TAILIEUCHUNG - Ebook Intensive care medicine ( 7th edition): Part 2

(BQ) Part 2 book "Intensive care medicine" includes: Hematologic and oncologic problems in the intensive care unit, pharmacology, overdoses and poisonings, transplantation, metabolism nutrition, psychiatric issues in intensive care, contemporary challenges in the intensive care unit,. | SECTION IX HEMATOLOGIC AND ONCOLOGIC PROBLEMS IN THE INTENSIVE CARE UNIT PATRICK F. FOGARTY CHAPTER 108 DISORDERS OF HEMOSTASIS IN CRITICALLY ILL PATIENTS JEREMIAH BOLES AND ALICE D. MA Disorders of hemostasis are common in critically ill patients. This chapter will review hemostasis pathophysiology of commonly encountered congenital and acquired bleeding disorders along with their associated symptoms laboratory findings and management. REVIEW OF NORMAL HEMOSTASIS Hemostasis can be broken into a series of steps occurring in overlapping sequence. Primary hemostasis refers to the interactions between the platelet and the injured vessel wall culminating in the formation of a platelet plug. The humoral phase of clotting or secondary hemostasis encompasses a series of enzymatic reactions resulting in a hemostatic fibrin plug. Finally fibrinolysis and wound repair occur. Each of these steps is carefully regulated and perturbations can predispose to either hemorrhage or thrombosis. Depending on the nature of the defect the hemorrhagic or thrombotic tendency can be either profound or subtle. Primary hemostasis begins at the site of vascular injury with platelets adhering to the subendothelium utilizing interactions between molecules such as collagen and von Willebrand factor vWF in the vessel wall with glycoprotein GP receptors on the platelet surface. Upon exposure to agonists present at a wounded vessel signal transduction leads to platelet activation. Via a process known as inside-out signaling the platelet membrane integrin a2bP3 also known as GP IIbIIIa undergoes a conformational change to be able to bind fibrinogen which cross-links adjacent platelets leading to platelet aggregation. Secretion of granular contents is also triggered by outside signals potentiating further platelet activation Fig. . Lastly the surface of the platelet changes to serve as an adequate scaffold for the series of biochemical reactions resulting in thrombin generation. Following .

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