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Anemia
| Question | Answer |
|---|---|
| RBC (erythrocytes) | carry oxygen throughout the body |
| hemoglobin | oxygen binds to; main component of RBC; percent of RBC in the volume of blood |
| Anemia | occurs when oxygen delivery is inadequate as a result of a deficient hematocrit or decreased hemoglobin |
| Anemia results in | reduced oxygen carrying capacity of the blood= less blood reaching the cells and tissues, may lead to hypoxia |
| tissue hypoxia | angina, fatigue, dyspnea on exertion, nigh cramps, increased heart and respiratory rate, stimulates erythropoietin release, increased erythropoietin stimulates RBC production in bone marrow may lead to bone pain, |
| Cerebral hypoxia | headache, dizziness, visual disturbances |
| severe anemia | may lead to heart failure |
| Most common cause of anemia | iron deficiency |
| Iron deficiency anemia occurs when | there is insufficient amount of mineral iron present in the body to produce the necessary hemoglobin to make RBCs; iron stores in the bone marrow will be the first to be depleted |
| Anemia develops as | hemoglobin production continues to decline |
| Iron deficiency can result from | nutritional iron deficiency, conditions causing internal blood loss, impaired iron absorption |
| iron deficiency anemia is most common in | older adults and women of childbearing age, most common nutritional deficiency in the US; |
| Iron deficiency anemia may result from chronic | occult blood loss caused by peptic ulcers, GI inflammation, hemorrhoids, cancer; may affect all major body systems depending on severity |
| altered hemoglobin synthesis | iron deficiency, thalassemia, chronic inflammation |
| altered DNA synthesis | Vitamin B12 malabsorption or deficiency; folic acid malabsorption or deficiency |
| bone marrow failure | aplastic anemia, red cell aplasia, myeloproliferative leukemia, cancer metastasis, lymphoma, chronic inflammation or infection, physical or emotional fatigue |
| acute or chronic blood loss | hemorrhage or trauma; chronic GI bleeding, menorrhagia |
| increased hemolysis | hereditary cell membrane disorder, defective hemoglobin, deficiency affecting glycolysis or cell oxidation, immune mechanisms and disorders, splenomegaly and hypersplenism, infection, erythrocyte trauma |
| iron deficiency anemia (etiology) | dietary deficiency Vegetarian, inadequate protein); decreased absorption (partial or total gastrectomy, chronic diarrhea, malabsorption syndrome); increased metabolic requirements (pregnancy, lactation); blood loss (GI bleed, menorrhagia), hemoglobinuria) |
| iron deficiency anemia (manifestations) | onset usually insidious; early signs-headache, pallor, lethargy, fatigue, short of breath, intolerance to cold; late signs- pica, glossitis, stomach irritation, cheilosis |
| iron deficiency anemia (therapies) | increase dietary intake of iron rich foods, oral or parenteral iron supplements |
| vitamin B12 deficiency (etiology) | usually occurs when insufficient b12 is consumed or absorbed; causes- resection of the stomach or ileum, loss of pancreatic secretions, chronic gastritis |
| Vitamin b12 deficiency | impairs cells division and maturation of cell nucleus= macrocytic misshapen RBCs with thin membrane=these cells are unable to carry adequate o2 and have shortened life span |
| pernicious anemia (form of b12 deficiency) | failure to absorb dietary b12; results from lack of gastric intrinsic factor (secreted by gastric mucosa), intrinsic factor (IF) binds with B12 and travels to ileum where it is absorbed, w/o IF body can't absorb b12 |
| vitamin b12 deficiency anemia (manifestations) | smooth, sore beefy red tongue; diarrhea, paresthesia, skin discoloration of hands and knuckles neurologic symptoms: diminished reflexes, confusion, memory loss, gait disturbances, peripheral neuropathy |
| Vitamin b12 deficiency anemia (therapies) | increased dietary intake of B12 foods (meat, eggs, dairy) oral or parenteral b12 supplement parenteral vitamin b12 caused by malabsorption or lack of intrinsic factor |
| Folic acid | required for DNA synthesis and normal maturation of RBCs; characterized by fragile, megaloblastic cells |
| folic acid is found in | leafy green vegetables, fruits, cereals, meats and is absorbed in the intestines |
| risk factors for folic acid anemia | chronically undernourished- alcohol abuse, older adults, total parenteral nutrition, drug abuse; pregnancy, celiac |
| alcohol abuse high risk for folic acid anemia because | alcohol suppresses folate metabolism, which forms folic acid |
| pregnancy and folic acid | should increase of folic acid intake to decrease risk of neural tube defects (foods, prenatal, supplements) |
| folic acid anemia (manifestations) | glossitis, cheilosis, diarrhea, pallor, progressive weakness, fatigue, SOB, heart palpitations; NO neurologic effects |
| sickle cell disease (manifestations) | moderate to severe lethargy, reduced tissue oxygenation and blood stagnation leading to altered LOC, sickle cell crisis, acute chest syndrome |
| folic acid anemia (therapies) | increased dietary intake, supplementation, folic acid supplementation in pregnancy |
| sickle cell crisis | trapping of sickled RBCs in the spleen and subsequent splenomegaly; reduced or absent RBC production by bone marrow leading to severe decrease hemoglobin, rarely hemolytic crisis |
| sickle cell acute chest syndrome | leads to an increase in hemoglobin sickling which exacerbates hypoxia and can be life threatening |
| sickle cell anemia (therapies) | mostly supportive; hydroxyurea :sickle cell crisis- rest, oxygen therapy, narcotic analgesia, vigorous hydration, Tx of precipitating factors: Acute chest syndrome- careful hydration, O2, transfusion, folic acid supplement :blood transfusion PRN, genetic |
| hemolytic anemia | characterized by premature destruction of RBCs, can be from intrinsic or extrinsic factors related to the RBC; intrinsic include (sickle cell and thalessaemia |
| thalassemia | inherited disorders of hemoglobin synthesis in which either the alpha or beta chains of the hemoglobin are missing or defective; more prevalent in certain populations |
| thalassemia (manifestations) | general symptoms include anemia, splenomegaly, bronze skin coloring, bone marrow hyperplasia, Thalassemia major- sever anemia, HF, liver and spleen enlargement from increased RBC destruction; fractures of long bones, ribs and vertebrae, accumulation iron |
| thalassemia (therapies) | regular blood transfusions, folic acid supplements, possible splenectomy, genetic counseling |
| acquired hemolytic anemia | mechanical trauma to RBCs (prosthetic heart valve, sever burn, hemodialysis, radiation); autoimmune disorders; bacterial or protozoal infections, immune system-mediated response(transfusion reaction), drugs, toxins, chemical agents, venoms |
| If the breakdown of heme units exceeds the liver's ability to conjugate and excrete bilirubin | jaundice develops |
| aplastic anemia | the bone marrow fails to produce all three types of blood cells leading to pancytopenia (deficiency of WBC and RBC) normal bone marrow is replaced by fat |
| aplastic anemia (manifestations) | onset may be insidious or sudden; fatigue, pallor, progressive weakness, exertional dyspnea, HA, tachycardia, HF; platelet deficiency leads to bleeding problems(bleeding gums, excessive bruising, nosebleeds), decreased WBC- risk in infection, sore throat, |
| aplastic anemia (therapies) | withdrawal of causative agent, blood transfusion, bone marrow transplant |
| Labs | hemoglobin, hematocrit, CBC; serum- iron, ferritin, iron binding capacity |
| Main treatment for anemia | treat the underlying cause |
| erythropoietin | may be ordered for Pt. with low erythropoietin levels, adequate iron must be present |
| nonpharmacologic therapy | nutrition changes high in iron, folic acid, b12 etc.; blood transfusion for blood loss as needed |
| neonatal anemia | may be caused by blood loss, hemolysis/erythrocyte destructions, and impaired RBC production; blood loss from placental bleeding, birth trauma, |
| physiologic anemia of NB | occurs as a result of the normal, gradual drop of hemoglobin in the first 6-12 weeks of life |
| anemia in children and infants | primary etiology of anemia is nutritional deficit due to excessive intake of mild, prolonged breast feeding, without adequate iron supplementation |
| anemia in adolescents | high requirements because of increased metabolic needs, expansion of blood volume, and increases of muscle mass, heavy menstrual bleeding |
| anemia in pregnant women | gain in plasma volume dilutes the RBCs and may be reflected as anemia, significant increase in iron required by the body due to rapid placental and fetal growth |
| risks of anemia during pregnancy | sepsis, maternal and perinatal mortality, low birth weight |
| women of reproductive age | heavy menstruation, high parity, use of IUD, vegetarian diet |
| Anemia in older adults common causes | iron deficiency, chronic disease or inflammation, chronic kidney disease; older adults do not adapt as well, increased risk of mortality, difficulty with mobility, hospitalization, decrease in ADLS |
| ferrous sulfate (indications) | treatment of choice for iron deficiency anemia, and prevention of deficiency |
| ferrous sulfate (adverse effects) | nausea, pyrosis, bloating, constipation, diarrhea; should be used cautiously in Pt. with peptic ulcer ulcerative colitis, regional enteritis: liquid preparations may stain teeth- dilute, administer with straw or dropper, rinse mouth; Toxicity- nausea, vom |
| ferrous sulfate (drug interactions) | vitamin c increases absorption but also side effects calcium decreases absorption |
| Ferrous sulfate (assessment) | H&H increase within 7 days and within 1month will rise at least 2gm/dL |
| folic acid (indications) | Tx of megaloblastic anemia resulting from deficiency, prophylaxis, initial Tx of megaloblastic anemia from b12 deficiency |
| folic acid (adverse effects) | nontoxic short term, long term may pose nonsignificant increased risk of some cancers |
| Epoetin Alfa (erythropoietin) | stimulate production of erythrocytes, alternative to infusions; mimics erythropoietin; given IV or subq |
| Epoetin Alfa (adverse effects) | hypertension related to increase in hematocrit; cardiovascular events hypertension, HF, thrombotic events including stroke or MI; monitor hemoglobin level should not be above 11 gm/dL |
| Epoetin Alfa (monitoring) | hemoglobin, iron, CBC, BUN, uric acid, creatinine, phosphorus, potassium |
| filgastin(Neupogen) | leukopoietic growth factor; mimics granulocyte colony stimulating factor; leukopoietic growth factors stimulate production of leukocytes |
| filgastin (adverse effects) | bone pain, leukocytosis |
Created by:
melsniv
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