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TOPIC: discuss the pathophysiology, clinical manifestations,

NURS530 Week 4 Presentation
Your presentation must: be 4-7 minutes long, can use PowerPoint slides

TOPIC: discuss the pathophysiology, clinical manifestations, evaluation, and treatment advances of: Disseminated Intravascular Coagulation.

Explain the processes or concepts in your own words using references to support your explanations.
Include all necessary physiology and pathophysiology in your explanation.
Use detailed explanations with master’s level terminology to teach or explain. Your classmates and professional colleagues are your audience.
Include at least one type of visual aid in your presentation, such as PowerPoint slides, diagrams, whiteboard use, etc.
Use APA format to style your visual aids and cite your sources.
Cite at least two references with on-screen citations.
Include a reference list in your visual aid or at the end of your slide set.

An Examination of Disseminated Intravascular Coagulation
Introduction
Disseminated intravascular coagulation (DIC) is a serious medical condition characterized by the excessive activation of coagulation pathways that leads to microvascular thrombosis and bleeding throughout the body (Levi & van der Poll, 2010). This condition can be triggered by a variety of underlying causes such as trauma, sepsis, cancer, obstetric complications, and other medical conditions. If left untreated, DIC can damage vital organs and tissues due to blocked circulation and result in multi-organ failure (Levi & van der Poll, 2010). Therefore, prompt diagnosis and treatment of DIC as well as its underlying trigger is crucial for improving patient outcomes.
Pathophysiology

The pathophysiology of DIC involves an excessive activation of coagulation that overwhelms the body’s natural anticoagulant mechanisms (Levi & van der Poll, 2010). Tissue factor released from damaged cells activates the extrinsic coagulation pathway, leading to a “cytokine storm” and systemic inflammatory response (Levi & van der Poll, 2010). This results in the overproduction of thrombin and fibrin, which depletes platelets and coagulation factors. Concurrently, fibrinolysis is impaired due to increased plasminogen activator inhibitor-1 (PAI-1) levels (Levi & van der Poll, 2010). The end result is microvascular thrombosis due to consumption of clotting factors and platelets as well as hemorrhage from impaired fibrinolysis.
Clinical Manifestations
Common clinical signs of DIC include bleeding, easy bruising, petechiae, ecchymoses, epistaxis, gastrointestinal bleeding, and heavy menstrual bleeding (Levi & van der Poll, 2010). Other manifestations involve organ dysfunction such as acute renal failure, liver damage, encephalopathy, and respiratory distress due to microvascular thrombosis. Laboratory findings indicative of DIC are thrombocytopenia, elevated D-dimer and fibrin degradation products, prolonged prothrombin time and partial thromboplastin time, and decreased fibrinogen levels (Levi & van der Poll, 2010).
Evaluation
The diagnosis of DIC is based on clinical presentation and confirmed via laboratory testing. The International Society on Thrombosis and Haemostasis has established diagnostic criteria that incorporates clinical symptoms and laboratory abnormalities (Taylor et al., 2001). Key lab tests include complete blood count with platelet count, prothrombin time, partial thromboplastin time, fibrinogen level, and D-dimer level. Imaging studies may help identify the underlying condition triggering DIC.
Treatment Advances
Treatment focuses on managing the cause of DIC and replacing depleted clotting factors. Platelet transfusions are given for bleeding or very low platelet counts below 50,000/μL (Levi & van der Poll, 2010). Fresh frozen plasma or cryoprecipitate replaces fibrinogen and coagulation factors. Antifibrinolytic drugs such as tranexamic acid reduce fibrinolysis. Low molecular weight heparin provides anticoagulation. For sepsis-induced DIC, activated protein C may lower mortality (Bernard et al., 2001). Novel targeted therapies under investigation include tissue factor pathway inhibitor and thrombomodulin (Levi & van der Poll, 2010). Prompt diagnosis and treatment of the precipitating condition prevents further coagulopathy.
Conclusion
In summary, DIC is a serious condition involving excessive coagulation activation leading to microvascular thrombosis and bleeding. Timely diagnosis and treatment of the underlying trigger is crucial for managing this coagulopathy and improving patient outcomes. Further research into new targeted therapies may help optimize DIC treatment.
References

Bernard, G. R., Vincent, J. L., Laterre, P. F., LaRosa, S. P., Dhainaut, J. F., Lopez-Rodriguez, A., … & Macias, W. L. (2001). Efficacy and safety of recombinant human activated protein C for severe sepsis. New England Journal of Medicine, 344(10), 699-709.
Levi, M., & van der Poll, T. (2010). Two-way interactions between inflammation and coagulation. Trends in cardiovascular medicine, 20(8), 254-259.
Taylor, F. B., Jr, Toh, C. H., Hoots, W. K., Wada, H., & Levi, M. (2001). Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thrombosis and haemostasis, 86(5), 1327-1330.

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