VTE Flashcards
Venous thrombi
Composed of RBC, fibrin, and some platelets
Mostly RBCs
VTE symptoms present when
Flow is obstructed
Vasc tissue is inflammed
DVTs and PEs
All PEs come from DVTs
Not all DVTs lead to PEs
Virchow’s triad
Conditions that increase clotting risk
Hypercoagulable state
Endothelial injury
Circulatory state
Hypercoagulable state
Abnormal clotting components
Ex. pregnancy, cancer
Endothelial injury
Abnormal surfaces in contact with blood flow
Ex. post-op, traumatic injury
Circulatory stasis
Abnormal blood flow
Ex. long period of immobility, hospitalization
Coagulation cascade overview
Cascade initiates -> increases production of thrombin -> results in clot formation
Factor II
Prothrombin
Factor IIa
Thrombin
Postthrombotic syndrome
Long-term complication of DVT
Caused by damaged venous valves
Pigmentation and skin hardening
DVT risk factors
Age > 40 years
HF, MI
Obesity
Pregnancy
Immobilization > 10 days
DVT non-pcol treatment
Bed rest w anticoag prn
Elevate feet
Pain management
Compression stockings
PE non-pcol treatment
Oxygen
Mechanical ventilation
Compression stockings
Ideal anticoagulant
Oral
Once daily dosing
Quick onset
Limited monitoring and drug interactions
Available and effective antidote
Wide therapeutic index
Low cost
UFH
Rapid parenteral anticoag
Variable response -> incr aPTT monitoring
Heparin associated thrombocytopenia (HAT)
Non-immune mediated
Mild platelet decrease
48-72 hours post-admin
Don’t need to d/c heparin
Heparin induced thrombocytopenia (HIT)
Immune mediated
7-14 days post-admin
Platelet decrease > 50% or to < 100,000 mm3