Can High Red Blood Cell Count Cause Ed – SRU taming. SRU is a “shock resuscitation unit”. It is the crucible of clinical training for residents of the University of Cincinnati Emergency Medicine Residency Training Program.
Sickle cell anemia (SCA) is one of the most common genetic disorders. A single point mutation in the beta-hemoglobin gene causes the hemoglobin molecule in patients with sickle cell anemia to be less soluble under deoxygenated conditions. It causes chronic hemolytic anemia and vasooculi, which leads to pain and tissue infarction with many secondary complications. (1) Given the morbidity of sickle cell anemia, these patients often present to the emergency department, raising questions about: what laboratory tests are necessary for these patients? And how do we interpret commonly ordered labs in these patients? This article will discuss the basics of these commonly ordered studies in hopes of determining when they are needed and how they can aid in the evaluation of sickle cell patients presenting to the emergency department.
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A normal red blood cell (RBC) has a typical lifespan of about 110 to 120 days and is subjected to considerable mechanical stress as it moves through capillaries millions of times during its lifetime. They repeatedly deform their membranes and lose this ability over time. Every day, the reticuloendothelial system destroys about 1% of the body’s red blood cells. In SCA, RBC membranes become irreversibly deformed after repeated sickling episodes and are removed from the circulation at a much younger age (about 20 days). For this reason, SCA is a disease of chronic extravascular hemolysis in which macrophages of the reticuloendothelial system phagocytize damaged red blood cells. Macrophages metabolize hemoglobin to unconjugated bilirubin, which is released into the plasma. As a result, unconjugated bilirubin levels are often slightly elevated in patients with sickle cell onset. In an acute pain crisis, unconjugated bilirubin may increase further due to increased hemolysis. (2, 3)
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In SCA, there is also some intravascular hemolysis, and free hemoglobin is released into the serum rather than metabolized in the reticuloendothelial system. Free hemoglobin binds to haptoglobin, a receptor for free hemoglobin. The haptoglobin-hemoglobin complex is transported to the liver and quickly removed from circulation. Haptoglobin levels decrease during hemolysis. In SCA, haptoglobin levels may be low because of the baseline level of hemolysis. It may decrease further during an acute crisis, but it may also be elevated because it is an acute phase reactant. (4) In general, haptoglobin may be indiscriminate in the initial workup of a SCA patient.
Another marker of hemolysis is LDH. It is a cytoplasmic enzyme found in almost all cells, including red blood cells. It catalyzes the reduction of pyruvate to lactate with concomitant oxidation of NADH to NAD+, an important step to provide further substrate for anaerobic metabolism. When cell death or tissue destruction occurs, LDH is released and is a marker of tissue damage and hemolysis. For these reasons, LDH is initially elevated in SCA. During acute vaso-occlusive crises (VOS), even in uncomplicated cases, LDH may increase further due to additional hemolysis and tissue infarction. (5) If the level is elevated 4 times the upper limit of normal in an acute exacerbation, there is some evidence that this indicates impending severe disease. (6) Therefore, LDH may serve as a prognostic marker in acute disease, but only if it is significantly elevated. In general, it may or may not increase during acute VOCs and is not specific.
Another laboratory test often ordered in the workup of SCA patients is the reticulocyte count. Reticulocytes are immature but already nucleated erythroid cells with residual RNA. In healthy individuals, reticulocytes reside in the bone marrow for approximately three days and then spend 1 day in the circulation before losing ribosomes and maturing into RBCs. At steady state, erythrocyte production equals erythrocyte loss, and approximately 1% of circulating erythrocytes are erythrocytes (normal range 0.5–2.0%). As anemia worsens and erythropoietin stimulation increases, the bone marrow releases reticulocytes at an earlier stage of their maturation and reticulocytes remain in the peripheral circulation longer. Therefore, the reticulocyte count is useful as a marker to assess the degree of erythropoiesis and the appropriateness of the bone marrow response in anemias. Absence of reticulocytosis in anemia usually indicates a bone marrow problem such as aplastic anemia. Because SCA is a chronic anemia, the reticulocyte count will initially be elevated (4-15%), and it is important to measure the fall in hemoglobin to ensure that the bone marrow is responding adequately. (78)
SCA is a disease that emergency physicians encounter frequently, given the acute exacerbations of the natural course of the disease and the many secondary complications that can occur.
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Unfortunately, there are no laboratory tests that can definitively determine whether a patient is in a pain crisis. The best approach is a good history and physical examination, and confidence in the patient’s reported pain.Open Access Policy Institutional Open Access Program Special Issues Guidelines Editorial Process Research and Publication Ethics Article Processing Costs Reviews.
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By Abdelnaby Khalyfa Abdelnaby Khalyfa Scilit Preprints.org Google Scholar View Publications 1, * and David Sanz-Rubio David Sanz-Rubio Scilit Preprints.org Google Scholar View Publications 2
Department of Child Health and Child Health Research Institute, University of Missouri School of Medicine, Columbia, MO 65201, USA
Received: March 7, 2021 / Revised: April 15, 2021 / Accepted: April 16, 2021 / Published: April 21, 2021
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Sleep is critical to overall health and quality of life, and sleep disturbances have been linked to several human diseases, including cardiovascular, metabolic, cognitive, and cancer-related changes. Obstructive sleep apnea (OSA) is the most common form of airway sleep-disordered breathing caused by repeated collapse of the upper airway during sleep. OSA has become a serious public health problem, and there is increasing evidence that untreated OSA can lead to the development of various diseases, including neurodegenerative diseases. In addition, OSA can cause decreased blood oxygenation and fragmentation of the sleep cycle. The generation of free radicals or reactive oxygen species (ROS) can occur and react with nitric oxide (NO) to form peroxynitrite, thereby reducing the bioavailability of NO. Hypoxia, a hallmark of OSA, refers to a decrease in tissue oxygen saturation and affects multiple types of cells, playing a role in cell-to-cell communication that is critical to the outcome of these interactions. Red blood cells (RBCs) are regarded as transporters of oxygen and nutrients in tissues, and these RBCs are important interorgan communication systems with additional functions, including involvement in the control of systemic NO metabolism, redox regulation, blood rheology and viscosity. Red blood vessels have been shown to cause endothelial dysfunction and increase cardiac damage. The mechanistic links between changes in RBC functional properties and the cardiovascular system are largely unknown. Extracellular vesicles (EVs) are secreted by most cell types and are released into biological fluids under both physiological and pathological conditions. EVs are involved in intercellular communication, transferring complex cargoes including proteins, lipids, and nucleic acids from donor cells to recipient cells. Improving our knowledge of the mechanisms of RBC-EV formation and their pathophysiological significance may help elucidate circulating EVs and translate their application into clinical practice. We will focus on the potential use of RBC-EVs as valuable diagnostic and prognostic biomarkers and state-specific cargo, as well as their potential as therapeutic vehicles for drug and gene delivery. The use of RBC-EV as a precision medicine in the diagnosis and treatment of patients with sleep disorders will improve the prognosis and quality of life of patients with cardiovascular disease (CVD).
Sleep is an integral part of life, and humans spend about one-third of our lives sleeping. Poor sleep quality and reduced sleep quantity can clearly lead to daytime sleepiness, reduced alertness and impaired mental functioning,
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