Anemia is a reduced level in a total number of red blood cells. Red blood cells carry hemoglobin, a protein that empowers them to carry oxygen to lungs and deliver it to all parts of the body. When their numbers are low, it is difficult for them to carry an adequate supply of oxygen. An inadequate reserve of oxygen causes symptoms of anemia. Blood is made up of two parts, the liquid part which is the plasma and the cellular part which is composed of different cell types. One of the most significant and abundant cells are the red blood cells (Nabili, 2017). Red blood cells are manufactured in the bone marrow. Detecting the reasons why the red blood cells level is low, will guide to an investigation if it is caused by factors such as increased blood loss in bleeding, the decreased production of RBCs in the bone marrow or from the excessive destruction of red blood cells (https://www.merkmanuals.com)
Anemia is also induced by other diseases. Some diseases can affect the body’s ability to produce red blood cells. In patients with kidney disease, anemia may develop because kidneys are not functioning well, in order to manufacture the hormone erythropoietin, that will prompt the bone marrow to make new and redder blood cells (American Society of Hematology,2010).
What type of anemia do you suspect Henry has? How would Henry’s red blood cells appear on a peripheral blood smear?
In Henry’s condition, his kidneys are unhealthy and damaged that’s why he is not producing enough erythropoietin, that yields in low productivity of red blood cells by the bone marrow, causing anemia. EPO is an endogenous hormone produced by peritubular fibroblasts in the renal cortex. 90% of this hormone is produced in the kidney. Anemia in chronic kidney disease is one of the cardinal signs of kidney dysfunction, however, it is not detected early because it happens gradually as the kidney function deteriorates. Epidemiologic data indicate that two-thirds of patients in early stages of kidney failure have low hemoglobin content; with a hemoglobin level of less than 11 g/dl (Taliercio,2010).
Iron deficiency anemia is prevalent in chronic kidney disease patients. Some may be treated with dialysis and some are not. Because patients in the early stages of kidney disease are encouraged to trim down the amount protein they eat, they may not be getting adequate quantity of iron from their diet. Modifications in iron metabolism and availability are likely important in clients affected by CKD and anemia. Patients with CKD, may also have iron deficiency secondary to blood loss in the gastrointestinal tract because they are more susceptible to bleeding, they may also have difficulty in mobilizing iron even though adequate stores of iron are available. Iron deficiency anemia happens when the body doesn’t have sufficient mineral iron, leading to abnormally low levels of red blood cells. That is because, iron is necessary to make hemoglobin, a protein in red blood cells that enables them to carry oxygen around the body. If one’s body doesn’t have enough hemoglobin, one’s tissues and muscles won’t get ample oxygen and won’t be able to work effectively (Ciccone,2013).
Analysis of blood smears are usually done in patients with anemia. Laboratory-initiated examinations of blood smears for patients with anemia are typically needed whenever the hemoglobin concentration is unpredictably low. This is bucked up since the consideration of the blood smear and red-cell indices is a logical step in the examination of any unexplained anemia. Modern automated instruments impart worthy information about the nature of anemia. They check not only a red-cell count, mean cell volume, mean cell hemoglobin (measure of the average amount of hemoglobin in an individual red cell), and the mean cell hemoglobin concentration (measure of the average concentration of hemoglobin in a cell) then also new variables that give information that beforehand could be derived only from a blood smear. A variety of histograms and scatterplots give a visual representation of red-cell characteristics (Nowrousian, 2012).
Because anemia can have many causes, other possibilities must be ruled out first before a diagnosis of CKD anemia can be made. Basic workup should include complete CBC count with differential, iron studies (ferritin, serum Fe, and total iron binding capacity, reticulocyte count, and guaiac test. Other blood tests such as thyroid-stimulating hormone (TSH), B12, and folate levels and a hemolysis panel (lactate dehydrogenase, haptoglobin), should be obtained if the history suggests these disorders, however, on top of these tests that may be conducted, a peripheral blood smear showing normocytic red blood cells with normochromic pattern would favor the diagnosis of anemia secondary to chronic kidney disease (Talierco,2010).
What is the physiological basis that would explain why Henry’s anemia would cause him to have the symptoms he is experiencing?
Henry’s symptoms such as, feeling tired, running out of breath in just doing simple tasks, feeling dizzy and having headaches are signs, that people with low amount of hemoglobin usually experience that may be categorized as mild to moderate kind of anemia. The reduced RBC mass and hemoglobin concentration that defines anemia result in a reduced oxygen-carrying capacity of the blood and reduced oxygen delivery to tissues. When less oxygen reaches one’s tissues and muscles, the heart has to work harder to move more oxygen-rich blood around the body, which can make one’s body tired easily. Fatigue is one of the most often signs of iron deficiency anemia. This is due to less oxygen reaching body tissues, depriving them of energy. Iron deficiency anemia may also manifest shortness of breath. Hemoglobin allows red blood cells to carry oxygen around the body. When hemoglobin is low in your body, the oxygen level is also low, meaning your muscles are not getting enough oxygen just for normal activities. Henry also experienced light-headedness in which low levels of hemoglobin in red blood cells are not enough to reach the brain, causing blood vessels in the brain to swell, thus causing pressure and headaches (Ciccone,2013).
Predict the cellular adaptation erythrocytes undergo when chronic hypoxia is present. How would this be evident on an oxygen-hemoglobin dissociation?

Erythropoietin functions in a classic negative feedback loop whereby increased synthesis in the kidney as a consequence of reduced oxygen delivery stimulates the release of mature RBCs into the bloodstream via interaction of the hormone with a response on RBC progenitor cells. Erythropoietin is produced in the kidney by cortical peritubular interstitial fibroblasts that increase synthesis of hormone in response to hypoxia. Under normal, basal conditions, the serum erythropoietin concentration is in the range of 0.01-0.003 U/ Ml. The circulating erythropoietin level typically increases 100 to 1000 fold in response to anemia and hypoxia in individuals with kidney disease. Regulation of erythropoietin synthesis by the peritubular fibroblasts is mediated primarily through binding of the transcription factor hypoxia-inducible factor (HIF), a dimer compromised of HIF-1? and HIF B subunits, to a hypoxia response element in erythropoietin gene and other related hypoxia-responsive genes, increasing their transcription. In the presence of hypoxia, HIF degradation is impaired and the transcription complex enhances transcription of the erythropoietin gene with subsequent translation and secretion of the hormone (Kimmel & Rosenberg, 2015). Normal basal erythropoiesis and the ability to increase RBC production in response to hypoxia and anemia are also being stimulated. However, adequate and enough nutrients are necessary for this process, such as supplies of iron, vitamin B12, and folate.
Chronic anemia-induced hypoxia triggers regulatory pathways that mediate long-term adaptive cardiac and cerebral changes, mainly at the transcriptional level. These adaptive mechanisms include a regulated cerebral blood flow and cardiac output, angiogenesis and cytoprotection triggered by hypoxia-inducible factor 1 alpha (HIF-1?), vascular endothelial growth factor (VEGF), neuronal nitric oxide synthase (nNOS) and Epo pathways. All these compensatory mechanisms purpose to improve oxygen delivery and to protect the brain and heart from hypoxic injury. Functional cardiac adaptations such as cardiac hypertrophy, increased cardiac output as well as, angiogenesis occurred along with the activation of HIF1?/VEGF and Epo/EpoR pathways under chronic anemia and hypoxia (Swenson & Bartsch, 2013).
References:
American Society of Hematology, 2010. http://www.hematology.org/patients/blood-disorders
/anemia/5225.aspx.
Ciccone,2013. Davis’s drug guide for rehabilitation professionals.
Braunstein. Merck Manual. https:www.merckmanuals.com/home/blood.disorders/anemia/overview-
Of anemia/network=o;matchtype={creative};device=c;device.
Kimmel ; Rosenberg, 2015. Chronic Renal Disease. ISBN-13:978-0124116023
Nabili,2017. Anemia. emedicinehealth.
Nowrousian,2012. Recombinant human erythropoietin (rhEPO) in clinical oncology.
Swenson ; Bartsch,2013. High altitude: Human adaptation to hypoxia.
Taliercio,2010. Anemia and chronic kidney disease: What’s the connection.

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