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ABSITE 2019-RM > Chapter 2: Hematology > Flashcards

Chapter 2: Hematology Flashcards

1
Q

Three initial responses to vascular injury

A

Vascular vasoconstriction, platelet adhesion, thrombin generation

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2
Q

Intrinsic coagulation cascade

A

Exposed collagen + prekallikrein + HMW kiniogen + Factor 12 -> activate factor 11 -> activate 9, then 8 -> activate 10, then add 5 -> Convert prothrombin (factor II) to thrombin -> thrombin then converts fibrinogen to fibrin

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3
Q

Extrinsic coagulation cascade

A

Tissue factor (injured cells) + factor 7 -> activate 10, then add 5 -> convert prothrombin to thrombin -> thrombin then converts fibrinogen to fibrin

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4
Q

Prothrombin complex (for intrinsic and extrinsic pathways)

A
  • 10, 5, Ca, platelet factor 3, prothrombin.
  • Forms on platelets
  • Catalyzes the formation of thrombin
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5
Q

Convergence point for intrinsic and extrinsic pathway

A

Factor 10

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6
Q

Inhibits factor 10

A

Tissue factor pathway inhibitor

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7
Q

Links platelets together (binds GpIIb /IIIa molecules) to form platelet plug -> hemostasis

A

Fibrin

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8
Q

Helps crosslink fibrin

A

XIII

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9
Q
  • Key to coagulation
  • Converts fibrinogen to fibrin and fibrin split products
  • Activates factors 5 and 13
  • Activates platelets
A

Thrombin

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10
Q
  • Key to anticoagulation
  • Binds and inhibits thrombin
  • Inhibits factors 9, 10, and 11
  • Heparin activates AT-III (up to 1000x normal activity)
A

Antithrombin III (AT-III)

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11
Q

Vitamin-K dependent; degrades factors 5 and 8; degrades fibrinogen

A

Protein C

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12
Q

Vitamin K dependent, protein C cofactor

A

Protein S

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13
Q

Released from endothelium and converts plasminogen to plasmin

A

Tissue plasminogen activator

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14
Q

Degrades factors 5 and 9, fibrinogen, and fibrin -> lost platelet plug

A

Plasmin

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15
Q

Natural inhibitor of plasmin, released from endothelium

A

Alpha-2 antiplasmin

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16
Q

Components of fibrinolysis

A

Tissue plasminogen activator, plasmin, alpha-2 antiplasmin

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17
Q

Factor: shortest half life

A

Factor 7

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18
Q

Factors: labile factors, activity lost in stored blood; activity not lost in FFP

A

Factors 5 and 8

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19
Q

Factors: only factor not synthesized in the liver (synthesized in the endothelium)

A

Factor 8

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20
Q

Factors: 2, 7, 9, 10, protein C and protein S

A

Vitamin-K dependent factors

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21
Q

Takes 6 hours to have effect

A

Vitamin K

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22
Q

Effect is immediate and lasts 6 hours

A

FFP

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23
Q

Prothrombin

A

Factor II

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24
Q

Half life: RBCs

A

120 days

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25
Q

Half-life: platelets

A

7 days

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26
Q

Half life: PMNs

A

1-2 days

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27
Q
  • From endothelium

- Decreases platelet aggregation and promotes vasodilation (antagonistic to TXA2)

A

Prostacyclin (PGI2)

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28
Q
  • From platelets
  • Increases platelet aggregation and promotes vasoconstriction
  • Triggers release of calcium in platelets -> exposes Gp2b/3a receptor and causes platelet-to-platelet binding; platelet-to-collagen binding also occurs (Gp1b receptor)
A

Thromboxane (TXA2)

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29
Q

Contains highest concentration of vWF-VIII; used in von Willebrand’s disease and hemophilia A (factor 8 deficiency), also has high levels of fibrinogen

A

Cryoprecipitate

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30
Q

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

A

FFP

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31
Q

Causes release of VIII and vWF from endothelium

A

DDAVP and conjugated estrogens

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32
Q

Measures 2, 5, 7, and 10; fibrinogen; best for liver synthetic function

A

PT

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33
Q

Measures most factors except 7 and 13 (thus does not pick up factor 7 deficiency); also measures fibrinogen

A

PTT

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34
Q

What do you want PTT for routine anticoagulation?

A

60 - 90 sec

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35
Q

ACT

A

activated clotting time

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36
Q

What do you want ACT (activated clotting time) for routine anticoagulation?

A

Want ACT 150 - 200 sec for routine anticoagulation, > 460 sec for cardiopulmonary bypass

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37
Q

INR: relative contraindication to performing routine procedures

A

INR > 1.5

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38
Q

INR: relative contraindication to central line placement, percutaneous needle biopsies, and eye surgery

A

INR > 1.3

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39
Q

Most common cause of surgical bleeding

A

Incomplete hemostasis

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40
Q

Most common congenital bleeding disorder

A

Von Willebrand’s disease

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41
Q
  • Reduced quantity of vWF

Tx: recombinant VIII:vWF, DDAVP, cryoprecipitate

A

Type 1 von Willebrand’s disease

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42
Q
  • Defect in vWF molecule itself, vWF does not work well

Tx: recombinant VIII:vWF, cryoprecipitate

A

Type 2 von Willebrand’s disease

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43
Q
  • Complete vWF deficiency (rare)

Tx: recombinant VIII:vWF, cryoprecipitate; (DDAVP will not work)

A

Type 3 von Willebrand’s disease

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44
Q

Lab findings of von Willebrand’s disease

A

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

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45
Q
  • VIII deficiency
  • Sex linked recessive
  • Prolonged PTT, normal PT
A

Hemophilia A

46
Q

Why may hemophilia A newborns not bleed at circumcision?

A

Factor 8 crosses the placenta

47
Q

Treatment for hemophiliac joint bleeding

A
  • Do not aspirate
  • Ice, keep joint mobile with ROM exercises
  • Factor 8 concentrate or cryoprecipitate
48
Q

Treatment for hemophiliac epistaxis, intracerebral hemorrhage, or hematuria

A

Recombinant factor 8 or cryoprecipitate

49
Q

Goals for hemophilia A pre and post op

A

Need levels 100% pre-op, keep at 80-100% for 10-14 days after surgery

50
Q
  • Sex-linked recessive
  • Prolonged PTT and normal PT
    Tx: Recombinant factor 9 or FFP
A

Hemophilia B - Factor 9 deficiency - Christmas Disease

51
Q

Goals for Hemophilia B pre and post op

A

Need levels 100% pre-op, keep at 30-40% for 2-3 days after surgery

52
Q

Prolonged PT.
Normal PTT.
Bleeding tendency.
Tx: Recombinant factor 7 concentrate or FFP

A

Factor 7 deficiency.

53
Q

Causes bruising, epistaxis, mucosal bleeding, petechiae, purpura.

A

Platelet disorders

54
Q

Platelet disorder: caused by H2 blockers, heparin

A

Acquired thrombocytopenia

55
Q

Platelet disorder: Gp2b/3a receptor deficiency on platelets (cannot bind to each other).
- Fibrin normally links the Gp1b/3a receptors together.
Tx: ?

A

Glanzmann’s thrombocytopenia

Tx: Platelets

56
Q

Gp1b receptor deficiency on platelets (cannot bind to collagen)
- vWF normally links Gp1b collagen.
Tx: ?

A

Bernard Soulier

Tx: Platelets

57
Q

How does uremia affect platelets?

A

Uremia inhibits platelet function.

Tx: hemodialysis (1st), DDAVP, platelets

58
Q

Thrombocytopenia due to antiplatlet antibodies (IgG PF4 antibody) results in platelet destruction.

  • Can also cause platelet aggregation and thrombosis.
  • Forms a white clot.
  • Can occur with low doses of heparin.
A

Heparin-induced thrombocytopenia (HIT)

59
Q

Treatment for heparin-induced thrombocytopenia (HIT)

A

Stop heparin, start argatroban (direct thrombin inhibitor) to anticoagulate

60
Q
  • Decreased platelets, low fibrinogen, high fibrin split products, and high d-dimer
  • Prolonged PT and prolonged PTT
  • Often initiated by tissue factor
    Tx: need to treat the underlying cause
A

Disseminated intravascular coagulation (DIC)

61
Q

Inhibits cyclooxygenase in platelets and decreases TXA2

62
Q

Aspirin pre-op recommendations

A

Stop 7 days before surgery; patients will have prolonged bleeding time

63
Q

Plavix pre-op recommendations

A

Stop 7 days before surgery; ADP receptor antagonist.

Tx: platelets

64
Q

Coumadin pre-op recommendations

A

Stop 7 days before surgery; consider starting heparin while Coumadin wears off

65
Q

Platelet pre-op recommendations

A

Want them > 50,000 before surgery, > 20,000 after surgery

66
Q

Surgery: can release urokinase, activates plasminogen -> thrombolysis.
Tx: e-aminocapropic acid (Amicar)

A

Prostate surgery

67
Q

Best way to predict bleeding risk

68
Q

Does normal circumcision rule out bleeding disorders?

A

No, they can still have clotting factors from the mother

69
Q

Picks up 99% of patients with bleeding disorder

A

Abnormal bleeding with tooth extraction or tonsillectomy

70
Q

Common with vWF deficiency and platelet disorders

71
Q

Common with bleeding disorders

A

Menorrhagia

72
Q

Present as venous or arterial thrombosis / emboli (e.g., DVT, PE, stroke)

A

Hypercoaguability Disorders

73
Q
  • 30% of spontaneous venous thromboses
  • MC congenital hypercoaguability disorder.
  • Causes resistance to activated protein C; the defect is on factor 5.
    Tx: heparin, warfarin
A

Factor V Leiden mutation

74
Q

Treatment for hyperhomocysteinemia

A

Folic Acid.

B12

75
Q

Tx: prothrombin gene defect G20210A

A

Heparin, warfarin

76
Q

Tx: protein C or S deficiency

A

Heparin, warfarin

77
Q
  • Heparin does not work in these patients
  • Can develop after previous heparin exposure
    Tx: recombinant AT-III concentrate or FFP (highest concentration of AT-III) followed by heparin, then warfarin
A

Antithrombin H1 deficiency

78
Q

Tx: dysfibrinogenemia, dysplasminogenemia

A

Heparin, warfarin

79
Q
  • Defect in platelet function; can get thrombosis

- Keep Hct

A

Polycythemia vera

80
Q

Causes of polycythemia vera

A

Primary: JAK2 mutation
Secondary: low oxygen tension (e.g.: living at high altitudes, smoking, carbon monoxide exposure)

81
Q
  • Procoagulant (get prolonged PTT, but are hyper coagulable)

- Caused by antibodies to cardiolipin and lupus anticoagulant (phospholipids)

A

Anti-phospholipid antibody syndrome)

82
Q 
Prolonged PTT (not corrected with FFP).
Positive Russell viper venom time, false-positive RPR test for syphillis.
Tx: heparin, warfarin
A

Anti-phospholipid antibody syndrome

83
Q

MC factor causing acquired hypercoagulability

84
Q

Causes of acquired hyper coagulability

A

Tobacco. Malignancy. Inflammatory states. IBD. Infections. OCPs. Pregnancy. Rheumatoid arthritis. Post-op patients. Myeloproliferative disorders.

85
Q

How does cardiopulmonary bypass result in hyper coagulability?

A

Activates Factor 12 (Hageman factor). Tx: heparin to prevent.

86
Q

Why does warfarin-induced skin necrosis occur?

A

Short half-life of proteins C and S, which are first to decrease in levels compared with the pro coagulation factors; results in relative hyperthrombotic state.
- Occurs when placed on coumadin without being heparinized first.

87
Q

Who is at risk for warfarin-induced skin necrosis?

A

Patients with relative protein C deficiency are especially susceptible.

88
Q

Key elements in the development of venous thromboses

A

Virchow’s triad (stasis, endothelial injury, hyper coagulability)

89
Q

Key element in the development of arterial thrombosis

A

Endothelial injury

90
Q

Risk factors for DVT

A

Stasis. Venous injury. Hypercoaguability.

91
Q

Post-op DVT Tx:
1st:
2nd:
3rd:

A

1st: Warfarin for 6 mo.
2nd: Warfarin for 1 yr.
3rd or significant PE: Warfarin for life.

92
Q

Indications for Greenfield filter

A
  • Contraindications to anticoagulation
  • Documented PE while on anticoagulation
  • Free-floating IVC, ilio-femoral, or deep femoral DVT
  • Recent pulmonary embolectomy
93
Q

When are temporary IVC filters indicated?

A

Can be inserted in patients at high risk for DVT (e.g. head injury patients on prolonged bed rest)

94
Q

Most common origin of PE

A

Ilio-femoral region

95
Q

Tx pulmonary embolism

A

Shock (despite massive interpose, pressors) -> OR.

No shock -> Heparin (thrombolytics have not shown an improvement in survival) or suction catheter-based intervention.

96
Q
  • Inhibits fibrinolysis by inhibiting plasmin

- Used in DIC, persistent bleeding following cardiopulmonary bypass, thrombolytic overdoses

A

Aminocaproic acid (Amicar)

97
Q

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

98
Q

Improve venous return but also induce fibrinolysis with compression (release of tPA (tissue plasminogen activator) from endothelium.

99
Q
  • Binds and activates anti-thrombin III
  • Reverse with protamine
  • Cleared by the reticuloendotehlial system
  • Does not cross placental barrier
100
Q

Risks of long-term heparin

A

Osteoporsis. Alopecia.

101
Q

Half-life / goal PTT of heparin

A

Half-life: 60-90 minutes.

Goal PTT: 60-90 seconds

102
Q

Cross reacts with NPH insulin or previous protamine exposure; 1% get protamine reaction (hypotension, bradycardia, and decreased heart function).

103
Q
  • Lower risk of HIT compared to unfractionated heparin
  • Binds and activates antithrombin III but increases neutralization of just 10a and thrombin
  • Not reversed with protamine
A

Low molecular weight heparin (ex, enoxaparin, fondaparinux)

104
Q
  • Reversible direct thrombin inhibitor
  • Metabolized in the liver
  • Half life: 50 minutes
  • Often used in patients with HITT
A

Argatroban

105
Q
  • Reversible direct thrombin inhibitor
  • Metabolized by proteinase enzymes in the blood
  • Half life: 25 minutes
A

Bivalirudin (Angiomax)

106
Q
  • Irreversible direct thrombin inhibitor
  • Most potent direct inhibitor or thrombin
  • High risk for bleeding complications
A

Hirudin (Hirulog; form leeches)

107
Q

Malayan pit viper venom; stimulates tPA release

108
Q
  • Activate plasminogen

- Need to follow fibrinogen levels: fibrinogen

A

Thrombolytics: Streptokinase, urokinase, tPA

109
Q

Treatment for thrombolytic overdose

A

e-aminocaproic acid (Amicar)

110
Q

Absolute contraindications to TPA

A

Active internal bleeding. Recent CVA or neurosurgery (

111
Q

Major contraindications to TPA.

112
Q

Minor contraindications to TPA.

A

Minor surgery. Recent CPR. A fib with MV disease. Bacterial endocarditis. Hemostatic defects (i.e. renal or liver disease). Diabetic hemorrhage retinopathy. Pregnancy.

ABSITE 2019-RM (33 decks)

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