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Chapter 2 - Hematology Flashcards

1
Q

What are the three initial responses to vascular injury

A

Vasoconstriction, platelet adhesion, thrombin generation

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2
Q

Intrinsic Pathway starts with?

A

exposed collagen, prekallikrein, HMW kininogen, factor XII

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3
Q

Intrinsic pathway steps?

A

collagen, prekallikrein, hmw kininogen, factor XII—> activate XI —-> IX, then add VIII—> activate X then add V —> convert prothrombin (factor II) to thrombin—> thrombin converts fibrinogen to fibrin

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4
Q

Extrinsic pathway starts with?

A

Tissue factor from incured cells + factor VII

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5
Q

Steps of extrinsic?

A

tissue factor + factor VII —> activate X then add V—> confert prothrombin to thrombin —>thrombin then converts fibrinogen to fibrin

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6
Q

What is the prothrombin complex and what does it do?

A

X, V, Ca, PF-3, Prothrombin. It forms on platelets and catalyzes the formation of thrombin

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7
Q

What is the convergence point for both intrinsic and extrinsic paths?

A

Factor X

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8
Q

What dies the Tissue factor pathwa inhibitor do?

A

Inhibits factor X

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9
Q

What does Fibrin do?

A

combines with platelets to form the platelet plug to create hemostasis

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10
Q

What does factor XIII do?

A

helps crosslink Fibrin

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11
Q

Why is thrombin the key to coagulation? What does it activate?

A

Converts Fibrinogen to Fibrin and Fibrin split products. It activates factors V and VIII. It activates platelets

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12
Q

What is Protein C, what does it do?

A

Vitamin K-dependen, degrades factors V and VIII, Degrades fibrinogen

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13
Q

What is protein S, what does it do?

A

Vitamin K dependent, cofactor of Protein C

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14
Q

TPA is released from where and does what?

A

Released from endothelium, converts plasminogen to plasmin

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15
Q

Plasmin does what?

A

degrades factor V and VIII, fibrinogen, and fibrin. Causes destruction of platelet plug.

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16
Q

What is Alpha-2 antiplasmin?

A

natural inhibitor of plasmin released from endothelium

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17
Q

What factor has the shortest half life?

A

VII

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18
Q

What factors’ activity is lost in stored blood but not FFP?

A

V and VIII

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19
Q

What factor is not synthesized in the liver? where is it synthesized?

A

VIII- synthesized in the endothelium

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20
Q

What are the vitamin K dependent factors?

A

II, VII, IX, C and S

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21
Q

How long does it take for Vitamin K to take effect?

A

6 hours

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22
Q

How long does it take FFP to work and how long does it last?

A

immediately. Lasts 6 hours

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23
Q

What is factor II?

A

Prothrombin

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24
Q

What is the normal half life of RBC’s? Platelets? PMN’s?

A

RBC: 120 days, platelets 7 days, PMN’s 1-2 days

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25
Q

Where is Prostacyclin released from and what does it do?

A

Endothelium. Decreases platelet aggregation and causes vasodilitation (antagonistic to TXA2)

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26
Q

Thromboxane (TXA2)- where is it released from, what does it do?

A

Platelets. Increases aggregation and promotes vasoconstriction. Triggers the release of Ca2+ in platelets. It exposes GpIIb/IIIa recepter and causes platelet-platelet and platelet to collagen binding. activates PIP system to further release calcium.

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27
Q

What is in high concentration in cryoprecipitate and what is it used for?

A

high concentrations of vWf VIII, use in von Willebrands disease and hemophilia A. Contains fibrinogen.

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28
Q

What is in FFP?

A

High levels of all factors including V and VIII, C, S, AT-III

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29
Q

Why are DDAVP and conjugated estrogens used in the setting of coagulopathy?

A

Cause release of VIII and vWF from endothelium

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30
Q

What factors does PT measure?

A

II, V, VII, X, fibrinogen- best for liver synthetic function

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31
Q

What does PTT measure?

A

All but VII and VIII- Does not pick up VII deficiency.

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32
Q

What is an ACT?

A

Activated clotting time. 150-200 for routine anticoagulation, 460 for Cardiopulmonary bypass

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33
Q

What level INR is a contraindication for surgical procedures?

A

> 1.5

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34
Q

What level INR is a contraindication for central line, PCT biopsies, and eye surgery?

A

> 1.3

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35
Q

What is the most common cause of surgical bleeding?

A

Incomplete hemostasis

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36
Q

What is the most common congenital bleeding disorder?

A

von willebrands

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37
Q

what is the inheritance of von willebrand’s disease?

A

I and II are AD. III is AR.

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38
Q

what does vWf do?

A

links GpIb receptor on platelets to collagen

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39
Q

In von willebrand’s, what is the PT and PTT? Bleeding time?

A

PT normal; PTT normal or abnormal; bleeding time long (ristocetin test)

40
Q

In these types of von willebrand’s disease there is a problem in vWf quantity

A

I- reduced, III- non. Treat with recombinant VIII:vWf. DDAVP, cryoprecipitate, conjugated estrogens.

41
Q

This type of Von willebrand’s disease has a problem in the quality of vWf

A

Type II. recombinant factors, cryoprecipitate

42
Q

What is Hemophilia A and what is its inheritance?

A

Factor VIII deficiency. Sex linked recessive.

43
Q

Does factor VIII cross the placenta?

A

Yes. Circumcision may not cause bleeding in hemophila A pts.

44
Q

What is the treatment for Hemophiliac joint?

A

no aspiration, ice, range of motion, factor VIII concentrate or cryoprecipitate.

45
Q

What is Hemophilia B and what is its inheritance?

A

Factor IX deficiency- Christmas disease. Sex linked recessive.

46
Q

What can cause an acquired thrombocytopenia?

A

H2 blockers, heparin

47
Q

What is Glanzmann’s thrombocytopenia?

A

GpIIb/IIIa receptor deficiency- cannot bind to each other. Fibrin normally links them together at this site. Tx with platelets

48
Q

What is Bernard Soulier?

A

GpIb receptor deficiency on platelets. Can’t bind to collagen. Tx with platelets.

49
Q

What does Uremia do to platelets and what is the treatment?

A

Inhibits platelet function. Tx with hemodialysis first, then DDAVP, Platelets.

50
Q

What does Ticlopidine do to platelets?

A

decreases ADP in platelets, prevens exposure of GpIIb/IIIa. Tx with platelets

51
Q

What does Dipyridamole do to platelets?

A

inhibits cAMP phosphodiesterase, increases cAMP, decreases ADP induced platelet aggregation. Tx with platelets

52
Q

What does Pentoxifyllene do to platelets?

A

inhibits platelet aggregation. Tx with platelets

53
Q

What does Clopidogrel do?

A

ADP receptor antagonist. Tx w/platelets

54
Q

PCN/cephalosporins do what to platelets?

A

bind platelets, can increase bleeding time.

55
Q

HIT is caused by what antibody?

A

IgG PF4- causes platelet destruction

56
Q

What type of clot does HIT cause?

A

White clot

57
Q

What is the treatment for HIT?

A

stop heparin, argatroban, hirudin, ancrod, or dextran

58
Q

What are the lab findings in DIC?

A

decreased platelets, prolonged PT and PTT, Low fibrinogen, high fibrin splits, high D-Dimer. Tx underlying cause

59
Q

How many days before surgery should ASA be stopped?

A

7

60
Q

How many days before surgery should coumadin be stopped?

A

7

61
Q

What should platelets be at before surgery? after surgery?

A

50k; 20k

62
Q

Prostate surgery has what effect bleeding?

A

can relase urokinase, activates plasminogen= thrombolysis. Treate with e Aminocaproic acid. Amicar.

63
Q

Tooth extraction or tonsillectomy will pick up what percentage of Pt’s with a bleeding disorder?

A

99%

64
Q

What is the most common cause of congenital hypercoagulability?

A

defect of factor V Leiden. resistance to activated protein C. Tx with heparin, warfarin

65
Q

What is the treatment of hyperhomocysteinemia

A

folic acid and B12 (10% of spontaneous DVT’s)

66
Q

What is the treatment for G20210 prothrombin gene defect?

A

heparin warfarin (5% of spontaneous DVT’s)

67
Q

How does Antithrombin III deficiency develop and how is it treated?

A

can develop after previous heparin exposure. Treat with recombinant AT-III or FFP.

68
Q

What antibody is the lupus anticoagulant, what does it do to PTT and to coagulation?

A

antiphospholipid antibodies. Cuases a procoagulant state. PTT is prolonged and is not corrected by FFP. Diagnose by positive russell viper venom time

69
Q

What are some causes of acquired hypercoagulability?

A

Tobacco (#1), malignancy, inflammatory state, Inflammatory Bowel disease, oral contraceptives, pregnancy, rheumatoied, postop, myeloproliferative

70
Q

How does cardiopulmonary bypass cause hypercoagulable state and what is the treatment?

A

Causes factor XII activation. Tx with heparin.

71
Q

What is the pathogenesis of warfarin skin necrosis?

A

no heparin bridge. Protein C and S have short half life. Transient hypercoaculable state. Protein C deficiency especially susceptible.

72
Q

What is Virchow’s Triad?

A

Stasis, Endothelial injury, hypercoagulable state

73
Q

What is the key element in the development of an arterial thrombus?

A

endothelial injury.

74
Q

How long must a pt be on warfarin for their 1st, 2nd, or 3rd DVT?

A

1= 6 months; 2= 1 year; 3 or significant PE= lifetime

75
Q

What are the indications for a greenfield filter?

A

contraindications to anticoagulation, documented PE on anticoagulation, free floating ileofemoral, IVC, or femoral DVT, those that have had pulmonary embolectomy

76
Q

Patient has pulmonary embolism and is in shock despite massive ionotropes, what do you do?

A

OR. If not in shock, give heparin (thrombolytics not proven to increase survival)

77
Q

What percentage on positive V/Q scans have negative duplexes?

A

1/3

78
Q

PE’s come from which site most commonly?

A

Iliofemoral region

79
Q

How does warfarin work?

A

prevents vitamin K dependent decarboxylation of glutamic resudues on vitamin K-dependent factors

80
Q

How does Dextran work?

A

Inhibits platelets and coagulation factors

81
Q

How do SCD’s work?

A

improve venous return but also induce fibrinolysis with compression (TPA)

82
Q

How does Heparin work?

A

potentiates antithrombin III

83
Q

How is heparin reversed?

A

Protamine (1-1.5 protamine/100U heparin) follow PTT’s

84
Q

What is the half life of heparin and how is it cleared?

A

60-90 minutes. Cleared by retuculoendothelial system

85
Q

What are the long term side effects of heparin? Does it cross Placenta?

A

osteoporosis, alopecia. No- warfarin does

86
Q

What are the problems/reactions of protamine?

A

cross reacts with NPH insulin or previous heparin exposure. 4-5% of patients get reaction- hypotension, bradycardia, decreased cardiac fxn

87
Q

How dies Hirudin work? is it reversible?

A

From leeches- direct thrombin inhibitor. Irreversible. Want PTT 60-90. High risk of bleeding.

88
Q

How does Argatroban work? where is it metabolized? half life?

A

Direct thrombin inhibitor; metabolized in the liver. half life 50 mins. Use for HITT

89
Q

How does Bivalirudin work? where is it metabolized? half life?

A

Reversible direct thrombin inhibitor, metabolyzed by proteinase enzymes in the blood; half life 25-30 mins.

90
Q

How does Ancrod work? where does it come from?

A

Malaysian pit viper venom; stimulates tPA release.

91
Q

How does Amicar (e-aminocaproic acid) work?

A

Inhibits fibrinolysis by inhibiting plasmin. Use in DIC, persistent bleeding after cardiopulmonary bypass, thrombolytic overdose.

92
Q

What are common thrombolytics? which one has high antigenicity?

A

urokinase, tPA, streptokinase. Streptokinase has high antigenicity

93
Q

What is required for thrombolytics to work?

A

Guidewire must get past obstruction

94
Q

What are acceptable Fibrinogen levels when using thrombolytics?

A

>

  1. <100 is associated with increased risk and severity of bleeding.
95
Q

What is an absolute contraindication to using thrombolytics?

A

active internal bleeding, recent CVA (<2 months), intracranial pathology

96
Q

Major contraindications to thrombolytics?

A

Recent surgery (<10 days); organ biopsy; left heart thrombus; active peptic ulcer; major trauma; uncontrolled htn

97
Q

Minor contraindications to thrombolytics?

A

Minor surgery; cpr; afib with mitral valve disease; bacterial endocarditits; hemostatic defects; hemorrhagic retinopathy; preggers

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