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Welcome Applicants!! 

Welcome Applicants!! . Morning Report Friday, October 28 th. Deep venous thrombosis. What is a DVT?. Etiology. Presence of a CVL* Genetic risk factors ( thrombophelia ) Underlying medical conditions Malignancy Sepsis Nephrotic syndrome Vasculitis Congenital heart disease.

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Welcome Applicants!! 

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  1. Welcome Applicants!! Morning Report Friday, October 28th

  2. Deep venous thrombosis

  3. What is a DVT?

  4. Etiology • Presence of a CVL* • Genetic risk factors (thrombophelia) • Underlying medical conditions • Malignancy • Sepsis • Nephrotic syndrome • Vasculitis • Congenital heart disease

  5. Risk Factors • Aging • Immobilization longer than 3 days • Pregnancy • Major surgery in the past 4 weeks • Trauma • IV drug use • Use of OCPs

  6. Clinical Features • Extremity pain/ tenderness • Swelling • Palpable cord • Discoloration (erythema) • Venous distention • Prominence of superficial veins • Cyanosis

  7. Diagnosis • Gold standard= venography • Doppler US • Adequate for Dx of lower extremity DVT • Not very sensitive for upper extremity DVT

  8. When to Consider Thrombophelia… • Positive family history • History of recurrent clots • Thrombi in unusual locations • Thrombosis at an early age

  9. Activated Protein C Resistance • Most common genetic disorder causing thrombophelia • 3-8% Caucasians • 1% African Americans • Caused by Factor V Leiden mutation •  Loss of the ability of the activated protein C to neutralize ongoing activation of the factor V molecule • Heterozygotes: threefold increased risk of DVT • Homozygotes: 30-fold increased risk

  10. Prothrombin 20210A Mutation • Second most common genetic risk factor • Mutation increased concentration of prothrombin in plasma 3-5 fold increase of thrombosis

  11. Hyperhomocysteinemia • Mutations in the genes for cystathionine and methylenetetrahydrofolatereductase elevated homocystine levels • Rarely causes arterial or venous thrombotic disease in childhood

  12. Deficiency of ATIII, Protein C or S • Homozygous AT deficiency is incompatible with life • Homozygous PC or PS deficiency  purpurafulminans within hours of birth • Heterozygotes: 50% increased risk of developing thromboembolism by middle age

  13. Lipoprotein (a) • Elevated levels associated with cardiac disease in adults • Also has anti-fibrinolytic properties which can  thrombotic disease • Serum levels >30mg/dL increase the likelihood of thromboembolism by a factor of seven

  14. Antiphospholipid Syndrome • Due to circulating antibodies against a protein-lipid complex • Can occur with or without rheumatologic disease • Can lead to pregnancy-related complications • Miscarriage

  15. Labs to Order

  16. Treatment • Acute life-threatening occlusions • Thrombolytic therapy • Acute non-life threatening occlusions • Initally… • Unfractionated heparin OR • Low-molecular weight heparin • Then… • Transition heparin to warfarin OR • Continue LMWH

  17. Treatment • Duration 3-6 months • May consider future prophylactic anticoagulation in patients with genetic predisposition during high-risk situations

  18. Complications • Pulmonary embolism • Recurrent thrombosis • Postphlebitic syndrome • Chronic pain, swelling and discoloration of the affected extremity

  19. Thanks for your attention!! Noon Conference: Class Housestaff! *Dr. Desselle will be coming by each class meeting to explain inservice scores as well as go over journal club presentations with the third years!*

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