxaparin used for?

A

ACS
Warfarin bridging (VTE tx)
and VTE prophylasix

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46
Q

What monitoring is done when giving enoxaparin?

A

None routinely

but-anti-Xa can be done for those with renal dz

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47
Q

Who cannot take enoxaparin?

A

Pt’s with severely reduced renal function (CrCl less than 20mL/min).

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48
Q

Who requires a reduced amount of enoxaparin?

A

Moderate renal dz

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49
Q

ADE of enoxaparin?

A

Bleeding

HIT (extremely rare)

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50
Q

What characteristics do both UFH and LMWH share?

A

both are used for ACS, Acute VTE, and VTE prophylaxis

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51
Q

Why might you choose to use UFH over LMWH?

A 
Renal dysfunction (enoxaparin accumulates)
shorter half life-so good for pt's about to have surgery
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52
Q

Why might you choose to use LMWH over UFH?

A

more predictable dose response curve
Doesn’t require routine monitoring
Heparin requires continuous infusion (so if a line is placed this is ok but no line means better to give sc)

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53
Q

What is the MOA of fondaparinux?

A

Synthetic pentasachharide - inhibits Xa via antithrombin (no IIa inhibition)

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54
Q

How is fondaparinux administered?

A

sc

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55
Q

who gets fondaparinux?

A

Acute VTE, and VTE prophylaxis

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56
Q

What monitoring needs to be done for those on fondaparinux?

A

No routine tests
Not for pt’s with renal dysfunction
decrease dose if CrCl less than 50, don’t use if CrCl less than 30

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57
Q

ADE of fondaparinux

A

Bleeding

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58
Q

What can be used to reverse Heparin

A

Protamine

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59
Q

What can be used to reverse enoxaparin?

A

Protamine

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60
Q

What can be used to reverse fondaparinux

A

Nothing-irreversible

give blood products

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61
Q

What are the oral direct Xa inhibitors?

A

(EAR)
Edoxaban
Apixaban
Rivaroxaban

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62
Q

What do all of the oral direct Xa inhibitors end with?

A

XAban

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63
Q

What is the MOA of rivaroxaban?

A

Directly inhibits Xa

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64
Q

How is rivaroxaban administered?

A

PO

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65
Q

What is Rivaroxaban given for?

A

stroke prevention for Non-valvular Afib
Tx of active VTE
Prevention of VTE after hip/knee replacement or having a VTE

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66
Q

What needs to be monitored for with Rivaroxaban?

A

Renal Function
Hepatic function-don’t use in severe hepatic dysfunction
P-glycoprotein and CYP 3A4 drug interaction

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67
Q

What are the renal dosing guidelines for Rivaroxaban?

A

Reduce if Mod-Mild

Don’t use if severe

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68
Q

ADE of rivaroxaban?

A

Bleeding

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69
Q

What is the reversible agent for Rivaroxaban?

A

No reversible agent available

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70
Q

How is Apixaban administered?

A

PO

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71
Q

What is Apixaban used for?

A

Stroke Prevention for non-valvular Afib
Tx of active VTE
Prevention of VTE after hip/knee replacement or having a VTE

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72
Q

What is monitored for with Apixaban?

A

Hepatic and renal dysfunction-not for use in severe

P-glycoprotein and CYP3A4 drug interactions

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73
Q

ADE apixaban

A

Bleeding

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74
Q

What reversible agent is available for Apixaban?

A

No reversible agent

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75
Q

How is Edoxaban administered?

A

PO

76
Q

What is Edoxaban used for?

A

Stroke prevention in pts with non-valvular Afib

Tx of active VTE

77
Q

What is the major difference between Edoxaban and the other two oral Xa inhibitors?

A

Edoxaban is no approved for hip/knee replacements,

or for prevention of additional VTE’s

78
Q

What needs to be monitored for with Edoxaban?

A 
Renal function (reduce if Mild, don't use if severe or than good)-really the only time you can use this without worry is if the pt has Moderate renal dz
Hepatic function-don't use in moderate or severe
P-glycoprotein drug interactions
79
Q

What is the “funny thing” about the monitoring for edoxaban?

A

Renal function can’t be too good - don’t give if greater than 95

80
Q

ADE edoxaban?

A

Bleeding

81
Q

Do any of the oral direct Xa inhibitors have a reversal agent?

A

no

82
Q

What drug interaction do all of the PO direct Xa inhibitors have in common?

A

PGP interactions

83
Q

Which of the PO direct Xa inhibitors have a CYP3A4 interaction?

A 
Apixaban
Rivaroxaban
(Not edoxaban)
84
Q

What intravenous forms of Direct Thrombin Inhibitors are there?

A

Argatroban

Bivalarudin

85
Q

What oral forms of of Direct Thrombin Inhibitors are there?

A

Dabigatran

86
Q

How is Bilvalirudin administered?

A

IV

87
Q

What is Bivalirudin used to tx?

A

ACS in pt’s undergoing PCI or coronary angioplasty

To tx confirmed or suspected HIT

88
Q

What needs to be monitored for when using Bivalirudin?

A 
Based on aPTT/ACT
Renal function (reduce if Moderate or if on hemodialysis)
89
Q

ADE of Bivalirudin?

A

Bleeding

90
Q

What reversal agent is available for Bivalirudin?

A

No reversal agent

91
Q

How is Argatroban administered?

A

IV

92
Q

What is Argatroban used for?

A

Tx pt’s with confirmed or suspected HIT

Those at risk of HIT undergoing PCI

93
Q

What two IV meds are used to tx HIT?

A

Argatroban

Bivalirudin

94
Q

What is monitored for with Argatroban?

A

Based on aPTT/ACT

Use caution in hepatic dysfunction

95
Q

ADE of Argatroban?

A

bleeding

96
Q

Reversal agent for Argatroban?

A

None

97
Q

How is Dabigatran administered?

A

PO

98
Q

What is Dabigatran used for?

A

Prevention of stroke and systemic embolism in pt’s with non-valvular fib
VTE tx and prevention of VTE after having VTE

99
Q

What needs to be monitored for in Dabigatran?

A 
Renal function (reduce if Moderate, do not use if severe)
Hepatic function-don't use in severe dysfunction
PGP drug interactions
100
Q

ADE of Dabigatran?

A 
Bleeding
GI upset (d/t coating)
101
Q

Reversal agent for Dabigatran?

A

None

102
Q

What factors does Warfarin inhibit?

A

II, VII, IX, X and proteins C and S

Also a Vitamin K antagonist

103
Q

What is Warfarin used for?

A

DVT/PE tx

Prevention of stroke in pt with Afib or heart valve replacement

104
Q

What are the monitoring parameters for Warfarin?

A

INR (therapuetic dose is 2-3)

105
Q

What are ADE of Warfarin?

A

Bleeding, bruising

106
Q

What is the MOA of Warfarin?

A

Blocks Vit K, causing either no, or a reduced amount of vitamin K in the body. Vitamin K is required to activate 2,7,9,and10. No vitamin K precursor - no activation

107
Q

What dose is preferable to start a new pt with Warfarin?

A

LOW-about 5mg/day

108
Q

What dose would you start a pt with Warfarin who is either
Older than 75
Critically ill
has a hepatic insufficiency?

A

Lower 2.5mg

109
Q

How do you adjust Warfarin dosage?

A

Adjust based on WEEKLY dose.
INR less than goal x 2 increase dose 10-20%
INR more than goal X2 decrease weekly dose by 10-20%

110
Q

What is the goal for INR for pt’s with
DVT/PE/aFib
Bioprosthetic valve-3 mos tx

A

2-3

111
Q

What is the goal INR for pt’s with
Mechanical mitral valve or any valve w/ r/f
Predisposition (leiden) who had a clot with the typical goal INR?

A

2.5-3.5

112
Q

What are the problems with Warfarin?

A 
Slow onset and offset (needs bridging)
dietary interactions (vit K)
Need for routine monitoring
Dose response variability
Narrow therapeutic index
Drug interaction (TONS OF THEM)
113
Q

When warfarin is stopped it takes about ____ days to return to baseline.

A

5

114
Q

If Warfarin is stopped and the pt is given Vit K it takes about ____ days to return to baseline

A

1

115
Q

How is vitamin K administered in the event of Warfarin excess?

A

Oral-NOT SC or IM-does not distribute properly (NEVER GIVE VIT K SC/IM)
Can be given IV - special instructions

116
Q

When Vitamin K is administered IV, in what way is it prepared?

A

IV Vit K 10mg dilutes with 50mL of NS and administered over 10-30 min. IV push will KILL THE PT!!

117
Q

What is special about the Novel ORAL anticoagulants?

A

Don’t require bridging!

118
Q

What Novel oral anticoagulants exist? (2)

A

Direct thrombin inhibitors

Factor Xa inhibitors

119
Q

What are the advantages of the new oral anticoagulants?

A

Faster onset and offset
No routine monitoring
Few drug/food interactions
Predictable dose-response

120
Q

What are the disadvantages of the new oral anticoagulants?

A

Limited clinical experience
$$$$$$
No antidote
renal excretion

121
Q

What is the MOA of ASA?

A

Inhibits the COX enzyme responsible for prostaglandin and TXA2 synthesis

122
Q

What is ASA used for?

A

Primary (off label) and secondary prevention of CAD
ACS tx
Chronic Stable Angina
PAD
Acute stroke/TIA tx and 2nd stroke prevention

123
Q

What needs to be monitored for with ASA?

A

Bleeding

124
Q

ADE

A

Bleeding

125
Q

MOA of Clopidogrel, prasugrel, and ticagrelor

A

P2Y12 platelet receptor antagnoist

126
Q

What is Clopidogrel (plavix) used for?

A

ACS and 2nd MI prevention
2nd stroke prevention
PAD

127
Q

What needs to be monitored for with Clopidogrel?

A

CYP2C19 drug and pharm interactions

128
Q

ADE Clopidogrel?

A

Bleeding

129
Q

What is Prasugrel used for?

A

ACS with PCI – if pt does not get PCI this drug is not the best choice.

130
Q

What dosage adjustments are very important to know when prescribing Prasugrel?

A

Reduce dose if weight less than 60kg
Do not use in pt’s with previous stroke
do not use in pt’s older than 75yo, unless they have DM or previous MI

131
Q

ADE of Prasugrel?

A

Bleeding

132
Q

How is Ticagrelor used?

A

Tx of ACS

133
Q

How is Ticagrelor monitored?

A

Hepatic function-don’t use in severe
Don’t use if signs of bleeding
CYP3A4 drug interaction

134
Q

ADE ticagrelor?

A

bleeding

135
Q

MOA of Dipyridamole?

A

ADP inhibitor which prevents platelet activation

136
Q

How is Dipyridamole administered?

A

XR formulation with ASA

137
Q

What is Dipyridamole used for?

A

Secondary stroke/TIA prevention

138
Q

Who cannot take Dipyridamole?

A

Those with severe renal or hepatic dysfunction

139
Q

ADE of Dipyridamole?

A

HA (resolves after couple days usually)

Bleeding

140
Q

MOA of cilostazol?

A

Inhibits phosophodiesterase III, preventing platelet activiation

141
Q

What is Cilostazol used for?

A

PAD with intermittent claudication (VERY SPECIFIC)

142
Q

What pt’s require dose adjustments for Cilostazol

A

CYP 3A4 and 2C19 drug interactions

143
Q

What needs to be monitored for with Cilostazol?

A

Platelets and WBC counts periodically

Signs of bleeding

144
Q

In what group of pt’s is Cilostazol contraindicated?

A

Heart Failure

145
Q

ADE of Cilostazol?

A

Bleeding
HA
GI upset

146
Q

What drug is a GP IIB/IIIA inhibitor?

A

Eptifibatide

147
Q

What is the MOA of GP IIB/IIIa inhibitors?

A

prevents platelets from cross linking with fibrinogen

148
Q

When is Eptifibatide used?

A

ACS during PCI in conjunction with heparin

149
Q

What must be monitored in use of Eptifibatide?

A

Renal function-decrease dose in Mild

Do not use in end stage renal disease

150
Q

ADE Eptifibatide

A

Bleeding

151
Q

What is the MOA of Vorapaxar?

A

Inhibits platelet PAR-1 to prevent platelet aggregation

152
Q

Who gets Vorapaxar?

A

Hx of MI

Established PAD

153
Q

How is Vorapaxar administered?

A

ONLY USED in conjunction with ASA or clopidogrel (only for really extreme circumstances)

154
Q

What groups should not use Vorapaxar?

A 
hx of stroke
TIA
intracranial hemorrhage
active bleeding
Severe hepatic dysfunction
155
Q

What interactions can occur with Vorapaxar?

A

CYP 3A4

156
Q

ADE Vorapaxar?

A

Bleeding

157
Q

Who do Fibrinolytics work?

A

Convert plasminogen to plasmin to break up fibrin

158
Q

What Medication is a Fibrinolytic?

A

t-PA (alteplase)

159
Q

When is t-PA (a fibrinolytic) administered in the event of a STEMI

A

If no PCI available, within 30 minutes door to needle time

160
Q

If PCI is available when must it occur in the event of a STEMI?

A

less than 90 minutes door to cath time

161
Q

What 2 options exist for tx for those with NSTEMI/UA

A
  1. Early invasive: PCI (if at high risk)

2. Conservative: Managed medically, see if sx resolve, undergo stress test

162
Q

If pt undergoes Fibrinolytics for a STEMI what must this be followed with?

A

Enoxaparin (LMWH) for 7 days prior

163
Q

If pt gets primary PCI what do we start and follow with?

A

Heparin (ITI), and Bivalirudin(DTI) infusion d/c’s after PCI complete
BP IIB/IIIa inhibitor (Eptifibatide) x 12-18hrs after PCI

164
Q

For pt’s getting medical management for ACS what medication must they follow with?

A

Heparin continuous infusion X 48 hours

165
Q

What medications must be given for chronic antiplatelet tx of MI

A 
ASA (for everyone) 
\+1 other medication 
Clopidogrel
or
Prasugrel
or
Tigagrelor
(ALL ADP blockers)
166
Q

How is acute VTE tx?

A

Continous heparin infusion

Start immediately x 5 days AND until INR 2-3 on warfarin therapy

167
Q

What value should be monitored for a pt being tx for VTE?

A

Baseline aPTT

check aPTT in 6 hours and adjust heparin based on result

168
Q

How long must a pt who has had a first occurrence of VTE stay on warfarin?

A

3 months

169
Q

How long must pt who has had a second occurrence of VTE stay on warfarin?

A

lifelong

170
Q

What is the INR goal range for pt’s on Warfarin

A

2-3 (2.5)

171
Q

If pt is admitted how often should INR be checked?

A

every day

172
Q

If pt is out-pt how often should INR be checked at first?

A

3-4 days

173
Q

What options are there for prevention of VTE?

A

UFH
Enoxaparin
Fondaparinux

Oral XA-inhibitors - can be used for hip/knee surgery prevention
Rivaroxaban
Apixaban

Direct thrombin inhibitor
Dabigatran

174
Q

There are two different types of stroke we covered, what are they?

A

Hemorrhagic

Ischemic

175
Q

What type of stroke can anti platelets be used to tx?

A

ischemic

176
Q

What meds are used to Tx ACUTE ischemic stroke?

A

Intravenous tPA

ASA (24h after IV tPA)

177
Q

What is the stroke tx protocol? (7 steps)

A
  1. Activate stroke team
  2. Tx within 4.5h of symptom onset (no tPA if over)
  3. CT scan r/o hemorrhage
  4. meet inclusion criteria for tPA
  5. Admin tPA 0.9 mg/kg over 1 hour w/ 10% bolus
  6. Avoid all antithrombotics for 24h (including ASA)
  7. Monitor closely for bleeding
178
Q

What do exclusion factors of tPA generally include

A

Bleeding risk

179
Q

What is the recommended tx for secondary stroke prevention?

A

ASA
Clopidogrel (if pt can’t tolerate ASA)
ASA plus dipyridamole (Aggrenox)
Warfarin for pts w/ cardioembolic stroke

180
Q

What is recommended tx for pt’s with PAD?

A

ASA daily
Clopidogrel- for pt’s who can’t tolerate ASA
Cilostazol-for pt’s with INTERMITTENT claudication

181
Q

Explain CHA2DS2-VASc score

A 
C-CHF (1)
H-HTN (1)
A-Age over 75 (2)
D-DM (1)
S-Stroke (2)
V-Vascular dz (1)
A-Age 65-74 (1)
S-Sex (female) (1)
Determines stroke risk
182
Q

Choice of antithrombotic in afib/flutter is based on ______?

A

Patient’s characteristics

183
Q

What antithrombotic should a pt with a hx of a mechanical heart valve be paced on?

A

Warfarin

184
Q

What antithrombotic should a pt with a hx of ACS be placed on?

A

Warfarin

185
Q

What antithrombotic should a pt with a hx of Severe kidney dysfunction be put on?

A

Warfarin

186
Q

If a pt has a CHA2DS2-VASc score greater than 2, what antithrombotic tx should they be on?

A 
Warfarin
Dabigatran
Rivaroxaban
Apixaban
Edoxaban
187
Q

If a pt has a CHA2DS2-VASc score of 1, what antithrombotic tx should they be on?

A

either no antithrombotic or
anticoagulant
asa

Pharm II exam 2 (3 decks)

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