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M2 Hematology > 9. Hypercoagulable States > Flashcards

9. Hypercoagulable States Flashcards

1
Q

under normal conditions, vascular endothelium is procoag or anticoag?

A

anticoag

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2
Q

perturbing the endothelium (injury, inflammation) converts it from what to what?

A

from anticoag to procoag

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3
Q

subendothelium is procoag or anticoag?

A

procoag. injury will expose this.

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4
Q

the first step in primary hemostasis is vasoconstriction. what causes this?

A

adrenergic activity, epinephrnie

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5
Q

definition of thrombus?

A

intravascular mass of fibrin + blood cells. endo product of primary and secondary hemostasis

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6
Q

thrombosis: definition?

A

act of forming a thrombus. may be physiologic of pathologic

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7
Q

define hypercoagulable state

A

thrombosis that occurs in circumstances under which you’d not usually expect thrombosis. due to excessive activation of blood coagulation (inc thrombogenic factors, decr anticoag factors)

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8
Q

what are the three things in Virchow’s Triad?

A
  • blood vessel wall damage
  • altered blood flow (stasis)
  • altered blood composition (hypercoagulability)
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9
Q

which of the Virchow’s triad components is most relevant for arterial thrombosis?

A

vessel injury. arteries are strong, can withstand injury. and very little stasis

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10
Q

which of the Virchow’s triad components is most relevant for venous thrombosis?

A

stasis, composition. vessel injury is less impt

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11
Q

major problems from venous thrombosis?

A
  • DVT

- Pulm Embolism

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12
Q

why does stasis lead to thrombosis?

A

hypoxic vascular endothelium will become procoagulant.

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13
Q

VTE: men vs women? young vs old?

A

men > women

incidence doubles with each 10 yr inc in age

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14
Q

define thrombophilia

A

hereditary or acquired predisposition to venous thromboembolism (VTE)

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15
Q

describe, in general, the VTE risk factor model

A

everyone has an intrinsic risk for thrombosis, from Genes and Acquired Risk Factors. then environment can make it worse, prophylaxis can make it less likely to get a thrombus

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16
Q

what are some environmental/situational risk factors for VTE?

A

pregnancy, surgery (wound healing), illness (inflammation), immobilization, trauma, air travel

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17
Q

what are some genetic risks for thrombosis?

A

anticoag deficiencies, Factor V leiden, prothrombin 20210A, Non-Type O blood type

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18
Q

what are some acquired risk factors for thrombosis?

A

age, cancer, obesity, hormone treatments, smoking

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19
Q

how does obesity contribute to a pro-thrombotic state?

A

incr FVIII due to inflammatory cytokines from adipose tissue

20
Q

how does pregnancy contribute to a pro-thrombotic state?

A

incr procoag factors (FVIII, vWF)

decr anticoag factors (protein S)

21
Q

what are two hematologic disorders that contribute to a pro-thrombotic state?

A

myeloproliferative disorders, PNH

22
Q

what are antiphospholipid antibodies (APA)?

A

autoantibodies directed against protein of phospholipid, plasma proteins that usually bind to phospholipids (ie, PS/PE on platelet surface)

23
Q

what can trigger APA?

A

meds, infections, another autoimmune disorder

24
Q

what is lupus anticoagulant? what does it do?

A

badly-named antibody. interferes with prothrombinase complex binding to phospholipid surface of platelet. somehow triggers thrombosis (we don’t know how)

25
Q

lupus anticoagulant: will it correct in a mixing study?

A

no, it is an antibody

26
Q

what are the requirements for Antiphospholipid Antibody Syndrome?

A

clinical event + persistent presence of an antiphospholipid antibody

27
Q

elevated coag factor levels: how defined? what is reason for elevation?

A

defined as >150%

can be either genetic or acquired (medical illness, obesity, APA)

28
Q

what are the major checkpoints for the clotting cascade?

A

VIIIa, Va, Xa, thrombin

29
Q

what does APC/S do?

A

inhibits Va, VIIIa

30
Q

what does antithrombin do?

A

inhibits Xa, thrombin

31
Q

a deficiency of APC/S or antithrombin will have what effect?

A

pro-coagulant, thrombin will proceed unchecked.

32
Q

What is Factor V Leiden mutation?

A

genetic mutation in Va which prevents the action of APC/S complex. pro-coagulant

33
Q

what is the prothrombin mutation?

A

genetic mutation that increases the levels of prothrombin. pro-coagulant

34
Q

define Activated Protein C Resistance

A

renders Va resistant to inactivation by activated protein C. Factor V Leiden is most common mutation. Can also be acquired.

35
Q

factor V Leiden mutation: what is penetrance?

A

asx in 90% of heterozygotes, even homozygoes may still be asx.

36
Q

how do we test for Factor V Leiden?

A

screening test for APC resistance. confirm with PCR, genetic test

37
Q

Prothrombin 20210A mutation: what is penetrance?

A

asx in 90% of heterozygotes. homozygotes have a higher risk of thrombus.

38
Q

what does Protein C do?

A

VitK-dependent factor, produced by liver. with its cofactor (protein S) inactivates factors V and VIII.

39
Q

what is an unusual risk associated with protein C and Protein S deficiency?

A

can have warfarin-induced skin necrosis

40
Q

Types of protein C deficiency?

A

Type I: activity low, antigen level low

Type II: activity low, antigen level normal

41
Q

what does Protein S do?

A

VitK-dependent factor, produced by liver. cofactor for Protein C; complex of C and S inactivates factors V and VIII

42
Q

Protein S deficiency: men v women?

A

women have lower levels than men, esp if preg or on OCPs

43
Q

Physiology of Protein S: what are the 3 forms in which it is found in the body? what happens in acute inflammatory states?

A

found bound to C4bBP protein, Free, or bound to Protein C.
in inflammatory states, more is bound to C4bBP protein, less available for Protein C binding. causes pro-coagulant state.

44
Q

describe the 3 types of Protein S deficiency

A

Type I: total antigen is low. could be acquired or congenital
Type II: normal level, activity is low
Type III: normal level, activity is low, due to binding to C4bBP, smoking, preg.

45
Q

what is the most severe/rare deficiency that yields a procoagulant state? by what age does it typically present?

A

hereditary antithrombin deficiency. typically VTE presents before age 35.

46
Q

what are the two types of antithrombin deficiency?

A

Type I: antigen low, activity low

Type II: antigen normal, activity low

M2 Hematology (15 decks)

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