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Advanced Principles of Anesthesia > Week 4 - Hematology and Anesthesia > Flashcards

Week 4 - Hematology and Anesthesia Flashcards

1
Q

What factor is synthesized by the endothelium?

A

von Willebrand factor (cofactor for adherence of platelets to subendothelial layer)

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2
Q

What is the basic outline of the phases of hemostasis?

A
  • Vasoconstriction
  • Primary Hemostasis (Platelet Plug – ends with unstable clot) – includes adhesion, activation, and aggregation
  • Secondary Hemostasis (ends with stable platelet plug) – Coauglation cascade (intrinsic, extrinsic, common)
  • Tertiary Hemostasis (fibrinolytic system)
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3
Q

Describe the vasoconstriction phase of hemostasis.

What are the mediators?

A

When endothelial lining of blood vessel is disrupted, the vessel contracts to cause a tamponade and decrease blood flow:

  • autonomic nervous system reflexes
  • thromboxane-A2
  • ADP

Areas adjacent to the injury vasodilate

  • distributes blood to surrounding organs/tissues
  • bring factors and platelets to injured site
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4
Q

What are the three stages of primary hemostasis?

A

Adhesion

Activation

Aggregation

*results in formation of unstable platelet plug

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5
Q

Describe the adhesion stage of primary hemostasis

A

vWF is mobilized from within the endothelial cells and emerges from the endothelial lining
-vWF makes the platelet “sticky” and allows them to adhere to the site of injury

Glycoprotein Ib receptors emerge from the surface of the platelet and adheres to vWF on the endothelial surface

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6
Q

Describe the activation stage of primary hemostasis. What mediators are released? (12)

A

Binding of GpIb to vWF causes platelet activation – platelets dislike structure swells and becomes oval and irregular
-GpIIb-IIIa receptor complex project on surface of the platelet

Binding of GpIb to vWF causes platelet degranulation releasing:
-vWF, fibrinogen, fibronectin, histamine, epi, platelet factor 4, platelet growth factor, serotonin, ADP, ATP, Thromboxane A2, thrombin

  • Thromboxane A2 and ADP will activate other platelets and recruit them to the sites
  • Thrombin activates coagulation factors (secondary hemostasis) and influence recruitment of platelets to injured site
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7
Q

Describe the aggregation stage of primary hemostasis

A

GpIIb-IIIa receptor complex links to other activated platelets

These mediators are responsible for platelet aggregation and form a primary unstable clot

  • in less threatening injuries, this may be enough to maintain hemostasis
  • in larger injuries, activation of coagulation cascade is required
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8
Q

What are examples of drugs that block the GpIIa-IIIb receptor complex?

A

Abciximab

Tirofiban

Eptifibatide

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9
Q

What are the clotting factors and their names?

A 
I - Fibrinogen*
II - Prothrombin*
III - Tissue factor or Thromboplastin*
IV - Calcium*
V - Proaccelerin
VI 
VII - Proconvertin
VIII - Antihemophiliac
vWF - von Willebrand
IX - Christmas
X - Stuart-Prower
XI - Plasma thromboplastin anteceden
XII - Hageman
XIII - Fibrin stabilizing*
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10
Q

What clotting factors are vitamin K dependent?

A

II
VII
IX
X

*warfarin is used to inhibit

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11
Q

All clotting factors are synthesized in the liver except which ones?

A

III - vascular wall and extravascular cell membranes - released from traumatized cells

IV (Calcium) - diet

vWF - endothelial cells

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12
Q

What are the factors in the intrinsic, extrinsic, and common pathways of the coagulation cascade?

A

Intrinsic = XII, XI, IX, VIII (12, 11, 9, 8)

Extrinsic = Tissue Factor (III) and VII (3 and 7)

Common = X, V, II, I

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13
Q

What causes activation of the extrinsic pathway of the coagulation cascade? What are the steps of activation?

A

Activated when injury occurs outside the vessel wall

i. e. organ trauma or crushing injuries
- tissue factor (factor III) activates factor VII which then activates the common pathway (factor X)

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14
Q

What causes activation of the intrinsic pathway of the coagulation cascade? What are the steps of activation?

A

Occurs with damage to blood vessels themselves

Injury –> Prekallikrein activates Factor XII –> XIIa activates XI w/ help from calcium –> XIa activates IX –> IXa and activated VIII with calcium activates Factor X

*Factor VIII is activated by Thrombine

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15
Q

What are the steps of activation in the common pathway of the coagulation cascade?

A

Factor X starts the common pathway

Factor V with help of Calcium (IV) converts Factor II (prothrombin) to Factor IIa (thrombin)

Thrombin (IIa) converts Factor I (fibrinogen) to Factor Ia (fibrin)

Factor XIII comes to stabilize the clot – forms cross-linked fibrin mesh to increase clot strength

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16
Q

What are the functions of Thrombin (factor IIa)?

A
  • Assists in activating factors V, VIII, I, and XIII
  • Recruits platelets to site of injury
  • Converts fibrinogen to fibrin (must be enough thrombin to activate fibrin)
  • Can also behave as anticoagulant – releases tPA from endothelial cells and stimulates protein C & S
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17
Q

What is the cell-based theory of coagulation and what are the three phases?

A

Newer concept that platelets, extrinsic and intrinsic pathways form a very interdependent relationship, not independently

Three Phases:

  • initiation
  • amplification
  • propagation

*explains why certain deficiencies fail to cause bleeding despite changes in lab values

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18
Q

Describe the initiation phase of the cell based theory of coagulation

A

Endothelial surface injury which exposes tissue factor (factor III)

  • TF makes the phospholipid surface acidic and less repellent to platelets
  • TF down-regulates anticoagulants that reside in the subendothelial layer (Antithrombin III)
  • TF activates Factor VII
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19
Q

Describe the amplification phase of the cell based theory of coagulation

A

Factor IX activates VIII, which activates X to produce more and more thrombin

Thrombin generation has a positive feedback to activate more clotting factors V, VIII, IX

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20
Q

Describe the propagation phase of the cell based theory of coagulation

A

All coagulation factors are actively influencing one another, promoting coagulation, and finally activating prothrombin, resulting in a large burst of thrombin

Enough thrombin must be present to convert fibrinogen to fibrin to the stable secondary hemostatic plug – from the burst of thrombin

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21
Q

Describe tertiary hemostasis/fibrinolytic system. What mediators are involved?

A

Counterbalance system that degrades fibrin

Starts with an increase in blood flow that washes away procoagulant mediators

  • thrombin: initially acting as a procoagulant now acts as an anticoagulant and activates other anticoagulant mediators
  • tissue factor pathway inhibitor: also calls to a stop to the fibrinolysis when clot has been digested
  • protein C & protein S: inhibit factor III, V, and VIII
  • antithrombin III: sequesters factors 9, 10, 11, 12, which inhibits thrombin
  • plasminogen is activated to plasmin which breaks down fibrin into fibrin degradation products
22
Q

What is the function of plasminogen in coagulation?

A
  • Plasminogen is synthesized in the liver and stored inactive as plasminogen
  • Plasminogen incorporates itself into the clot – when activated, it turns to plasmin and causes fibrin to degrade into fibrin degradation products
  • The blood then removes the waste products of the clot
23
Q

What is a normal platelet count value?

A

150,000 to 300,000

Thrombocytopenia = <100,000
Surgical risk = <50,000
Spontaneous bleeding = <20,000

*normal platelet count only counts the actual number of platelets present and doesn’t imply normal platelet function

24
Q

What does the PT (prothrombin time) lab evaluate? What is normal?

A

Evaluates Extrinsic Factors (III and VII) as well as Common pathway (X, V, II, I, XIII)

Normal = 12-14 seconds (reagent dependent – different at different labs)

  • test for warfarin
  • fails to ID specific factor, the existing problem may or may not cause bleeding
  • INR also evaluates extrinsic and common pathways independent of different lab settings – normal = 1.5-2.5
25
Q

What does the aPTT (activated partial thromboplastin time) lab evaluate? What is normal?

A

Evaluates Intrinsic Pathway (XII, XI, IX, VIII) as well as Common Pathway (X, V, II, I, XIII)
*identifies abnormalities in all factors except III and VII

Normal = 25-32 seconds

*test for heparin (intraop heparin is assess w/ ACT - normal = 90-150)

26
Q

How much must a factor deficiency be decreased by before evidence of prolonged PT or PTT can be appreciated?

A

30%

27
Q

What are the components of a TEG lab?

A

Clot Initiation:
-R time = clotting factors

Clot Strength:

  • K value = fibrinogen
  • Alpha angle = fibrinogen
  • Maximum amplitude = platelets, fibrinogen, factor II/III

Clot Stabilization:
-LY-30 = fibrinolysis

28
Q

What is a normal fibrinogen lab value? How do you treat a low level?

A

Normal >150 mg/dl (200-350)

Treat with fibrinogen or cryoprecipitate

29
Q

What does the D-Dimer lab measure? What is normal?

A

Measures degradation by-products of fibrinolysis

Normal = <500 mg/ml

30
Q

What does cryoprecipitate contain?

A

Fibrinogen, Factor VIII, Factor XIII, and vWF

  • used for hypofibrinogenemia (low fibrinogen levels)
  • 1 units cryo per 10kg body weight will raise fibrinogen level by 50 mg/dl
31
Q

What does prothrombin complex concentrate contain?

A

PCC 3 Factor contains 2, 9, 10

PCC 4 Factor contains 2, 7, 9, 10 (vitamin K dependent factors)
*can be used to reverse warfarin

32
Q

What is the universal donor and receiver for PRBC and Plasma?

A

PRBC:

  • donor = O
  • receiver = AB

Plasma:

  • donor = AB
  • receiver = O
33
Q

What phase of hemostasis does each of the following act?

  • Antiplatelet
  • Anticoagulants
  • Thrombolytics/Fibrinolytic
  • Antifibrinolytics
A

Antiplatelet = Primary

Anticoagulants = Secondary

Thrombolytics/Fibrinolytics = Tertiary (encourage breakdown of clot)

Antifibrinolytics = Tertiary (inhibit breakdown of clot) – i.e. TXA

34
Q

What are the anticoagulant recommendations for the management of patients with drug-eluding stents?

A

12 months of anti-platelet and ASA therapy

*bare metal stent - 4-6 weeks of anti-platelet and ASA

35
Q

What are the types of von Willebrand’s disease?

A
  • Quantitative or Qualitative deficiency in vWF
  • Usually inherited, but can be acquired

Type I = Quantitative deficiency (decreased number)
Type II = Qualitative deficiency (decreased function)
Type III = no vWF is detected

36
Q

What lab value is affected in von Willebrand’s disease?

A

will have elevated aPTT (factor VIII is intrinsic pathway)

normal PT (extrinsic pathway)

37
Q

How do you treat each type of von Willebrand’s disease?

A

Type I (Quantitative) and Type II (Qualitative) = DDAVP – causes release of vWF from endothelial cells

Type III = vWF concentrates sometimes with Factor VIII

38
Q

What factors are deficient in Hemophilia A, B, and C?

A

Hemophilia A = Factor VIII deficiency (most common 75%)

Hemophilia B = Factor IX deficiency

Hemophilia C = Factor XI

*inherited - on X gene and X linked recessive so affects mainly men

39
Q

What lab value is affected with hemophilia?

A

PTT will be prolonged (intrinsic pathway)

-then look at specific factor activities and mutation testing of genes

40
Q

How do you treat hemophilia?

A

Replace missing or nonfunctional clotting factor – in serious, life threatening bleeding maintain factor level above 50%

*if pt has severe deficiency the replacement factors can be seen as foreign and antibodies form against the factor

Hemophilia A - DDAVP is helpful in mild VIII deficiency because it stimulates release of vWF which stabilizes factor VIII

41
Q

What is Heparin-Induced Thrombocytopenia (HIT)?

A

Autoimmune life-threatening complication of exposure to heparin
-HYPERcoagulable state

HIT antibody activates platelets and this results in the removal of IgG coated platelets from body causes thrombocytopenia

  • bleeding is rare, at risk for blood clots
  • onset 5-10 days but can be less than 24 hours in previously exposed pts (w/in 3 months)
42
Q

What lab value is affected by HIT?

A

If platelet drop >50% or <100,000 in any pt receiving heparin

43
Q

How do you treat HIT?

A

Halt platelet activation – stop all heparin (includes heparin containing medications)

Therapeutic-dose anticoagulation with non-heparin anticoagulant (argatroban, bivalirudin, apixaban, rivaroxaban, dabigatran) – warfain is not a good option due to initial transient hypercoagulable state caused by depletion of protein C

*do not delay treatment for lab testing

44
Q

What is the Four T score that assesses risk of HIT?

A

Degree of Thrombocytopenia
Timing
Thrombotic events
Alternative causes for low platelets

45
Q

What are the types of HIT?

A

HIT Type I = non immune and caused by direct effect of heparin on platelets
*mild transient platelet drop that occurs within first 2 days after heparin (non clinically significant)

HIT Type II = IgG immunce mediated and antibodies to Platelet Factor 4
*clinically significant

46
Q

What is Disseminated Intravascular Coagulation?

A

Systemic process with potential for causing both thrombosis and hemorrhage

Process of coagulation and fibrinolysis becomes abnormal and (often massively) activated

*caused by some underlying pathology – does not occur in isolation

47
Q

What is the sequence of events in DIC?

A

Procoagulant exposure

Coagulation (can lead to consumption coagulopathy)

Fibrinolysis (generates fibrin degradation products – large amounts can interfere with fibrin clot formation and platelet aggregation)

End organ damage (from decreased perfusion, thrombosis, and or bleeding and underlying cause)

48
Q

What is acute/decompensated DIC? What will the labs look like?

A
  • Rapid onset and large amounts of procoagulant substances
  • Rapid consumption of coagulation factors and platelets that outpace their production
  • Liver is unable to remove FDPs (high levels can operate as a pathologic anticoagulant)
  • At risk for BLEEDING from consumption coagulopathy

LABS: prolonged PT/PTT, low fibrinogen, elevated D-Dimer, thrombocytopenia

49
Q

What is chronic/compensated DIC? What will labs look like?

A
  • Continuous or intermittent exposure to smaller amounts of procoagulants
  • Coagulation factors and platelet production are able to keep up with consumption rate
  • Liver is able to clear FDPs
  • THROMBOSIS risk, but many pts are asymptomatic

LABS: normal or mildly prolonged PT/PTT, normal fibrinogen, elevated D-Dimer, normal platelets

50
Q

What is Factor V Leiden Thrombophilia?

A

Gene mutation that makes factor V resistant to the inactivation by protein C – protein C cannot suppress coagulation due to resistance from Factor V

Higher risk for development of DVT

About 5% of caucasians

Advanced Principles of Anesthesia (31 decks)

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