VTE Patho + Prophylaxis Flashcards
(54 cards)
3 Fxns of endothelial in BVs
1) barrier: hide shit in sub-endo
2) Antithrombotic + antiplatelet secretions
3) Fibrinolytic secretions
Primary Hemostasis
Platelet aggregation + activation
- damage to BV— collagen + vWF —- bind to cells + activate —- release serotonin, thromboxane A2, ADP—- binds to IIa/IIb receptors === activation of platelets + conformation change
— can bind to fibrinogen to clump together
Secondary hemostasis
coagulation cascade
— damage: TF release that activates cascade—— prothrombin—- thrombin
- thrombin cleaves fibrinogen to fibrin
stabilize clots
What is the 3 fxns of thrombin
1) cleave fibrinogen to fibrin
2) recruit + activate platelets
3) increase thrombin release (+ feedback)
What are some examples of inhibitors of coagulation
antithrombin , heparin, Protein C + S
What is thrombosis
process that occurs with inappropriate or over-activation of hemostasis in an not injured or slightly injured BV
Arterial thrombus vs venous thrombus
Arterial: results from ruptured plaque (atherosclerotic) in arteries —- causes MI, stroke, PAD
Venous: forms from slowing /decrease BF in venous system —- DVT or PE (normally result of trauma or surgery)
T or F: most PEs start from thrombus formed in deep veins of legs that travel to LS of heart + go to lungs
F- RS of heart
Why do DVTs and PEs not cause HAs
—- clots that form in venous system ; they gets stuck in lungs before getting into the LS of the heart + impact BF to the heart itself
Which type of DVT have a higher risk of thrombus embolization
Deep veins —- specifically we care more about the proximal ones (closer to the lungs)
—- aka anything about the knee—-scary
Superficial ones: smaller + closer to surface
T or F: VTEs are the 2nd most common cause of CVD in Canada
T
T or F: 1/3 of people with VTE will get recurrent episodes
T
T or F: 50% of VTEs occur in pts without RFs
T
What is Virchow’s triad
Stasis of BF: slow turbulent BF (not laminar)
— increase conc of shit near BV surface + increase change of interaction
Hypercoagulability: more likely to clot
BV injury : activation of primary + secondary hemostasis
What are conditions that increase clotting risk (hypercoagulability)
Protein C or S deficiency
Prothrombin gene mutation
Anthiphospholipid Ab
Antithrombin deficiency
Factor V Leiden
Pregnancy
Estrogen therapy
Malignancy
What are Strong RF of VTE
fracture of hip or leg
hip or knee surgery
major trauma /surgery
SC injury
Moderate RF of VTE
Chemo
HF
RF
pregnancy (postpartum)
previous VTE
malignancy
hormone replacement therapy
thrombophilia
Weak RF of VTE
bed rest > 3 days
immobility for LT (prolonged travel)
age
obesity
pregnancy
varicose veins
SS of DVT
unilateral swelling, pain, cramping, warm
T or F: if have DVT/PE, you may have elevated D dimer
T- D dimer is breakdown product of fibrin
SS of PE
cough, chest tightness, SoB, dizzy, palpitations, tachypnea, tachycardia, hypoxemia, fever, distended neck veins
What is the Wells Criteria
Scoring system to determine what type of test to use
—- gives risk of VTE —- and what to do for there
If pt low risk of VTE based on Well’s criteria, what test do we do
D dimer test
—- high sensitivity but low specificity
—- good at ruling OUT (if - : don’t have VTE)
If pt moderate to high risk of VTE based on wells criteria, what do we do next
Use more specific testing
DVT: compression ultrasonography
PE
- spiral CT: use more often (use X rays to look into body)
- ventilation perfusion scan : give radioactive shit to see if mismatch bw ventilation + perfusion around body