Treating Pernicious Anemia

The lack of intrinsic factor in the stomach leads to a vitamin B-12 deficiency. Vitamin B-12 is necessary for production of normal, healthy red blood cells. Without B-12, red blood cells become to large(macrocytic) and do not carry enough oxygen to supply the body. Without enough oxygen the body can not function normally and a person is said to be anemic (Pernicious Anemia, n.d.).

However, absorption cannot occur in the absence of IF. Once in the circulation B12 binds to a transport protein and is taken to the liver, bone marrow, and other proliferating cells. Most individuals with normal absorption have no issue acquiring the needed daily amount. The cause of Malabsorption of both folate and B12 is from lack of IF, gastric surgery, inflammatory bowel disease, celiac disease, and hyperthyroidism (Buttaro, Trybulski, Polgar Bailey, Sandberg-Cook, 2013). Healthy adults may consider taking supplemental crystalline vitamin B12 (Stabler, 2013). However, treatment is not necessary for asymptomatic anemia. Deficiency related to IF indicates a need for 1000 mcg of B12 intramuscular injections weekly for eight weeks and then monthly for life. Treatment for macrocytic anemia resulting from folate insufficiency is 1 mg of folic acid PO daily until the patient achieves an adequate hemoglobin level and indefinitely if patient has an underlying illness or an inadequate diet (Buttaro, Trybulski, Polgar Bailey, Sandberg-Cook,

Otherwise known as G6PD deficiency, people with an extreme case of this illness would experience hemolytic anemia, fever, and fatigue after eating fava beans or take drugs like primaquine. This is due to the fact that people with favism lack sufficient amount of the enzyme G6PD, which is important for protecting cells from chemical elements that would otherwise destroy the cells. The substances mentioned above act as the catalysts for the production of free radicals (un-paired electrons). As these un-paired electrons seek to pair with electrons in red blood cells with deficient amount of G6PD, it causes the cell membranes to burst. The loss of red blood cells when left untreated can cause the person to have kidney failure, heart failure, and death. As of now, there is no treatment for G6PG

Iron deficiency anemia, one of the most common types of anemia, is a blood disorder where

Then anemia as previously meantioned kills red blood cells. Causing a veriaty of different trouble across the board with the body, along with substanial fatigue. This type of anemia is called low iron-anemia, which goes along with its cause. for this reason it is obvious to see why doctors and scientist believe that iron defiecency is one of the causes for lupus. Low iron enemia as well as chronic enemia wich is passed down through heretity is also suspected to be one of the reasons for lupus.

19. Following surgery for stomach cancer, Joe has been diagnosed with pernicious anemia. Which of the following is most likely the cause of this problem? A. he may not be absorbing vitamin B12 from his diet since the operation because of less intrinsic factor

How are you? You gave a good response to this week's discussion question. In which you state, "There are four different types of anemia". I agree that there are four anemias that are commonly known. However, there are more than four hundred kinds of anemia (1). It is amazing how one illness can have so many manifestations. I hope this helped.

Immune-Mediated Hemolytic Anemia (IMHA) is one of the most severe autoimmune disorders that kills between 29-77% of dogs each year [1]. The disease is usually found in large and middle aged dogs. IMHA is a pathologic process that results in premature destruction of red blood cells when an immune response directly or indirectly targets red blood cells of all ages[ 2]. IMHA can be caused by various factors, but categorized in two ways. IMHA can be an idiopathic autoimmune event (primary IMHA) or associated with trigger factors (secondary IMHA) such as imbalance of immune cells caused by another underlying disease, toxin, drug, or vaccine [3]. The most common clinical signs of IMHA may be acute or chronic, depending upon the rate of hemolysis. If the patient is in a chronic state, they will have symptoms such as lethargy, jaundice, decreased physical activity, diarrhea, or discoloration of urine, which most mistake for a urinary tract infection. If there is a more rapid hemolysis occurring, the first symptom to happen may be an acute collapse from the dog [1]. Although the mortality rate of IMHA is fairly high, there are treatment options to improve tissue oxygen delivery and to suppress the immune response to prevent some of the major complications that occur with IMHA [1]. Depending on the severity of the patients IMHA, a blood transfusion may be required, but if not then most cases are treated with immunosuppressant therapy such as glucocorticoid therapy, adjunct

Sickle -cell anemia is a very important subject to touch on in today’s time because many people honestly do not know what this is. Sickle -cell anemia is a severe hereditary form of anemia in which a mutated form of hemoglobin distorts the red blood cells into a crescent shape at low oxygen levels (SCDAA par .1). Also it is one of the most common diseases in the African American race. There are other races that this particular disease would show up in such as the Hispanics, and people of the South American descent. According to the American Society of Hematology there are a count for 70 ,000 to 100 ,000 African Americans suffering from this disease (American Society of Hematology par .1). Statistics also state that 1 in 12 African Americans even have the sickle cell trait (ASH par .4). By doing simple math, that means that over the course of a year, there are over 1 ,000 babies being born in the United States with that disease. I know if I was shocked by those numbers, there are others out there who would be shocked too. I believe there should be more awareness thrown out there about sickle cell anemia because, it takes 2 parents with the trait to bring a child into this world unknowingly with the full blown disease. Throughout many countries sickle -cell often times gets sucked under the radar, when it really should be front in center because of the severity of this disease. Sickle -cell does not go away in a few days with a little bit of rest or medication, like the

Pernicious anemia is typically caused by a weakened stomach lining, or an autoimmune condition where the body attacks the intrinsic factor or the stomach lining. Biermer’s disease is rarely hereditary, this is called Congenital Pernicious anemia this is where babies do not make enough intrinsic factor or there is something going wrong with the absorption process in the small intestine. The prevalence of Pernicious anemia is estimated to be diagnosed in 1/769 people while Congenital Pernicious anemia is estimated to be

When the activity of the GPI-anchored proteins is reduced the mutation is then able to develop into the dominant gene in the creation of red blood cells. The complement system then recognizes the red blood cells as foreign cells causing the complement system to attack the mutation and when this occurs, red blood cells are destroyed faster than the normal 120 day life span, which leads to the deficiency of red blood cells and all the nutrients that they carry. In PNH, the red blood cells are missing two of the complement regulating proteins that are needed for GPI-anchored proteins to attach them to the cell membrane and since the two proteins are missing a lot of the nutrients and are in a deficient amount, it can lead to hemolytic anemia, iron deficiency anemia, aplastic anemia, blood clots, myelodysplasia, acute myelogenous leukemia, and even

The body adjusts to an extreme blood loss by allowing the circulating volume of blood to expand at the expense of the extravascular fluid. In this case, the adjustment of the circulating volume produces a delayed anemia. We also need to consider that the loss of the blood causes an opening, allowing the extravascular fluid to enter the stream, diluting the

Fanconi anemia (fan-KO-nee uh-NEE-me-uh), or FA, is a rare, inherited blood disorder that generally leads to bone marrow failure. While it is rare, only effecting less than 2% of the world's population is more commonly seen in South Africa. It is named after the Swiss pediatrician who first published information after clinical observations in 1927. FA is the result of a genetic defect in a cluster of proteins responsible for the DNA repair. As a result, the majority of FA patients develop cancer, most often acute myelogenous leukemia and around 90% develop bone marrow failure by the age of 40. About 60–75% of FA patients are plagued with congenital defects, commonly short stature, abnormalities of the skin, arms, head, eyes, kidneys, and ears, and developmental disabilities. Also around 75% of FA patients have some form of endocrine problem, with varying degrees of severity. Life expectancy for someone with Fanconi's Anemia is approximately 22 years.

The environment plays a significant role in the inheritance and expression of sickle cell anemia. Things like, cold/windy weather, decreased air quality, dehydration, anything that causes an increased physiological need for oxygen ie - increasing HR/BP and vasoconstriction or altering erythrocyte oxygen binding can potentially cause an SCA attack/incident (Tewari 2015). The majority of environmental factors affecting the severity of sickle cell anemia are related to fetal hemoglobin (HbF) concentrations (the most studied genetic modulator of SCA) and α thalassemia. High concentrations of HbF (in those affect by SCA, HbF is typically about 20%) prevents clinically significant sickle hemoglobin (HbS) polymerization (formation of sickled erythrocytes).

This wide range of test reflects the increased risk that older people have of many diseases and the difficulty of reaching a diagnosis in chronic tiredness.