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Anesthesia Pharm Exam 3 > Coagulation and Transfusion > Flashcards

Coagulation and Transfusion Flashcards

1
Q

Regulators of Hemostasis

A
  • vascular extracelular matrix and endothelial reactivity
  • platelets
  • coagulation proteins
  • inhibitors of coagulation
  • fibrinolysis
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2
Q

Clot Formation

A
    • coagulation cascade!*
  • tissue factor release
  • factor VIIa generation
  • plt activation
  • cellular and humoral activation pathways
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3
Q

Clot Prevention

A
  • PGI2 (prostacyclin) tPA, heparin sulfate, antithrombin III, protein C, endothelium derived relaxing factor (EDRF)
  • these are expressed to inhibit plt activation, fibrin formation, and provide for vascular patency
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4
Q

Platelet Activation

A
  • receptors on platelets bind to damaged blood vessel wall
  • form bridges w VWF to initiate platelet adhesion
  • once adhered, platelet surface receptor changes and causes platelet aggregation
  • upon aggregation, they expose surface factors that ativate coagulation cascade forming a hemostatic plug
  • issues: abnormalities in platelet number or function
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5
Q

How does aspirin work?

A
  • inhibits the synthesis of platelet thromboxaneA2 (factor that causes platelets to aggregate) by irreversible acetylation (inactivation) of cyclooxygenase
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6
Q

How does ibuprofen work?

A
  • block both prostaglandin and thromboxane formation by reversibly inhibiting COX activity
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7
Q

Aspirin, Ibuprofen MOA (visual)

A
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8
Q

Coagulation Cascade Visual

A
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9
Q

Inherited (Genetic) Hypercoagulability Risk Factors

A
  • inherited antithrombin deficieny
  • prothrombin G20210A mutation
  • Factor V Leiden
  • Dysfibrinogememia
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10
Q

Prothrombin G20210A Mutation

A
  • these pts have higher prothrombin levels (precursor for thrombin)
  • 2% population
  • heterozygous = 3x risk of thrombus
  • homozygous = very rare
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11
Q

Factor V Leiden

A
  • gene mutation so that procoagulant factor V is not inactivated by protein C
  • 5% presence in population
  • heterozygous = 3x risk of thrombus
  • homozygous = 18x risk of thrombus
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12
Q

Dysfibrinogememia

A
  • high levels or structurally defective fibrinogen, variants are either more or less susceptible to clot formation
  • high levels = 2x increase arterial thrombus
  • fibrinogen >450mg/dL = poor outcome for CVA pts
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13
Q

Protein C Deficiency

A
  • genetic anticoagulant issue
  • circulating anticoagulant
  • vitamin K dependent proteins that inhibit procoagulant factors V and VIII
  • decrease = 5x increased risk of VTE
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14
Q

Antithrombin III Deficiency

A
  • protease inhibitor that binds to thrombin
  • heparin facilitates this
  • heterozygous deficiency in 50% of pop
  • acquired ATIII deficiency after Heparin or DIC
  • homozygous ATIII deficiency is fatal
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15
Q

Lipoprotein(a)

A
  • inhibits fibrinolysis - similar to plasminogen
  • increased levels associated w VTE and CAD
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16
Q

tPA abnormalities

A
  • 2-3x increased risk of VTE
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17
Q

Exogenous Causes of HYPERcoagulability (visual)

A
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18
Q

Coagulopathic States Associated w Increased Risk of Bleeding (just because of genetics or comorbidities)

A
  • hemophilia
  • inherited plt disorders
  • von Willebrand dx
  • liver failure
  • renal failure (uremia)
  • DIC
  • dilutional coagulopathy
  • anticoagulant/antiplatelet therapy
  • other coagulation disorders (factor deficiencies)
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19
Q

Risk Factors for Bleeding in Surgical Patients (iatrogenic reasons)

A
  • advanced age
  • small body size, preop anemia (low RBC volume)
  • antiplatelet/antithrombotic drugs
  • preexisting coagulopathy
  • prolonged operation (long bypass time)
  • emergency operation (no preop labs)
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20
Q

Risk Factors for Bleeding in Surgical Patients (comorbidities)

A
  • HF
  • COPD
  • HTN
  • PVD
  • liver/renal failure
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21
Q

Antiphospholipid Antibodies

A
  • disease state associated w hypercoagulability
  • ie: lupus anticoagulants, anticardiolipin antibody, anti-B2-glycoprotein-1 antibody
  • thought to be 2/2: decreased thrombomodulin expression, increased TF expression, impaired protein C anticoagulation pathway
  • at risk for recurrent thrombotic events
  • usually require anticoagulation (coumadin)
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22
Q

Liver or Renal Failure

A
  • decreased production of anticoagulant factors (ATIII, Protein C and S, plasminogen)
  • increases platelet activation
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23
Q

Blood Stasis

A
  • pre-op or post-op immobility
  • low CO, afib
  • Virchow’s Triad
  • metabolic syndrome
  • cancer
  • age
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24
Q

Virchow’s Triad

A
  • low flow state
  • endothelial damage
  • dysfunctional blood components
25
Q

Metabolic Syndrome

A
  • abdominal obesity
  • HTN
  • increased glucose
  • increased cholesterol
  • associated w endothelial dysfunction and increased platelet aggregation
26
Q

HIT

A
  • 0.5-5% incidence in pts tx w heparin in past 5 days
  • unexplained drop in platelets by 50% (<150,000)
  • 7% to 50% of heparin-treated patients generate heparin-PF4 antibodies, especially following cardiovascular surgery (also ortho and neuro)
  • antibody T1/2 90 days
  • increased risk of thrombosis
    • if HIT suspected, start treatment immediately, don’t wait for labs!*
27
Q

Heparin/HIT MOA

A
  • heparin binds to platelet factor 4 (PF4)
  • antibodies recognize the complex, release microparticles that stimulate thrombin aggregation and thrombin are formed
  • excessive thrombus leads to endothelial damage and TF production and more prothrombosis
  • increased risk of DVT, VTE, PE, MI, CVA, arterial occlusion
  • -* thrombus risk 40-75%
28
Q

High Risk HIT Pops

A
  • females
  • malignancy
  • high PF4 titer
  • increased risk of DVT, VTE, PE, MI, CVA, arterial occlusion
29
Q

HIT Diagnosis

A
  • platelet drop by 50% (<150,000)
  • new thrombus within 5-14 days of heparin tx
  • R/O sepsis, IABP destruction of platelets, drug induced thrombocytopenia
30
Q

Rapid Onset HIT S/S

A
  • platelet drop within minutes to hours 2/2 previous exposure to heparin within past 3 months
  • hypotension, pulmonary hypertension, and/or tachycardia, occur 2 to 30 minutes after intravenous heparin bolus
  • observed intraoperatively and can present as anaphylaxis, usually accompanied by acute thrombocytopenia
  • can also occur days to weeks after stopping heparin (“delayed onset HIT”), and should be considered if a recently hospitalized, heparin-treated patient presents with thrombosis
31
Q

HIT Treatment

A
  • STOP heparin and eliminate all sources (flushes)
  • initiate anticoagulation w direct thrombin inhibitor (ie: lepirudin, argatroban, desirudin, or bivalirudin)
32
Q

Direct Thrombin Inhibitor

A
  • argatoban
  • lepirudin
  • desirudin
  • bivalirudin
33
Q

Risk Factors for Bleeding

A
  • advanced age
  • low preop RBC volume
  • antiplatelet or antithrombotic medications preop
  • redo or emergency surgery
  • comorbidities on previous flashcards
34
Q

Thrombocytopenia

A
  • platelet <50,000
  • high risk for bleeding!
35
Q

Hemophilia

A
  • recessive X linked disorder

- A: factor VIII deficiency

  • 1:5k - 10k males
  • recombinant Factor VIII

- B: factor IX deficiency

  • 1:20k - 34k makes
  • recombinant Factor IX
36
Q

von Willebrand Factor

A
  • glycoprotein that allows platelet adhesion and aggregation under arterial flow
  • a carrier for coagulation factor VIII
37
Q

von Willebrand Disease

A
  • partial quantitative deficiency (Type I) may respond to DDAVP
  • qualitative deficiency (Type II) has 4 variants
  • total deficiency (Type III)
  • can be acquired
38
Q

Treatment for von Willebrand Disease

A
  • measure vWF activity
  • administer factor VIII/vWF concentrate, IGG, cryoprecipitate, plasma pheresis
  • short t1/2 of vWF may require redosing
39
Q

DIC

A

- thrombocytopenia (platelets <100k in 50-60% and <50k in 10-15%)

  • >4 dats ICU or 50% decrease in ICU = 4-6x mortality
  • coagulopathy: prolonged PT or aPTT, bleeding
  • fibrinogen consumption: low levels indicate severe DIC, fibrinogen and D-dimer are innacurate
  • reduced antithrombin and Protein C levels
40
Q

PT

A
  • prothrombin time
  • normal 11-13 seconds
  • addresses the extrinsic and common coagulation pathways
  • primarily used to monitor long-term use of anticoagulant therapy through the INR
41
Q

aPTT

A
  • activated partial thromboplastin time
  • normal is 25-38 seconds
  • adresses the intrinsic and common coagulation pathways
  • used to monitor heparin therapy, screen for hemophilia A and B, detect clotting inhibitors
42
Q

Fibrinogen

A
  • normal is 2-4 g/L
  • decreased levels indicate DIC, liver disease or dilutional coagulopathy
  • fibrinogen (Factor I) is a glycoprotein synthesized in the liver and cleaved by thrombin to produce fibrin monomer, the basis of clot formation
43
Q

Platelet Aggregation Studies

A
  • done if pt has normal platelets but is not clotting
  • used to classify qualitative platelet abnormalities in adhesion, release, or aggregation
  • normal range is >65%
44
Q

TEG (visual)

A
45
Q

Components

A
46
Q

PRBCs remain in circulation for how long?

A
  • 120 days
  • old or dysfunctional cells removed by the spleen
  • shelf life up to 42 days
  • old = increased 2,3 DPG (10% at 42 days)
47
Q

Synthesis of PRBC

A
  • synthesis dependent upon erythropoietin and iron
  • erythropoietin increases w anemia or hypoxia
48
Q

CADET face Right

A
  • increases HbB affinity for 02

CO2

Acid

DPG

Exercise

Temperature

49
Q

Universal Donor

A

Type O

50
Q

Universal Acceptor

A

Type AB

51
Q

Rh Compatibility

A

Rh- gets Rh-

Rh+ can get either Rh- or Rh+

always give Rh- to Rh- women of childbearing age

52
Q

Acute Hemolytic Reaction

A
  • ABO incompatibility
  • occurs in 1:30k
  • s/s = agitation, N/V, dyspnea, fever, flushing, hypotension, tachycardia, HgBnuria
  • renal failure from ATN or DIC is worst case scenario
  • fever, nonhemolytic rxn occurs 0.1-1% of transfusions
53
Q

Platelets

A

T1/2 7-10 days

  • 150 - 300,000
  • transfused in 4- or 8-packs (can expect plt count to increase 15-30)
  • total count and function of plts important
    • avoid elective surgery w platelet count <50k*
    • see if pt was taking ASA or ibuprofen*
54
Q

FFP

A
  • contains procoagulants, anticoagulants, albumin, and immunoglobulins from plasma that aren’t in PRBCs
  • indicated for the treatment of complex coagulopathies in which multiple coagulation factors and inhibitors are depleted
  • must be kept cold between 1C (34F) and 6C (42F)
  • can be kept thawed 5 days at these temps
  • ABO compatibility but not Rh
  • AB is universal donor for FFP
  • INR >1.5 times normal to be effective tx
55
Q

Adverse Side Effects of FFP

A
  • 1-3% risk of allergic reaction
  • Hypocalcemia w high volume FFP (tx w calcium chloride 500-1000 mg or 1/2 to 1 amp)
  • TRALI occurs 1:2k to 1:7.5k transfusions (but incidence is down since FFP from males)
56
Q

Albumin

A
  • colloid osmotic pressure of 5% albumin similar to that of plasma
  • volume expander
  • no effect on hepatic or renal function
  • no effect on coagulation parameters
57
Q

Hydroxyethyl Starches

A
  • synthetic colloids
  • effective volume expanders
  • high dose (>20 ml/kg) may affect bleeding
58
Q

Cryoprecipitate

A
  • 150-250mg fibrinogen per unit
  • each bag contains 5-10 u of cryoppt
  • each unit increases plasma fibrinogen 100mg/dL/5kg body weight
  • proper level of fibrinogen not known (>150-200mg/dL?)
59
Q

Recombinant Factor VIIa (NOVOseven)

A
  • indicated for hemophilia w F8, F9 antibodies and F7 deficiency
  • dose 90-100 ug/kg (up to 400ug have been given without thrombosis)
  • used for trauma and surgical bleeding (but not supported by literature)
  • initial dose 20-70 ug/kg
  • decreases bleeding and re-ops but increases CVA and thrombosis

Anesthesia Pharm Exam 3 (6 decks)

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