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Pernicious anemia occurs when the body can’t produce enough red blood cells (RBCs) due to vitamin B12 deficiency or lack of intrinsic factor. Pharmaceutical management includes lifelong vitamin B12 replacement, such as hydroxocobalamin intramuscular (IM) injections (Gilbert, 2017). Depending on symptoms and severity, patients without neurological symptoms may receive 1000 mcg IM injections every day or every other day during the initial week of treatment, then weekly for three to four weeks, and followed by once-monthly injections (Gilbert, 2019). Dosing for pediatrics requires 100 mcg once daily for a week, then every 3 to 4 days for 2 to 3 weeks, and a maintenance dose monthly (“Cyanocobalamin,”2019). Although IM injections are more commonly utilized, oral vitamin B12 has been effective in treating pernicious anemia. Evidently, dosages of 1000 to 2000 mcg daily are just as effective as IM injections. (Rodriguez & Shackelford, 2019). Patient preference should be taken into consideration as many patients prefer tablets over injection due to pain. Individuals with vitamin B12 deficiency who choose nonpharmaceutical management would need adequate intake of foods fortified with vitamin B12, including meat, poultry, eggs, and dairy products (“Cyanocobalamin,” 2019). The recommended adequate intake for individuals ages 14 years and older is 2.4 mcg daily and 2.6 mcg for pregnant women (Langan & Goodbred, 2017). Long term use of proton pump inhibitors or H2 blockers, certain seizure medications, and metformin may potentially cause vitamin B12 deficiency (Langan & Goodbred, 2017). Individuals ages 50 and older have a higher risk of deficiency, which can be due to the lack of stomach acid and the intrinsic factor which prevents the small intestine from absorbing vitamin B12 (Rodriguez & Shackelford, 2019). Strict vegetarians who don’t eat any animal or dairy products or vitamin B12 supplements are also a contributing factor to pernicious anemia. Therefore, patients older than 50 years and vegetarians should consume foods fortified in vitamin B12 or take supplements. Pernicious anemia is also associated with certain autoimmune and genetic diseases, including type 1 diabetes, autoimmune thyroid disease, and autoimmune gastritis (Rodriguez & Shackelford, 2019).

Thalassemia is an autosomal recessive disorder impairing the production of hemoglobin, specifically, the alpha and beta chains (Linder & McCance, 2019). Beta-thalassemia is caused by a mutation of the beta-globin gene that decreases the production of beta-globin resulting in ineffective erythropoiesis and anemia. Alpha-thalassemia occurs when there is a deletion of some or all of the alleles within the HBA1 and HBA2 genes. When there is a loss of the alpha-globin alleles, there is no or limited production of normal hemoglobin and instead, abnormal hemoglobin is produced that can’t effectively carry oxygen resulting in anemia (Linder & McCance, 2019). Chronic management depends on the severity of the thalassemia. According to Martin and Drucilla (2016), the standard of care guidelines for patients with thalassemia incorporates blood transfusions and chelation therapy. To improve anemia and suppress incorporates blood transfusions and chelation therapy. To improve anemia and suppress ineffective erythropoiesis, blood transfusions are needed when hemoglobin levels are less than 6 g/dl or when levels drop less than 7 g/dl for two consecutive times (Martin & Drucilla, 2016). Chelation therapy will begin one year after the chronic blood transfusion to lower the liver iron concentration (LIC). The standard recommendation is to maintain LIC below 7 mg/g or a ferritin level between 500-2500 ng/ml (Martin & Drucilla, 2016). Chelating agents include Exjade, Jadenu, and Ferriprox and are weight-based. For example, the initiating therapy for Exjade oral tablet for patients 2 years of age and older with transfusional iron overload is 20 mg/kg/day whereas patients with iron overload but are non-transfusion-dependent is 10 mg/kg/day (“Exjade,” 2019). According to Linder and McCance (2019), a cure for thalassemia is by allogenic hematopoietic stem cell transplantation (HSCT) from a matched donor, especially for children, as it can eliminate the lifelong need for blood transfusions and drugs to maintain iron levels. Patients with thalassemia may also take folic acid for RBC production. Risk factors include family history and certain ancestries, including African Americans and people of Mediterranean and Southeast Asia (Linder & McCance, 2019). Complications that can cause moderate to severe thalassemia include iron overload and infections. It is recommended that foods fortified in iron, such as cereal red meats, should be consumed in moderately-low amounts.


Cyanocobalamin. (2019). Retrieved from https://www.drugs.com/ppa/cyanocobalamin.html

Exjade. (2019). Retrieved from https://www.drugs.com/pro/exjade.html

Gilbert, L. (2017). Diagnosis and treatment of pernicious anemia. Practice Nurse, 47(4), 20-23. Retrieved from https://search-ebscohost-com.lopes.idm.oclc.org/login.aspx?direct=true&db=hch&AN=122680895&site=eds-live&scope=site

Langan, R. C., & Goodbred, A. J. (2017). Vitamin B12 deficiency: Recognition and management. American Family Physician, 96(6), 384-389. Retrieved from https://www.aafp.org/afp/2017/0915/p384.html

Linder, L. A., & McCance, K. L. (2019). Alterations of hematologic function in children. In V. L. Brashers & N. S. Rote (Eds.), Pathophysiology: The biologic basis for disease in adults and children (8th ed., pp. 992-1016). St. Louis, MO: Elsevier.

Martin, M., & Drucilla, H. (2016). Clinical management of patients with thalassemia syndromes. Clinical Journal of Oncology Nursing, 20(3), 310-317. doi:10.1188/16.CJON.310-317

Rodriguez, N. M., & Shackelford, K. (2019). Pernicious anemia. StatsPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK540989/



Anemias are extremely common in today’s healthcare world (Woo & Osborn, 2016, p 865). Overall the same underlying foundation of anemia is that there is a decrease in the ability of the blood to carry oxygen to the rest of the body (Woo & Osborn, 2016, p.865). There are many types of anemia usually based on size and hemoglobin content, but all share the same base trait (Woo & Osborn, 2016, p.865).

Iron deficiency anemia is an anemia that is caused by a decreased hemoglobin concentration that is caused by a decrease in red blood cell production due to the lack of iron available needed to make red blood cells (Sanjeevaiah & Sushmith, 2019). This type of anemia is classified as microcytic-hypochromic anemia (Sanjeevaiah & Sushmith, 2019). This anemia could be caused by another disease process that uses all of the body’s available and stored iron reserves (Sanjeevaiah & Sushmith, 2019). The two main causes of this anemia are GI bleeding and menstruation (Sanjeevaiah & Sushmith, 2019). Treatment includes increasing iron-rich foods in the patient’s diet, then adding an iron supplement of 325 mg/day, and finally ferritin intravenous infusions depending on the severity of the anemia (Woo & Osborn, 2016, p871).

Folic acid deficiency anemia is when there is an issue with folate absorption leading to a decreased amount of fully mature red blood cells (Woo & Osborn, 2016, p.868). In developed countries, this is seen most with chronic alcoholism (Woo & Osborn, 2016, p868). This type of anemia is classified as macrocytic-normochromic anemia (Woo & Osborn, 2016, p868). Treatment includes an increase of folic acid in the patient’s diet, oral supplementation, and eventually subcutaneous administration depending on the severity (Woo & Osborn, 2016, p872).

Pernicious Anemia is where there is a lack of vitamin b12 due to underlying causes such as malabsorption and causes red blood cells to be unable to mature (Woo & Osborn, 2016, p868). This type of anemia can be autoimmune and possibly heredity (Woo & Osborn, 2016, p868). This anemia is macrocytic-normochromic anemia that actually develops over a long period of time (Woo & Osborn, 2016, p868). This type of anemia is usually seen in patients who are extreme dieting, or vegetarians, vegans, and patients with Chron’s disease (Woo & Osborn, 2016, p868). Treatment includes dietary modifications to increase oral consumption of foods rich in vitamin b12, oral supplementation, and eventually intramuscular injections over the course of a month, depending on the severity of the anemia (Woo & Osborn, 2016, p872). Anemia of Chronic disease is usually associated with a chronic low hemoglobin count and is caused by the destruction of red blood cells, decreased production of red blood cells, or decreased iron metabolism (Woo & Osborn, 2016, p869). Anemia of chronic disease is thought to be a cellular immune response and is caused internally without a stimulus from an outside source (Sanjeevaiah & Sushmith, 2019). This anemia is normocytic-normochromic anemia is most cases but in a small amount, it is microcytic-normochromic (Sanjeevaiah & Sushmith, 2019). The treatment for this type of anemia is mainly focusing on the underlying disease process that is causing the anemia and reversing it (Woo & Osborn, 2016, p873).

Sickle Cell Anemia occurs when some red blood cells have an abnormal gene known as hemoglobin S is activated and glutamic acid is replaced by valine causing the physical structure of the red blood cell to be altered and form a sickle shape (Sanjeevaiah & Sushmith, 2019). This anemia is classified as normocytic-normochromic anemia (Woo & Osborn, 2016, p869). The issue occurs when the patient experiences a trigger, such as dehydration or cold weather, causing the lower partial pressures of oxygen in the body to reduce tension on the red blood cell causing them to take on the sickle form (Woo & Osborn, 2016, p869). This change leads to two issues; hemolytic anemia and vaso-occlusion (Woo & Osborn, 2016, p869). The treatment for this type of anemia is to address hydration status, oxygenation status, and pain management for patients experiencing a crisis (Woo & Osborn, 2016, p876). Initial treatment is education on how to avoid triggers and to stay adequately hydrated (Woo & Osborn, 2016, p876). Additional therapies include immunizations, and oral supplementation of multivitamins (Woo & Osborn, 2016, p876).

In terms of age and gender, there are no differences in treatment options, but there is a higher incidence of certain anemias in certain groups (Sanjeevaiah & Sushmitha, 2019). For example, women are more likely to have iron deficiency anemia while African American males are more likely to get sickle cell anemia (Woo & Osborn, 2016, p865-879).


Sanjeevaiah, A., & Sushmitha, A. (2019). The Prevalence and Type of Anaemia in Asymptomatic Adults in a Rural Population. Journal of Evidence Based Medicine and Healthcare, 8, 551. https://doi-org.lopes.idm.oclc.org/10.18410/jebmh/2019/114

Woo, T. & Osborn, K. (2016). Anemia. T.M. Woo (Eds). Pharmacotherapeutics for Advanced Practice Nurse Prescribers (4th edition pp. 865-879). Philadelphia: PA. F.A. Davis Company



Lenalidomide (Revlimid) is an immunomodulatory agent to treat various cancers including multiple myeloma (MM), myelodysplastic syndrome, and lymphoma due to its antineoplastic, antiangiogenic, and pro-erythropoietic properties (Chen, Zhou, & Palmisano, 2017). Lenalidomide activates T cells and natural killer T (NKT) cells, increases NKT cells and inhibits pro-inflammatory cytokines. It is a thalidomide derivative that inhibits proliferation and induces apoptosis of certain hematopoietic tumor cells. Common adverse effects include neutropenia and thrombocytopenia, but other adverse effects are disease-specific. For instance, patients with MM have increased risk of venous and arterial thromboembolism, myocardial infarction, and stroke; therefore, thromboprophylaxis is recommended (“Revlimid,” 2019). Due to its induced neutropenic and thrombocytopenic effects, complete blood counts (CBC) should be monitored. For patients with MM, CBCs are done every week for the initial two cycles, on days 1 and 15 of cycle 3, and every 4 weeks afterward (Chen et al., 2017). Patients should be monitored for signs of infection and bleeding or bruising. Other common adverse effects include fatigue, diarrhea, back pain, upper respiratory infections, insomnia, anemia, rash, cough, dyspnea, muscle cramps/spasms, hypokalemia, swelling of the limbs, and decreased appetite (Cruz, 2016). In addition, lenalidomide is contraindicated in pregnant women as it may cause birth defects, such as absence or short limbs, absence of bone, and congenital heart disease, or embryo-fetal death (“Revlimid,” 2019). Lenalidomide is also seen in semen so men should use condoms during intercourse and up to 28 days after discontinuation of the drug (Cruz, 2016). Furthermore, hepatotoxicity, thyroid disorders, increased mortality in patients with chronic lymphocytic leukemia (CLL), tumor flare reactions, and impaired stem cell mobilization as been seen in patients taking lenalidomide (“Revlimid,” 2019). Possible drug interactions include digoxin, erythropoietic agents, and estrogen-containing medications. Evidently, co-administered with lenalidomide, digoxin plasma levels increased, which requires monitoring, and erythropoietic and estrogen-containing therapies may increase the risk of thrombosis (“Revlimid,” 2019). However, coadministration of lenalidomide and warfarin had no alteration on prothrombin time and international normalized ratio, so warfarin can be administered for its prophylactic use (Chen et al., 2017).


Chen, N., Zhou, S., & Palmisano, M. (2017). Clinical pharmacokinetics and pharmacodynamics of lenalidomide. Clinical Pharmacokinetics, 56(2), 139-152. doi:10.1007/s40262-016-0432-1

Cruz, M. P. (2016). Lenalidomide (Revlimid): A thalidomide analogue in combination with dexamethasone for the treatment of all patients with multiple myeloma. Pharmacy and Therapeutics, 41(5), 308, 310-313. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4849339/#__sec1title

Revlimid. (2019). Retrieved from https://www.drugs.com/pro/revlimid.html

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