NUR 9211 Hematology 2018

Vaglio, S., Calizzani, G., Lanzoni, M., Candura, F., Profili, S., Catalano, L., . . . Grazini, G. (2013). The demand for human albumin in Italy. Blood Transfusion, 11, 26-32.

Merriam-Webster. (2018). Plasma. Retrieved from Merriam-Webster Dictionary: https://www.merriam-webster.com/dictionary/plasma  

Busher Janice T. Serum Albumin and Globulin. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 101. Available from: https://www.ncbi.nlm.nih.gov/books/NBK204/

Busher Janice T. Serum Albumin and Globulin. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 101. Available from: https://www.ncbi.nlm.nih.gov/books/NBK204/

Merriam-Webster. (2018). Globulin. Retrieved from Merriam-Webster Dictionary: https://www.merriam-webster.com/dictionary/globulin

ReferencesHuether, S.E., Rote, N.S., & McCance, K.L. (2019). Structure and function of the hematologic system. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 890-925). St. Louis, MO: Elsevier.McCance, K.L., & Rote, N.S. (2019). Alterations of erythrocyte, platelet, and hemostatic function. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 926-962). St. Louis, MO: Elsevier.

    Albumin does not diffuse freely through intact vascular endothelium. Hence, it is the major protein providing the critical colloid osmotic or oncotic pressure that regulates passage of water and diffusable solutes through the capillaries. Albumin accounts for 70% of the colloid osmotic pressure. It exerts a greater osmotic force than can be accounted for solely on the basis of the number of molecules dissolved in the plasma, and for this reason it cannot be completely replaced by inert substances such as dextran. Reference:Busher Janice T. Serum Albumin and Globulin. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 101.  https://www.ncbi.nlm.nih.gov/books/NBK204/

Reeves, H. M., & Winters, J. L. (2013). The mechanisms of action of plasma exchange. British Journal of Haematology, 164, 342-351.

It has been hypothesized that the bulk removal of immunoglobulinby plasmaphoresis might lead to the removal of negative feedbackon the antibody-producing cells.Reference: Reeves, H. M., & Winters, J. L. (2013). The mechanisms of action of plasma exchange. British Journal of Haematology, 164, 342-351.

ReferencesMcCance, K.L., & Rote, N.S. (2019). Alterations of erythrocyte, platelet, and hemostatic function. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 926-962). St. Louis, MO: Elsevier.

Jones and Bartlett Learning. (2017). Nurses Drug Handbook. Burlington: Jones and Bartlett Learning.

Also known as Familial Essential Thrombocythemia, this chronic condition occurs because of excessive platelet production due to a defect in bone marrow megakaryocyte progenitor cells.McCance, K. L., & Rote, N. S. (2018). Alterations in Erythrocyte, Platelet, and Hemostatic Functions. In S. E. Huether, & K. L. McCance, Pathophysiology. A Biologic Basis for Disease in Adults and Children (pp. 926-962). St. Louis: Elsevier.

Aspirin achieves its antithrombotic effect by permanently inactivating platelet cyclooxygenase (COX)-1, thus blocking TXA2 biosynthesis. While low-dose aspirin given once daily is known to inhibit platelet TXA2 biosynthesis by approximately 97 to 99% in healthy subjects, the same aspirin regimen is unable to fully inhibit platelet TXA2 production in approximately 80% of ET patients.Low-dose aspirin is currently recommended for the primary or secondary prevention of atherothrombosis in ET, despite the lack of direct, randomized evidence for its efficacy and safety in this setting. The present results argue against the adequacy of a conventional aspirin regimen for a substantial proportion of ET patients and suggest the need of a properly sized, randomized trial testing the efficacy and safety of a twice daily regimen of antiplatelet prophylaxis. Although twice-daily dosing may reduce compliance as compared to a once-daily regimen, such an approach has been used successfully for stroke prevention in patients with cerebrovascular disease. We conclude that the abnormal magakaryopoiesis that characterizes ET is responsible for shorter lasting antiplatelet effects of low-dose aspirin through faster renewal of platelet COX-1. This abnormal biochemical and functional phenotype can be reverted to a normal pattern of platelet response by modulating the aspirin dosing interval but not the dose. Reference:Pascale, S., Petrucci, G., Dragani, A., Habib, A., Zaccardi, F., Pagliaccia, F., . . . Patrono, C. (2012). Aspirin-insensitive thromboxane biosynthesis in essential thrombocythemia is explained by accelerated renewal of the drug target. American Society of Hematology, 1-33. doi:doi:10.1182/blood-2011-06-359224

ReferencesHuether, S.E., Rote, N.S., & McCance, K.L. (2019). Structure and function of the hematologic system. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 890-925). St. Louis, MO: Elsevier.