BL - Hereditary and Acquired Thrombotic Disorders Flashcards
Thick muscular vessel
High pressure/
flow
High oxygen
Artery
Thin, pliable vessel
Low pressure/slow flow
Low oxygen
vein
Platelets more important in
Arterial
Blood clotting factors more important in
Venous
Virchow’s Triad
VENOUS STASIS
ALTERED VESSELS
ALTERED COAGULABILITY
Trauma Post-surgery Immobility/Inactivity Obesity Pregnancy Estrogens/Birth control Malignancy Age
Risk Factors for Venous Thrombosis
- Factor V Leiden
- Prothrombin gene mutation
- Protein C deficiency
- Protein S deficiency
- Antithrombin deficiency
These are all?
Inherited hypercoagulable disorders
Risk Factors for Venous Thrombosis
~inflammatory damage
~mechanical injury
~hypoxia
ALTERED VESSELS
-clotting factors ( increased factors VII, VIII, XI)
-hematologic disorders
-**Malignancy
Vasculitic/proinflammatory disorders
-Disseminated intravascular coagulation ( DIC)
Acquired hypercoagulable states
Risk Factors for Venous Thrombosis
SOB, acute versus gradual Diminished exercise capacity chest pain syncope cardiac arrest/death
Pulmonary embolism (PE)
-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
Venous thrombosis-Limb
~immobility
~paralysis
~reduced flow states
VENOUS STASIS
Blood work for DVT concerns
- elevated D-Dimer*
- Negative D-Dimer rules out thrombosis
Acquired hypercoagulable states
- clotting factors ( increased factors VII, VIII, XI)
- hematologic disorders
- **Malignancy
- Vasculitic/proinflammatory disorders
- Disseminated intravascular coagulation ( DIC)
Inherited hypercoagulable disorders
- Factor V Leiden
- Prothrombin gene mutation
- Protein C deficiency
- Protein S deficiency
- Antithrombin deficiency
~inflammatory stimuli
~consumption of endogenous anticoagulants
ALTERED COAGULABILITY
VENOUS STASIS
ALTERED VESSELS
ALTERED COAGULABILITY
Virchow’s Triad
Treatment for acute clot is:_____
heparin/tPA
_____ used to prevent additional clots
Warfarin
Strongest risk factor for clot?
Malignancy
D-dimers can only be formed when crosslinked fibrin has been degraded by plasmin through ______.
fibrinolysis
Do blood clots form in the lung?
Nope, they travel there
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
tPA
D-dimers can only be formed when crosslinked fibrin has been degraded by _____through fibrinolysis.
plasmin
Warfarin acts by inhibiting the activity of ______dependent enzymes (Factors II, VII, IX, X, Protein C, Protein S)
vitamin K
thrombus can break off and travel through major veins, right heart into pulmonary artery until it becomes lodged
PE
Blood flow through pulmonary artery is impaired by thrombus, Lung tissue past thrombus cannot participate in gas exchange, tissue can:
infarct (Pulmonary infarct)
Warfarin acts by inhibiting the activity of vitamin K dependent enzymes (Factors ____________)
II, VII, IX, X, Protein C, Protein S
Increased pulmonary vascular resistance can lead to_______
right ventricular dysfunction
Increased airway resistance d/t bronchoconstriction
Decreased pulmonary compliance
in PE
If clot burden is high ( saddle embolus-both PA affected)->
cardiovascular arrest and death in PE
______ inactivates activated clotting factors
Heparin
Warfarin______ treat the acute clot-do not give alone for acute event!
does NOT
Reduction of vitamin K by warfarin dependent factors takes at least____ days regardless of INR
4-5
Due to an autosomal dominant mutation of the factor V gene that leads to partial resistance to inactivation through proteolytic cleavage by protein C.
Factor V Leiden (Activated Protein C Resistance)
vitamin K-dependent plasma protein that, when activated, inactivates factors Va and VIIIa to inhibit coagulation.
Deficiency is inherited in an autosomal dominant fashion.
Protein C Deficiency
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.
Protein S Deficiency
regulates coagulation by inactivating thrombin as well as factors Xa, IXa, XIa and XIIa.
deficiency is inherited in an autosomal dominant fashion.
Antithrombin Deficiency
Oral anticoag drug?
Warfarin/ Coumadin
-Pregnancy
-active thrombosis
-DIC
-nephrotic syndrome
-use of warfarin
-birth control
Can cause?
Acquired low levels occur of Protein S
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
Antiphospholipid syndrome
Is factor 5 Leiden a deficiency
NO
it is a mutation
Protein C cant break down this factor 5
it sticks around and clots
Anticardiolipin Antibodies
Lupus anticoagulant
Beta2-glycoprotein-I antibodies
Antiphospholipid syndrome positive for one of these three antibodies
Antiplatelet therapy for arterial thrombosis
______ therapy for venous thrombosis
Anticoagulant
Most inherited hypercoagulable states do not cause:
arterial thrombosis
______ therapy for arterial thrombosis
Anticoagulant therapy for venous thrombosis
Antiplatelet
