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Comprehensive Prep > 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 kininogen + 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

Factor XIII: function

A

Helps crosslink fibrin

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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
A

Antithrombin III (AT-III)

Heparin activates AT-III (up to 1000x normal activity)

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11
Q

Protein C: function

A

degrades factors 5 and 8; degrades fibrinogen

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12
Q

Protein S: function

A

Protein C cofactor

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13
Q

Tissue plasminogen activator: origin and function

A

Released from endothelium and converts plasminogen to plasmin

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14
Q

Plasmin: function

A

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

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15
Q

Alpha-2 antiplasmin: origin and function

A

Released from endothelium, natural inhibitor of plasmin

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16
Q

Factor: shortest half life

A

Factor 7

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17
Q

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

A

Factors 5 and 8

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18
Q

Factors: only factor not synthesized in the liver

A

Factor 8, synthesized in the endothelium

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19
Q

Vitamin K: onset of action

A

6 hours

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20
Q

FFP: onset and duration of action

A

Works immediately, lasts 6 hours

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21
Q

Prothrombin is also known as…

A

Factor II

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22
Q

Half life: RBCs

A

120 days

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23
Q

Half-life: platelets

A

7 days

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24
Q

Half life: PMNs

A

1-2 days

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25
Q

Prostacyclin (PGI2) - origin and action

A

From endothelium - decreases platelet aggregation and promotes vasodilation (antagonistic to TXA2)

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26
Q

Thromboxane (TXA2) - origin and action

A

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)
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27
Q

Cryoprecipitate contains…

A

highest concentration of vWF-VIII; high levels of fibrinogen

Used in von Willebrand’s disease and hemophilia A (factor 8 deficiency)

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28
Q

FFP contains…

A

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

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29
Q

DDAVP and conjugated estrogens: function

A

Causes release of VIII and vWF from endothelium

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30
Q

Lab: PT measures…

A

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

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31
Q

Lab: PTT measures…

A

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

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32
Q

What do you want PTT for routine anticoagulation?

A

60 - 90 sec

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33
Q

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

A

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

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34
Q

Most common congenital bleeding disorder

A

Von Willebrand’s disease

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35
Q

Type 1 von Willebrand’s disease: description and Tx

A

Reduced quantity of vWF

Tx: recombinant VIII:vWF, DDAVP, cryoprecipitate

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36
Q

Type 2 von Willebrand’s disease: description and Tx

A

Defect in vWF molecule itself, vWF does not work well

Tx: recombinant VIII:vWF, cryoprecipitate

37
Q

Type 3 von Willebrand’s disease: description and Tx

A

Complete vWF deficiency (rare)

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

38
Q

Lab findings: von Willebrand’s disease

A

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

39
Q

Hemophilia A: inheritance, description, lab findings, Tx

A

Sex linked recessive

VIII deficiency

Prolonged PTT, normal PT

Tx - for hemophiliac epistaxis, intracerebral hemorrhage, or hematuria: rFactor 8 or cryoprecipitate

Tx - for joint bleeding: Do not aspirate - Ice, keep joint mobile with ROM exercises - Factor 8 concentrate or cryoprecipitate

40
Q

Why do hemophilia A newborns not bleed at circumcision?

A

Factor 8 crosses the placenta

41
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

42
Q

Hemophilia B: inheritance, description, lab findings, Tx

A

Sex-linked recessive

Factor 9 deficiency

Prolonged PTT and normal PT

Tx: rFactor9 or FFP

AKA Christmas Disease

43
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

44
Q

Factor 7 deficiency: lab findings, Tx

A

Prolonged PT. Normal PTT.

Tx: rFactor7 or FFP

45
Q

S&S: Platelet disorders

A

Bruising, epistaxis, mucosal bleeding, petechiae, purpura.

46
Q

Acquired thrombocytopenia

A

Platelet disorder: caused by H2 blockers, heparin

47
Q

Glanzmann’s thrombocytopenia: description and Tx

A

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

Tx: Platelets

48
Q

Bernard Soulier: description and Tx

A

Gp1b receptor deficiency on platelets (cannot bind to collagen) - vWF normally links Gp1b collagen

Tx: Platelets

49
Q

Uremia inhibited platelet function: treatment

A

hemodialysis (1st), DDAVP, platelets

50
Q

Heparin-induced thrombocytopenia (HIT): description, Tx

A

Thrombocytopenia due to antiplatelet 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.

Tx: stop heparin, start argatroban (direct thrombin inhibitor) to anticoagulate

51
Q

Disseminated intravascular coagulation (DIC): description and Tx

A

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

52
Q

Aspirin: mechanism of action

A

Inhibits cyclooxygenase in platelets and decreases TXA2

53
Q

Blood thinners: pre-op recommendations

A

Aspirin: stop 7 days before surgery; patients will have prolonged bleeding time

Plavix: stop 7 days before surgery; ADP receptor antagonist. Tx: platelets

Coumadin: stop 7 days before surgery; consider starting heparin

54
Q

Platelet pre-op recommendations

A

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

55
Q

Bleeding after prostate surgery…

A

Can release urokinase, activates plasminogen -> thrombolysis

Tx: e-aminocapropic acid (Amicar)

56
Q

Most sensitive history finding (99% of patients with bleeding disorder)

A

Abnormal bleeding with tooth extraction or tonsillectomy

57
Q

Common with vWF deficiency and platelet disorders

A

Epistaxis

58
Q

Factor V Leiden: description and Tx

A

MC congenital hypercoaguability disorder - 30% of spontaneous venous thromboses

Causes resistance to activated protein C; the defect is on factor 5.

Tx: heparin, warfarin

59
Q

Hyperhomocysteinemia: treatment

A

Folic Acid. B12

60
Q

prothrombin gene defect G20210A: treatment

A

Heparin, warfarin

61
Q

protein C or S deficiency: treatment

A

Heparin, warfarin

62
Q

Heparin does not work in these patients…

A

Antithrombin H1 deficiency. Can develop after previous heparin exposure

Tx: recombinant AT-III concentrate or FFP (highest concentration of AT-III) followed by heparin, then warfarin

63
Q

dysfibrinogenemia, dysplasminogenemia: treatment

A

Heparin, warfarin

64
Q

Polycythemia vera: description ,causes, treatment

A

Defect in platelet function; can get thrombosis

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

Tx:

65
Q

Anti-phospholipid antibody syndrome: description, cause

A

Hypercoagulabe with prolonged PTT (not corrected with FFP). Positive Russell viper venom time, false-positive RPR test for syphillis.

Caused by antibodies to cardiolipin and lupus anticoagulant (phospholipids)

Tx: heparin, warfarin

66
Q

Causes of acquired hypercoagulability

A

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

67
Q

How does cardiopulmonary bypass result in hypercoagulability?

A

Activates Factor 12 (Hageman factor).

Tx: heparin to prevent.

68
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.

69
Q

Who is at risk for warfarin-induced skin necrosis?

A

Patients with relative protein C deficiency are especially susceptible.

70
Q

Key elements in the development of venous thromboses

A

Virchow’s triad (stasis, endothelial injury, hypercoagulability)

71
Q

Key element in the development of arterial thrombosis

A

Endothelial injury

72
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.

73
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
74
Q

Pulmonary embolism: treatment

A

Shock (despite massive interpose, pressors) -> OR. No shock -> Heparin (thrombolytics have not shown an improvement in survival) or suction catheter-based intervention.

75
Q

Aminocaproic acid (Amicar): mechanism

A

Inhibits fibrinolysis by inhibiting plasmin. Used in DIC, persistent bleeding following cardiopulmonary bypass, thrombolytic overdoses

76
Q

Warfarin: mechanism

A

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

77
Q

What is the mechanism behind SCDs?

A

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

78
Q

Heparin: mechanism

A

Binds and activates anti-thrombin III.

Reverse with protamine. Cleared by the reticuloendothelial system.

Does not cross placenta.

79
Q

Risks of long-term heparin

A

Osteoporosis. Alopecia.

80
Q

Half-life / goal PTT of heparin

A

Half-life: 60-90 minutes. Goal PTT: 60-90 seconds

81
Q

protamine reaction

A

Cross reacts with NPH insulin or previous protamine exposure

1% get protamine reaction (hypotension, bradycardia, and decreased heart function).

82
Q

Low molecular weight heparin (ex, enoxaparin, fondaparinux)

A

Binds and activates antithrombin III but increases neutralization of just 10a and thrombin

Lower risk of HIT compared to unfractionated heparin. Not reversed with protamine

83
Q

Argatroban: mechanism

A

Reversible direct thrombin inhibitor - Metabolized in the liver - Half life: 50 minutes - Often used in patients with HITT

84
Q

Bivalirudin (Angiomax): mechanism

A

Reversible direct thrombin inhibitor - Metabolized by proteinase enzymes in the blood - Half life: 25 minutes

85
Q

Hirudin (Hirulog; form leeches)

A

Irreversible direct thrombin inhibitor - most potent direct inhibitor or thrombin

High risk for bleeding complications

86
Q

Ancrod: mechanism

A

Malayan pit viper venom; stimulates tPA release

87
Q

Thrombolytics: Streptokinase, urokinase, tPA

A

Activate plasminogen - need to follow fibrinogen levels

88
Q

Treatment for thrombolytic overdose

A

e-aminocaproic acid (Amicar)

89
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.

Comprehensive Prep (45 decks)

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