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Hematology > Hematology Week 2: Introduction to Thrombophilia > Flashcards

Hematology Week 2: Introduction to Thrombophilia Flashcards

1
Q

Virchow’s Triad

3 listed

A
  • Alteration of blood flow
  • Endothelial injury
  • Hypercoagulable state (inherent/acquired)
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2
Q

VTE AKA

A

Venous Thromboembolism

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3
Q

Thrombosis High-Risk Patients

3 listed

A
  • Males
  • >55
  • recently hospitalized
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4
Q

DVT AKA

A

Deep Venous Thrombosis

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5
Q

circulatory stasis involves

A

alteration of blood flow

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6
Q

Circulatory stasis: Things that contribute to a clot in arteries

A

Turbulence

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7
Q

Circulatory stasis: Things that contribute to a clot in venous

A

Stasis

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8
Q

Circulatory stasis

A

Arterial: turbulence

Venous: Stasis

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9
Q

Alteration of blood flow consequences

A

Disruption of laminar flow via stasis or turbulence

  • allows platelets to interact with endothelium
  • activates endothelium
  • prolongs exposure of activated clotting factors
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10
Q

Common Causes of Alteration of blood flow in the arteries/cardiac/aortic

3 listed

A
  • Aneurysms
  • Dilated atrium
  • Ulcerated atherosclerotic plaques
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11
Q

Causes of Altered blood flow in the venous system

9 listed

A
  • Prolonged immobilization
  • Paget-Schroetter syndrome axial or subclavian vein can be compressed
  • Clot in iliac veins (pregnancy) left iliac vein is compressed by the right iliac artery
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12
Q

Common Causes of Hyperviscosity

3 listed

A
  • polycythemia (primary, secondary)
  • Sickle Cell Anemia
  • Increased plasma proteins
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13
Q

Causes of arterial endothelial injury

12 listed

A

commonly affected due to high flow rates

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14
Q

Indications for inheritable Hypercoagulable States

5 listed

A

age <40

unprovoked thrombosis

FHx of thrombosis

Thrombosis at an unusual site

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15
Q

Contraindicators of inherited hypercoagulable states

A

NOT associated with arterial thrombosis (Stroke, TIA, MI, etc)

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16
Q

Inherited hypercoagulability conditions

5 listed

A
  • Factor V Leiden
  • Factor II hyperprothrombinemia
  • AT deficiency
  • Protein C deficiency
  • Protein S deficiency
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17
Q

Procoagulant gains of function conditions

2 listed

A
  • Factor V Leiden
  • Factor II hyperprothrombinemia
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18
Q

inherited conditions with a weaker risk of VTE

2 listed

A
  • Factor V Leiden
  • Factor II hyperprothrombinemia
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19
Q

Factor V Leiden Genetic inheritance pattern

A
  • Autosomal Dominant
  • can be traced back to a single mutational event 25k years ago
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20
Q

accounts for half of all heritable thrombophilias

A

Factor V Leiden

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21
Q

Found in 12-18% of all patients with VTE

A

Factor V Leiden

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22
Q

Factor V Leiden subtype increased risks

A

Heterozygotes patients with a NON-O BLOOD TYPE have more FVIII and have 2-4x more risk of VTE

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23
Q

Risk of recurrence of VTE with Factor V Leiden

A

Negligible recurrence risk

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24
Q

Risks of heterozygotes of Factor V Leiden

A

5% will have VTE

non-O blood type has increased risks

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25
Q

What does Factor 5 do?

A

factor 5 associated with factor 10 to link the intrinsic and extrinsic pathways

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26
Q

Factor V in Factor V Leiden

A

Factor V is less susceptible to the inhibition of the anticoagulant protein Protein C

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27
Q

Factor V Leiden Etiology

A

arginine to glutamine substitution at R506

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28
Q

Factor II Hyperprothrominemia Genetic inheritance and consequences

A
  • Autosomal dominant
  • nearly exclusively caucasian
  • 3-4 fold increased risk of thrombosis
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29
Q

Factor II Hyperprothrombinemia Genetics

A

Autosomal Dominant

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30
Q

Factor II Hyperprothrombinemia VTE recurrence risk

A

Negligible recurrence risk

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31
Q

Factor II Hyperprothrombinemia Pathophysiology

A

gain of function mutation in 3’ unstranslated region resulting in increased plasma prothrombin levels by 25%

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32
Q

Factor II Hyperprothrombinemia gene

A

prothrombin 20210A untranslated region causing high efficiency mRNA

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33
Q

More rare inherited conditions of hypercoagulability

3 listed

A
  • AT Deficiency
  • Protein C deficiency
  • Protein S Deficiency
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34
Q

inherited conditions of hypercoagulability with greater risk of VTE

3 listed

A
  • At Deficiency
  • Protein C Deficiency
  • Protein S Deficiency
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35
Q

Inherited conditions of hypercoagulability that are measured by activity or antigen levels

3 listed

A

At Deficiency

Protein C Deficiency

Protein S Deficiency

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36
Q

Protein C Deficiency Genetics

A

Autosomal Dominant >160 mutations

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37
Q

Protein C Deficiency epidemiology

3 listed

A
  • .2-.5% of population
  • 2-5% of all VTE patients
  • initial VTE episode is spontaneous in 2/3 of patients
38
Q

Protein C deficiency Caveats

A
  • Homozygotes are rare but typically fatal (born with purpura fulminans)
  • Heterozygotes Risk of warfarin skin necrosis because it is a vitamin K antagonist
39
Q

Protein S deficiency Genetics

A

Autosomal Dominant

40
Q

Protein S deficiency epidemiology

A

rare <1% of population

41
Q

most difficult to Dx Inherited condition of hypercoagulability

A

Protein S deficiency

42
Q

Protein S deficiency Homozygotes

A

Rare but typically fatal (born with purpura fulminans

43
Q

Protein S deficiency Caveat

A
  • can be a physiologic phenomenon during pregnancy
  • Risk of Warfarin skin necrosis
44
Q

Protein S deficiency pathophysiology

A

Protein S is a cofactor for Protein C to put the brakes on Factor V

45
Q

Antithrombin Deficiency Genetics

A

Autosomal Dominant (mostly)

46
Q

Antithrombin Deficiency Epidemiology

A

0.02% of population

1% of all VTE cases particularly in pregnancy

Half of affected patients have spontaneous VTE

Much higher o

47
Q

Antithrombin Deficiency Acquired form

A

Nephrotic Syndrome (more common than Antithrombin Deficiency)

48
Q

Which inherited hypercoagulable condition carries the highest risk for VTE?

A

Antithrombin Deficiency

49
Q

Antithrombin Function

A

Antithrombin inhibits thrombin

50
Q

Inherited Conditions of hypercoagulability association with pregnancy morbidity

A

No significant association

51
Q

Inherited Conditions of hypercoagulability association with arterial thrombosis

A

No significant association

52
Q

Heritable thrombophilias Overview

A
53
Q

Clots usually occur in a vein where?

A

Around a valve

54
Q

Tissue Factor can also be expressed on________ to contribute to _________

A

White Cells, clotting

55
Q

Neutrophils NETs can contribute to?

A

Clotting

56
Q

Hypoxia in valve areas can contribute to?

A

Clotting

57
Q

Treatment of unprovoked clots

A

nowhere does thrombophilia affect treatment decisions, if a patient has a clot they have a pretty high risk to have another clot regardless of how they got it

58
Q

Acquired Hypercoagulable Conditions

5 listed

A
59
Q

Acquired Hypercoagulable Conditions Arterial Thrombosis possible

A
  • Heparin-induced thrombocytopenia
  • Antiphospholipid syndrome
  • Cancer
60
Q

Heparin-induced Thrombocytopenia

A

1/5000 patients typically using unfractionated heparin and cardiac surgery

61
Q

Heparin-induced thrombocytopenia pathophysiology

A
  • prothrombotic, potentially fatal complication of heparin treatment
  • demonstrate anti-PF4/heparin antibodies
62
Q

Heparin-induced thrombocytopenia mechanism

A

positively charged PF4 molecules are stored in alpha granules of platelet interact with negatively charged heparin polysaccharide causing a conformational change of the PF4 molecule that is immunogenic quickly developing IgG antibodies within 4-5 days

antibodies complex with platelets which have Fc receptors which cause antibody activation of platelets which release more PF4 causing a cycle

63
Q

HIT AKA

A

Heparin-induced Thrombocytopenia

64
Q

HIT Treatment

A

stop heparin and put them on another anticoagulant

65
Q

Antiphospholipid Syndrome in vitro vs in vivo

A
  • autoimmune hypercoagulable state
  • causes prolongation of PTT in vitro
  • In vivo causes clotting
66
Q

Antiphospholipid syndrome antibody to

A

ß2GP1

67
Q

Antiphospholipid syndrome pathophysiology

A

ß2GP1 conformational change can become immunogenic which can upregulate complement activity, upregulating endothelial proteins, increasing tissue factor expression, activates platelets, interferes with trophoblasts (pregnancy morbidity)

68
Q

Antiphospholipid syndrome how is it diagnosed

A

Clinicopathologic diagnosis

patient with thrombotic episode or a pregnancy morbidity by the loss of pregnancy after 10 wks gestation or lost 3 pregnancies before 10 weeks gestation, preterm labor before 34 weeks gestations eclampsia or preeclampsia

69
Q

Antiphospholipid syndrome Transiency

A

need to prove that the antibodies are persistent because 10% of healthy subjects need to have transient antibodies 12 weeks apart the same type of the 3

70
Q

Antiphospholipid syndrome clinical presentation

3 listed

A

DVT in lower extremity but PE is less common

arterial thrombosis

microvascular clotting: least common and the most deadly woul be called catastrophic Antiphospholipid syndrome)

71
Q

Catastrophic Antiphospholipid syndrome

A

microvascular clotting in Antiphospholipid syndrome

72
Q

Cancer and thrombosis epidemiology

A
73
Q

Hypercoagulability Estrogen and hormone replacement therapy

A
  • also true for testosterone
  • confers increased risk for thrombosis
  • most risk in the first year
74
Q

Hypercoagulability and pregnancy

A

can increase risk of clot by 10x

75
Q

Hypercoagulability and pregnancy how many thromosis occur post partum?

A

1/3

76
Q

Hypercoagulability and pregnancy thrombosis prevalence

A

0.86 per 1000 deliveries

77
Q

Hypercoagulability and pregnancy mechanism of increased risk

5 listed

A
  • decreased protein S levels
  • Increased fibrinogen and prothrombin
  • increased estrogen
  • impaired fibrinolysis
  • vascular congestion
78
Q

Symptoms of DVT

4 listed

A
  • swelling
  • pain
  • redness
  • heat
79
Q

Symptoms for pulmonary embolism

5 listed

A

tachypnea is the most reliable symptom

80
Q

Symptoms for pulmonary embolism most reliable symptom

A

Tachypnea

81
Q

Symptoms for pulmonary embolism most common symptoms

A

chest pain and tachypnea

82
Q

pulmonary embolism picture

A
83
Q

D-Dimer Test

A

best test for thrombosis

84
Q

Clinical and pathophysiologic aspects of thrombosis

5 listed

A
85
Q

How are D-dimers formed?

A
86
Q

d-dimer is only detectable if?

A

Factor XIIIa has crosslinked fibrin

87
Q

Arterial vs venous thrombosis

A
88
Q

Arterial vs venous thrombosis

A
89
Q

Clot in iliac veins (pregnancy) the ____________ is compressed by the ________________.

A

left iliac vein is compressed by the right iliac artery

90
Q

Clotting in Paget–Schroetter

A

axial or subclavian vein can be compressed

Hematology (26 decks)

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