NUR 631 APEA MyQBank Assignment: Hematology

Assessment Description

APEA MyQBank questions correlate directly with your success on the 3P High Stakes Exam. To prepare for the APEA MyQBank exam, review the CareOnPoint materials for this topic prior to completing this assignment.

Complete the following:

Take the APEA MyQBank: Hematology in Exam Mode.

Following the exam, upload the certificate of completion, showing the completion of all assigned exam modules, to the assignment dropbox.

If your score is 79% or lower, complete the “APEA MyQBank Remediation Plan,” located on the college page of the Student Success Center under the APRN Core Courses: 3P Courses tab, and upload it per the instructor’s direction.

APEA MyQBank percentage scores will be converted to assignment grade points according to the scoring guide found in the Class Resources.

Adults over the age of 65 are more likely to develop anemia of chronic disease, which is a mild to moderate anemia caused by reduced erythropoiesis and impaired iron use in those with chronic systemic disease or inflammation (McCance et al., 2019). It is thought that the elderly is more likely to develop chronic anemia due to a combination of “decreased erythrocyte lifespan, suppressed erythropoietin production, ineffective bone marrow erythroid progenitor response to erythropoietin, and altered iron metabolism and iron sequestration in macrophages.” One of the primary hallmarks of chronic illness anemia during treatment is that patients do not react to traditional iron replacement therapy. There is limited evidence that treatment with erythropoietin and ways to improve iron storage can be done; nonetheless, transfusion may impair the fate of critically ill persons (McCance et al., 2019). The primary goal of treatment is to address the underlying problems.

Endothelial injury is described as endothelial function damage caused by a variety of events such as atherosclerosis, bacterial toxins, exogenous chemicals, or radiation. Cigarette smoke has been discovered to influence the pathophysiology of atherosclerosis due to the toxins emitted, which include metals, free radicals, nicotine, and aldehydes (Ding et al., 2020). These drugs greatly increase the quantity of low-density lipoproteins oxidized, lowering nitric oxide, and increasing blood viscosity, resulting in thrombus formation. It also causes an inflammatory response by secreting macrophages and other inflammatory chemicals, which stimulate chemokines and increase the formation of atherosclerotic plaques.

Several processes, including atrial fibrillation, can cause hemodynamic alterations that raise the likelihood of thrombus development. The left atrial appendage (LAA) is a primordial left atrial remnant seen in the left atrioventricular groove. The blood flow velocity is lowered during atrial fibrillation due to the impaired contraction of the LAA, which functions as a reservoir during left ventricular systole, leading in the establishment of an arterial thromboembolism. Repeated atrial fibrillation events resulted in fibrosis, damage, and inflammation within the LAA, increasing the risk of thrombus dislodgement and propensity to ischemic stroke (Ding et al., 2020).

Hypercoagulability raises the risk of thrombosis, which can be caused by poor protein synthesis or action in homeostasis, as well as secondary causes from clinical diseases (Ding et al., 2020). Antiphospholipid syndrome (APS) is an example of an acquired cause of hypercoagulability. APS is an autoimmune condition in which the individual’s antibodies assault the plasma membrane’s phospholipids and binding proteins. The antibodies bind to platelets, endothelial cells, or the surface of the placenta, causing endothelial injury and promoting thrombus formation.

Ding, W. Y., Gupta, D., & Lip, G. Y. H. (2020). Atrial fibrillation and the prothrombotic state: revisiting Virchow’s triad in 2020. Heart (British Cardiac Society)106(19), 1463–1468.

McCance, K. & Huether, S., (2019). Pathophysiology: The biologic basis for disease in adults and children(8th Edition). St. Louis, MO: Elsevier Mosby.

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