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SBM hematology > hypercoagulable states > Flashcards

hypercoagulable states Flashcards

1
Q

thrombus:

A
  • fibrin + blood cells

- end result of coagulation cascade

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2
Q

thrombosis:

A
  • act of forming a thrombus

- pathological or physiologic

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3
Q

virchow’s triad:

A

1) vascular damage
2) decreased flow
3) altered blood composition (hyper coagulability)

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4
Q

thrombophilia:

A

acquired or hereditary predisposition to VENOUS thromboembolism

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5
Q

acquired thrombophilia sources

A 
Medical illness
- Inflammation
Surgery
- Wound healing
Obesity
- Increased factor VIII due to inflammatory cytokines associated with adipose
- Increased PAI-1 produced by fat cells
Cancer
- Tumor associated procoagulant molecules and cytokines
Medications
- Estrogen
Pregnancy
- Increased pro-coagulant factors (e.g., VIII, vWF)
- Decreased anticoagulant factors (e.g., protein S)
Hematologic disorders
- Myeloproliferative disorders
- Paroxysmal nocturnal hemoglobinuria
Heparin induced thrombocytopenia (HIT)
Hyperhomocysteinemia
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6
Q

what are antiphospholipid antibodies (APA)?

A

autoantibodies directed against protein component of phospholipids and plasma proteins usually bound to phospholipids

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7
Q

subtypes of APA

A

Lupus anticoagulant
Anti b2-GP1
Anti-prothrombin
Anti-cardiolipin

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8
Q

causes of APA

A
  • medications
  • infections
  • autoimmune disorder
  • primary autoimmune phenomenon
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9
Q

APA increases risk of?

A
  • VTE

- repeated pregnancy loss

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10
Q

lupus anticoagulant mechanism

A

interferes with the prothrombinase complex (X, V, II) so it is an anticoagulant in vitro and will NOT correct with mixing studies. however, in vivo it is a trigger for thrombosis, often in older people, for unknown reasons.

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11
Q

diagnosis of APA

A
  • one clinical event and positive test (2x 12 weeks apart)
  • clinical events include thrombosis or unexplained lost pregnancy
  • lab test criteria include positive lupus anticoagulant, ACA (IgG or IgM) at moderate or high titer (>40 GPL, MPL), or Anti-beta-2GP-I in titer >99th percentile
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12
Q

factor V leiden mechanism

A
  • APC resistance in factor V due to gene mutation
  • Va can’t be inactivated by APC
  • Resistance can be acquired through cancer, pregnancy, contraceptives, lupus anticoagulants
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13
Q

factor V leiden risk

A
  • heterozygote 3 fold increase
  • homozygote 18 fold increase
  • very little arterial risk, only venous
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14
Q

factor V leiden labs

A
  • Screen with test for APC resistance
  • Confirm with PCR for gene mutation
  • Genetic test; therefore requires informed consent
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15
Q

Prothrombin G20210A mechanism and risk

A
  • point mutation in prothrombin
  • risks similar to factor V leiden
  • little risk of arterial
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16
Q

Prothrombin G20210A labs

A
  • PCR for gene mutation
17
Q

hereditary protein C deficiency characteristics

A
  • autosomal dominant
  • homozygote usually lethal
  • ## little role in arterial
18
Q

hereditary protein C deficiency risk

A
  • 7 fold increased risk of venous thrombosis

- warfarin can induce vitamin K decrease and lead to hyper coagulation in small skin vessels causing skin necrosis

19
Q

hereditary protein C deficiency labs

A
  • test activity, if low measure antigen to differentiate types I and II
20
Q

acquired protein C deficiency causes

A
  • warfarin
  • DIC
  • liver disease
  • septis
21
Q

hereditary protein S deficiency mechanism and characteristics

A
  • autosomal dominant
  • homozygotes usually lethal
  • longer half life than protein C
  • ## warfarin risk
22
Q

hereditary protein S deficiency subtypes

A
  • quantitative - I and III

- qualitative - II

23
Q

hereditary antithrombin deficiency mechanism

A
  • similar to protein C deficiency
  • type I is quantitative and type II is qualitative
  • homozygote is lethal
  • lab test, test activity first and then antigen
24
Q

clues to hereditary thrombophilia

A 
Idiopathic
VTE at young age
Unusual locations
Family history (hereditary)
Recurrent obstetric complications
25
Q

consider testing

A 
Any VTE, age <50
Idiopathic VTE, any age
VTE in unusual sites
Recurrent VTE
VTE + Family history
VTE in pregnancy or OCP
Relatives of those with known thrombophilia
Recurrent pregnancy loss or complications

SBM hematology (14 decks)

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