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Pharmacology II - Emily Britton > Hematology Pharm > Flashcards

Hematology Pharm Flashcards

1
Q

3 components of Virchow’s triad are?

A

Hypercoaguable state, vascular wall injury, circulatory stasis

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2
Q

Coagulation along with _________ and wound healing are largely responsible for maintaining the circulation as a ________ hemodynamic system in a normal state of equilibrium, referred to as hemostasis

A

fibrinolysis / closed

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3
Q

Number one reason people in the community are on anticoagulants

A

afib

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4
Q

Review coagulation cascade

A

slide 4

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5
Q

With the extrinsic pathway, damage outside blood vessels triggers the release of __________ (Factor III, TF) from damaged cells

A

thromboblastin

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6
Q

With the extrinsic pathway, THROMBOBLASTIN activates _______. VIIa when complexed on the surface of the platelet with ______ (factor IV) and thromboblastin (IIIa) activates factor ____.

A

VII / calcium / factor X (Xa)

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7
Q

Summary for extrinsic

A

Damage -> release of thromoboblastin -> thromboblastin (III) activates VII and combines with IV which activates factor X (3 to 7 and 4 activates 10)

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8
Q

With the intrinsic pathway there is trauma to the blood itself or exposure of blood to collagen in a traumatized blood vessel wall which activates factor ____. XIIa activates factor _____ and that factor activates factor ____. Ixa when complexed on the platelet surface with activatged VIII:C and ca++ activates factor ____(Xa)

A

XII / XI / IX / X

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9
Q

With the common pathway, activated X (Xa) when complexed on the platelet surface with activated factorV (Va) aand calcium (factor IV) on the platelet surface, converts _______ to _______.

A

prothrombin (factor II) / thrombin (Iia)

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10
Q

With the common pathway, IIa converts ______ to ______ and in the presence of factor XIII, cross-linking occurs.

A

fibrinogen (I) to fibrin (Ia)

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11
Q

Heparin acts as a catalyst to markedly accelerate the rate at which ________ (heparin cofactor) neutralizes ______ and factor Xa

A

ATIII / thrombin

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12
Q

Heparin basically speeds up ______ to neutralize _____ and ____

A

ATIII / thrombin / Xa

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13
Q

Heparin MOA

A

speeds up ATIII reaction at least 1000 fold. Heparin induces a conformational change that makes the reactive site more accesible to the protease. Once the thrombin is bound to ATIII, the heparin molecule is released.

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14
Q

Is heparin safe in pregnancy?

A

Yes, it does not cross the placenta

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15
Q

Heparin only acts on _________ factors. This means that it stops further clots from forming but doesn’t break up and lyse clots.

A

unbound

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16
Q

Heparin is cleared by the reticuloendothelial system which is basically a system of __________

A

phagocytes

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17
Q

Heparin resistance is when _____ doses are required to obtainthe desired aPTT or ACT

A

higher

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18
Q

Heparin resistance can be due to what?

A

Increased concentration of Factor VIII, accelerated of the drug with massive PE, inherited or acquired ATIII deficiency (inherited usually has a normal response to heparin)

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19
Q

Heparin resistance in someone with Acquired ATIII deficiency in patients with cirrhosis, nephrotic syndrome, or DIC is treated with what?

A

2 units FFP to proved ATIII or ATIII concentrate

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20
Q

Heparin toxicity can result in what?

A

bleeding, thrombocytopenia (HIT), Abnormal LFTs, infrequent risk of osteoporosis or spontaneous vertebral fractures

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21
Q

The vertebral fractures that can happen with heparin is related to what?

A

somehow the calcium that is involved in the clotting cascade

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22
Q

HIT show when in treatment naïve patients?

A

7-14 days after initiation of therapy

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23
Q

With HIT, if patient previously exposed to heparin, thrombocytopenia may occur ______

A

earlier

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24
Q

Type II HIT

A

heparin dependent antiplatelet IgG antibodies

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25
Q

Is HIT reversible?

A

Yes, stop the heparin

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26
Q

In a minority of patients, HIT may be associated with thrombotic complications including ____ ______ with platelet-fibrin clots (white clots). This is termed HITTS. Clots associated with HITTs can be treated with ______

A

arterial thrombosis / Argatroban

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27
Q

Review slide 17

A

HIT pathophysiology ( remember this is an immune mediated type of reaction)

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28
Q

Protamine sulfate acts as a _______ ______ by complexing with strongly acidic (cationic) and anionic heparin to form a stable _______

A

heparin antagonist / salt

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29
Q

The complexes formed by prtoamine and heparin are removed by the ___________ system

A

reticuloendothelial

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30
Q

Protamine has a rapid onset of about 5 min and lasts about ___ hrs

A

2 hours

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31
Q

Protamine is used to ______ heparin after CPB procedures and others where higher molecular weight heparin was used for anticoagulation.

A

neutralize

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32
Q

LMWH (anti-factor Xa agents) are not as susceptible to protamine antagonism. If emergency reversal is needed, protamine will neutralize about ___% of anti-Xa activity of LMWHs.

A

65%

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33
Q

Protamine dosing is determined by what?

A

dose of heparin, route of heparin admin, time elapsed since heparin was administered

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34
Q

How fast is protamine administered?

A

slow IV 10mg/ml over 1-3 min. 50 mg/10 minutes maximum

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35
Q

What happens with rapid IV injection of protamine

A

acute histamine-related hypotension, bradycardia, pulmonary HTN, transient flusing, dyspnea

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36
Q

What 3 things do you want to watch when administering protamine?

A

BP, PA pressures, airway pressures (wheezing)

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37
Q

Hypersensitivity reaction from protamine sulfate can be anaphylactoid or anaphylaxis. An anaphylactoid reaction is due to ______ activation by the heparin-protamine complexes release of lysosomal enzymes from neutrophils with prostaglandins and thromboxane generation.

A

compliment

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38
Q

Who is susceptible to protamine hypersensitivity reactions?

A

hypersensitive to fish, previous protamine reversal of heparin, protamine containing insulin (NPH), previous vasectomy

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39
Q

Pretreatment for protamine hypersensitvity

A

corticosteroid and antihistamine

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40
Q

Heparin _________ happens when there is re-anticoagulation after protamine administered. Usually 8-9 hrs but 30 min to 18 hrs after CPB reported.

A

rebound

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41
Q

Overdose of protamine may result in _______ theoretically because it has anticoagulant and anti-platelet effects when given alone or in excess of heparin.

A

bleeding

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42
Q

LMWH drugs are Factor ____ inhibitors

A

Xa / Dalteparin (Fragmin) , Enoxaparin (lovenox), Tinzaparin (Innohep)

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43
Q

LMWH MOA: Inhibition of Factor ____ by ______. Have some Factor Iia inhibition effect

A

Xa / antithrombin

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44
Q

T/F aPTT and Pt levels are relatively insensitive with LMWH therapy

A

TRUE

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45
Q

According to JAMA 2018: rates of VTE were not reduced with ______ guided dosing, and almost half of the patients never reached prophylactic anti-Xa levels and achieving those levels did not decrease VTE rates.

A

anti-Xa

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46
Q

Can you use LMWH AKA with HIT patients?

A

NO

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47
Q

What should you do to the dose of LMWH in patients with chronic renal insufficiency?

A

decrease the dose

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48
Q

How is LMWH eliminated?

A

renally

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49
Q

Fondaparinux AKA

A

Arixtra

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50
Q

Fondaparinux MOA: Synthetic indirect specific inhibitor of Factor ____

A

Xa

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51
Q

Fondaparinux is ______ mediated, has no effect on factor ______ no effect on ______ function.

A

ATIII / IIa / platelet

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52
Q

Advantages of Fondaprinux

A

fixed-dose SQ daily, not associated with HIT, stop if platelets fall below 100,000

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53
Q

T/F Fondaparinux has the same risk of spinal or epidural hematoma as LMWHs

A

TRUE

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54
Q

Fondaparinux in a nutshell

A

Xa only, less indication, less risk of thrombocytopenia, but same risk of spinal and epidural hematomas

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55
Q

Betrixaban (Bevyxxa) is an ORAL ____ inhibitor and only approved for preventing clots in the _______ patient

A

Xa / acute hospitalized

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56
Q

Danaparoid sodium (Orgaran) is a ___________ - not a LMWH or true heparin. Almost exclusively anti ______ activity. Relatively low cross reactivity for patients with history of HIT - but STILL may cause HIT

A

heparinoid / Xa

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57
Q

Oral Xa inhibitors

A

Rivaroxaban (Xarelto) / Apixaban (Eliquis) / Edoxaban (Savaysa)

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58
Q

Review charts on slide 33 and 34

A

pharmacokinetic comparison of Oral Xa inhibitors. Know that Rivaroxaban has the most protein binding

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59
Q

How many days before surgery should coumadin be stopped?

A

5 days

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60
Q

Dabigatrin (pradaxa) should be stopped __ to ___ days if CrCl is > 50 ml/min and ___ to ___ days if CrCl is <50 ml/min.

A

1-2 days / 3-5 days

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61
Q

Rivaroxaban (xarelto ) should be stopped how long before surgery

A

24 hrs

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62
Q

Apixaban (Eliquis) should be stopped ___ hrs before high/moderate procedural bleeding risk and ____ hrs for low procedural bleeding risk.

A

48 hrs / 24 hrs

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63
Q

Resumption of all NOAC after surgery is as soon as adequate hemostasis has been established BUT coumadin should not be resumed until __ to ____ hrs post surgery

A

12 to 24 hrs

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64
Q

Dabigatran should be stopped 4 to 6 days if CrCl is less than or equal ____ ml/min

A

30 ml/min

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65
Q

Oral Xa Reversal general measures

A

d/c medication, mechanical compression, surgical hemostasis, transfusional support

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66
Q

If an oral Xa inhibitor needs to be reversed and the last dose was within 2 hrs you can administer ________ _______. HD is _________.

A

activated charcoal / not beneficial

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67
Q

Other treatments for Oral Xa inhibitors

A

PCC, FEIBA, rFVIIa

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68
Q

Reversal agent for Oral Xa inhibitors

A

Andexanet

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69
Q

Andexanet is only approved for ____ and _____

A

eliquis and xarelto

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70
Q

Andexanet alpha (Andexxa) reverses Factor ___ inhibitors. It is recombinant human factor ___.

A

Xa / Xa

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71
Q

Andexanet binds _________ to Factor Xa inhibitors for ______ reversal

A

competitively / complete

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72
Q

Andexxa black box warning

A

thromboembolic events, ischemic events, cardiac arrest, sudden death. May also cause UTIs, Pneumonia, infusion related reactions

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73
Q

Review Andexxa dosing chart on slide 40

A

now

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74
Q

Ciraparantag is still listed as _______ but reverses Xa inhibitos, IIa inhibitors, Fondaparinux and heparin. It’s MOA is it binds to anticoagulants through a ______ bond

A

investigational / hydrogen

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75
Q

Argatroban is a DIRECT _____ _______

A

thrombin inhibitor

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76
Q

Argatroban is a SMALL molecule that is highly selective and ________direct thrombin inhibitor (Factor IIa). It binds rapidly to the apolar region of both circulating and ____ ____ thrombin

A

reversible / clot-bound

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77
Q

_______ is used for the prevention and treatment of thrombosis in patients with HIT or HITTS

A

argatroban

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78
Q

Argatroban produces dose dependent increases in ___, ____ , ____, ____

A

aPTT, ACT, PT and TT

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79
Q

Goal for aPTT for someone on Argatroban

A

1.5 to 3 times baseline (<100 sec)

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80
Q

Is there a reversal agent for Argatroban?

A

No

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81
Q

T/F For CABG patients receiving argatroban, use the same target ACT as with heparin

A

TRUE

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82
Q

Direct Thrombin Inhibitors include Bivalirudin (Angiomax) and Lepirudin (Refluidin). Hirudin is the polypeptide that is responsible for the anticoagulant properties of the saliva of the ______ ______

A

medicinal leech

83
Q

Hirudin analogs have a higher risk of bleeding because it binds ________ to the active catalytic and substrate recognition sites of BOTH circulating and clot-bound thrombin (Factor Iia)

A

irreversibly

84
Q

Is there a reversal agent for Hirudin analogs

A

NO, and it binds irreversibly

85
Q

Indication for Hirudin analogs

A

thrombosis associated with HIT

86
Q

Hirudin analogs are excreted by the ______ and dose should be adjusted in ______ impairment

A

kidneys / renal

87
Q

Antihirudin antibodies form in ____% of patients and may be associated with an __________ anticoagulant effect of lepirudin.

A

40% / increased

88
Q

Hirudin analogs are good for patients that are totally allergic to heparin and can’t take _____

A

LMWH

89
Q

Dabigatran (Pradaxa) is what?

A

Oral direct thrombin inhibitor

90
Q

Dabigatran is ___% renal eliminated and ___% liver metabolism. Unfortunately it interacts with ____ inhibitors

A

80% / 20% / PgP

91
Q

Dabigatran bleeding or overedose is treatable with activated charcoal if last dose taken within 2hrs. It can also be removed by ___ (62-68% of circulating Dabigatran). In fact there is even a specific antidote which is ___________ and __________

A

HD / Idarucizumab and Ciraparantag

92
Q

Idarucizumab (Praxbind) is a ________ antibody fragment

A

humanized.

93
Q

Idarucizumab (Praxbind) has _______ binding to dabigatran with 350 times greater affinity than thrombin. Two bolus doses will provide reversal in ___ minutes

A

noncompetitve / 10 minutes

94
Q

Reverse AD trial with Praxbind reported the median time from reversal to procedure was____ hrs for invasive procedure. Among bleeding patients who were reversed, the median time to investigator-reported hemostasis was ___ hrs.

A

1.6 / 2.5

95
Q

Review chart on slide 50

A

DOAC reversal algorithm

96
Q

Warfarin MOA: INDIRECT anticoagulant that alters the synthesis of blood coagulation factors ___________ by interfering with the action of Vitamin K and as well as proteins __ and __ which are natural ________

A

II, VII, IX, X / C and S / anticoagulants

97
Q

Factors II, VII, IX, and X are biologically inactvie unless 9-12 of the amino terminal glutamic acid residues are ___________. Vit K is required for this ______

A

carboxylated / carboxylation

98
Q

T/F With Warfarin you are at risk of developing a clot in the first day or two of therapy because you’re actually inhibiting the protein C and S which are natural anticoagulants

A

TRUE

99
Q

Warfarin has no effect on normal factors already in the _____ when the drug is started.

A

blood

100
Q

Warfarin decreases the total amount of each Vit. K dependent coagulation factor made by the liver by ___ to ____ %. In addition, the factors made are undercarboxylated resulting in diminished biological activity (10-40% of normal)

A

30 to 50%

101
Q

Antidote for warfarin toxicity/bleeding is _____, but takes up to ___ hrs for synthesis of new fully carboxylated coagulation proteins.

A

Vitamin K1 / 24 hours

102
Q

Would you ever give Vitamin K SQ

A

NO

103
Q

For immediate hemostatic competence in someone with warfarin toxicity, what should be given? Why?

A

FFP 10-20 ml/kg, because it contains all the clotting factors and AT3

104
Q

Review slides 54 and 55

A

Warfarin reversal summary

105
Q

Warfarin is pregnancy category ___

A

X

106
Q

Lots of drug interactions with _______. Any herbal that starts with a G as well as abx, other blood thinngers, NSAIDS, Tylenol and antiepileptics.

A

warfarin

107
Q

Most NOAC DO NOT require bridge therapy as they are only held ___ to ___ hr prior to procedure.

A

24-48 hrs

108
Q

Calculates stroke risk of not on an anticoagulant

A

CHADS-VASC

109
Q

Calculates bleeding risk

A

HAS BLED

110
Q

Low/Minor bleeding risk procedures

A

GI endoscopy, cardiac cath, cardiac device implantation, catheter ablation of afib, dental extractioin, dermatologic sugery, cataract removal

111
Q

Major/high bleeding risk procedures

A

Intraabdominal surgery, intrathoracic surgery, major orthopedic surgery, peripheral arterial revascularization, urologic surgery

112
Q

Bridge Therapy indications for High risk patients

A

Mechanical heart valve, older aortic valve prosthesis, stroke or TIA within 6 months, AFIB with CHADs2 score of 5 or 6, AFIB with stroke or TIA within 3 months, rheumatic valvular heart dz, VTE within 3 months or severe thrombophilia

113
Q

Bridge Therapy indications for moderate risk patients

A

Mechanical heart valve, bileaflet aortic valve + afib, prior stroke/TIA, HTN ,DM, CHF, > 75y/o. Afib with CHADs of 3 or 4. VTE within last 3 to 12 months, active CA, recurrent VTE

114
Q

T/F Bridge therapy for high risk patients would include therapeutic doses of SC LMWH or IV UFH

A

TRUE

115
Q

T/F Bridge therpay for moderate risk patients would include therapeutic or low dose LMWH and therapeutic dose IV UFH

A

TRUE

116
Q

Bridge therapy for low risk patients

A

Mechanical heart valve without Afib no other risk factors for stroke, Afib with CHADS 0-2 with no previous stroke, single VTE over 12 months ago with no other risk factors

117
Q

T/F Bridge therapy for low risk patients includes low dose SC LMWH or NO therpay at all.

A

TRUE

118
Q

Hold the bridge therapy ____ hrs pre-procedure if using LMWH. It is recommended to use __% dose for last dose pre-procedure

A

24 hrs / 50%

119
Q

Resume bridge therapy within __ to __ hrs for LMWH and within ___ hrs for UFH.

A

24 - 72 hrs / 24 hrs

120
Q

According to the 2017 and 2019 updates it states there is a questionable benefit of bridge therapy. There was no reduction in thromboembolic events and an increased risk of bleeding. 40-60% of anticoagulant interruptions may be unecessary so continue anticoagulation if bleeding risk is very low. The AHA 2019 AFib guidelines support bridging if the patient is VERY high risk of ______.

A

stroke.

121
Q

What are some thrombolytic agents?

A

Aletplast, Reteplase, Tenecteplase, Streptokinase, Urokinase

122
Q

With thrombolytic agents t-PA binds to fibrin and plasminogen and converts bound plasminogen to ________.

A

plasmin

123
Q

**Streptokinase has no intrinsic ________ activity, but forms a stable 1:1 complex with plasminiogen causing conformational changes that expose the active site that cleaves free plasminogen to _______.

A

enzymatic / plasmin

124
Q

Urokinase is a two chain serine protease isolated _______ kidney cells that converts plasminogen to plasmin.

A

human

125
Q

Urokinase and streptokinase lack fibrin specificity which results in an inducced systemic _______ state

A

lytic

126
Q

T/F Urokinase and tPA are very expensive

A

TRUE

127
Q

___________ requires a loading dose to overcome plasma antibodies that inactivate the protein. These antibodies are the result of prior streptococcal infections

A

streptokinase

128
Q

Absolute contraindications for thromobolytic agents like streptokinase and urokinase, t-PA

A

active internal bleed, trauma or surgery within 14 days (depends on surgery), recent head trauma, brain bleed, BP > than or equal to 200/120, Traumatic CPR and pregnancy

129
Q

Relative contraindications for thrombolytic agents like t-PA

A

chronic servere HTN ,PUD, on other anticoagulants, any other known bleeds, significant liver dz

130
Q

Major toxicity of t-PA is hemorrhage due to lysis of fibrin in “physiological thrombi” at sites of vascular injury. A systemic lytic state that results from systemic formation of plasmin which produces fibrinogenolysis and destruction of other ________ factors

A

coagulation

131
Q

With thrombolytic agents fibrinolytic activity can last __ to ___ hrs after discontinuation of the drug. Monitor _____ concentrations or ______ times during therapy for patients who exhibit bleeding.

A

7-24 hrs / fibrinogen / thrombin

132
Q

Epsilon Aminocaproic Acid is AKA _______

A

Amicar

133
Q

Amicar is a ____________ for excessive bleeds or surgical complications

A

procoagulant

134
Q

How does Amicar work?

A

inhibitor of fibrinolysis and indirect inhibitor of plasmin’s anti-platelet effects

135
Q

Amicar is used in treatment of excessive bleeding resulting from systemic ________ or urinary fibrinolysis.

A

hyperfibrinolysis

136
Q

What drug allows completion of surgery after stopping oozing in patients with cirrhosis as well as reduces bleeding and transfusion requirements after CPB

A

Amicar

137
Q

Amicar inhibits activation of plasminogen inhibiting fibrinolysis which results in INDIRECT inhibition of __________ anti-platelet effects

A

plasmin’s

138
Q

Amicar should be loaded over ___hr. Avoid rapid IV infusion secondary to hypotension, bradycardia, and/or arrhythmias.

A

1

139
Q

Low molecular weight Dextran, Dextran 40 has a molecular weight of about 40,000 Dalton’s. It causes expansion of intravascualr volume and prevents thromboembolism by decreasing blood _______

A

viscosity.

140
Q

__________ formation from dextran infusion may make subsequent cross-matching of blood difficult

A

Rouleaux

141
Q

Tranexamic Acid (TXA) is a a hemostatic agent that works as a ________ inhibitor of several ________ binding sites to reduce plasmin

A

competitive / plasminogen

142
Q

Spray-dried fibrin sealant that contains purifiied human plasma-derived FIBRINOGEN and THROMBIN

A

Raplixa

143
Q

NovoSeven RT is a recombinant coagulation factor ____

A

VIIa

144
Q

rFVIIa is used for the management of patients with _________________ and _____________

A

Hemophilia A or B / congenital factor VII deficiency

145
Q

rfVIIa works in the ____________ pathway. rFVIIa binds to activated platelet receptors or TF and then activates factor ____ and subsequently generates ________ and ____________

A

extrinsic / X / thrombin and fibrin

146
Q

Off-label use for RFVIIa ( oh and this shit is EXPENSIVE)

A

warfarin induced bleeding that can’t wait reversal with FFP or Vit. K, Spont intracranial hemorrhage, massive bleeding.

147
Q

Most $ignificant complication of RFVIIa is __________. (myocardial/cerebral ischmia or infaction)

A

thromboembolic

148
Q

Kcentra contains Factors II, VII, IX, X-inactive as well as _________.

A

heparin

149
Q

FEIBA contains factors II, VII (active), IX, X and the active factor VII may increase risk of ____________.

A

thrombosis

150
Q

Profilnine has factors II, IX, X and trace VII but no ______________.

A

heparin

151
Q

Platelet adhesion review: vWF (Factor VIII:vWF) is manufactured and released from endothelial cells. The Factor VIII:vWF promotes platelet _______ to damaged vascular walls.

A

adhesion

152
Q

________ disesase is the most common inherited coagulation defect

A

vonWillebrand’s disease

153
Q

Platelet ACTIVATION: _______(factor IIa) combines with the thrombin receptor on the platelet surface to activate the platelet. This changes the shape of the platelet and releases ____ and _______ which are meidators that promote platelet _______.

A

Thrombin / ADP and Thromboxane 2 / aggregation

154
Q

Platelet AGGREGATION is mediated by Thromboxane A2 and ADP which uncover fibrinogen receptors. Fibrinogen, which is Factor ____ attaches to the receptors linking the platelets to eachother

A

1

155
Q

Aspirin is a ___________ cyclo-oxygenase inactivator that persists for the life of the platelet which is __ to ___ days

A

irreversible / 8-12 days

156
Q

The end result of aspirin is it affects _______________ so that platelet aggregation is impaired

A

thromboxane A2

157
Q

NSAIDs will depress thromboxane A2 production by platelets but is temporary and lasts only about __ to ___ hrs.

A

24-48 hrs

158
Q

Thienopyridine ADP receptor Antagonists

A

Clopidogrel, Ticlopidyne, Prasugrel, Tricagrelor

159
Q

Platelet Glycoprotein (GP Iib/IIIa) Receptor Inhibitors

A

Abciximab, Eptifibatide, Tirofiban

160
Q

Thienopyridine ADP receptor antagonists bind selectively and non-competitively to a low affinity, ADP receptor binding site on the surface of platelets, thereby inhibiting ADP binding to the receptor. The receptor is to be considered ________ modified by the drug

A

irreversibly

161
Q

Plavix is a ________. The other thing about Plavix is CYP2C9 is required for metabolism and ________ inhibits this CYP enzyme

A

prilosec

162
Q

With Plavix, __ to __% inhibition is achieved after the first day of therapy with a steady state reached in 3-7 days.

A

40-60%

163
Q

Stop Plavix ____ days prior to surgery.

A

7 days

164
Q

Ticlodipine has a long plasma t1/2. ________________ can normalize prolonged bleeding time in 2 hrs. Platelet transfusions can also be used to reverse the effects. Stop __ to ____ days prior to surgery

A

methylprednisolone / 10 to 14 days

165
Q

With Prasugrel, half of the platelets are inhibited within ___ hr, with steady state achieved in 3-5 days.

A

1 hour

166
Q

With prasugrel, this is considered ________ and should be stopped ____ days prior to surgery

A

irreversible / 7 days

167
Q

What’s nice about Tricagelor (Brillinta) is that it is _______ and only has to be stopped ____ days prior to surgery

A

reversible / 5 days

168
Q

Adverse effects of clopidogrel, Prasugrel, and Tricagelor

A

Bleeding, N/V, Rash and diarrhea, severe neutropenia

169
Q

Adverse effects of Ticlopidine

A

> 50% have diarrhea or rash (rash is most common), nausea, dyspepsia,

170
Q

The most serious adverse effects of Ticlopidine is severe neutropenia, agranulocytosis, TTP, apalastic anemia and increased bleeding. What will have to be done if this needs treated.

A

Blood products as there is no reversal agent

171
Q

Cangrelor is an IV ______ inhibitor. It was approved in 2015 but DO NOT ADMIN with ______ inhibitor. It’s nice because it is reversible by stopping the infusion and platelet function will return to normal within 1 HR.

A

P2Y12 / G2b3a

172
Q

VerifyNow P2Y12 test measures the percentage of ________ function. _____% inhibition is considered safe to proceed with surgery or regional anesthesia.

A

platelet / <20%

173
Q

Dipyridamole (Persantine) is an oral medication that is considered to be a platelet aggregation inhibitor. It’s MOA for inhibiting platelet aggregation is not well understood. It’s not proven to be effective when used _______. Should be used in combination with ASA or _____________.

A

alone / warfarin

174
Q

Someone taking Dipyridamole with ASA should stop both medications ___ days prior to surgery

A

7 days

175
Q

Aggrenox is a combination drug of Dipyridamole and ASA used for the prevention of ________ thrombosis.

A

cerebral

176
Q

Vorapaxar (Zontivity) is used to reduce stroke and MI in high risk patients. It’s MOA is a protesase-activated receptor (PAR) 1 ______________. It blocks thrombin receptor so it can’t activate platelets. No true reversal so would have to give blood products if someone is bleeding.

A

antagonist

177
Q

GP Iib/IIIa Receptor Inhibitors interact with platelet glycoprotein Iib/IIIa to inhibit _______________ binding to activated platelets inhibiting platelet aggregation and clot retraction

A

fibrinogen

178
Q

Abciximab (Reopro) is a fab fragment of a monoclonal antibody that binds selectively to GP Iib/IIIa receptros and dissociates _____ from it. Has a slightly _____ DOA that the rest in this class.

A

slowly / longer

179
Q

Eptifibatide (Integrelin) is a synthetic cyclic heptapeptide that is _______ reversible

A

rapidly

180
Q

Tirofiban (Aggrastat) is a synthetic nonpeptide __________ derivative that is _______ reversible

A

tyrosine / rapdily

181
Q

GP Iib/IIIa Receptor inhibitors adverse effects include bleeding (minimal local petechiae to major hemorrhage) but it is NOT associated with an increased number of major bleeding episodes in patients requiring subsequent _______ surgery.

A

CABG

182
Q

Apciximab has a higher _______ _________ rate when compared to others in its class

A

allergic reaction

183
Q

DDAVP is considered a __________. It is a synthetic analog of ADH (posterior pituitary hormone) that causes endothelial cells to release what 3 things.

A

procoagulant / vWF, tissue type plasminogen activator, prostaglandins

184
Q

DDAVP promotes platelet _______________ to the vascular endothelium. No matter what it’s being used for the patient may be at an increased risk of developing ____________.

A

adhesiveness / clots

185
Q

T/F DDAVP may minimize intraoperative blood loss and transfusion requirements in patients undergoing cardiac surgery or spinal fusion surgery

A

TRUE

186
Q

How fast and how long does DDAVP work

A

Increases platelet adhesion within 30 minutes and lasts 4-6 hrs

187
Q

DDAVP side effects

A

hypo or hypertension, hyponatremia, nausea

188
Q

What is Xigirs ( no longer used)

A

Recombinant human activated protein C

189
Q

Full anticoagulation is a _________ contraindication to regional anesthesia because hematoma formation appears as likely with removal as during insertion of epidural catheters

A

absolute

190
Q

Temporary intraoperative anticoagulation with heparin is acceptable for someone with an epidural catheter as long as catheter insertion precedes heparin admin by ____hr (24 hours for cardiac surgery). Indwelling neuraxial catheters should be removed __ to __ hrs after the last heparin dose and after evaluating the patient’s coagulation status.

A

1 hr / 2-4 hrs

191
Q

T/F ASA and NASAIDS do not appear to be associated with an increased risk of epidural hematoma. The risk is increased if these are combined with other anti-platelet drugs or anticoagulants.

A

TRUE

192
Q

Neuraxial blockade in someone that is taking Clopidogrel/Prasugrel should have stopped taking the drug for at least ___ days

A

7 days

193
Q

Neuraxial blockade in someone that is taking Ticlopidine should have stopped taking the drug for at least _____ days

A

14 days

194
Q

Neuraxial blockade in someone that is taking Abciximab should have stopped the infusion at least ____ to ____ hrs prior to neuraxial

A

24 to 48 hrs

195
Q

Neuraxial blockade in someone that is taking Eptifibatide or Tirofiban should have stopped taking it at least __ to ____ hrs prior to neuraxial

A

4 to 8

196
Q

Low dose coumadin takers need to have an INR of < ___ to place or remove catheter

A

<1.5

197
Q

With SQ heparin there is ___ contraindication to the use of neuraxial techniques. However, patients on heparin >4 days should have platelet count checked to rule out ____

A

NO / HIT

198
Q

Partial anticoagulation with LMWH/Fondaparinux (Factor Xa inhibitors) poses a significant risk of epidural hematoma with ____________ blockade

A

neuraxial

199
Q

With LMWH high doses, needle placement requires a delay of at least ___ hrs.

A

24

200
Q

If LMWH in use, needle placement should occur at least _ to __ hrs after last dose. If epidural catheter is inserted it should be done __ to ___ hours prior to any dose of postoperative LMWH (single day dosing). Twice daily dosing should be delayed until __ hrs post-op. Catheters should be removed befor initiating twice daily dosing.

A

10 to 12 hrs / 6 to 8 hrs / 24 hrs

201
Q

Removal of epidural catheter should be done __ to ___ hrs before any dose of LMWH

A

2 to 4 hrs

202
Q

Removal of epidural catheter should occur __ to __ hrs after any dose and __ hrs before subsequent doses

A

10 to 12 hrs / 2 hours

203
Q

T/F It is safe for neuraxial procedures for someone on DOACs?

A

False, currently all have a black box warning for use with neuraxial anesthesia

204
Q

To simplify, D/C all DOAC __ days (dabigatran and Xa inhibitors) prior to neuraxial anesthesia and restart ____ hrs post procedure for low bleed risk and ___ to ___ hrs for high bleed risk

A

4 days / 24 hours / 48-72 hrs

Pharmacology II - Emily Britton (5 decks)

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