23 - Clotting Disorders VTE Flashcards
3 Key Mechanisms
that facilitate
HEMOSTASIS
Vascular Constriction
Primary Platelet Plug Formation
Primary Hemostasis
Clot PROPAGATION through FIBRIN formation
Secondary Hemostasis
Define:
Designed to stop bleeding at the site of vascular injury through complex interactions between the vascular endothelium, platelets, procoagulant proteins, anticoagulant proteins, and fibrinolytic proteins
HEMOSTASIS
3 Pathways of Coagulation Cascade
Intrinsic
12 -> 11 > 11a > 9 > 9a > Xa
Common
X -> Xa
EXtrinsic
8a -> Xa
Xa
Prothrombin (2) –> Thrombin (2a)
Inhibitors of Coagulation Cascade
ANTI-THROMBIN 3
Inactivatesthe serine proteases:
IIa IXa Xa XIa XIIa
2 9 10 11 12
Protein C & Protein S
attenuates coagulation cascade by proteolysis of 2 cofactors:
Va & VIIIa
5 8
Protein C & S = affected by Factor V Leiden
Defects in these –> ↑CLOTTING / ↑THROMBOSIS
Factor V Leiden
Mutation in Factor V Leiden
VVV
Most COMMON defect in natural AC system
VVV
Resistance to inactivation by Protein C** & **S
↑CLOTTING / ↑THROMBOSIS
3 Types of Thrombosis
Thrombosis
formation of an innapropriate fibrin-platelet aggregate on:
Thrombosis
formation of an innapropriate fibrin-platelet aggregate on:
- *Mural**
- *endothelium** of blood or lymphatic vessel
Cardiac
within the heart
- *Thromboembolus**
- *free in lumina of blood** or lymphatic vessel
What is this score used for?
CHADS2 –> CHA2DSVASc
ISCHEMIC STROKE RISK
AFIB
Helps determine if you should be on an
Anticoagulant or NOT
Risk Factors for VTE:
VIRCHOW’S TRIAD
+
Important ones
B H V
Blood Stasis
Hypercoagulable State
Vascular Injury
Age > 40 / CANCER / TOTAL JOINT ARTHROPLASTY
HORMONAL THERAPY / PREGNANCY
Risk Factors for VTE:
Virchow’s Triad
BLOOD STASIS
BLOOD STASIS
Heart Disease
BED REST / IMMOBILIZATION / PARALYSIS
Left Ventricular Dysfunction
Venous Obstruction
Valve Damage from Hypoxemia
CVA
Risk Factors for VTE:
Virchow’s Triad
HYPERCOAGULABLE STATE
HYPERCOAGULABLE STATE
Activation of clotting Cascade
Clotting Factor Deficiencies
Mutation in Factor V Leiden
resistance to inactivation by protein C or S mechanism
MALIGNANCY
PREGNANCY / HORMONE REPLACEMENT
H/O Blood Clots
Risk Factors for VTE:
Virchow’s Triad
VASCULAR INJURY
VASCULAR INJURY
TRAUMA / SURGERY
Total Joint Artheroplasty = Hip Surgery
Heart Valve Replacement
Atherosclerosis / Atheromatous Plaque
Indwelling Vascular Catheters
VTE & PREGNANCY
HYPERCOAGULABLE STATE
Virchows Triad - VTE Risk Factors
Pregnancy –> ↑VTE Risk by 4-5x
more common in 1st half of pregnancy
20x ↑ risk in POST-partum
Reasons:
Hypercoagulability: ↑Factor 6/8 Fibronogen & Von WIllebrand Factor
Hormonal induced: ↓Venous capacitance& ↓Venous Outflow
Mechanical Obstructionbyuterus
Additional Risk Factors:
Heart Disease / Sickle / Lupus / Obesity
HTN / Smoking / Diabetes / Anemia
VTE & OCPs
HYPERCOAGULABLE STATE
Virchows Triad - VTE Risk Factors
Oral Contraception –> 3-6x VTE Risk
highest in 1st 6-12 months
Proposed Mechanisms:
↑Prothrombin ↑Factor 7/8/10
↑Fibrinogen&↑Prothrombin Frag 1/2
↑Resistance to Activated Protein C
↓Levels of Protein S
Cancer-Associated Thrombosis
HYPERCOAGULABLE STATE
Virchows Triad - VTE Risk Factors
VTE is 4-7x higher in Cancer patients
Additional Risk Factors:
Female / Older Age
BLACK / Prothrombotic Mutations
DM / Obesity / Previous VTE
Atherosclerosis / Inflammation
What is this Score used for?
PADUA PREDICTION SCORE
Risk factors for:
VTE** in **HOSPITALIZED MEDICAL PATIENTS
4+ = High risk –> thromboProphylaxis
<4 = could consider prophylaxis