A | B |
IRON DEFICIENCY ANEMIA | Iron deficiency anemia is caused by an inadequate supply of iron for RBC formation. It is the most common type of anemia. The body cannot make hemoglobin without iron. Iron deficiency leads to fewer RBCs, microcytic (small) RBCs, and hypochromic (pale) RBCs. The RBCs also may be malformed. |
iron loss due to | bleeding is the usual cause of iron deficiency anemia. Menstrual blood loss is the com- mon cause in adult females. Chronic, occult (hidden) blood loss may occur from disorders such as bleeding ulcers, gas- trointestinal inflammation, hemorrhoids, and cancer |
s/s iron deficiency anemia | iron deficiency can cause brittle, spoon-shaped nails; cheilosis (cracks at the corners of the mouth); a smooth, sore tongue; and pica (a craving to eat unusual sub- stances, such as clay or starch). |
VITAMIN B12DEFICIENCY (PERNICIOUS) ANEMIA/ pernicious anemia | required for RBC formation and maturation. is impaired absorption of the nutrient from the GI tract. Intrinsic factor, a substance secreted by the gastric mucosa, binds with dietary vitamin B12 so it can be absorbed by the body. deficit interferes with maturation of red blood cells. Great numbers of large, immature RBCs move into the circulation. These cells are fragile and incapable of carrying oxygen in adequate amounts. neurologic function, |
VITAMIN B12DEFICIENCY (PERNICIOUS) ANEMIA/ pernicious anemia signs and symptoms | smooth, sore, beefy red tongue and diarrhea, paresthesias (altered sen- sations, such as numbness or tingling) in the extremities and problems with proprioception (the sense of one’s position in space) also may develop. |
FOLIC ACID DEFICIENCY ANEMIA | required for normal production and maturation of red blood cells. absorbed from the intestines and is found in green, leafy vegetables; fruits; cereals; and meats. deficiency produces an anemia character- ized by fragile, megaloblastic (big and immature) cells |
FOLIC ACID DEFICIENCY ANEMIA risk | more common among people who are chronically malnourished (e.g., older adults, alcoholics, and drug users). People receiving total parenteral nutrition (TPN) . Pregnant women, |
SICKLE CELL DISORDERS | genetically transmitted, inherited as an autosomal recessive trait. an autosomal recessive inheritance pattern, a person must inherit the abnormal gene from both parents for the disorder to be fully expressed. characterized by abnormal hemoglobin, hemoglobin S (HbS), in the RBCs. This abnormal hemoglobin affects how RBCs respond to stress. When blood oxygen levels fall, the cells deform and become sickle shaped . When blood oxygen levels fall, the cells deform and become sickle shaped. These deformed RBCs clump together and obstruct small blood vessels . The damaged RBCs break down (hemolysis), leading to anemia. |
SICKLE CELL DISORDERS signs and symptoms | Sickling is usually marked by an abrupt onset of intense pain, often in the abdomen. The acute pain also may occur in the chest, back, or joints. The client also has manifesta- tions of anemia and may become jaundiced as bilirubin is released when red blood cells are destroyed. |
THALASSEMIA | abnormal hemoglobin synthesis. |
Manifestations of THALASSEMIA | include liver and spleen enlargement from increased red cell destruction. The RBCs are small and fragile; their distinctive bull’s eye appearance has caused them to be called target cells. Stress on the bone marrow to produce RBCs can lead to thinning of bones and fractures. |
ACQUIRED HEMOLYTIC ANEMIA | esults when RBCs are damaged by outside factors |
ACQUIRED HEMOLYTIC ANEMIA CAUSES | Mechanical trauma (prosthetic heart valves, severe burns, hemodialysis, or radiation). a Antibody reactions after infection. a Immune responses (transfusion reactions). a Drugs, toxins, chemical agents, or venoms. |
ACQUIRED HEMOLYTIC ANEMIA | spleen enlarges removes large numbers of damaged or destroyed RBCs. Bilirubin released from the hemoglobin of damaged RBCs can cause jaundice. |
Aplastic Anemia | bone marrow fails to produce RBCs. may follow injury to stem cells in bone marrow caused by radiation, cer- tain chemicals, or an immune response. |
Cause aplastic anemia | Benzene, arsenic, nitrogen mustard, certain antibiotics (especially chloram- phenicol), and chemotherapeutic drugs. associated with some viral infections, such as mononucleosis, hepatitis C, and HIV |
Aplastic anemia Signs and Symptoms | pancytopenia; that is, they have decreased numbers of red blood cells, white blood cells, and platelets fatigue, pallor, progressive weakness, dyspnea with exertion, headache, tachycardia, and, ultimately, heart failure. Platelet deficiency may cause bleeding problems. A deficiency of white blood cells increases the risk of infection. |
Myelodysplastic syndrome (MDS or myelodysplasia) | a group of stem cell disorders characterized by abnormal-appearing bone marrow and ineffective blood cell production |
Risk factors for MDS | Exposure to environmental toxins such as radiation and benzene and cancer treatment with radiation and chemotherapy are identified |
Signs and Symptoms MDS | asymptomatic or may complain of weakness and fatigue, dyspnea, and pallor. The spleen may be enlarged, and some clients with MDS develop skin lesions |
Blood Transfusion | Nursing Implications for Blood Transfusions: Record baseline VS Stay with client for 1st 15 minutes Monitor for transfusion reaction: warm feelings, chills, itching, weakness, fainting, difficulty breathing If reaction occurs: STOP transfusion immediately and notify RN, take VS, save blood bag and return to lab, collect urine and blood samples per protocol, monitor client and intervene as physician orders. Equipment: Y-tubing with filter, NS, Blood Check ID band, blood type Information verified by 2 nurses Take baseline VS, including temperature Stay 15 minutes, infuse no more than 25 mL if possible, monitor for reaction Infuse within 4 hours Monitor for transfusion reaction: Allergic: (pruritus, resp distress, urticaria) flushing. May give diphenhydramine (Benadryl) if expect minor reaction to blood Hemolytic: ABO incompatibility (flank pain, chest pain, fever, chills, tachycardia, tachypnea) If reaction-- stop blood immediately. Maintain IV access with NS. Take VS. Notify provider. Follow facility policy (e.g. send urine sample, CBC, send bag and tubing to lab for analysis) |
Dietary Modifications iron deficiency anemia or folic acid deficiency anemia | Meats, poultry, and fish provide iron that is readily absorbed. The iron contained in vegetables and grains is less readily absorbed, but accounts for most of the daily iron intake |
Sources of Iron | a Beef, beef liver, pork, ham, chicken, turkey, tuna, shrimp, clams, tofu a Dried beans, green beans, green peas, spinach, broccoli a Potatoes, whole grains, brown rice |
Folic acid Sources | Asparagus, okra, spinach and other greens, broccoli a Green beans and other legumes, dried beans a Fortified grain products (corn flakes, oatmeal, pasta) |
B12 Sources | Meat, poultry, eggs a Fish and shellfish a Milk and cheese |
B12 Treatment | Vitamin B12 (cobalamin) injections, Vitamin B 12 po |
Sickle Cell Treatment | Meds: Folic acid supplements and Hydroxyurea Blood transfusions Genetic counseling Pain medication: Diluadid (hydromorphone) IV hydration and Oxygen Elevate HOB Keep room warm--over 72 degrees Assess circulation and for s/s infection Immunizations ID triggers |
Hemophilia A | Group of hereditary clotting factor deficiencies, passed from mother to son as a sex-linked recessive gene. Lack of clotting factor: Deficiency of factor VIII |
Leukemia | White blood cell disorder “Blasts” Immature, nonfunctional WBC’s RBC’s and Platelets crowded out anemia and bleeding |
Hemophilia A Diagnostic and Treatment | Diagnostic Tests: Platelet count, Coagulation studies (APTT, bleeding time, prothrombin time), Clotting factor assays Interdisciplinary Care: Medications Fresh frozen plasma or Factor VIII (recombinant DNA) -- “Cryoprecipitate |
Spleen: | (largest lymphoid organ, located in LUQ) Filter’s blood Produces lymphocytes (WBC active in immune response) Stores blood and platelets |