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BL/DD USMLE and Basics > BL - Hereditary and Acquired Thrombotic Disorders > Flashcards

BL - Hereditary and Acquired Thrombotic Disorders Flashcards

1
Q

Thick muscular vessel
High pressure/
flow
High oxygen

A

Artery

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2
Q

Thin, pliable vessel
Low pressure/slow flow
Low oxygen

A

vein

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3
Q

Platelets more important in

A

Arterial

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4
Q

Blood clotting factors more important in

A

Venous

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5
Q

Virchow’s Triad

A

VENOUS STASIS
ALTERED VESSELS
ALTERED COAGULABILITY

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6
Q 
Trauma
Post-surgery
Immobility/Inactivity
Obesity
Pregnancy
Estrogens/Birth control
Malignancy
Age
A

Risk Factors for Venous Thrombosis

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7
Q
  • Factor V Leiden
  • Prothrombin gene mutation
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin deficiency

These are all?

A

Inherited hypercoagulable disorders

Risk Factors for Venous Thrombosis

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8
Q

~inflammatory damage
~mechanical injury
~hypoxia

A

ALTERED VESSELS

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9
Q

-clotting factors ( increased factors VII, VIII, XI)
-hematologic disorders
-**Malignancy
Vasculitic/proinflammatory disorders
-Disseminated intravascular coagulation ( DIC)

A

Acquired hypercoagulable states

Risk Factors for Venous Thrombosis

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10
Q 
SOB, acute versus gradual
Diminished exercise capacity
chest pain
syncope
cardiac arrest/death
A

Pulmonary embolism (PE)

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11
Q

-impaired venous return with blood flow
edema develops due to increased hydrostatic pressure, pain present

  • blood flow through alternative routes leads to dilated superficial veins
  • redness and warmth of the affected area
A

Venous thrombosis-Limb

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12
Q

~immobility
~paralysis
~reduced flow states

A

VENOUS STASIS

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13
Q

Blood work for DVT concerns

A
  • elevated D-Dimer*

- Negative D-Dimer rules out thrombosis

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14
Q

Acquired hypercoagulable states

A
  • clotting factors ( increased factors VII, VIII, XI)
  • hematologic disorders
  • **Malignancy
  • Vasculitic/proinflammatory disorders
  • Disseminated intravascular coagulation ( DIC)
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15
Q

Inherited hypercoagulable disorders

A
  • Factor V Leiden
  • Prothrombin gene mutation
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin deficiency
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16
Q

~inflammatory stimuli

~consumption of endogenous anticoagulants

A

ALTERED COAGULABILITY

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17
Q

VENOUS STASIS
ALTERED VESSELS
ALTERED COAGULABILITY

A

Virchow’s Triad

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18
Q

Treatment for acute clot is:_____

A

heparin/tPA

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19
Q

_____ used to prevent additional clots

A

Warfarin

20
Q

Strongest risk factor for clot?

A

Malignancy

21
Q

D-dimers can only be formed when crosslinked fibrin has been degraded by plasmin through ______.

A

fibrinolysis

22
Q

Do blood clots form in the lung?

A

Nope, they travel there

23
Q

For arterial thrombi, in the acute setting, heparin (to prevent further clot formation) and a fibrinolytic
agent such as______(to lyse the existing clot) are indicated

A

tPA

24
Q

D-dimers can only be formed when crosslinked fibrin has been degraded by _____through fibrinolysis.

A

plasmin

25
Q

Warfarin acts by inhibiting the activity of ______dependent enzymes (Factors II, VII, IX, X, Protein C, Protein S)

A

vitamin K

26
Q

thrombus can break off and travel through major veins, right heart into pulmonary artery until it becomes lodged

A

PE

27
Q

Blood flow through pulmonary artery is impaired by thrombus, Lung tissue past thrombus cannot participate in gas exchange, tissue can:

A

infarct (Pulmonary infarct)

28
Q

Warfarin acts by inhibiting the activity of vitamin K dependent enzymes (Factors ____________)

A

II, VII, IX, X, Protein C, Protein S

29
Q

Increased pulmonary vascular resistance can lead to_______

A

right ventricular dysfunction

30
Q

Increased airway resistance d/t bronchoconstriction

A

Decreased pulmonary compliance

in PE

31
Q

If clot burden is high ( saddle embolus-both PA affected)->

A

cardiovascular arrest and death in PE

32
Q

______ inactivates activated clotting factors

A

Heparin

33
Q

Warfarin______ treat the acute clot-do not give alone for acute event!

A

does NOT

34
Q

Reduction of vitamin K by warfarin dependent factors takes at least____ days regardless of INR

A

4-5

35
Q

Due to an autosomal dominant mutation of the factor V gene that leads to partial resistance to inactivation through proteolytic cleavage by protein C.

A

Factor V Leiden (Activated Protein C Resistance)

36
Q

vitamin K-dependent plasma protein that, when activated, inactivates factors Va and VIIIa to inhibit coagulation.
Deficiency is inherited in an autosomal dominant fashion.

A

Protein C Deficiency

37
Q

vitamin K-dependent plasma protein that facilitates the anticoagulant activity of activated protein C. As with protein C, deficiency is inherited as an autosomal dominant trait.

A

Protein S Deficiency

38
Q

regulates coagulation by inactivating thrombin as well as factors Xa, IXa, XIa and XIIa.

deficiency is inherited in an autosomal dominant fashion.

A

Antithrombin Deficiency

39
Q

Oral anticoag drug?

A

Warfarin/ Coumadin

40
Q

-Pregnancy
-active thrombosis
-DIC
-nephrotic syndrome
-use of warfarin
-birth control
Can cause?

A

Acquired low levels occur of Protein S

41
Q

provokes blood thrombosis in a/v as well as pregnancy-related complications

The diagnostic criteria require one clinical event, i.e. thrombosis or pregnancy complication, and two blood tests spaced at 12 weeks apart that test positive for one of the three antibodies

A

Antiphospholipid syndrome

42
Q

Is factor 5 Leiden a deficiency

A

NO
it is a mutation
Protein C cant break down this factor 5
it sticks around and clots

43
Q

Anticardiolipin Antibodies
Lupus anticoagulant
Beta2-glycoprotein-I antibodies

A

Antiphospholipid syndrome positive for one of these three antibodies

44
Q

Antiplatelet therapy for arterial thrombosis

______ therapy for venous thrombosis

A

Anticoagulant

45
Q

Most inherited hypercoagulable states do not cause:

A

arterial thrombosis

46
Q

______ therapy for arterial thrombosis

Anticoagulant therapy for venous thrombosis

A

Antiplatelet

BL/DD USMLE and Basics (55 decks)

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