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Anticoagulation Flashcards

1
Q

Warfarin

A

-Coumadin
-Inhibits factors VII, IX, X, II, proteins C and S
-Duration: 2- 5 days
-Reversal: fresh frozen plasma, vitamin K ((phytonadione), PCC (Kcentra), aPCC (FEIBA)

-Warfarin MOA:
-Inhibits VKORC (a protein that reduces Vitamin K to activate it)
-Inhibits creation of Vitamin K dependent factors: X, IX, VII, II (1972) and protein and C and S
-Contraindicated in pregnant patients
-Warfarin reversal agents and their times to onset
-Administer Vit K (6 hours)
-FFP (<1 hour)
-Prothrombin Concentrate Complex (immediate)

-Patient started on Coumadin and develops skin necrosis:
-Warfarin induced skin necrosis
-Seen in patients with protein C and S deficiency
-Short half-life of protein C and S (natural anticoagulants)= brief period hypercoagulable with initial inhibition of protein C & S
-Important to bridge with Lovenox when starting coumadin

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2
Q

FFP

A

-Contains factors VII, IX, X, II (diluted), fibrinogen, proteins C and S
-Onset: 1-4 hours; duration of action: less than/ equal to 6 hours
-Large administration of volume (200 mL per unit)

FFP - All coag factors, protein C and S, ATIII and fibrinogen. Highest concentration of ATIII

-When to use FFP: any coagulation disorder including Antithrombin III deficiency

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3
Q

Vitamin K (phytonadione)

A

-Cofactor for hepatic production of factors VII, IX, X, II
-Onset: 6-10 hours (PO;) 1-2 hours (IV)
-IV if major bleeding, or emergent procedure (≤6 hours)
-

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4
Q

PCC (Kcentra®)

A

-Contains factors, including VII, IX, X, II (at a concentration 25x FFP)
-Onset: 5-15 minutes
-Duration of action: 6-8 hours
-Contains heparin – contraindicated in patients with HIT
-Contraindicated in disseminated intravascular coagulation (DIC) due to high risk of thrombosis

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5
Q

aPCC (FEIBA®)

A

-Contains factors VIIa (activated), IX, X and II
-Onset: 15-30 minutes
-Duration of action: 8-12 hours
-Consider use in patients with HIT
-Higher thrombotic risk due to activated factor VII

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6
Q

Heparin

A

-Binds antithrombin III (ATIII)
unfractionated heparin (UFH): Inhibits thrombin and some factor Xa
Enoxaparin (Lovenox): Inhibits factor Xa and thrombin
Reversal: protamine
Consider pre-medicating with corticosteroids and antihistamines in those with prior exposure to protamine or fish allergy (potential for anaphylactoid reactions)
Protamine can cause hypotension and bradycardia

Heparin – cleared by reticuloendothelial system (macrophages, spleen). SE = osteoporosis and alopecia
Lovenox vs heparin – Lovenox has lower bleeding risk, mortality, and recurrent DVT risk

-Determine effectiveness of Lovenox
-Check factor Xa levels
-Unlike heparin, Lovenox weakly reversed by protamine

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7
Q

Dabigatran (Pradaxa)

A

Inhibits thrombin
Reversal: Idarucizumab (Praxbind- Binds to both thrombin-bound and free dabigatran with higher affinity than thrombin); PCC; Reversed with dialysis

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8
Q

Direct Oral Anticoagulants

A

Direct Oral Anticoagulants: Apixaban (Eliquis), Betrixaban (Bevy), Edoxaban (Savaysa), Rivaroxaban (Xarelto)
Direct Oral Anticoagulants: Apixaban (Eliquis), Betrixaban (Bevyxxa), Edoxaban (Savaysa), Rivaroxaban (Xarelto)

Reversal: Andexanet alfa (Andexxa); PCC

andexanet alfa/ Andexxa= decoy- receptor for factor Xa inhibitor molecules

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9
Q

Intravenous Direct Thrombin Inhibitors

A

Intravenous Direct Thrombin Inhibitors: Argatroban, Bivalirudin (Angiomax)
Inhibits thrombin
Reversal: FFP

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10
Q

Thrombolytics

A

Alteplase (Activase®, Cathflo Activase®), Tenecteplase (TNKase®)
-Initiates fibrinolysis by binding to fibrin in a
thrombus, converting plasminogen to plasmin
-Reversal: Cryoprecipitate, Aminocaproic acid (Amicar- Binds competitively to plasminogen; blocking binding of plasminogen to fibrin and the subsequent conversion to plasmin, resulting in fibrinolysis

-MOA tPA:
-Activates plasminogen, breaks down fibrinogen
-Reverse= aminocaproic acid
-Contraindications:
-Absolute= active internal bleeding, recent CVA or neurosurgery, recent GI bleed, intracranial pathology
-Relative= surgery past 10 days, recent organ biopsies, recent delivery, recent major trauma, uncontrolled hypertension

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11
Q

Antiplatelets

A

Bleeding associated with Plavix: Tx is platelets

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12
Q

Uremia

A

Uremia inhibits release of vWB
Best acute (emergent) treatment for bleeding with uremia is DDAVP. HD takes too long, but used for all other cases

Uremic platelet dysfunction – first line is DDAVP. Cryo is 2nd. HD is 3rd

Platelet disorder will have what coagulation lab abnormality: increased bleeding time (PT and PTT not reliably affected)

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13
Q

Direct thrombin inhibitors

A

Fondaparinux – direct thrombin inhibitor (factor IIa)
Argatroban = Administered IV, liver metabolism. Follow PTT
Bivalirudin = Administered IV, renal metabolism. Follow PTT
Dabigatran (Pradaxa) = oral, Idarucizumab is the reversal, Can also be dialyzed

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14
Q

Direct Factor Xa inhibitors

A

Direct Factor Xa inhibitors – Hold 2-3 days before surgery
Rivaraxaban (Xarelto) – oral –. Avoid in patients with kidney disease, metabolized in kidney
- Reversal - Andexanet alfa or PCC
Apixaban (Eliquis). – oral – avoid this in patients with liver disease – hepatic clearance
- Reversal Andexanet alfa or PCC
Need to adjust for renal insufficiency. Less bleeding cx vs warfarin with above

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15
Q

Continuation of Statin therapy

A

Continuation of Statin therapy perioperatively decreases all-cause mortality

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16
Q

Insulin pre-operatively

A

Insulin pumps should be continued at sleep basal rates;
On the morning of surgery, take 50% of intermediate-acting (NPH) or long-acting insulin
Short-acting insulin should be held
Regular insulin is considered short acting and should be held

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17
Q

TEG parameters

A

R value = Time elapsed until clotting begins = represents activation of clotting factors = if high, give FFP
- 5-10 minutes is normal
MA (maximum amplitude) – measures function of platelets and fibrin – represents maximum clot strength
- < 50 mm = transfuse platelets if the patient is actively bleeding. Can also give DDAVP
Alpha angle = speed of clot strengthening, estimates fibrinogen level
- < 45 degrees = deficiency in fibrinogen = Give Cryoprecipitate
LY30 (lysis at 30 minutes) – measure of fibrinolysis – normal is 0-3%
- > 3% = Give tranexamic acid
K time – Give cryo if high
- 1-3 minutes is normal

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18
Q

Prothrombin complex

A

Facto V, X, calcium, platelet factor 3, prothrombin  forms on platelets catalyzes the formation of thrombin

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19
Q

Thrombin

A

Thrombin (Factor II) = key to coagulation
Converts fibrinogen (factor I) to fibrin (factor Ia)
Activates V and VIII and platelets

Fibrin + platelets = platelet plug
Fibrin cross links platelets by binding GpIIb/IIIa

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20
Q

Antithrombin III Key to anticoagulation

A
  • Binds and inhibits thrombin (II)
  • Inhibits factor II (thrombin), IX, X, XI
  • Heparin activates AT-III
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21
Q

Protein C

A

inhibits factor V and VIII, and degrades fibrinogen

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22
Q

Activated Clotting Time

A

Want ACT 150-200 for full dose AC, >480 for cardiac bypass

*useful measure of anticoagulation during major cardiovascular surgery

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23
Q

Cryoprecipitate

A

Cryoprecipitate – Has highest levels of vWF-VIII, fibrinogen
- Used in von-Willebrand’s and hemophilia A (VIII)

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24
Q

Glanzmann’s thrombocytopenia

A

Glanzmann’s thrombocytopenia - GpIIb/IIIa receptor deficiency on platelets, prevents fibrin from linking platelets together
Prolonged bleeding time, normal PT, PTT
Fibrin usually binds the receptors together.
Dx: platelet function analyzer
Tx: Platelets

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25
Q

Bernard Soulier

A
  • GpIb receptor deficiency on platelets (Can’t bind to collagen).
    Prolonged bleeding time, normal PT, PTT
    Dx: platelet function analyzer
    Tx: platelets
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26
Q

Hemophilia A

A

Hemophilia A – Give factor VIII (best) or cryo
Hemarthrosis -> do no aspirate tx Give factor VIII Ice,
Can get alloantibodies if given factorsIf patient has high inhibitory titers  give factor VII
For major surgery Preop levels: 80 to 100 percent for hemophilia A, taper post op levels to 50% for 10-14 days

-Factors missing in Hemophilia A:
-Hemophilia A = Factor VIII, prolongation of PTT
-Tx= factor VIII or cryo

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27
Q

Hemophilia B

A

Hemophilia B – Give factor IX or FFP
Hemarthrosis -> do no aspirate tx Give factor IX
If patient has high inhibitory titers  give factor VII
For major surgery Preop levels: 60 to 80 percent for hemophilia A, taper post op levels to 50% for 10-14 days

-Factors missing in Hemophilia B:
-Hemophilia B= Factor IX, prolongation of PTT
-Tx= factor IX or FFP

28
Q

Von Willebrand’s disease

A

Von Willebrand’s disease
MC congenital bleeding issue
Epistaxis = MC sx
PT normal, PTT can be normal or high
Prolonged bleeding time (ristocetin test) = dx
Type I (Autosomal Dominant) - MC 70% mild symptoms. Low level of vWF. #1 treatment for surgical prophylaxis = DDAVP. #1 treatment for acute bleeding recombinant VIII:vWF.
Type II (Autosomal Dominant) - defect in vWF. Tx: Recombinant factor VIII:vWF, Some variants can be treated with Cryo or DDAVP
Type III (Autosomal recessive) - Complete deficiency of vWF. most severe. Tx: Recombinant VIII:vWF,. DDAVP and cryo will not work for type III

-Von Willebrand’s Disease
-Type I: MC, reduced quantity of vWf, tx= desmopressin (for most patients) or cryoprecipitate -Type II: Dysfunctional vWF, tx= desmopressin or cryoprecipitate
-Type III: Complete absence of vWF, desmopressin does not work, tx= cryoprecipitate or Factor VIII replacement

29
Q

Anti-thrombin III deficiency

A

Will have heparin resistance
Tx: Recombinant ATIII or FFP (Has highest concentration of anti-thrombin III) then try heparin again. 2nd line is switch to direct thrombin inhibitor

-Tx= ATIII concentrate or FFP, prior to heparin admin; then start on long-term anticoagulant

30
Q

Anti-phospholipid syndrome

A

Anti-phospholipid syndrome
Thrombosis, venous AND arterial
Anti-cardiolipin and lupus anticoagulant antibodies
Cardiolipin is a mitochondrial phospholipid.
Hypercoagulable AND elevated PTT (does not correct with FFP)
Tx: heparin and warfarin

-Antiphospholipid syndrome:
-Hx: symptoms of Lupus, prior DVTs, recurrent pregnancy losses
-Prolonged PTT but are hypercoaguable
-Caused by antibodies to cardiolipin and lupus anticoagulant
-Tx: heparin bridge to coumadin

31
Q

HIT

A

HIT
- IgG ab to platelet factor 4. IgG binds to heparin after formation of heparin-platelet factor 4 complex
- Patients develop a white clot
- Arterial and venous clots
- Dx: ELISA ab test (quickest to get) Highly sensitive, low specificity. If positive, then get serotonin release assay (send out)
o If ELISA is positive, then start argatroban
- Platelet transfusion is contraindicated
- Tx: argatroban (Liver metabolism), bivalirudin (renal excretion), Lepirudin (renal excretion), or fondaparinux then warfarin

-Patient on coumadin undergoes surgery and following surgery platelets drop >50%:
-Concern for Heparin Induced Thrombocytopenia
-Suspicion with 4Ts score (thrombocytopenia, timing, thrombosis, and other possible causes)
-ELISA testing anti-platelet-factor-4 for initial screening
-Serotonin release assay for confirmation
-Stop heparin immediately with sufficient clinical suspicion
-Start safe anticoagulation (argatroban= classic; bivalirudin or fondaparinux also options)

32
Q

Phlegmasia cerulea dolens

A

Phlegmasia cerulea dolens – blue leg. Can lead to gangrene of leg. Occurs with Ileofemoral DVT.
- Tx: catheter directed thrombolytic. If threatened  open thrombectomy.
- 50% of these people have CA somewhere
Phlegmasia alba dolens – white leg, less severe

33
Q

Post thrombotic syndrome

A

Pain, cramping, swelling, sensation of heaviness, ulcers
Prevent with catheter directed thrombolytics for early DVT
Can affect patients up to 2 years after dx – chronic valvular disruption

34
Q

MCC of death after gastric bypass

A

PE

35
Q

CABG just had an MI

A

Don’t do CABG if the patient just had an MI. 15% mortality

36
Q

Bergman’s triad

A

Bergman’s triad – mental status change, petechia, dyspnea.
- Fat emboli

37
Q

May-Thurner syndrome

A

May-Thurner syndrome
Compression of left common iliac vein by right common iliac artery and sacrum
Predisposes patients to thrombosis
MC presentation  acute left iliofemoral DVT with left leg swelling
Treatment is AC, thrombolytics and stent placement

38
Q

Preventing hypothermia in the OR

A

Best measure  increase temperature in the room and forced warm air (bair hugger)

39
Q

SCD

A

SCD – improves venous return but also promotes fibrinolysis (release of tPA)
Left leg 2X more common for DVT left iliac vein compressed by right iliac artery = May-Thurner syndrome

40
Q

Bridging

A

Only need to bridge patients for elective surgery if CHADSVASC score is > 7 or CHADS score > 5
Prosthetic mitral valve has a much high risk of thrombosis vs prosthetic aortic valve (higher flow rate)
Bridging is not needed for aortic valves!!

41
Q

Thrombotic thrombocytopenic purpura

A

-Moschcowitz syndrome
-Deficiency or inhibition of ADAMTS13, which leaves large von Willebrand factor multimers to increase platelet adhesion and activate coagulation in arterioles and capillaries
Sx: thrombocytopenic purpura, neurologic manifestations due to microvascular disease in the brain, kidney injury or hematuria due to microvascular disease in the kidney, hemolytic anemia due to destruction of red cells, and fever

42
Q

Coagulation factors not synthesized in liver

A

Factor VIII, desmopressin

43
Q

Factor with the shortest half-life

A

Factor VI

44
Q

Patient presents with DVT and strong family history of DVT. What heritable blood clotting disorders would be on your differential?

A

-Factor V Leiden
-Prothrombin Gene Defect 20210
-Protein C and S Deficiency
-Antithrombin 3 Deficiency
-Hyperhomocystenemia

45
Q

Patients with hyperhomocysteinemia, how to treat this?

A

-Folic acid and B12

46
Q

PT/ PTT

A

-Coumadin= WEPT = Warfarin Extrinsic pathway PT
-PTT = intrinsic pathway

-Factors measured by PT/INR:
-Measures external pathway: factors II, VII, IX, X (1972)
-Best test for liver synthetic function
-Goal INR of 2-3 generally in anticoagulated patients

-Factors measured by PTT: all except VII
-Goal of 60-90 in anticoagulated patients

47
Q

Timing of surgery

A

Percutaneous angioplasty – wait 2 weeks before surgery
Bare metal stent – elective surgery delayed till 30 days
DES – elective surgery delayed until 6 months

48
Q

Any patient undergoing major intra-abdominal/pelvic operation for cancer or inflammatory bowel disease

A

needs 4 weeks anticoagulation

49
Q

PE

A

S1Q3T3 pattern for PE on EKG. A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain

Massive PE – hypotension!
- If low risk of bleed Treat with SYSTEMIC tPA
- If high risk of bleed (intracranial hemorrhage, s/p trauma/surgery)  catheter directed tPA

-MC VS change: tachycardia, tachypnea
-Respiratory alkalosis
-MC EKG finding: sinus tachycardia
-Classic S1Q3T3 finding is uncommon: classically associated with right ventricular strain due to pulmonary embolism. Characterized by a deep S wave in lead I, a pathological Q wave in lead III, and an inverted T wave in lead III.
-New Right bundle branch block
-Dx:
-CT Pulmonary Arteriogram= study of choice
-D-Dimer: sensitive- good for ruling out PE; high false positive rate
-Tx=
-Anticoagulation: Heparin bolus followed by drip for goal PTT 60-90
-Indications for thrombolytics: hemodynamic instability, right heart strain on echocardiogram
-Pulmonary embolectomy (Trendelenburg Procedure): uncommon, surgical option if contraindication for thombolytics

50
Q

AC after PE or DVT

A

In patients requiring anticoagulation for treatment of DVT or pulmonary embolism and no history of cancer:
 3 months anticoagulant therapy is recommended with dabigatran, rivaroxaban, apixaban over WARFARIN!!!

Provoked DVT/PE – Usually stop at 3 months
Unprovoked distal DVT – Usually stop at 3 months
Unprovoked PE or unprovoked proximal DVT  LIFE LONG AC
Recurrent VTE  lifelong AC
Any CA history and VTE  lovenox or direct oral anticoagulation. LIFELONG unless malignancy resolved.

51
Q

IVC filter

A

PE with IVC filter placed – comes from ovarian (Gonadal) veins, superior to IVC, or UE
Placement of IVC filters increases risk of DVT, IVC thrombosis, IVC perforation, can erode into duodenum or aorta
IVC filter perforated into duodenum  Ex lap, duodenal repair, IVC filter removal and IVC repair
IVCF filter indications
- DVT and low cardiopulmonary reserve (severe pulm HTN,RHF)
- Large, unstable, free floating IVC clot

52
Q

Homocystinuria

A

Homocystinuria – Inherited condition – autosomal recessive
Causes thrombosis in ARTERIES
Toxic metabolites to brain  seizures
Skeletal abnormalities  interferes with collagen cross linking
Tx: Pyridoxine vitamin B6, folate, B12

53
Q

Superficial vein thrombosis

A

Superficial vein thrombosis – if low risk (< 5 cm length, away from deep vein system)  NSAIDS and compression stockings
If high risk >5 cm length, near deep vein system  needs AC

54
Q

Distal DVT below the knee treatment

A

(2 options): Need to do 1 because it can extend into larger veins
- Anti-coagulate
- Repeat US surveillance

55
Q

DVT associated with a central line

A

If you find a DVT associated with a central line, and still need the line, the recommendation is to start AC, and remove the line in 5 days to avoid embolus

56
Q

Frailty index

A

In patients over 65, the likelihood of developing periop complications is best measured by frailty index

57
Q

Thromboxane TXA2 (COX-1)

A

Secreted by platelets
Increases platelets aggregation and promotes vasoconstriction
Trigger release of Ca in platelets → exposes GpIb and GpIIb/IIIa receptors and causes platelet to platelet binding.
ASA irreversibly binds cyclooxygenase, decreasing TXA production for the life of the platelet (platelets don’t have nuclear material) – results in decreased TXA production and decreased platelet aggregation

58
Q

Prostacyclin PGI2 (COX-2)

A

Secreted from the endothelium.
Decreases platelet aggregation, promotes vasodilation, causes bronchodiliation
Increases cAMP in platelets
ASA irreversibly binds cyclooxygenase, but cyclooxygenase is re-synthesized in endothelium (has nuclear membrane unlike platelets) – results in normal PGI production and platelet inhibition

59
Q

Omentum

A

Has a dense amount of tissue factor used as hemostatic agent

60
Q

Blood transfusions

A

Stored PRBC lasts 3 weeks
Type and screen – Looks for preformed abs to minor HLA antigens.
Type and crossmatch – same as above but holds units
MCC of mortality from transfusion is TRALI

Blood is tested for Hep B, Hep C, HIV, West Nile, HTLV
MC contaminant in transfusions- staph epidermidis
MC contaminant in platelets  staph epidermidis
Platelets (stored at room temperature) are MC product to have contamination
Platelets lasts for 5 days stored
All blood products have risk of transmitting HIV and hepatitis C EXCEPT albumin and immunoglobulins

61
Q

CMV negative prbc

A

CMV negative prbc – given to
1. CMV sero-negative pregnant mothers
2. Organ/bone marrow transplant donor/recipient
3. HIV
4. Low birth weight infants

62
Q

Platelet transfusion indications

A

Platelet transfusion indications – one 6 pack of platelets = 1 unit = should raise platelets by 50,000
- <10,000 (has high risk for spontaneous bleeding))
- <20,000 with infection or bleeding risk (post op patients)
- <50,000 only with active bleeding or pre-procedure
- Contraindication for transfusion of platelets: TTP, HUS, HELLP, HITT

63
Q

Platelet transfusion indications

A

-One 6 pack of platelets = 1 unit = should raise platelets by 50,000
- <10,000 (has high risk for spontaneous bleeding))
- <20,000 with infection or bleeding risk (post op patients)
- <50,000 only with active bleeding or pre-procedure
- Contraindication for transfusion of platelets: TTP, HUS, HELLP, HITT

64
Q

Acute hemolytic transfusion reaction

A

Acute hemolytic transfusion reaction – 2/2 to ABO incompatibility
- Preformed recipient abs against donor RBC ABO antigens
- Type II hypersensitivity reaction. Hemolysis.
- Chills, fevers, Hypotensive, DIC, these patients are really sick
- Will see RED URINE (hemoglobinuria)
- Hemolytic anemia
- Dx: low haptoglobin (<50), high free hgb, high Unc-bili, high LDH
- Tx: fluids and pressors

65
Q

Febrile (nonhemolytic) transfusion reaction

A

Febrile (nonhemolytic) transfusion reaction = MC transfusion reaction
- Sx: FEBRILE is the key to the presentation!!!!, But NO hemolysis
- Cytokines released from DONOR WBC
- MC occurs with platelets!!
- Tx: WBC/platelet filter for future transfusion

66
Q

Urticaria

A

Urticaria – OR JUST ANY RASH (at IV site)
- From recipient antibodies to donor plasma proteins
- MCC is IgA deficient patient with preformed IgE antibodies to IgA
- Tx: 1st slow the transfusion rate, 2nd Histamine blockers, supportive

67
Q

TRALI

A

Transfusion-related acute lung injury
Donor abs binds to recipients WBC then lodge in lung
-acute, noncardiogenic pulmonary edema associated with hypoxia that occurs during or after a transfusion

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