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Anemia

QuestionAnswer
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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