Pathophysiology of Anemia and Nursing Care Implications - Research Paper Example

June 22, Anemia Anemia is a very common blood functioning disorder and it is affecting people at an alarming rate in developing or poor countries. The name anemia is a derivation from two Greek words that collectively mean “without blood” (Uthman 3). Anemia in simple words could be described as “any condition characterized by an abnormal decrease in the body’s total red blood cells mass” (Uthman 3). According to this definition, anemia could be understood as the reduction in the mass of circulating blood cells that subsequently reduces hemoglobin levels. Anemia in itself is not considered as an isolated disease but could be termed as the root cause of other problems. It happens when our body fails on making healthy Red Blood Cells and leads to fatal diseases like cancer, thalassemia etc (Uthman 4). To understand how anemia gets itself rooted within a person’s body it becomes important to first understand what is the importance of Red Blood Cells in our body and why their deficiency cause anemia. Importance of Red Blood Cells in the physiologic structure of Blood It is a common assumption that human body has large proportion of blood but this is not true. Actually, blood makes up only a small fraction of our body’s volume i-e blood accounts for only seven present of the total body volume. Various systems in our body hugely depend upon blood circulation and its confinement most importantly the Circulatory system and Reticuloendothelial System (Uthman 7). Blood may appear to be like an inert liquid to the naked eye but in real sense it is living and breathing tissue just like any other body part. It consists of cells suspended in a liquid medium. Plasma is that liquid medium which accounts for about 60 percent of the total blood volume and it comprises of 93 percent water (Uthman 9). Besides water, it also consists of two types of proteins called albumin and globulins. Plasma also contains proteins that are involved in the coagulation of blood and are called coagulation factors. If we take plasma out of the blood and let it clot or coagulate then the resulting fluid is called serum. The quantity of nutrients and other substances in serum helps evaluating anemia during laboratory testing. Forty percent of total blood volume is constituted by Blood Cells and the Red Blood Cells (RBCs or Erythrocytes) formulate the largest proportion while the other constituents are the White Blood Cells (Leukocytes) and Platelets. RBCs have nuclei in the DNA and are self-replicating cells that are made in the bone marrow. RBCs account for half of the total blood cells in the body and their only function is to keep hemoglobin healthy. All blood cells are produced by hematopoiesis in the bone marrow (Coyer, and Lash 77). The major raw material essentials for this process are proteins, vitamin B12, folic acid, and iron (Coyer, and Lash 77-82). Hemoglobin is a protein which serves as a carrier for oxygen from the lungs to the tissues and this is done through a delicate balancing act. Hemoglobin has to hold on to oxygen molecules with just the right amount of force (Uthman 9). It consists of four smaller protein molecules called Globin Subunits and each of these encloses an unusual molecule called Heme. Each Heme molecule contains one atom of Iron. Iron is the most essential part of hemoglobin without which there will be no hemoglobin and without hemoglobin there will be no blood (Uthman 9). Due to the delicate structure hemoglobin has, any type of natural or artificial toxic substance can cause the hemoglobin molecule to denature i-e be permanently altered. The various tasks of RBCs include protecting hemoglobin from getting corrupted, continually synthesizing certain molecules that destroy the toxins, maintain the correct PH and to keep the Iron atoms intact (Uthman 10-11). This explains why any malfunctioning in the production of RBCs can cause serious troubles to the whole body. Causes of Anemia: Anemia can be caused by three conditions: Hypervolemia or Excessive Blood Loss Anemia: This refers to the decrease in total blood volume due to the decrease in mass of the red blood cells. It could be Chronic or long-term bleeding and Acute or not long-term. Acute bleeding happens when there is heavy blood loss from a wound or disease over a short time period like in an accident or a bleeding ulcer. The blood is just as thick and concentrated as it is in the normal state but there is less of it left in the body (Uthman 14). Anemia becomes evident when the maximum level of hemodilution occurs, usually within 3 days after the acute blood loss (Coyer and Lash 77). Hemodilution occurs in response to decreased blood volume when fluid moves from the interstitium into the intravascular space to expand the plasma volume (Coyer and Lash 77). In chronic bleeding, the patient experiences gradual blood loss and often this loss of RBCs and Hemoglobin are left undetected. The blood loss in this scenario can take weeks or months and the body has time to adapt to it by starting its own IV. In this process the normal drinking water is reserved from the kidneys and used to thin the circulating blood. The decrease in blood viscosity from the lower number of red blood cells, along with increased intravascular fluid, causes the blood to flow faster through the CV system and the flow becomes more turbulent. This process causes pressure on the ventricles, the heart dilates, and heart valve dysfunction develops (Coyer, and Lash 77). Chronic or Acute blood loss can be caused by Stomach Ulcers, Stomach or Colon Cancer, Gastritis, Child Birth, Surgery, Trauma, Blood donations, Hemorrhoids, Heavy Menstruation etc. When anemia develops because of hemorrhage, the reduction in red blood cell numbers causes a decrease in blood volume and the cardiovascular (CV) system becomes hypovolemic (Coyer and Lash 77). Hemolysis or Excessive Red Blood Cells destruction Anemia: The pathophysiology of hemolytic anemia involves the destruction of erthythrocytes and the subsequent acceleration of erythropoiesis (Coyer and Lash 78). Hemolytic anemia may be inherited or acquired (Cavendish 47). Hemolytic anemia produces hemolysis within the blood vessels or lymphoid tissue that filters blood (Coyer and Lash 78). Immunohemolytic anemia is caused by extravascular hemolysis and associated with autoimmune mechanisms or drug reactions. In simple words it can be understood as some health conditions cause the early death of RBCs, the life span of which is usually around 110 to 120 days after which they break down and are removed. Due to this, the bone marrow speed up new cells production process and a failure in this process causes decrease in red blood cells count. These raptured and dysfunctional RBCs lead to Hemolysis Anemia (Uthman). It could be caused by infections, poisons, medications, medical procedures like Hemodialysis or a procedure involving heart-lung bypass machine. Hypoxia or Decreased Red Blood Cells Production: This is a condition when body stops producing the required ratio of RBCs or it is producing enough RBCs but they are not properly functioning. When anemia becomes severe, the body directs blood to the vital organs, such as the heart and the brain, and renal blood flow decreases (Uthman). Decreased renal blood flow in turn causes an activation of the renin-angiotensin system response, leading to salt and water retention (Coyer, and Lash 78). This process increases blood volume to improve kidney function without changing tissue hypoxia in other organs (Uthman). Physiologic Compensation: The physiologic compensation of decreased red blood cells production is as follows:- Increased Cardiac Output: This is the heart’s response to tissue hypoxia. In anemia, Hypoxia contributes to the changes in the CV and respiratory systems by causing the blood vessels to dilate and the heart to contract more forcefully, which further increases the demand for oxygen (Uthman). Tissue hypoxia causes the rate and depth of breathing to increase. Hemoglobin releases that oxygen to the tissues more rapidly (Uthman). Therefore, because of less peripheral vessel resistance and thinner, less viscous blood, the cardiac output can rise without causing the blood pressure to go up. Redistribution of Blood Flow: In anemia, all the body organs conjoin to protect the two most oxygen demanding organs the heart and the brain. The skin and kidney are the main sacrificing donors (Uthman). Small blood vessels in the skin contract which causes greater resistance to blood flow, resulting in partial diversion of blood. This diversion causes the clinical condition Pallor (paleness of skin) in anemia (Uthman 16). Kidney is a very vital organ but is endowed with more blood flow than it needs which it sacrifices in the process of adaptation to anemia (Uthman). Decreased Hemoglobin Oxygen Affinity: Increased oxygen extraction of anemic blood by the tissues produces increased concentration of de-oxyhemoglobin in the RBCs produces 2,3-iphosphoglycerate (2,3- DPG) that is elaborated within the red cell (Uthman 16). 2,3- DPG causes hemoglobin to bind oxygen less avidly and to give up as much to the starved tissue and due to this the electron-accepting cargo is ripped from hemoglobin (Uthman). Classification of Anemia Classification by Morphology: This includes Cystic or cell size, color/ chromic, and the shape of RBCs (Wiwanitkit 4). Information about the appearance of RBCs helps in its classification and could be provided by hemoglobin measurements, hematocrit and red cell indices. The mean corpuscular volume, mean hemoglobin, mean corpuscular hemoglobin concentration and RBCs distribution width formulate Red cells indices (Wiwanitkit 4). For measuring iron storage, serum ferritin concentration is used. This helps in diagnosing iron deficiency anemia. Classification by Etiology: This classification is based on the bone marrow factory concept (Wiwanitkit 4). Anemia can be caused by either inadequate /impaired production of RBCs, increased rate of destruction or excessive loss of cells. Blood loss results from acute traumatic conditions or chronic diseases. Increased destruction occurs in hemolytic anemia. Impaired cell production could be caused by either hereditary condition due to a disorder in the red cell membrane likeSperocytosis and Elliptocytosis, or disorders in enzymes within the red cells (Wiwanitkit 4). Types of Anemia There are over 400 types of anemia, most common of which are as follows: 1.Microcytic Anemia: In microcytic hypochromic anemia, red cells are small and have a reduced amount of hemoglobin (Coyer, and Lash 79). Common diseases of this type of anemia are: Iron Deficiency Anemia: It is the most common form of anemia. It represents a problem of iron demand on red blood cell development that cannot be met with current iron stores. Iron is required for hemoglobin synthesis, oxygen and electron transport and DNA synthesis (Cavendish 47). Each milliliter of blood contains 0.5 mg of iron and loss of 500 milliliters of blood creates a loss of 250 milliliters or 25% of the body’s iron reserves (Braun and Anderson 396-397). In this type the iron demands of body increases while the intake decreases. The major causes include inadequate iron intake, chronic hemorrhage, malabsorption and high iron demands in conditions like adolescence, infancy, pregnancy or lactation (Braun and Anderson 396-397). Excessive loss of body iron could be caused by heavy blood loss, gastrointestinal ulcers and cancer or hemorrhoids. Thalassemias and sideroblastic anemia: Thalassemias are a group of inherited disorders characterized by decreased rate of production or failure to synthesize normal globin chains (Vacanti, Sikka, and Urman 64). Or it could be understood as the disorder resulting from the imbalance between alpha and beta chains of hemoglobin molecule. Beta-thalassemia occurs when one beta-chain is reduced and if both the beta-chains get defected then the severe anemia condition called Thalassemia major or Cooley’s Thalassemia occurs (Vacanti, Sikka, and Urman 64). Alpha-thalassemia occurs due to the defect in two alpha-chains. Thalassemia is an inherited condition typically affecting people from Mediterranean, African, Middle Eastern and South Asian descent (Coyer, and Lash 77-82). Its clinical features include anemia hemolysis, and bone marrow hyperplasia. Treatment is based on the severity of the anemia and for patients with severe anemic conditions bone marrow transplantation proves curative. Regular blood transfusion is required for severe thalassemia (Vacanti, Sikka, and Urman 64). Sideroblastic anemia could be either inherited or acquired (Coyer, and Lash 79). The etiology of its acquired form is not known yet but it occurs due to other conditions like alcoholism, drug reaction, copper deficiency or hypothermia (Coyer, and Lash 79). Inherited Sideroblastic anemia that occurs from an X-linked transmission pattern affect only males and autosomal transmission affects only females (Coyer, and Lash 79). Individuals having sideroblastic leukemia show signs like bronze colored skin, iron overload, enlargement of spleen and liver. 2. Macrocytic Anemias: Macrocytic anemia occurs when the bone marrow produces very large cells called macrocytes (Coyer, and Lash 80). Their pattern of chromatic deposits in the nucleus is also altered. Hemoglobin proportion also increases according to the size of cell. The MCHC remains normal, producing normochromic cells (Coyer, and Lash 80). The early or premature death of these cells decreases the numbers of their circulation and leads to anemic conditions. Because both folic acid and vitamin B12 are required for normal hematopoiesis and cells maturation that is why any deficiency in these cause malabsorption syndrome and lets macrocytic anemia happen (Coyer, and Lash 80). Probable anemic conditions in macrocytic anemia are as follows: Pernicious Anemia (Vitamin B12 Deficiency): Pernicious means highly destructive which indicates the kind of damage it can produce. In this type of anemia there is an impaired absorption of vitamin B12, owing to an autoimmune disorder (Cavendish 48). In autoimmune disorder the body’s immune system attacks the body’s own tissues destroying the parietal (wall) cells of the stomach (Cavendish 48). The stomach lining then fails to produce a substance called intrinsic factor, which is required to promote the absorption of vitamin B12 from food (Cavendish 48). A deficiency of vitamin B12 stops the production of normal RBCs in the bone marrow. It is usually found in people above 30 and older (Cavendish 48). It takes at least 20-30 years to develop. Folate Deficiency: Folate (folic acid) is a very important vitamin in helping red blood cells to mature. Folate deficiency is most common in people over 75 years of age but pre-menopausal women can develop folate deficiency and are recommended to take folic acid during pregnancy to reduce the risk of neural tubal defects occurring in the fetus (Brown and Cutler 150-155). Its primary cause is the lack of dietary intake of folic acid. Alcoholism is also associated with folate deficiency due to hepatic damage. Alcoholism can lead to poor appetite which results in poor intake of folic acid. Malabsorption conditions such as coeliac disease and other bowel inflammatory disease, poor appetite, older age group and poverty are other causative factors (Brown and Cutler 150-155). Drugs such as methotrexate, cholestyramine, and some anticonvulsants like phenytoin may also lead to folate deficiency (Brown and Cutler 150-155). Excessive hemolysis of red blood cells in conditions such as sickle cell disease and thalassemia also may result in folate deficiency. It is also associated with the potential development of cancer. Megaloblastic Anemia: It is a major form of anemia and stems from the deficiency of both folic acid and vitamin B12 (Cavendish 47). This badly affects the production of red blood cells and the bone marrow produces large abnormal red blood cells. Those suffering from intestinal disorders (such as Crohn’s disease) that affect the absorption of nutrients are prone to this type of anemia (Cavendish 47). 3. Normocytic Anemias: The classification of normocytic anemia is based on the proliferative status of the erythroid component in the bone marrow and the corresponding number of reticulocytes in peripheral blood (Cualing, Bhargava, and Sandin 74). Anemia with decreased red cell production (non-hemolytic normocytic anemia) and anemia with reticulocytosis (i-e increased destruction of red cells blood loss) are its two sub classes (Cualing, Bhargava, and Sandin 74). This is the less common type of anemia and the diseases that cause normocytic anemia are as follows: Aplastic Anemia: It is a life threatening type of anemia and is developed by the inability of the bone marrow to produce not only red blood cells but white blood cells and platelets as well (Cavendish 47-48). Although it’s actual cause is unknown but it is believed that genetics or injury to the bone marrow incurred by chemotherapy, radiation therapy, environmental toxins and infections can contribute to the onset of aplastic anemia. These factors may prevent the bone marrow from producing stem cells that are the progenitors (initial versions) of all cells in the body (Cavendish 47-48). Autoimmune Hemolytic Anemia: Hemolytic anemia is a result of premature or excessive destruction of red blood cells in the blood stream. It may stem from an autoimmune disorder in which the body produces antibodies to red blood cells destroying them prematurely (Mulholland, Lillemoe, and Doherty 73). It is further categorized as the presence of either warm antibodies or cold antibodies. Warm Antibody Hemolytic Anemia: It is the most commonly found immunohemolytic anemia affecting females above 40 years of age. In patients with warm antibody hemolytic anemia, the spleen is the primary source of destruction of the red cells by the red pulp macrophages (Mulholland, Lillemoe, and Doherty 73). Warm antibodies are predominantly IgG. It is usually idiopathic but may also be caused by lymphomas, leukemia etc. Splenectomy is a successful treatment for this type of anemia (Mulholland, Lillemoe, and Doherty 73). Cold Agglutin Immune Hemolytic Anemia: It is a less common anemic condition and occurs in cooler places. This stems as a result of vascular obstruction and not hemolysis. Cold antibodies are predominantly IgM and since spleen does not contain receptors to bind IgM, no destruction of red blood cells occurs (Mulholland, Lillemoe, and Doherty 73). Rather, IgM causes complement fixation with destruction of red cells predominantly in the liver, or there is agglutination of red cells in peripheral circulation leading to peripheral red cell destruction (Mulholland, Lillemoe, and Doherty 73). In patients having IgM hemolytic anemia, Splenectomy is not successful. Signs and Symptoms of Anemia As mentioned above, anemia has various types and varying causes, so, the signs of anemia vary according to their underlying causes and types. But there are some of the common symptoms that are found in almost all types of Anemias. These symptoms include Pallor: This is caused by the shunting of blood flow away from skin (Uthman 18). Tachycardia: This means fast heart rate and is caused by increased cardiac output. Dyspnea: This means shortness of breath and usually occurs from exertion. Although an anemic person’s respiratory system is healthy but the tissues in the body starve for oxygen and there is not enough hemoglobin to get them enough air. If the person exerts himself too much then the tissues send signals to the respiratory system for delivering more oxygen and this is why the anemic patient experiences shortness of breath (Uthman 18). Frequent Fatigability: This stems from the oxygen starvation experiences by the tissues. Dizziness and Fainting: This is caused by the lack of oxygen in the brain. Tinnitus: The buzzing or roaring sounds or ringing like noises that an anemic person presumably hears are an outcome of the increased cardiac output. The rushing of blood through the vessels in the ear region is perceived as sounds by the patient and is termed medically as Tinnitus. Headaches: Headaches are a common symptom is almost all types of Anemias. Miscellaneous Symptoms: More common symptoms include dimmed vision due to the oxygen starvation of brain, loss of appetite, nausea, palpitations and constipation. Heart Failure: This may happen due to the increased cardiac output condition faced by the anemic patient. The more blood per minute the heart is called on to deliver, the higher becomes the risk of its failure. Works Cited Braun, Carrie Ann. and Cindy, M Anderson. Pathophysiology: Functional Alterations in Human Health. Lippincott Williams & Wilkins, 2006. Print Brown, Marvelle. and Tracy, Cutler. Haematology Nursing. John Wiley & Sons, 2012. Print Cavendish , Marshall. Diseases and Disorders. 1. Marshall CavendishCorporation, 2007. Print. Coyer, Sharon M, and Ayhan Aytekin Lash. "Pathophysiology of Anemia and Nursing Care Implications." MEDSURG Nursing. 17.2 (2008): . Cualing, Hernani. Parul, Bhargava. and Ramon, L. Sandin. Non-Neoplastic Hematopathology and Infections. John Wiley & Sons, 2012. Print. Mulholland, Michael. Keith, Lillemoe. and Gerard, Doherty. Greenfields Surgery: Scientific Principles & Practice. 5. Lippincott Williams & Wilkins, 2010. Print. Uthman, Ed. Understanding Anemia. Univ. Press of Mississippi,1998. Print. Uthman, Edward. "Anemia Pathophysiologic Consequences, Classification, and Clinical Investigation." http://web2.airmail.net. Edward O. Uthman, 1997-2000. Web. 18 Jun 2012. . Vacanti, Charles. A, Pankaj. K Sikka, and Richard, D Urman. Essential Clinical Anesthesia. Cambridge University Press, 2011. Print. Wiwanitkit, Viroj. Tropical Anemia. Nova Publishers, 2006. Print. Read More