Acquired Disorders_Neonatal Hemostasis_Thrombophilia and Anticoag Therapy

Acquired Disorders_Neonatal Hemostasis_Thrombophilia and Anticoag Therapy

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Unformatted text preview: MLS 483 ­ Clinical Hemostasis II Study Guide 3 Topics: Acquired Disorders, Neonatal Hemostasis, Thrombophilia, and Anticoagulant Therapy 2. Objectives: ​ At the conclusion of this unit, the student will be expected to complete the following objectives with a grade of C or better on course evaluations. Specifically, the student will be able to: 1. Assess acquired bleeding disorders of hemostasis (ex. DIC, Vitamin K Deficiency, Liver Disease, etc.). Specifically address clinical manifestations, pathophysiology, expected laboratory results, reasoning behind expected laboratory results, treatment options, and means of differentiation. 2. Assess hypercoagulable conditions of hemostasis (ex. Antithrombin Deficiency, Protein C Deficiency, Factor V Leiden, Prothrombin 20210, etc.). Specifically address clinical manifestations, risk factors, pathophysiology, expected laboratory results, reasoning behind expected laboratory results, treatment options, and diagnostic mechanisms. 3. Differentiate arterial and venous thrombi. 4. Investigate Deep Vein Thrombosis and Pulmonary Embolism. Address definitions, clinical applications, related laboratory testing, risk factors, and treatment options. 5. Calculate the International Normalized Ratio (INR), utilizing and explaining the appropriate components. 6. Evaluate anticoagulant therapies. Specifically, describe examples of each, modes of action, reasons for use, adverse effects, laboratory tests used for monitoring, and treatment in cases of overdose. 7. Examine the Lupus Anticoagulant. Specifically address its definition, pathophysiology, related clinical implications, expected laboratory results, and diagnostic testing protocol. 8. Analyze automated methodologies utilized in hemostasis laboratory testing. 9. Compare and contrast newborn hemostasis testing results with adult values. 10. Investigate normal and abnormal hemostatic conditions of a neonate. 11. Examine testing methods related to acquired disorders, hypercoagulable disorders, and anticoagulant therapy. Include a discussion of methodology, purpose, principle, procedural notes, reagents involved, results interpretation, clinical implications, reasons for spurious results, and troubleshooting mechanisms. 12. Correlate laboratory results with hemostatic disease processes and/or clinical manifestations 13. Given a specific diagnosis, predict hemostasis testing results that would likely manifest in that condition. 14. Diagnose abnormal and normal conditions given specific laboratory results and/or patient history and clinical manifestations. Required Reading​ : 1. McKenzie: Chapters 32, 33, 36, Required References​ : 1. McKenzie, SB: ​ Clinical Laboratory Hematology (2nd​ ​ ed)​ . Upper Saddle River, NJ. Prentice Hall, 2010. MLS 473 lecture notes 1. Complete the table. MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 1 of 12 Factor V Leiden Prothrombin 20210 Protein C Deficiency Protein S Deficiency Antithrombin Deficiency Clinical Findings Autosomal dominant – single point mutation at codon 506 of factor V gene; glutamine for arginine Mutation at 20210 of prothrombin gene; guanine for adenine Heterozygous​ recurrent thrombosis & PE Homozygous​ serious complications Homozygous​ severe at birth Heterozygous​ similar to PC deficiency; arteriole thrombosis Autosomal dominant Homozygous Heterozygous – recurring DVT at a young age Pathophysiology & Physiologic Effect Alters Factor V’s response to PC – NOT THE AMOUNT OF FACTOR V Lab Evaluation & Therapy Clot based modification of aPTT; Diagnostic: PCR for mutation determination Elevated prothrombin levels PCR; testing prothrombin alone is not definitive Type 1: Quantitative Type 2: Qualitative Skin necrosis because of oral anticoagulants Types 1 – decreased total PS, free PS, PS activity Type 2 – Normal total PS and free PS, decreased PS activity Type 3 – Normal total PS, decreased free PS and PS activity Type 1 – Quantitative defect Type 2 – Molecular defect (Qualitative) AT​ ​ inhibits serine proteases​ inhibits fibrin formation Immunological: total PS​ ​ ELISA; free PS​ monoclonal antibodies Functional: measures ability of PS to serve as a cofactor for APC Chromogenic assay Progressive activity assay Heparin Cofactor Assay 2. Compare/contrast arterial and venous thrombi. Arterial: Platelets and fibrin​ ​ little WBCs and RBCs Pathophysiology: form at sites where endothelium is damage i.e.plaques Complications: embolus Labs: hyperhomocystinemia, CRP, TPA, lipidemia Venous: RBCS trapped in fibrin, less platelets Pathophysiology: form at sites where endothelium is damage i.e. direct trauma Complications: thrombophlebitis, DVT, pulmonary embolism 3. Differentiate hypercoagulable disorder subtypes: Antithrombin Deficiency Type I Type II (Active Site Defect) Type II (Heparin­binding Site Defect) MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 2 of 12 Protein C Deficiency Type I Type II Protein S Deficiency Type I Type II Type III 4. Discuss the conditions of DVT (deep vein thrombosis) and PE (pulmonary embolism). Include definitions, clinical applications, pathophysiology, risk factors, associated laboratory testing, and treatment. 5. Briefly discuss the pathophysiology leading to the thrombophilic tendencies of the following disorders/conditions: Heparin Cofactor II Deficiency Hyperhomocysteinemia Dysfibrinogenemia Elevated Factor VIII Factor XII Deficiency MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 3 of 12 Plasminogen Deficiency TTP HIT HUS Malignancy Pregnancy/Oral Contraceptives 6. Discuss each item as it relates to the Lupus Anticoagulant. Definition Naming Confusion Clinical Manifestations & Applications Pathophysiology Implications for the Laboratory Diagnostic Protocol 7. Address each item as it relates to screening tests for the Lupus Anticoagulant. MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 4 of 12 Dilute Russell’s Viper Venom Time (dRVVT) Plasma Clot Time (PCT) Kaolin Clotting Time (KCT) Purpose / Principle Reagents and/or Procedural Notes Interpretation of Results 8. Discuss normal and abnormal bleeding disorders that can arise in newborns. Include a description of clinical manifestations and pathophysiology. 9. Complete the following table to compare neonatal and adult hemostatic testing/results. Normal ​ Neonatal​ Reference Normal ​ Adult​ Reference Age Adult Level Interval Interval Reached Platelet Count (x 109​ ​ /L) MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 5 of 12 Platelet Aggregation Testing PT (seconds) aPTT (seconds) Thrombin Time (seconds) Plasminogen Antithrombin Coagulation Factors Fibrinogen Group Fibrinogen Factor V Factor VIII Factor XIII Prothrombin Group Factor II Factor VII Factor IX Factor X Contact Group Factor XI Factor XII PK HMWK 10. Discuss how each of the following lab tests could (or could not) be used to help differentiate liver disease and DIC. PT and/or aPTT Platelet Count MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 6 of 12 D­Dimer Blood Smear Morphology Factor VIII Assay Factor IX Assay Factor X Assay 11. Address the items listed for each disorder. Disseminated Intravascular Coagulation Clinical Manifestations Pathophysiology (Causes/Triggers) Expected Lab Results (​ explain why that would be the expected result in this condition) Treatment Options Liver Disease Clinical Manifestations Pathophysiology MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 7 of 12 Expected Lab Results (​ explain why that would be the expected result in this condition) Treatment Options Vitamin K Deficiency Clinical Manifestations Pathophysiology (and Causes/Triggers) Expected Lab Results (​ explain why that would be the expected result in this condition) Treatment Options Primary Fibrinogenolysis Clinical Manifestations Pathophysiology Expected Lab Results (​ explain why that would be the expected result in this condition) Treatment Options 12. Complete the table related to anticoagulant therapy. Oral Anticoagulants Unfractionated Heparin (ex. Coumadin) Mode of Action MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 8 of 12 Reasons for Use Laboratory Monitoring (list the tests used and significance of results) Potential Complications Antidote (in case of overdose) MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 9 of 12 13. Explain why some hospital patients are receiving oral anticoagulants and heparin therapy simultaneously. 14. What is the INR? How is it calculated (explain the parameters used in the calculation)? How are the results interpreted (include a discussion of normal, therapeutic, and therapeutic ranges)? 15. Calculate the INR based on the following information: Patient PT = 18.9 seconds Normal Reference PT = 12.3 seconds Thromboplastin ISI = 1.2 How would you classify these results (normal, increased, decreased, therapeutic, etc.)? Discuss how these results might influence this patient’s dosage of oral anticoagulant (Coumadin). 16. Complete the table. Low Molecular Weight Thrombolytic Therapy Antiplatelet Therapy Heparin Mode of Action Indications for Use Laboratory Monitoring MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 10 of 12 Potential Complications Examples 17. What effect do thrombolytic agents have on laboratory results. 18. Discuss laboratory tests used in the evaluation of hypercoagulable states: Antithrombin III . Protein C Protein S MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 11 of 12 Plasminogen Antiplasmin D­Dimer 19. Explain the principle behind each of the following hemostasis lab testing methodologies: Electromechanical Methodology Optical Density Methodology Chromogenic Methodology MLS 483 Clinical Hemostasis II 2012 Acquired Disorders, Neonatal Hemostasis, Thrombosis, and Anticoagulant Therapy Study Guide 3 Page 12 of 12 ...
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  • Summer '16
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  • Biology, anticoagulant therapy, Neonatal Hemostasis, Clinical Hemostasis, Clinical Hemostasis II

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