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ABSITE > 2 Hematology > Flashcards

2 Hematology Flashcards

1
Q

What are the initial steps of primary hemostasis?

A

Subendothelial collagen exposure –> Platelet adhesion–> shape change –> granulation release (ADP, TXA2) –> Recruitment –> hemostatic plug (Aggregation)

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2
Q

What are the three initial responses to vascular injury?

A

Vascular vasoconstriction
Platelet adhesion
Thrombin generation

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3
Q

What initiates the intrinsic pathway?

A

Exposed collagen
Prekallikrein
HMW kininogen
Factor XII

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4
Q

What are the steps in the intrinsic pathway?

A

Exposed collagen/prekallikrein/HMW kininogen/factor XII

  • -> activates XI
  • -> activate IX, then add VIII
  • -> activate X, then add V
  • -> convert prothrombin (Factor II) to thrombin
  • -> thrombin then converts fibrinogen to fibrin
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5
Q

What initiates the extrinsic pathway?

A

Cellular injury –> release of tissue factor

Factor VII

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6
Q

What are the steps in the extrinsic pathway?

A

Cellular injury leads to release of tissue factor - reacts with VII

  • -> Activates X, then add V
  • -> convert prothrombin to thrombin
  • -> thrombin then converts fibrinogen to fibrin
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7
Q

What are the steps in the common pathway?

A

Prothrombin (Factor II) is converted to thrombin

–> Thrombin then converts fibrinogen to fibrin

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8
Q

What is the prothrombin complex?

A

X, V, Ca, platelet factor 3 and prothrombin
Forms on platelets
Catalyzes the formation of thrombin

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9
Q

What is the convergence point for both coagulation pathways?

A

Factor X

Needed for conversion of prothrombin to thrombin

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10
Q

Function of Tissue factor pathway inhibitor?

A

Inhibits factor X

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11
Q

Function of Fibrin

A

Links platelets together
Binds GpIIb/IIIa molecule
Forms a platelet plug - hemostasis

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12
Q

Role of XIII

A

Helps crosslink fibrin

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13
Q

Functions of thrombin

A

Key to coagulation
Converts fibrinogen to fibrin and fibrin split products
Activates factors V and VIII
Activates platelets

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14
Q

Function of Antithrombin III

A

Key to anticoagulation
Binds and inhibits thrombin
Inhibits factors IX, X and XI
Heparin activates AT-III (up to 1000x normal activity)

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15
Q

Function of Protein C

A

Vitamin K-dependent
Degrades factors V and VIII
Degrades fibrinogen

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16
Q

Function of Protein S

A

Vitamin K-dependent

Protein C cofactor

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17
Q

What enzymes regulate fibrinolysis?

A

Tissue plasminoagen activator
Plasmin
Alpha-2 antiplasmin

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18
Q

Function of Tissue plasminogen activator

A

Released from endothelium

Converts plasminogen to plasmin

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19
Q

Function of Plasmin

A

Degrades factors V and VIII, fibrinogen and fibrin

Causes degradation of platelet plug

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20
Q

Function of Alpha-2 antiplasmin

A

Natural inhibitor of plasmin

Releases from endothelium

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21
Q

Which factor has the shortest half-life?

A

Factor VII

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22
Q

Which factors are liable - activity is lost in stored blood, but not lost in FFP?

A

Factors V and VIII

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23
Q

Which factors is NOT synthesized in the liver? Where is is synthesized?

A

Factor VIII

Synthesized in endothelium

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24
Q

Which factors are vitamin K-dependent?

A

II, VII, IX, X

Proteins C & S

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25
Q

How long does it take for Vitamin K to be effective?

A

6 hours

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26
Q

How long does it take for FFP to be effective? How long does it last?

A

Immediate

Lasts 6 hours

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27
Q

Which factor is prothrombin?

A

Factor II

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28
Q

What is the normal half life of RBCs?

A

120 days

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29
Q

What is the normal half life of platelets?

A

7 days

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30
Q

What is the normal half life of PMNs?

A

1-2 days

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31
Q

Function and source of Prostacyclin (PGI2)

A

From endothelium
Decreases platelet aggregation, promotes vasodilation
Antagonistic to TXA2

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32
Q

Function and source of Thromboxane (TXA2)

A

From platelets
Increases platelet aggregation and vasoconstriction
Triggers release of calcium in platelets - exposes GpIIb/IIIa receptors and causes platelet-to-platelet binding
Platelet-to-collagen binding also occurs (GpIb receptors)

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33
Q

Contents of cryoprecipitate

A

Highest concentration of vWF-VIII
Used in von Willibrand’s disease, Hemophillia A (Factor VIII deficiency)
Has high levels of fibrinogen

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34
Q

Contents of fresh frozen plasma

A

High levels of all coagulation factors, protein C, protein S, and AT-III

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35
Q

Function of DDAVP and conjugated estrogens

A

Causes release of VIII and vWF from endothelium

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36
Q

What does PT assess?

A

Measures II, V, VII, X, fibrinogen

Best for liver synthetic function

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37
Q

What does PTT assess?

A

Measures all factors, except VII and XIII, fibrinogen

Goal PTT 60-90sec

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38
Q

Goal Activated Clotting Time?

A

Routine anticoagulation ACT 150-200sec

For pardiopulmonary bypass >460sec

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39
Q

INR level that is a relative CI for surgical proceedures

A

INR > 1.5

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40
Q

INR level that is a relative CI for central line placement, percutaneous needle biopsies or eye surgery

A

INR > 1.3

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41
Q

What is the most common cause of surgical bleeding?

A

Incomplete hemostasis

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42
Q

What is the most common congenital bleeding disorder?

A

Von Willebrand’s disease

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43
Q

Inheritance patterns for vW disease

A

Type I/II - AD

Type III - AR

44
Q

Function of vWF

A

GpIb receptor on platelets to collagen

45
Q

Coagulation test results in vWF disease

A

PT normal
PTT can be normal or abnormal
Prolonged bleeding time (ristocetin test)

46
Q

Which form of vWF disease is the most common? Symptoms?

A

Type I

Mild symptoms

47
Q

Which form of vWF disease has the most severe bleeding?

A

Type III

48
Q

What is the defect in Type I vWF disease? Treatment?

A

Reduced quantity of vWF

Tx: recombinant VIII:vWF, DDAVP (increased release of vWF), cryoprecipitate

49
Q

What is the defect in Type II vWF disease? Treatment?

A

Defect in vWF molecule itself, doesn’t work well

Tx: Recombinant VIII:vWF, cryoprecipitate

50
Q

What is the defect in Type III vWF disease? Treatment?

A

Complete deficiency of vWF

Ts: Recombinant VIII:vWF, cryoprecipitate

51
Q

Why do you not give DDAVP in type II/III vWF disease?

A

Because they have crappy vWF (type II) or no vWF (type III), trying to increase the release of vWF will have no effect

52
Q

Hemophilia A

A

VIII deficiency
Sex-linked recessive
Prolonged PTT, normal PT
Sx: joint bleeding, epistaxis, ICH, hematuria

53
Q

What are goals of VIII in Hemophilia A for surgery?

A

Need levels 100% pre-op

Keep >80% post-op for 10-14 days

54
Q

How do you treat Hemophilia A with joint bleeding?

A

Do NOT aspirate
Ice, keep joint mobile with ROM exercises
Give factor VIII concentrate or cryoprecipitate

55
Q

How do you treat Hemophilia A with epistaxis, ICH or hematuria?

A

Recombinant factor VIII or cryoprecipitate

56
Q

Why do Hemophilia A patients not bleed at circumcision?

A

Factor VIII crosses the placenta

57
Q

Hemophilia B

A

IX deficiency (Christmas disease)
Sex-linked recessive
Prolonged PTT, normal PT
Tx: Recombinant factor IX or FFP

58
Q

Factor VII deficiency

A

Prolonged PT and normal PTT
Bleeding tendency
Tx: recombinant factor VII concentrate or FFP

59
Q

Symptoms of platelet disorders

A

Bruising, epistaxis, mucosal bleeding, petechiae, purpura

60
Q

Causes of acquired thrombocytopenia

A

H2 blockers

Heparin

61
Q

Glanzmann’s thrombocytopenia

A

GpIIb/IIIa receptor deficiency on platelets - they cannot bind to each other
Fibrin normally links the receptors
Tx: Platelets

62
Q

Bernard Soulier thrombocytopenia

A

GpIb receptor deficiency on platelets - they cannot bind to collagen
vWF normally links GpIb to collagen
Tx: Platelets

63
Q

Uremia platelet dysfunction

A

Inhibits platelet function

Tx: hemodialysis, DDAVP, platelets

64
Q

Heparin-induced thrombocytopenia - Type I

A 
Self limited
Onset 2-3 days
Platelets ~100,000
Occurs in 10-20% patients
No antibodies
Tx: Monitor patient - do not need to stop Heparin
65
Q

Heparin-induced thrombocytopenia - Type II

A 
Severe
Onset 5-10 days
Platelets 10-20,000
Antiplatelet antibodies (IgG PF4)
Can also cause platelet aggregation/thrombosis
White clot
Test: Platelet factor 4(PFE4) antibody; seretonin assay
Tx: Stop heparin, start argatroban
66
Q

What is argatroban?

A

Direct thrombin inhibitor

67
Q

Disseminated intravascular coagulation (DIC)

A

Decreased platelets, low fibrinogen, high fibrin split products, high D-dimer
Prolonged PT/PTT
Initiated by tissue factor
Tx: treat underlying cause (i.e. sepsis)

68
Q

Anticoagulation effect of ASA

A

Inhibits cyclooxygenase in platelets and decreases TXA2
Platelets lack DNA - cannot re-synthesize COX, need to wait for new platelets to form
Stop 7 days before surgery - prolonged bleeding time
Reversal - platelets

69
Q

Anticoagulation effect of Clopidogrel (Plavix)

A

ADP receptor antagonist
Stop 7 days before surgery
Reversal - platelets

70
Q

Anticoagulation effect of Coumadin

A

Inhibits Vitamin K decarboxylation of clotting factors

Stop 7 days before surgery - bridge with Heparin

71
Q

Operative platelet goals for surgery?

A

Pre-op >50,000

Post-op >20,000

72
Q

Thrombolytic problems in prostate surgery?

A

Cane release urokinase, activates plasminogen, which causes thrombolysis
Tx: g-aminocaproic acid (Amicar)

73
Q

How do hypercoagulability disorders present?

A

Venous or arterial thrombosis
Emobli
DVT, PE, stroke

74
Q

Factor V Leiden mutation

A

Most common congenital hypercoagulability disorder
Factor V is resistance to activated protein C
Tx: heparin, warfarin

75
Q

Hyperhomocysteinemia

A

Hypercoagulability
Tx: Folic acid B12
(This is why they assess it in stroke patients)

76
Q

Prothrombin gene defect G20210 A

A

Hypercoagulabiltiy

Tx: Heparin, warfarin

77
Q

Protein C or S deficiency

A

Hypercoagulability

Tx: Heparin, warfarin

78
Q

Antithrombin III deficiency

A

Hypercoagulability
Can develop after previous heparin exposure (development of antibodies)
NOTE: Heparin will no longer work for them
Tx: recombinant AT-III concentrate or FFP, followed by Heparin, then warfarin

79
Q

Dysfibinogenemia, dysplasminogenemia

A

Hypercoagulability

Tx: heparin, warfarin

80
Q

Polycythemia vera

A

Defect in platelet function and extra RBCs, causes thrombosis
Keep Hct <48, platelets <400 before surgery
Tx: Phlebotomy, ASA

81
Q

Anti-phospholipid antibody syndrome

A

Not always associated with SLE
Procoagulant
Prolonged PTT but hypercoagulable
Caused by antibodies to cardiolipin and lupus anticoagulant (phospholipids)
Dx: prolonged PTT (not corrected with FFP), positive Russell viper venom time, false-positive RPR test for syphillis
Tx: Heparin, warfarin

82
Q

Causes of acquired hypercoagulability

A 
Tobacco*
Malignancy
Inflammatory states
Inflammatory bowel disease
Infections
Oral contraceptives
Pregnancy
Rheumatoid arthritis
Post-op status
Myeloproliferative disorders
83
Q

Cardiopulmonary bypass effect on hypercoagulability

A

Activates factor XII (Hageman factor)

Tx: Heparin to prevent

84
Q

Warfarin-induced skin necrosis

A

Occurs when starting coumadin without bridging with heparin
Due to short half-life of protein C/S; procoagulant factors outlive them
Patients with relative protein C deficiency are especially susceptible
Tx: Heparin if occurs

85
Q

Key elements in the development of venous thromboses

A

Virchow’s triad

Stasis, endothelial injury, hypercoagulability

86
Q

Key elements in the development of arterial thromboses

A

Endothelial injury

87
Q

Risk factors for DVT

A

Stasis, venous injury and hypercoagulability

88
Q

Post-operative treatment of DVT

A

1st - Warfarin for 6 months
2nd - Warfarin for 1 year
3rd or significant PE - Warfarin for lifetime

89
Q

Indications for IVC filters?

A

CI to anti-coagulation
Documented PE while on anti-coagulation
Free-floating IVC, ilio-femoral, or deep femoral DVT
Recent pulmonary embolectomy

90
Q

Treatment of pulmonary embolism

A

Shock, despite massive inotropes/pressors –> go to OR

Stable - Heparin (thrombolytics not shown to have an improvement in survival) or suction catherter-based intervention

91
Q

Most common source of PE

A

Ilio-femoral region

92
Q

g-Aminocaproic acid (Amicar)

A

Anti-fibrinolytic
Inhibits plasmin
Uses: DIC, persistent bleeding following cardiopulmonary bypass, thrombolytic overdose

93
Q

Warfarin (Coumadin)

A

Prevents vitamin K-dependent decarboxylation of glutamic residues on vitamin K-dependent factors

94
Q

Sequential compression devices

A

Improves venous return

Induces fibrinolysis - release of tPA (tissue plasminogen activator) from endothelium

95
Q

Heparin

A

Binds and activates anti-thrombin III (1000x more activity)
Reversed with protamine (binds heparin)
Half-life 60-90min
Cleared by reticuloendothelial system
Safe in pregnancy (does not cross placenta)

96
Q

Side effects of long-term use of Heparin

A

Osteoporosis, alopecia

97
Q

Protamine

A

Reverses Heparin by binding to it
Cross reacts with NPH insulin or previous protamine exposure
1% get protamine reaction

98
Q

Symptoms of protamine reaction

A

Hypotension
Bradycardia
Decreased heart function

99
Q

Low molecular weight heparin

enoxaparin, fondaparinux

A

Binds and activates antithrombin II, but increases neutralization of just Xa, Thrombin
Not reversed with protamine
Lower risk of HIT compared to unfractionated heparin

100
Q

Argatroban

A

Reversible direct thrombin inhibitor
Metabolized in lifer
Half-life is 50 min
Used in patients with HITT

101
Q

Bivalirudin (angiomax)

A

Reversible direct thrombin inhibitor
Metabolized by protinase enzymes in the blood
Half-life of 25 minutes

102
Q

Hirudin (Hirulog)

A

From leeches
Irreversible direct thrombin inhibitor
Most potent direct inhibitor of thrombin
High risk for beleding complications

103
Q

Ancrod

A

Malayan pit viper venom

Stimulates tPA release

104
Q

Thrombolytic medications

A

Streptokinase (high antigenicity)
Urokinase
tPA

105
Q

MOA thrombolytic medications

A

Activate plasminogen
Need for follow fibrinogen levels (<100 associated with increased risk/severity of bleeding
Tx for thrombolytic overdose: g-aminocaproic acid (Amicar)

106
Q

Contraindications to thrombolytic use

A 
Absolute:
- Active internal bleeding
- <3mo CVA/neurosurgery
- intracranial pathology
- recent GI bleed
Major:
- <10d surgery, organ biopsy, delivery
- Left heart thrombus
- Active peptic ulcer
- Recent major trauma
- Uncontrolled HTN
- Recent eye surgery
Minor:
- Minor surgery
- Rcent CPR
- Afib with mitral valve disease
- Bacterial endocarditis
- Hemostatic defects (renal or liver disease)
- Diabetic hemorrhagic retinopathy
- Pregnancy

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