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N929 - Anesthesia Pharmacology > Anticoagulants, Antiplatelets, Thrombolytics > Flashcards

Anticoagulants, Antiplatelets, Thrombolytics Flashcards

1
Q

anticoagulants

A

prevent clot formation or extension of existing clot

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2
Q

anti-platelet agent

A

reduce platelet aggregation on the surface of the platelet

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3
Q

thrombolytics

A

converts endogenous plasminogen to the fibrinolytic enzyme plasmin to dissolve newly formed blood clots

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4
Q

herbal agents

A

have various mechanisms of anticoagulation

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5
Q

what is the primary source of endogenous anticoagulation factors?

A

capillary endothelium

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6
Q

prevention of blood coagulation outside the body

A
  • siliconized containers (stored donated blood)
  • heparin in CPB or artificial kidney machines
  • citrate ion
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7
Q

tissue plasminogen inhibitor

A

polypeptide produced by endothelial cells; acts a a natural inhibitor of the extrinsic pathway by inhibiting TF-VIIa complex

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8
Q

protein C pathway (APC)

A

consists of four key elements:

  • protein C
  • thrombomodulin
  • endothelial protein C receptor
  • protein S
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9
Q

protein C

A

enzyme with potent anticoagulant, profibrinolytic, and anti-inflammatory properties; activated by thrombin to form activated protein C and acts by inhibiting activated factors V and VIII

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10
Q

SERPIN (serine protease inhibitors)

A
  • antithrombin, previously known as ATIII
  • main inhibitor of thrombin
  • binds and inactivates thrombin, factor IIa, and factor Xa
  • enzymatic activity enhanced by the presence of heparin
  • AT synthesized in the liver and plasma half-life is 2.5-3.8 days
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11
Q

AT deficiency

A
  • hereditary estimated 1 in 2000-5000

- acquired deficiency (i.e. prolonged heparin infusions of >4-5 days) decreased plasma AT activity by 50-60% of normal

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12
Q

citrate ion

A
  • any substance that deionizes the blood calcium will prevent blood coagulation
  • negatively charged citrate combines with positively charged calcium in the blood to cause an un-ionized calcium compound
  • citrate ion removed by the liver
  • liver damage or MTP –> can greatly increase citrate and lead to hypocalcemia
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13
Q

types of anticoagulants

A
  • vitamin K antagonists
  • un-fractionated heparin
  • low molecular weight heparin and fondaparinux
  • direct thrombin inhibitors
  • direct oral anticoagulants
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14
Q

coumarin

A
  • precursor to modern day coumadin

- vitamin K antagonist

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15
Q

Vitamin K Antagonist drug

A

coumadin (warfarin)

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16
Q

Vitamin K Antagonist MOA

A
  • inhibition of vitamin K resulting in defective vitamin K dependent coagulation proteins (II, VII, IX, and X)
  • blocks action of vitamin K
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17
Q

Vitamin K Antagonist PK/PD

A
  • rapidly, completely absorbed
  • 97% protein bound
  • e ½ 24-36 hours after oral admin
  • crosses placenta
  • metabolized to inactive metabolites excreted in bile and urine
  • onset 3-4 days
  • DOA 2-4 days
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18
Q

Vitamin K Antagonist dose/route

A

2.5-10 mg orally (varies)

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19
Q

Vitamin K Antagonist clinical use

A

effective prevention of thromboembolisms

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20
Q

Vitamin K Antagonist INR 2-3

A

Afib, tx VTE/PE, prevent VTE, tissue heart valves

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21
Q

Vitamin K Antagonist INR 2.5-3.5

A

mechanical heart valve, prevent recurrent MI, hx VTE with INR 2-3

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22
Q

Vitamin K Antagonist considerations

A
  • not to be used in parturient, teratogenic
  • measured by PT/INR
  • affects factors for varied amounts of time
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23
Q

Vitamin K Antagonist surgical management

A
  • minor – d/c 1-5 days preop for PT 20% within baseline; restart 1-7 days postop
  • immediate surgery (24-48 hours) or active bleeding – give vitamin K [2.5-20 mg oral, 1-5 mg IV]
  • emergency – FFP or 4-factor concentrate (Kcentra)
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24
Q

unfractionated heparin MOA

A
  • naturally occurring polysaccharide that inhibits coagulation
  • released endogenously by mast cells and basophils
  • unfractionated derived from porcine intestine or bovine lung; enhance the naturally occurring effects of antithrombin
  • binds to AT enhances 1000x ability of AT to inactivate coagulation enzymes
  • neutralized thrombin so no conversion of fibrinogen to fibrin
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25
Q

unfractionated heparin PK/PD

A
  • large molecule weight, only about 1/3 binds to AT, so this is responsible for anticoagulation effect
  • poor lipid solubility, cannot cross lipid barriers
  • bound to plasma proteins
  • DOA 1.5-4 hours
  • degraded by enzyme in blood (heparinase)
  • monitored by biologic activity
  • dose-dependent relationship with elimination ½
  • decrease in body temp prolongs elimination ½
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26
Q

unfractionated heparin VTE prophylaxis dose

A

5,000 units SubQ Q8-12 hours

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27
Q

unfractionated heparin VTE treatment dose

A

5,000 units IV + continuous infusion for goal PTT 1.5-2.5x control

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28
Q

unfractionated heparin CPB dose

A

400 units/kg IV

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29
Q

unfractionated heparin vascular intervention dose

A

100-150 units/kg IV

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30
Q

unfractionated heparin clinical uses

A
  • SQ VTE and PE prophylaxis (ERAS, ortho, post-MI, hemodialysis)
  • warfarin bridge
  • vascular or non CPB cases (ACT > 200-300 seconds)
  • interventional aneurysm clipping/coil (ACT >250 seconds)
  • CPB (ACT > 400-480 seconds)
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31
Q

unfractionated heparin considerations

A
  • 1 unit of activity = amount of heparin that maintains the fluidity of 1 mL of citrated plasma for 1 hour after re-calcification
  • safe in obstetrics does not cross placenta
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32
Q

unfractionated heparin monitoring

A
  • aPTT 1.5-2.5x pre drug value
  • ACT 3-5 min post admin; 30 min-1hr intervals post admin
  • HEPTEM
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33
Q

unfractionated heparin side effects

A
  • hemorrhage, hematoma
  • HIT (heparin induced thrombocytopenia)
  • allergic reaction
  • hypotension with large dose
  • altered protein binding
  • chronic exposure –> reduce AT activity
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34
Q

unfractionated heparin reversal

A

protamine 1-1.5 mg for each 100 units of heparin

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35
Q

intraspinal hematoma

A
  • incidence 0.1 per 100,000
  • more likely to occur in anticoagulated or thrombocytopenic patients, patient with neoplastic disease, liver disease, or alcoholism
  • IV heparin and neuraxial anesthesia –> 1 hour delay between needle placement and heparin admin; catheter removed 1 hour before heparin admin and 2-4 hours after last dose; monitor PTT or ACT
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36
Q

heparin induced thrombocytopenia

A
  • heparin-dependent antibodies that aggregate platelets and leads to consumption which produces thrombocytopenia
  • clinical suspicion confirmed with lab test for antibodies
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37
Q

mild/type 1 HIT

A
  • 30-40% heparin treated patients
  • non-immune mediated
  • plt count <100,000
  • typically presents 3-15 days post initiation of therapy
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38
Q

severe/type 2 HIT

A
  • 0.5-6% heparin treated patients
  • immune mediated
  • plt count <50,000
  • typically presents 6-10 days after initiation of therapy
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39
Q

heparin allergic reaction

A
  • heparin obtained from animal tissues, caution used for those with preexisting allergy
  • fever, urticaria, hemodynamic changes
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40
Q

AT deficiency

A
  • AT deficiency = resistance to heparin
  • no antithrombin means nothing for heparin to bind to
  • occurs in up to 22% of patients undergoing cardiac surgery
  • patients who received intermittent or continuous heparin therapy may manifest a progressive, paradoxical reduction in AT
  • decrease may paradoxically increase thrombotic tendency
  • treatment - restore normal values; 2-4 units FFP in adults, or AT concentrate
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41
Q

Low Molecular Weight Heparin (LMWH)

A

Derived from unfractionated heparin by chemical depolymerization –> fragments 1/3 size of heparin

42
Q

Low Molecular Weight Heparin (LMWH) drug

A

Enoxaparin (Lovenox)

43
Q

Low Molecular Weight Heparin (LMWH) MOA

A
  • binds to and accelerates AT; inhibits factors Xa and IIa (Xa>IIa)
  • decreased thrombin activity and prevention of fibrin clot formation
44
Q

Low Molecular Weight Heparin (LMWH) PK/PD

A
  • low molecular weight
  • less protein binding
  • elimination ½ 24 hours
45
Q

Low Molecular Weight Heparin (LMWH) advantages

A
  • decreased dosing frequency (1x daily)
  • less need for monitoring
  • more predictable PK response
  • fever effects on plts
  • reduced risk for HIT
46
Q

Low Molecular Weight Heparin (LMWH) disadvantages

A
  • more expensive
  • surgery delayed for 12 hours post dose
  • protamine only neutralizes 65%; more complete reversal with FFP
47
Q

Direct Oral Anticoagulants (DOACs) types

A
  • Direct thrombin IIa inhibitor

- Direct factor Xa inhibitor

48
Q

Direct Oral Anticoagulants (DOACs) uses

A
  • tx VTE
  • prevent embolic stroke
  • prophylaxis in patients undergoing surgery
49
Q

Direct Oral Anticoagulants (DOACs) advantages

A
  • rapid onset with peak in 24 hrs
  • predictable PD
  • minimal drug interactions
  • no required routine lab monitoring
50
Q

Direct Thrombin IIa Inhibitor drug

A

Dabigatran (Pradaxa)

51
Q

Direct Thrombin IIa Inhibitor PK/PD

A
  • metabolized via renal elimination (~80%)

- elimination ½ 12 hours

52
Q

Direct Thrombin IIa Inhibitor monitoring

A

coagulation assay –> dilute thrombin time, aPTT, ROTEM (but less specific than thrombin time)

53
Q

Direct Thrombin IIa Inhibitor reversal

A

idarucizumab (Praxbind); specific to dabigatran; binds with 350 fold higher affinity than thrombin, ½ 45 min

54
Q

Direct Factor Xa Inhibitor drugs

A

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

55
Q

Direct Factor Xa Inhibitor PK/PD

A

hepatic metabolism (~65-70%)

56
Q

Direct Factor Xa Inhibitor monitoring

A
  • coagulation assay –> anti Xa (not widely available)
  • PT can be helpful for rivaroxaban only
  • ROTEM not sensitive
57
Q

management of DOAC-treated patients undergoing surgery

A
  • minimal bleeding risk - no DOAC interruption likely safe
  • low bleeding risk - recommend stop DOACs for 24 hours prior to elective surgery
  • high bleeding risk - interruption of DOAC therapy 48 hours prior to elective surgery (longer for dabigatran and impaired renal fxn)
58
Q

antiplatelet agents

A
  • COX inhibitors
  • P1Y12 receptor antagonists
  • Glycoprotein IIB/IIIA inhibitors
59
Q

antiplatelet therapy MOA

A
  • suppress platelet function (inhibit aggregation) for the prevention of thrombosis
  • indicated for patients at risk for CVA, MI, or other vascular thrombosis complications
60
Q

Cyclooxygenase Inhibitors

A

Aspirin

NSAIDs

61
Q

Aspirin MOA

A
  • inhibit platelet aggregation
  • inhibit thromboxane A2 synthesis by interfering with COX 1 and 2 isoenzymes and subsequent release of ADP by plts and their aggregation
  • acetyl group of ASA causes acetylation of COX
62
Q

Aspirin PK/PD

A

irreversible effects, last the life of a platelet (8-12 days)

63
Q

Aspirin dose

A

81-325 mg PO

64
Q

Aspirin perioperative management

A
  • primary prophylaxis – should be continued in perioperative period up to/including DOS; may be held for a few days at discretion of surgeon or procedural physician due to heightened risk for perioperative bleeding
  • secondary prophylaxis – should be continued in perioperative period up to/including DOS; stopping needs explicit discussion with CV physician
65
Q

Aspirin definite surgical contraindications

A

HOLD ASA –> intracranial, middle ear, posterior eye, intramedullary spine; possibly in prostate surgery

66
Q

NSAIDs

A

Ketorolac, Naprosyn, Ibuprofen

67
Q

NSAIDs MOA

A

same MOA as aspirin but reversibly depress thromboxane A2 synthesis by platelets

68
Q

NSAIDs PK/PD

A

temporary 24-48 hours

69
Q

NSAIDs surgical considerations

A

often held prior to surgery

70
Q

P2Y12 Receptor Antagonists drugs

A

Clopidogrel (Plavix)

Ticagrelor (Brillinta)

71
Q

P2Y12 Receptor Antagonists MOA

A

inhibitors of platelet activation/aggregation through irreversible binding of its active metabolite to P2Y12 class of ADP receptors on plts

72
Q

P2Y12 Receptor Antagonists PK/PD

A
  • clopidogrel – prodrug must be metabolized by CYP450 to produce active metabolite that inhibits plt aggregation for life of platelet
  • Ticagrelor – no need for hepatic activation
73
Q

P2Y12 Receptor Antagonists clinical use

A
  • secondary prevention of MI, CVA
  • coronary stent
  • ACS
  • PAD
  • BMS or DES
74
Q

P2Y12 Receptor Antagonists surgical considerations

A
  • d/c 7 days before elective surgery

- plt transfusion useful for emergent surgery and restoring hemostasis

75
Q

Platelet Glycoprotein IIb/IIIa Antagonists Drugs

A

Abciximab (ReoPro)
Tirofiban (Aggrastat)
Eptifibatide (Integrilin)

76
Q

Platelet Glycoprotein IIb/IIIa Antagonists MOA

A
  • act at the corresponding fibrinogen receptor that is important for plt aggregation
  • blocks fibrinogen, and thus the final common pathway of platelet aggregation
77
Q

Platelet Glycoprotein IIb/IIIa Antagonists PK/PD

A
  • renal excretion

- half-life 2.5 hrs (except abciximab half-life is 12 hrs with clinical effects lasting 48 hrs

78
Q

Platelet Glycoprotein IIb/IIIa Antagonists clinical use

A
  • ACS
  • angioplasty failures
  • stent thrombosis
79
Q

Platelet Glycoprotein IIb/IIIa Antagonists surgical considerations

A
  • their effects can be monitored with ACTs and reversible with the clearance of the drug
  • ACT maintained between 200-400 seconds
  • plt counts monitored and therapy d/c if thrombocytopenia develops (<100,000)
  • drug can be reversed with plt transfusion
80
Q

herbal anticoagulants

A
  • garlic
  • ginkgo
  • ginseng
  • black cohosh
  • fish oil
  • feverfew
81
Q

garlic

A

inhibits plt aggregation, d/c 7 days before surgery

82
Q

ginkgo

A

inhibits plt activating factor, d/c for 36 hrs before surgery

83
Q

ginseng

A

inhibits plt aggregation and lowers blood glucose; check PT/PTT/glucose, d/c for 24 hours (preferably 7 days)

84
Q

black cohosh

A

claims to be useful for menopausal symptoms; contains small amounts of anti-inflammatory compounds including salicylic acid

85
Q

fish oil

A

claims to prevent/treat athersclerotic CV disease (800-1500 mg/day); also used to decrease triglycerides; dose dependent bleeding risk increases with dose >3g/day

86
Q

feverfew

A

claims to prevent migraines; increases risk of bleeding b/c it individually inhibits plt aggregation; has additive effects with other antiplatelet drugs; additive effects with warfarin

87
Q

fibrinolysis

A
  • plasminogen = serum protein that is absorbed into the clot at its formation
  • plasminogen cleaved into plasmin which breaks down fibrin and fibrinogen
  • tissue plasminogen activator and urokinase-type plasminogen activators are released from the capillary endothelium
88
Q

fibrin specific thrombolytics

A
  • alteplase
  • reteplase
  • tenecteplase
89
Q

non-fibrin-specific thrombolytics

A

-streptokinase

90
Q

thrombolytics MOA

A
  • converts plasminogen to the active form plasmin, plasmin breaks down fibrin
  • more capable of dissolving newly formed clots (platelet rich and weaker fibrinogen bonds)
91
Q

thrombolytics clinical use

A
  • restore circulation through previously occluded vessel (STEMI, acute ischemic stroke, acute massive PE)
  • contraindicated in trauma, severe HTN, active bleeding, pregnancy
92
Q

thrombolytics treatment considerations

A
  • common risk –> hemorrhage or bleeding
  • often 6 hour window for treatment
  • efficacy of thrombolytic depends on the age of the clot, older clot has more cross-linking and are more compacted = more difficult to dissolve
93
Q

thrombolytics adverse effects

A
  • bleeding

- re-thrombosis

94
Q

alteplase t-PA MOA

A

fibrin specific thrombolytic drug synthesized by endothelial cells

95
Q

alteplase t-PA PK/PD

A

short ½ life – about 5 min

96
Q

alteplase t-PA clinical use

A

limited to use in the first 3-6 hours of ischemic stroke

97
Q

alteplase t-PA route

A

systemic IV admin or directly into embolism

98
Q

streptokinase MOA

A
  • protein produced by beta-hemolytic streptococci
  • not enzyme, but non-covalently binds to plasminogen and converts it to plasminogen-activator complex that acts on other plasminogen molecules to generate plasmin
99
Q

streptokinase PK/PD

A

e ½ about 20 min

100
Q

streptokinase considerations

A
  • bacterial product may stimulate antibody production and subsequent allergic reactions
  • least expensive of the thrombolytic drugs

N929 - Anesthesia Pharmacology (12 decks)

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