NUR 631 Topic 4 DQ 1

Sample Answer for NUR 631 Topic 4 DQ 1 Included After Question

Answer both of the following discussion questions for your discussion response using the “Discussion Forum Sample.”

  1. Anemia of chronic disease is a common occurrence in elderly patients. What is the pathophysiological mechanism behind this disease process?
  2. Virchow’s triad refers to states that can produce hypercoagulability. What are the three categories? Give an example for each and explain the pathophysiological changes seen.

A Sample Answer For the Assignment: NUR 631 Topic 4 DQ 1

Title: NUR 631 Topic 4 DQ 1

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. https://doi.org/10.1136/heartjnl-2020-316977

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

A Sample Answer For the Assignment: NUR 631 Topic 4 DQ 1

Title: NUR 631 Topic 4 DQ 1

Anemia of chronic disease (ACD), also known as anemia of inflammation (AI), is a type of anemia that occurs in individuals with chronic systemic disease or inflammation. It is characterized by mild to moderate anemia, which is caused by various mechanisms that affect erythropoiesis (the production of red blood cells) and iron utilization. There are several underlying factors that contribute to the development of ACD. Firstly, there is a decrease in the lifespan of red blood cells, leading to their premature destruction. Secondly, there is a suppression of erythropoietin production, which is a hormone responsible for stimulating red blood cell production in the bone marrow. Thirdly, the bone marrow’s response to erythropoietin is impaired, resulting in reduced production of red blood cells. Lastly, there are alterations in iron metabolism and sequestration in macrophages (a type of immune cell).

During chronic inflammation, a variety of cytokines are released by immune cells and affected tissues. Some of these cytokines include tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), interleukin-1β (IL-1β), IL-3, and IL-6. These cytokines contribute to the development of ACD by affecting iron metabolism. IL-6, in particular, has a significant impact on hepatocytes (liver cells) and increases the release of a peptide called hepcidin. Hepcidin plays a crucial role in regulating iron levels in the body. It acts by inhibiting the activity of ferroportin, which is the primary transporter

responsible for exporting iron from macrophages into the bloodstream. Increased levels of hepcidin, as seen in chronic inflammation, lead to decreased ferroportin activity and reduced iron release from macrophages. This results in iron sequestration within macrophages and a reduced availability of iron for erythropoiesis.

The features of ACD are similar to those observed in other conditions such as chronic obstructive pulmonary disease (COPD), critical illness after acute events like surgery or trauma, myocardial infarction, sepsis, and in the elderly. Additionally, ACD shares some characteristics with anemia seen in multiple myeloma and malignant lymphoma. Understanding the mechanisms involved in ACD is important for its diagnosis and management. Treating the underlying chronic disease or inflammation is often necessary to improve anemia in these individuals. Additionally, strategies to optimize iron utilization and address erythropoietin deficiencies may be employed in the management of ACD.

Virchow’s triad is a concept that describes the three major factors contributing to the formation of blood clots, also known as thrombosis. These factors include:

Vessel wall injury: Damage or injury to the blood vessel wall is a significant factor in thrombosis. Conditions such as smoking, chronic high blood pressure, and atherosclerosis (caused by elevated levels of lipids in the blood) can lead to vessel wall damage. When the vessel wall is injured, it disrupts the normal flow of blood, leading to turbulence and the formation of eddy currents. This disrupted flow increases friction within the vessel, promoting the formation of blood clots.

Blood flow abnormalities: Abnormalities in blood flow can contribute to thrombosis. Conditions that disrupt normal blood flow patterns, such as atrial fibrillation, left ventricular wall akinesis (impaired movement of the heart wall), valvular heart disease, prolonged immobility (e.g., bedridden patients or long periods of travel), surgery, and trauma, can increase the risk of clot formation. These conditions can lead to stasis (sluggish blood flow) or turbulent blood flow, creating an environment conducive to clot formation.

Altered blood constituents leading to hypercoagulability: Changes in the composition of blood constituents can make it more prone to clotting, resulting in hypercoagulability. Soluble coagulation factors, such as fibrinogen and tissue factor, as well as cells like platelets, play key roles in the clotting process. Platelets are involved in the formation of atherosclerotic plaques and can aggregate to form clots. Plasma fibrinogen, in addition to influencing blood viscosity and flow, interacts with plasminogen binding and participates in the final stages of clot formation. Elevated levels of fibrin D-dimer, which are products of fibrin degradation, indicate increased thrombus formation and fibrin turnover in the bloodstream. Understanding Virchow’s triad helps identify the underlying mechanisms that contribute to thrombosis. By addressing these factors, healthcare professionals can implement preventive measures and treatment strategies to reduce the risk of blood clot formation and its associated complications.

McCance, K. L., Huether, S. E., Brashers, V. L., Rote, N. S., & McCance, K. L. (2019d). Pathophysiology: The biologic basis for disease in adults and children. Elsevier.