Hematology Pharm Flashcards
3 components of Virchow’s triad are?
Hypercoaguable state, vascular wall injury, circulatory stasis
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
fibrinolysis / closed
Number one reason people in the community are on anticoagulants
afib
Review coagulation cascade
slide 4
With the extrinsic pathway, damage outside blood vessels triggers the release of __________ (Factor III, TF) from damaged cells
thromboblastin
With the extrinsic pathway, THROMBOBLASTIN activates _______. VIIa when complexed on the surface of the platelet with ______ (factor IV) and thromboblastin (IIIa) activates factor ____.
VII / calcium / factor X (Xa)
Summary for extrinsic
Damage -> release of thromoboblastin -> thromboblastin (III) activates VII and combines with IV which activates factor X (3 to 7 and 4 activates 10)
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)
XII / XI / IX / X
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 _______.
prothrombin (factor II) / thrombin (Iia)
With the common pathway, IIa converts ______ to ______ and in the presence of factor XIII, cross-linking occurs.
fibrinogen (I) to fibrin (Ia)
Heparin acts as a catalyst to markedly accelerate the rate at which ________ (heparin cofactor) neutralizes ______ and factor Xa
ATIII / thrombin
Heparin basically speeds up ______ to neutralize _____ and ____
ATIII / thrombin / Xa
Heparin MOA
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.
Is heparin safe in pregnancy?
Yes, it does not cross the placenta
Heparin only acts on _________ factors. This means that it stops further clots from forming but doesn’t break up and lyse clots.
unbound
Heparin is cleared by the reticuloendothelial system which is basically a system of __________
phagocytes
Heparin resistance is when _____ doses are required to obtainthe desired aPTT or ACT
higher
Heparin resistance can be due to what?
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)
Heparin resistance in someone with Acquired ATIII deficiency in patients with cirrhosis, nephrotic syndrome, or DIC is treated with what?
2 units FFP to proved ATIII or ATIII concentrate
Heparin toxicity can result in what?
bleeding, thrombocytopenia (HIT), Abnormal LFTs, infrequent risk of osteoporosis or spontaneous vertebral fractures
The vertebral fractures that can happen with heparin is related to what?
somehow the calcium that is involved in the clotting cascade
HIT show when in treatment naïve patients?
7-14 days after initiation of therapy
With HIT, if patient previously exposed to heparin, thrombocytopenia may occur ______
earlier
Type II HIT
heparin dependent antiplatelet IgG antibodies
Is HIT reversible?
Yes, stop the heparin
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 ______
arterial thrombosis / Argatroban
Review slide 17
HIT pathophysiology ( remember this is an immune mediated type of reaction)
Protamine sulfate acts as a _______ ______ by complexing with strongly acidic (cationic) and anionic heparin to form a stable _______
heparin antagonist / salt
The complexes formed by prtoamine and heparin are removed by the ___________ system
reticuloendothelial
Protamine has a rapid onset of about 5 min and lasts about ___ hrs
2 hours
Protamine is used to ______ heparin after CPB procedures and others where higher molecular weight heparin was used for anticoagulation.
neutralize
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.
65%
Protamine dosing is determined by what?
dose of heparin, route of heparin admin, time elapsed since heparin was administered
How fast is protamine administered?
slow IV 10mg/ml over 1-3 min. 50 mg/10 minutes maximum
What happens with rapid IV injection of protamine
acute histamine-related hypotension, bradycardia, pulmonary HTN, transient flusing, dyspnea
What 3 things do you want to watch when administering protamine?
BP, PA pressures, airway pressures (wheezing)
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.
compliment
Who is susceptible to protamine hypersensitivity reactions?
hypersensitive to fish, previous protamine reversal of heparin, protamine containing insulin (NPH), previous vasectomy
Pretreatment for protamine hypersensitvity
corticosteroid and antihistamine
Heparin _________ happens when there is re-anticoagulation after protamine administered. Usually 8-9 hrs but 30 min to 18 hrs after CPB reported.
rebound
Overdose of protamine may result in _______ theoretically because it has anticoagulant and anti-platelet effects when given alone or in excess of heparin.
bleeding
LMWH drugs are Factor ____ inhibitors
Xa / Dalteparin (Fragmin) , Enoxaparin (lovenox), Tinzaparin (Innohep)
LMWH MOA: Inhibition of Factor ____ by ______. Have some Factor Iia inhibition effect
Xa / antithrombin
T/F aPTT and Pt levels are relatively insensitive with LMWH therapy
TRUE
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.
anti-Xa
Can you use LMWH AKA with HIT patients?
NO
What should you do to the dose of LMWH in patients with chronic renal insufficiency?
decrease the dose
How is LMWH eliminated?
renally
Fondaparinux AKA
Arixtra
Fondaparinux MOA: Synthetic indirect specific inhibitor of Factor ____
Xa
Fondaparinux is ______ mediated, has no effect on factor ______ no effect on ______ function.
ATIII / IIa / platelet
Advantages of Fondaprinux
fixed-dose SQ daily, not associated with HIT, stop if platelets fall below 100,000
T/F Fondaparinux has the same risk of spinal or epidural hematoma as LMWHs
TRUE
Fondaparinux in a nutshell
Xa only, less indication, less risk of thrombocytopenia, but same risk of spinal and epidural hematomas
Betrixaban (Bevyxxa) is an ORAL ____ inhibitor and only approved for preventing clots in the _______ patient
Xa / acute hospitalized
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
heparinoid / Xa
Oral Xa inhibitors
Rivaroxaban (Xarelto) / Apixaban (Eliquis) / Edoxaban (Savaysa)
Review charts on slide 33 and 34
pharmacokinetic comparison of Oral Xa inhibitors. Know that Rivaroxaban has the most protein binding
How many days before surgery should coumadin be stopped?
5 days
Dabigatrin (pradaxa) should be stopped __ to ___ days if CrCl is > 50 ml/min and ___ to ___ days if CrCl is <50 ml/min.
1-2 days / 3-5 days
Rivaroxaban (xarelto ) should be stopped how long before surgery
24 hrs
Apixaban (Eliquis) should be stopped ___ hrs before high/moderate procedural bleeding risk and ____ hrs for low procedural bleeding risk.
48 hrs / 24 hrs
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
12 to 24 hrs
Dabigatran should be stopped 4 to 6 days if CrCl is less than or equal ____ ml/min
30 ml/min
Oral Xa Reversal general measures
d/c medication, mechanical compression, surgical hemostasis, transfusional support
If an oral Xa inhibitor needs to be reversed and the last dose was within 2 hrs you can administer ________ _______. HD is _________.
activated charcoal / not beneficial
Other treatments for Oral Xa inhibitors
PCC, FEIBA, rFVIIa
Reversal agent for Oral Xa inhibitors
Andexanet
Andexanet is only approved for ____ and _____
eliquis and xarelto
Andexanet alpha (Andexxa) reverses Factor ___ inhibitors. It is recombinant human factor ___.
Xa / Xa
Andexanet binds _________ to Factor Xa inhibitors for ______ reversal
competitively / complete
Andexxa black box warning
thromboembolic events, ischemic events, cardiac arrest, sudden death. May also cause UTIs, Pneumonia, infusion related reactions
Review Andexxa dosing chart on slide 40
now
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
investigational / hydrogen
Argatroban is a DIRECT _____ _______
thrombin inhibitor
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
reversible / clot-bound
_______ is used for the prevention and treatment of thrombosis in patients with HIT or HITTS
argatroban
Argatroban produces dose dependent increases in ___, ____ , ____, ____
aPTT, ACT, PT and TT
Goal for aPTT for someone on Argatroban
1.5 to 3 times baseline (<100 sec)
Is there a reversal agent for Argatroban?
No
T/F For CABG patients receiving argatroban, use the same target ACT as with heparin
TRUE
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 ______ ______
medicinal leech
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)
irreversibly
Is there a reversal agent for Hirudin analogs
NO, and it binds irreversibly
Indication for Hirudin analogs
thrombosis associated with HIT
Hirudin analogs are excreted by the ______ and dose should be adjusted in ______ impairment
kidneys / renal
Antihirudin antibodies form in ____% of patients and may be associated with an __________ anticoagulant effect of lepirudin.
40% / increased
Hirudin analogs are good for patients that are totally allergic to heparin and can’t take _____
LMWH
Dabigatran (Pradaxa) is what?
Oral direct thrombin inhibitor
Dabigatran is ___% renal eliminated and ___% liver metabolism. Unfortunately it interacts with ____ inhibitors
80% / 20% / PgP
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 __________
HD / Idarucizumab and Ciraparantag
Idarucizumab (Praxbind) is a ________ antibody fragment
humanized.
Idarucizumab (Praxbind) has _______ binding to dabigatran with 350 times greater affinity than thrombin. Two bolus doses will provide reversal in ___ minutes
noncompetitve / 10 minutes
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.
1.6 / 2.5
Review chart on slide 50
DOAC reversal algorithm
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 ________
II, VII, IX, X / C and S / anticoagulants
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 ______
carboxylated / carboxylation
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
TRUE
Warfarin has no effect on normal factors already in the _____ when the drug is started.
blood
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)
30 to 50%
Antidote for warfarin toxicity/bleeding is _____, but takes up to ___ hrs for synthesis of new fully carboxylated coagulation proteins.
Vitamin K1 / 24 hours
Would you ever give Vitamin K SQ
NO
For immediate hemostatic competence in someone with warfarin toxicity, what should be given? Why?
FFP 10-20 ml/kg, because it contains all the clotting factors and AT3
Review slides 54 and 55
Warfarin reversal summary
Warfarin is pregnancy category ___
X
Lots of drug interactions with _______. Any herbal that starts with a G as well as abx, other blood thinngers, NSAIDS, Tylenol and antiepileptics.
warfarin
Most NOAC DO NOT require bridge therapy as they are only held ___ to ___ hr prior to procedure.
24-48 hrs
Calculates stroke risk of not on an anticoagulant
CHADS-VASC
Calculates bleeding risk
HAS BLED
Low/Minor bleeding risk procedures
GI endoscopy, cardiac cath, cardiac device implantation, catheter ablation of afib, dental extractioin, dermatologic sugery, cataract removal
Major/high bleeding risk procedures
Intraabdominal surgery, intrathoracic surgery, major orthopedic surgery, peripheral arterial revascularization, urologic surgery
Bridge Therapy indications for High risk patients
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
Bridge Therapy indications for moderate risk patients
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
T/F Bridge therapy for high risk patients would include therapeutic doses of SC LMWH or IV UFH
TRUE
T/F Bridge therpay for moderate risk patients would include therapeutic or low dose LMWH and therapeutic dose IV UFH
TRUE
Bridge therapy for low risk patients
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
T/F Bridge therapy for low risk patients includes low dose SC LMWH or NO therpay at all.
TRUE
Hold the bridge therapy ____ hrs pre-procedure if using LMWH. It is recommended to use __% dose for last dose pre-procedure
24 hrs / 50%
Resume bridge therapy within __ to __ hrs for LMWH and within ___ hrs for UFH.
24 - 72 hrs / 24 hrs
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 ______.
stroke.
What are some thrombolytic agents?
Aletplast, Reteplase, Tenecteplase, Streptokinase, Urokinase
With thrombolytic agents t-PA binds to fibrin and plasminogen and converts bound plasminogen to ________.
plasmin
**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 _______.
enzymatic / plasmin
Urokinase is a two chain serine protease isolated _______ kidney cells that converts plasminogen to plasmin.
human
Urokinase and streptokinase lack fibrin specificity which results in an inducced systemic _______ state
lytic
T/F Urokinase and tPA are very expensive
TRUE
___________ requires a loading dose to overcome plasma antibodies that inactivate the protein. These antibodies are the result of prior streptococcal infections
streptokinase
Absolute contraindications for thromobolytic agents like streptokinase and urokinase, t-PA
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
Relative contraindications for thrombolytic agents like t-PA
chronic servere HTN ,PUD, on other anticoagulants, any other known bleeds, significant liver dz
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
coagulation
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.
7-24 hrs / fibrinogen / thrombin
Epsilon Aminocaproic Acid is AKA _______
Amicar
Amicar is a ____________ for excessive bleeds or surgical complications
procoagulant
How does Amicar work?
inhibitor of fibrinolysis and indirect inhibitor of plasmin’s anti-platelet effects
Amicar is used in treatment of excessive bleeding resulting from systemic ________ or urinary fibrinolysis.
hyperfibrinolysis
What drug allows completion of surgery after stopping oozing in patients with cirrhosis as well as reduces bleeding and transfusion requirements after CPB
Amicar
Amicar inhibits activation of plasminogen inhibiting fibrinolysis which results in INDIRECT inhibition of __________ anti-platelet effects
plasmin’s
Amicar should be loaded over ___hr. Avoid rapid IV infusion secondary to hypotension, bradycardia, and/or arrhythmias.
1
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 _______
viscosity.
__________ formation from dextran infusion may make subsequent cross-matching of blood difficult
Rouleaux
Tranexamic Acid (TXA) is a a hemostatic agent that works as a ________ inhibitor of several ________ binding sites to reduce plasmin
competitive / plasminogen
Spray-dried fibrin sealant that contains purifiied human plasma-derived FIBRINOGEN and THROMBIN
Raplixa
NovoSeven RT is a recombinant coagulation factor ____
VIIa
rFVIIa is used for the management of patients with _________________ and _____________
Hemophilia A or B / congenital factor VII deficiency
rfVIIa works in the ____________ pathway. rFVIIa binds to activated platelet receptors or TF and then activates factor ____ and subsequently generates ________ and ____________
extrinsic / X / thrombin and fibrin
Off-label use for RFVIIa ( oh and this shit is EXPENSIVE)
warfarin induced bleeding that can’t wait reversal with FFP or Vit. K, Spont intracranial hemorrhage, massive bleeding.
Most $ignificant complication of RFVIIa is __________. (myocardial/cerebral ischmia or infaction)
thromboembolic
Kcentra contains Factors II, VII, IX, X-inactive as well as _________.
heparin
FEIBA contains factors II, VII (active), IX, X and the active factor VII may increase risk of ____________.
thrombosis
Profilnine has factors II, IX, X and trace VII but no ______________.
heparin
Platelet adhesion review: vWF (Factor VIII:vWF) is manufactured and released from endothelial cells. The Factor VIII:vWF promotes platelet _______ to damaged vascular walls.
adhesion
________ disesase is the most common inherited coagulation defect
vonWillebrand’s disease
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 _______.
Thrombin / ADP and Thromboxane 2 / aggregation
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
1
Aspirin is a ___________ cyclo-oxygenase inactivator that persists for the life of the platelet which is __ to ___ days
irreversible / 8-12 days
The end result of aspirin is it affects _______________ so that platelet aggregation is impaired
thromboxane A2
NSAIDs will depress thromboxane A2 production by platelets but is temporary and lasts only about __ to ___ hrs.
24-48 hrs
Thienopyridine ADP receptor Antagonists
Clopidogrel, Ticlopidyne, Prasugrel, Tricagrelor
Platelet Glycoprotein (GP Iib/IIIa) Receptor Inhibitors
Abciximab, Eptifibatide, Tirofiban
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
irreversibly
Plavix is a ________. The other thing about Plavix is CYP2C9 is required for metabolism and ________ inhibits this CYP enzyme
prilosec
With Plavix, __ to __% inhibition is achieved after the first day of therapy with a steady state reached in 3-7 days.
40-60%
Stop Plavix ____ days prior to surgery.
7 days
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
methylprednisolone / 10 to 14 days
With Prasugrel, half of the platelets are inhibited within ___ hr, with steady state achieved in 3-5 days.
1 hour
With prasugrel, this is considered ________ and should be stopped ____ days prior to surgery
irreversible / 7 days
What’s nice about Tricagelor (Brillinta) is that it is _______ and only has to be stopped ____ days prior to surgery
reversible / 5 days
Adverse effects of clopidogrel, Prasugrel, and Tricagelor
Bleeding, N/V, Rash and diarrhea, severe neutropenia
Adverse effects of Ticlopidine
> 50% have diarrhea or rash (rash is most common), nausea, dyspepsia,
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.
Blood products as there is no reversal agent
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.
P2Y12 / G2b3a
VerifyNow P2Y12 test measures the percentage of ________ function. _____% inhibition is considered safe to proceed with surgery or regional anesthesia.
platelet / <20%
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 _____________.
alone / warfarin
Someone taking Dipyridamole with ASA should stop both medications ___ days prior to surgery
7 days
Aggrenox is a combination drug of Dipyridamole and ASA used for the prevention of ________ thrombosis.
cerebral
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.
antagonist
GP Iib/IIIa Receptor Inhibitors interact with platelet glycoprotein Iib/IIIa to inhibit _______________ binding to activated platelets inhibiting platelet aggregation and clot retraction
fibrinogen
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.
slowly / longer
Eptifibatide (Integrelin) is a synthetic cyclic heptapeptide that is _______ reversible
rapidly
Tirofiban (Aggrastat) is a synthetic nonpeptide __________ derivative that is _______ reversible
tyrosine / rapdily
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.
CABG
Apciximab has a higher _______ _________ rate when compared to others in its class
allergic reaction
DDAVP is considered a __________. It is a synthetic analog of ADH (posterior pituitary hormone) that causes endothelial cells to release what 3 things.
procoagulant / vWF, tissue type plasminogen activator, prostaglandins
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 ____________.
adhesiveness / clots
T/F DDAVP may minimize intraoperative blood loss and transfusion requirements in patients undergoing cardiac surgery or spinal fusion surgery
TRUE
How fast and how long does DDAVP work
Increases platelet adhesion within 30 minutes and lasts 4-6 hrs
DDAVP side effects
hypo or hypertension, hyponatremia, nausea
What is Xigirs ( no longer used)
Recombinant human activated protein C
Full anticoagulation is a _________ contraindication to regional anesthesia because hematoma formation appears as likely with removal as during insertion of epidural catheters
absolute
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.
1 hr / 2-4 hrs
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.
TRUE
Neuraxial blockade in someone that is taking Clopidogrel/Prasugrel should have stopped taking the drug for at least ___ days
7 days
Neuraxial blockade in someone that is taking Ticlopidine should have stopped taking the drug for at least _____ days
14 days
Neuraxial blockade in someone that is taking Abciximab should have stopped the infusion at least ____ to ____ hrs prior to neuraxial
24 to 48 hrs
Neuraxial blockade in someone that is taking Eptifibatide or Tirofiban should have stopped taking it at least __ to ____ hrs prior to neuraxial
4 to 8
Low dose coumadin takers need to have an INR of < ___ to place or remove catheter
<1.5
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 ____
NO / HIT
Partial anticoagulation with LMWH/Fondaparinux (Factor Xa inhibitors) poses a significant risk of epidural hematoma with ____________ blockade
neuraxial
With LMWH high doses, needle placement requires a delay of at least ___ hrs.
24
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.
10 to 12 hrs / 6 to 8 hrs / 24 hrs
Removal of epidural catheter should be done __ to ___ hrs before any dose of LMWH
2 to 4 hrs
Removal of epidural catheter should occur __ to __ hrs after any dose and __ hrs before subsequent doses
10 to 12 hrs / 2 hours
T/F It is safe for neuraxial procedures for someone on DOACs?
False, currently all have a black box warning for use with neuraxial anesthesia
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
4 days / 24 hours / 48-72 hrs
