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Pharm II Exam 3 > Antithrombotics: Afib & Stroke > Flashcards

Antithrombotics: Afib & Stroke Flashcards

1
Q

Which thrombus is platelet rich?

A

White thrombus (ACS, non-cardioembolic stroke)

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2
Q

Which thrombus forms in the veins?

A

Red thrombus

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3
Q

Which thrombus is fibrin and RBC rich?

A

Red thrombus

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4
Q

Which thrombus forms in the arteries?

A

White thrombus

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5
Q

Thromboembolism locations?

A

Pulmonary embolism (PE) - lungs, Cerebrovascular accident - brain, Acute MI - heart, DVT - Lower extremity

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6
Q

Mediators of platelet aggregation?

A

TXA2, ADP, 5-HT

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7
Q

What role does TXA2 play in aggregation?

A

Platelet activation/vasoconstriction

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8
Q

What is TXA2?

A

Thromboxane A2: activated by platelets during hemostasis

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9
Q

What role does ADP play in aggregation?

A

Platelet activation

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10
Q

What is ADP?

A

Adenosine diphosphate: triggers binding of fibrinogen to platelet receptor GPIIb/IIIa, links platelets

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11
Q

What role do 5-HT receptors play in platelet aggregation?

A

Platelet aggregation/vasoconstriction

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12
Q

What are 5-HT receptors?

A

Serotonin receptors, can activate blood platelets

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13
Q

Which anticoagulant medication targets TXA2?

A

Aspirin

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14
Q

Which anticoagulant medication targets ADP?

A

P2Y12i’s (clopidogrel, ticagrelor)

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15
Q

Which medications interact with 5-HT R’s?

A

Serotonin (SSRI’s, prozac)
*agonists that may cause bleeding !

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16
Q

Targets for antiplatelet drug therapy?

A

TXA2, ADP, GPIIb/IIIa

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17
Q

Will the coagulation cascade go through the final common pathway if it starts with the extrinsic or intrinsic pathway?

A

BOTH, does not matter if it starts with extrinsic or intrinsic pathway - will go through final common pathway/lead to clot formation

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18
Q

What is the primary difference that can be quickly assessed/lead to certain drugs being used earlier on depending on the situation?

A

The mediated factors released in the intrinsic vs. extrinsic pathway

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19
Q

Common pathway?

A
  1. Factor Xa is activated by binding with Ca2+ and clotting factor V (forming a prothrombinase complex)
  2. The prothrombinase complex (Factor Xa, Ca2+, & clotting factor V) and platelet phospholipids activate prothrombin (factor II) to become thrombin (factor IIa)
  3. Thrombin (factor IIa) cleaves fibrinogen (factor I) into fibrin (factor Ia)
  4. Thrombin cleaves stabilizing factor (XIII) into factor XIIIa
  5. Factor XIIIa binds with calcium & creates fibrin crosslinks to form the clot
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20
Q

Intrinsic pathway?

A
  1. Begins when factor XII is exposed to collagen, kallikrein, and kininogen from a damaged surface and is activated to factor XIIa
  2. Factor XIIa activates factor XI into XIa
  3. With a calcium ion, factor XIa activates factor IX into IXa
  4. Factor IXa, factor VIIIa, and calcium form a complex to activate factor X into factor Xa
  5. Common pathway

*Factor VIII is found in the blood and is often activated by thrombin (factor IIa)

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21
Q

Extrinsic pathway?

A
  1. Begins w/ injury to endothelial tissue releasing tissue factor (factor III) into the blood
  2. Trauma causes factor VII to become factor VIIa
  3. Tissue factor binds with factor VIIa and Ca2+ to activate factor X to factor Xa
  4. Common pathway
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22
Q

Do heparin and warfarin interfere with the clotting pathway prior to or after factor Xa is formed?

A

Prior to Xa

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23
Q

Can meds directly block factor Xa?

A

Yes!

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24
Q

Normal activity of antithrombin?

A

Binds factors IIa, IXa, Xa, XIa, XIIa to inactivate them
*can be leveraged to our benefit w/ meds

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25
Q

Does heparin have a direct or indirect effect on thrombin?

A

Indirect (via antithrombin), acts like catalyst in an enzymatic reaction

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26
Q

Antithrombin sites of activity are mostly along the which part of the coagulation pathway?

A

Mostly along intrinsic pathway to the common pathway of coagulation cascade

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27
Q

Indications for use of unfractioned heparin (UFH)?

A

Ischemic heart disease (generally during PCI), During cardioversion for for A-fib, VTE prophylaxis, VTE treatment, to keep lines open for patients during surgery/dialysis, etc.
VTE = venous thromboembolism

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28
Q

Which clotting factors does UFH inhibit?

A

Factors X and II

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29
Q

When is UFH administered as a continuous infusion?

A

for ACS and warfarin bridging (VTE treatment)

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30
Q

When is UFH administered as a subcutaneous injection?

A

for VTE prophylaxis

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31
Q

What should be monitored with UFH therapy?

A

aPTT

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32
Q

Goal level aPTT with UFH?

A

2-2.5x control (approximately 60-80 sec)

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33
Q

Adverse effects of UFH?

A

Bleeding, HIT (heparin induced thrombocytopenia), Osteoporosis

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34
Q

What is Heparin induced thrombocytopenia (HIT)?

A

Antibody mediated adverse effect of heparin that is strongly associated with thrombosis/platelet clotting (resulting in platelet levels dropping)

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35
Q

Monitoring parameters for HIT?

A

-If platelets fall >50% from baseline w/ nadir (lowest count) > 20,000
-If platelets start to fall on day 5-10 of tx
-If thrombosis occurs while on heparin
-Rule out other causes of thrombocytopenia

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36
Q

What is thrombocytopenia?

A

Platelet deficiency in the blood

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37
Q

Treatment for HIT?

A

Stop heparin, treat w/ IV direct thrombin inhibitor

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38
Q

What should be avoided in HIT treatement?

A

*DO NOT administer platelets
*DO NOT give warfarin, or give direct oral anticoagulant (DOAC) to patients until platelets return to normal

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39
Q

Which complex acts on resting platelets in HIT?

A

Anti-heparin/PF4 IgG immune complex

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40
Q

When to use Low molecular weight heparin (LMWH)?

A

Commonly used for ACS, can be used for warfarin bridging, DVT prophylaxis

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41
Q

Types of LMWH?

A

Enoxaparin (Levenox), Dalteparin, Tinzaparin

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42
Q

Enoxaparin (Levenox) administered how often?

A

Every 12 hours if CrCl > 30

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43
Q

Which factors does LMWH act on?

A

Inhibit factor Xa > IIa

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44
Q

How is LWMH administered for ACS, warfarin bridging (acute VTE tx), and VTE prophylaxis?

A

Subcutaneous injection

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45
Q

Monitoring for LWMH?

A

Not routinely done, may monitor Anti-Xa level in peds or at risk pts

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46
Q

Dosing of LWMH in reduced renal function?

A

If CrCl <30reduce Levonox to q24hrs
If CrCl <10 or acute renal failure —> Switch to Heparin
**Not for use in patients w/ severe renal dysfunction

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47
Q

What is considered acute renal failure?

A

Any change in CrCl of 0.3 or more from baseline

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48
Q

Adverse effects of LWMH?

A

Bleeding, HIT is extremely rare

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49
Q

How do fibrinolytics break up clots?

A

t-PA (alteplase) binds to fibrin in thrombus and converts plasminogen to plasmin to break up fibrin

50
Q

When are fibrinolytics used?

A

Will use in ischemic stroke, might use for PE, sometimes used for ACS

51
Q

Mortality benefit of fibrinolytics last how long?

A

Only 3 hours

52
Q

Window for t-PA administration to stop progression/loss of some function?

A

3-4.5 hours (morbidity benefit post 3 hours, but no mortality benefit)

53
Q

Which is the active form: plasminogen or plasmin?

A

Plasmin- breaks down the clot (active form)

54
Q

Types of fibrinolytics?

A

t-PA/Alteplase, Reteplase, Tenectaplase

*Also streptokinase and urokinase (older agents, not used as much)

55
Q

How is t-PA/alteplase administered?

A

Recombinant IV drug therapy

56
Q

About how long does it take to form a clot in the atria?

57
Q

A-fib can lead to what?

A

Stroke and systemic embolism (tx aims to prevent this)

58
Q

Decide antithrombotic treatment for A-fib/flutter based on what?

A

Stroke risk, bleeding risk, patient characteristics/preferences

59
Q

Guidelines recommend use of what therapy in patients w A-fib/A-flutter?

A

Antithrombotic therapy

60
Q

Which antithrombotics are preferred for A-fib/A-flutter?

A

Anticoagulant > Antiplatelet > nothing (both better than no tx)

61
Q

How to determine stroke risk?

A

CHADSVAS score

62
Q

C in CHADSVAS score?

A

Congestive HF/LV dysfunction (+1 point)

63
Q

H in CHADSVAS score?

A

HTN (+1 point)

64
Q

First A in CHADSVAS score?

A

Age >/= 75 yrs (+ 2 points)

65
Q

D in CHADSVAS score?

A

DM (+1 point)

66
Q

First S in CHADSVAS score?

A

Stroke (TIE/TE) (+2 points)

67
Q

V in CHADSVAS score?

A

Vascular Disease (+1 point)

68
Q

Second A in CHADSVAS score?

A

Age 65-74 yrs (+1 point)

69
Q

Second S in CHADSVAS score?

A

Sex - female (+1 point)

70
Q

Risk & therapy indications w/ CHADSVAS score of 0 (male) or 1 (female)?

A

Low risk, no anticoagulation tx

71
Q

Risk & therapy indications w/ CHADSVAS score of 1 (male)?

A

Moderate risk, oral anticoagulation should be considered

72
Q

Risk & therapy indications w/ CHADSVAS score of 2 or greater (male and female)?

A

High risk, oral anticoagulation is recommended

73
Q

Consider alternatives to anticoagulation in patients with what HAS-BLED score?

A

Score > or = 3

74
Q

Choice antithrombotic in a-fib/a-flutter in patients w/ mechanical heart valve?

75
Q

Choice antithrombotic in a-fib/a-flutter in patients w/ severe kidney dysfunction (CrCl < 15)?

76
Q

Choice antithrombotic in a-fib/a-flutter in patients w/ CHADSVAS score of > or = 2?

A

Warfarin, Dabigatran, Rivaroxaban, Apixaban, Edoxaban

77
Q

Choice antithrombotic in a-fib/a-flutter in patients w/ CHADSVAS score of 1?

A

Anticoagulant, Aspirin, or no antithrombotic

78
Q

All DOACs have different doses based on what?

A

Indication

79
Q

DOACs can’t be used in what kind of A-fib?

A

Valvular A-fib

80
Q

What class of anticoagulants are recommended over VKAs (vitamin K antagonists) in American, European, & Canadian guidelines?

A

DOAC’s
*subject to change w/ rapid changes to literature
*except in situations where VKAs are preferred (i.e. severe renal dysfunction, mechanical heart valve, etc.)

81
Q

Which DOAC reduces stroke better than VKA, and has an increased risk of GI bleed and MI?

A

Dabigatran

82
Q

Which DOAC reduces the risk of bleeding compared to traditional therapy?

83
Q

One of the major studies that concluded DOACs are recommended over Warfarin in A-fib per updated guidelines?

A

ENGAGE AF-TIMI 48: Edoxaban vs. Warfarin in patients w/ A-fib

84
Q

Among patients with nonvalvular A-fib, how does edoxaban compare with warfarin in preventing stroke or systemic embolism?

A

No difference in DOAC vs. Warfarin when it comes to anticoagulation activity in A-fib, yet DOACs are safer when it comes to bleeding risks

85
Q

Which is more expensive: Warfarin or Edoxaban?

A

Edoxaban (~$1,000/yr vs. $60/yr for Warfarin)

86
Q

Which patient preferences may determine choice of antithrombotic therapy in A-fib/A-flutter?

A

Regular INR monitoring, Inconsistent diet, cost & insurance coverage, other meds (drud-drug interactions), difficulty w/ remembering doses

87
Q

Which type of stroke accounts for 88% of strokes?

A

Ischemic stroke

88
Q

What are the two types of ischemic stroke?

A

Cardioembolic, non-cardioembolic

89
Q

What is an ischemic stroke?

A

Blood clots stop flow of blood to area of the brain

90
Q

What is a hemorrhagic stroke?

A

Blood leaks into brain tissue due to rupture of weakened or diseased blood vessels

91
Q

Goals of therapy in stroke treatment?

A

Reduce neurologic injury to prevent mortality & long term disability (acute ischemic stroke), and prevent reoccurrence (secondary stroke prevention)

92
Q

Therapy administered up to 3 hours post-stroke signs and symptoms present has what benefit?

A

Mortality benefit

93
Q

Therapy administered up to 4.5 hours post-stroke signs and symptoms present has what benefit?

A

Morbidity benefit

94
Q

What 2 medications are used to treat acute ischemic stroke?

A

IV t-PA (Alteplase) and Aspirin PO

95
Q

How long after administering t-PA should you wait before starting Aspirin tx?

A

Wait 24-48 hours after t-PA before giving ASA

96
Q

Step 1 of stroke treatment protocol?

A

Activate stroke team

97
Q

Step 2 of stroke treatment protocol?

A

Treat as early as possible (w/in 4.5 hours of sx onset)

98
Q

Step 3 of stroke treatment protocol?

A

CT scan/rule out hemorrhage

99
Q

Step 4 of stroke treatment protocol?

A

Meet inclusion & exclusion criteria fr t-PA

100
Q

Step 5 of stroke treatment protocol?

A

Administer t-PA with 10% given as initial bolus over 1 min

101
Q

Step 6 of stroke treatment protocol?

A

Avoid all antithrombotic therapy (including Aspirin) for 24 hours

102
Q

Step 7 of stroke treatment protocol?

A

Monitor patient closely for BP, response, possible hemorrhage

103
Q

Inclusion criteria for t-PA (Alteplase) use in acute ischemic stroke?

A

-Age 18 & up
-Clinical dx of ischemic stroke causing measurable neurological deficit
-Time of sx onset well established to be less than 4.5 hrs before treatment initiation

104
Q

Exclusion criteria for t-PA (Alteplase) use in acute ischemic stroke?

A

-Active internal bleeding (ex. GI/GU bleed w/in 21 days)
-Recent use of anticoagulant (ex. Warfarin) and elevated PT (>15 sec)/INR
-SBP > 185 mmHg or DBP > 110 mmHg at time of treatment

105
Q

Secondary stroke prevention methods?

A

Statins, BP reduction, Smoking cessation, Antiplatelet treatment

106
Q

When should statins be used for secondary stroke prevention?

A

In patients with presumed atherosclerotic origin

107
Q

Which statins are recommended if necessary for secondary stroke prevention?

A

High-intensity statins: Atorvastatin, Rosuvastatin

108
Q

Desired BP reduction levels for secondary stroke prevention?

A

<140/90 mmHg

109
Q

Which meds for BP reduction in secondary stroke prevention?

A

CCB/ACEi/HCTZ > BB

110
Q

What can be used in place of antiplatelet treatment if stroke is cardioembolic (from A-fib) for prevention of secondary stroke?

A

Anticoagulation (DOACs or Warfarin)

111
Q

Non-cardioembolic antiplatelet treatment for secondary stroke prevention?

A

Aspirin/Clopidogrel (Plavix)/Aggrenox

112
Q

What is Aggrenox?

A

Aspirin plus ER dipyridamole (combo drug)

113
Q

In what circumstances would a patient qualify for anticoagulant tx but we would refrain from giving it?

A

Pregnancy, elderly w/ fall risk, etc. (aspirin or maybe clopidogrel instead)

114
Q

Heparin is helpful because…?

A

Can be reversed more quickly/short half-life in case of need for immediate surgery

115
Q

Is heparin cleared renally?

A

No, safe for acute renal failure

116
Q

If CrCl is <30, do you reduce the dose or frequency of Lovenox (enoxaparin)?

A

Reduce frequency (ex. reduce to once daily vs. twice daily)

117
Q

What type of clots would benefit from fibrinolytics?

A

Will use in ischemic stroke, sometimes in PE, sometimes in ACS

118
Q

Risk w/ finrinolytics?

A

Will break up any clot, may cause bleeding

119
Q

Would fibrinolytics be used in stable DVT or stable PE?

120
Q

What does the HASBLED tool measure?

A

Risk of bleeding if on an anticoagulant

Pharm II Exam 3 (6 decks)

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