DVT (a) PDF

Atherosclerosis Definition Chronic cardiac Venous thromboembolism (VTE): A clot formation in the venous circulation and is manifested as: Three primary components coagulation cascade (Virchow’s triad): Deep vein thrombosis (DVT) and Pulmonary embolism (PE). Venous stasis, (flow of blood) Vasc...

Atherosclerosis Definition Chronic cardiac Venous thromboembolism (VTE): A clot formation in the venous circulation and is manifested as: Three primary components coagulation cascade (Virchow’s triad): Deep vein thrombosis (DVT) and Pulmonary embolism (PE). Venous stasis, (flow of blood) Vascular injury, Hypercoagulability Blood + keep in the same state (balanced) HemoStasis: It keeps the blood in fluidized state What is Homeostasis? prevent loss from damaged blood vessels (balanced flow) Intact endothelium Platelets Mechanisms include: In vivo Anticoagulant Procoagulant mechanism Other name for it? Thrombocytes Access amount of platelets? Production of platelets? Thrombocytosis Thrombopoeisis Fragments of Megakaryocytes Loss their shape Clotting coagulation factors: Platelets What happens when injured? To provide close barrier = stop bleeding Serotonin Ca2+ Granules in platelets: contains: enzymes ADP Platelet-derived growth factor (PDGF) During hemostasis: three phases in rapid sequence / factor involves in clot formation: 1: Vascular spasms: immediate vasoconstriction 2: Platelet plug formation 3: Coagulation (blood clotting) Clot retraction Other events: Fibrinolysis Reorganization Repair and regeneration A blood clot is a gel that contains formed elements of the blood entangled in fibrin threads Homeostasis: Main events Drugs for clotting disorders Age: double with each 10 years after 50. History of VTE: strongest Visuals: Damage to valves, obstruction, ↑ blood viscosity and immobility. = VTE symptoms Conditions associated with venous stasis include: Major medical illness (Heart failure, AMI) That need high general anesthesia < 30 minutes Venous stasis: slowed blood flow Major surgery Paralysis (e.g., stroke, spinal cord injury) DVT (a) Polycythemia vera = high RBC production Risk factors for VTE Obesity Swelling Legs Thighs Varicoseveins. Dilating of veins (e.g., knee and hip replacement), • major orthopedic surgery (especially fractures of the pelvis, hip, or leg), or Platelets plug formation Vascular injury may result from trauma indwelling venous catheters. malignancy; activated protein C resistance deficiency of protein C, protein S, or anti-thrombin; factor VIII or XI excess; Hypercoagulable states include anti-phospholipid antibodies; and other situations. Estrogens and SERMs also linked to venous thrombosis Symptoms of DVT and PE risk factors Assessment of the patient’s status should focus on the search for Thrombus formation at the damaged blood vessel: Extrinsic pathway (shorter) Activation of prothrombinase Contrast venography allows visualization of the entire venous system in the lower extremity and abdomen. Coagulation : basic three steps Three steps: Intrinsic pathway Conversion of prothrombin to thrombin Conversion of fibrinogen to insoluble fibrin (insoluble) Pulmonary angiography allows visualization of the pulmonary arteries. unilateral leg pain, swelling persist after a night’s sleep, Patients with DVT frequently present with: and cyanosis of the skin chronic lower extremity swelling, pain, tenderness that lead to skin discoloration Post thrombotic syndrome (PTS): a long term complication of DVT Diagnosis ulceration < 0.5 mg/L Positive for d-dimer Consider PE Normal range? If more ? used frequently for the initial evaluation of patients with suspected VTE. Ultrasonography, CT and ventilation-perfusion scans: are substantially elevated in patients with acute thrombosis. D-dimer is a degradation product of fibrin blood clots in blood: If PE 4x the normal number? signs, symptoms, and risk factors low = 0 intermediate = 2 - 3 Clotting pathways Triggering step: Modified Wells Criteria: evaluating the Pretest Probability of DVT: Explosive in nature Completed in 15 seconds high probability of having acute DVT = > 3 In General Surgical Patients Tissue trauma Extrinsic: No inhibitory mechanisms to counter this pathway Monitoring Modified Caprini Risk Assessment Model for VTE PT (10-30 sec) Less = clotting More = bleeding Differences Between Extrinsic & Intrinsic exposure of Collagen to Factor XII & Thrombocytes Triggering step: Slow to proceed Takes 2 to 6 minutes Intrinsic: Many inhibitory or antagonistic mechanisms Monitoring Less = bleeding More = clotting aPTT Activated partial thrombin time 29-39 sec