ANEMIA

Is a condition that results from an insufficient supply of healthy RBC to oxygenate the body tissue adequately.

ETIOLOGY: Is caused by one of three race : production of healthy RBC ; RBC destruction (hemolysis) Loss of blood (Erythropoiesis - the RBC production that takes place in the bone marrow) Healthy RBC include precursor cells (Reticulocytes) and adequate supply of Fe, VitB12, folic acid, protein, pyridoxine, presence of copper. If any of these factors are missing the RBC will be fragile, misshapen, abnormal size, lacking Hgb or few. Maybe inherited or nutritional (food intake) destruction of RBC can be due to: Extrinsic Causes: o Physical trauma o Prosthetic heart bulbs o Thrombotic thrombocytopenic purpura o Antibodies triggering Iso-immune & auto-immune reactions. o Infectious agents and toxins such as Malaria Intrinsic Causes: o Defective Hgb o Sickle cell disease o Membrane abnormalities resulting in osmotic injury to the cells o Exposure to certain drugs and chemical condition such as: hypersplenism/neoplasma is additional causes of hemolysis. o May also be due to acute blood lost, mostly common seen in trauma/blood vessel rapture or chronic blood loss like GI tract hemorrhaging (melena) and menses.

3. Infection Viral Hepa infection mononucleus Epstein-bars Virus Bacterial clostridia, gram negative sepsis Protozoa , malaria, leishmaniasis, toxoplasmosis 4. Drugs and Chemical Chemotherapeutic Agent Anticonvulsant Antimetabolic Certain Oral Contraceptives Toxic Chemical Thrombotic Thrombocytopenic purpura and chemolytic uremic syndrome 5. Physical Effects Trauma, Burns, Prosthetic Values and surfaces, snake venom 6. Chronic Disease and Malignancies Renal and Hepatic Diseases Chronic infection Neoplasma Collagen Vascular Disease

Etiologic Categories of Anemia

1. Genetic Hgb pathics Thalassemias Enzyme abnormalities of the glycolytic pathways Detection of the RBC cytoskeleton Hereditary sphyrocytosis Fancori anemia Nutritional Fe deficiency Cobalamin/VitB12 deficiency Folate deficiency Alcoholism, generalized malnutrition and starvation Hemorrhage Immunologic antibody mediated abnormalities

PHATOPHYSIOLOGY: The transport of O2 is impaired w/ anemia Hgb/ no. of RBC is too low to carry adequate O2 to tissue and hypoxia develops. The body attempts to compensate to tissue hypoxia in major ways: 1. A shift in O2-Hgb disconnection curved to the to facilitate the removal of move O2 by tissue at the same partial pressure of O2. 2. Redistribution of blood from tissue of low O2 needs to tissues of O2 needs. 3. Cardiac Output achieved rate/ stroke volume to meet O2 demand of the tissue 4. of RBC production resulting from erythropoiesis synthesis by the kidneys response to tissue hypoxia. CLINICAL MANIFESTATIONS: 1. The bodies primarily response to hypoxia deeper depending in the severity of blood lost the chronicity of the anemia, the clients age and person of other disorder. 2. Client with mild anemia (Hgb = 10-12 g/dl) are usually asymptomatic 3. (Hgb = <6-10 g/dl) may suffer from dyspnea, palpitation, diaphoresis and chronic fatigue 4. (Hgb = <6g/dl) such as those chronic renal disease

2.

MEDICAL MANAGEMENT: (GOAL OF CARE) 1. Alleviate and Controlling the causes: a. Supplemental Therapy: i. FeSO4 (Oral) (IM) Z-technique b. Nutritional Therapy i. Excellent source of Fe c. Surgery to repair sites of hemorrhages d. Speelectomy e. Removal of toxic agents that causes abresia f. Stem cell/ Bone Marrow Transplantation g. Corticosteroid Therapy h. Immunosuppressive Therapy 2. Relieving the manifestation: a. O2 Therapy b. EPO (Erythropoiety) R : subQ A : ( production of RBC) c. Fe replacement Nursing condsideration: (Pregnancy) Fe best taken after meal 2 hours after meal + juice Expect black and constipation d. Blood Transfusion

Food Rich in Fe and VitB12 and Folic Acid

[Excellent Source] Almonds, asparagus, bran, beans, carrots, cauliflower, celery, egg yolk, graham bread, kidney, liver, lettuce, oatmeal, oyster, beans, spinach and full wheat (cooked foods in iron pans) [Good Source] Apricots, beef, cabbage, cornmeal, cucumber, duck, goose, lamb, mushroom, orange, pepper, potato, prunes, radish, raisins, pineapple and tomatoes [Vit B12] Red meats, liver, dairy products and eggs [Folic Acid] Asparagus, broccoli, spinach, lettuce, lemon, melon, green leafy vegetable, fish, legumes, liver, mushrooms, milk, egg and yeast, wheat germ, kidney beans, dry peas, beans and nuts (food should not cook with excessive heat and large amount of H2O.

CLINICAL MANIFESTATION [Severe Anemia] Hgb = < 6g/dl AREA

General

Skin Eye Ears Mouth Lungs Heart GI

GUT Muscle Nervous System

CM Pallor, Severe fatigue, malaise, weakness, light headedness, fever, extreme dyspnea, headache, vertigo, sensitivity to cold and weight loss Pallor, jaundice, dry skin, brittle nails, spoon shape concave nails with longitudinal ridges Blurred vision, sclera jaundice, retinal hemorrhage Vertigo and Tinnitus Red glossy bright red, sore tongue Dyspnea and orthopnea Tachycardia, palpitations, ,murmurs, angina, HPN and anemic cardiomegaly failure, MI -Anorexia, dysphagia, abdominal pain, hema -tenesis, tarry stool, hepatomegaly,spleenomegaly Amenorrhea, menorrhagia, fertility, hematuria Back pain, external tenderness, severe bone and joint pain Headache, confusion, peripural metopathy, porresthesia, loss of balance, mental depression, coping difficulty (life-threatening condition)

THALASSEMIAS
Type of Anemia cause by erythrocytes production. Is a group of genetic disorder that result in adequate normal Hgb production IDA (iron-deficiency anemia) affects both synthesis of Thalassemias disrupt the globulin this disorder includes: a. Alpha Thalassemias i. A relatively benign and asymptomatic condition b. Beta Thalassemias i. (minor) a mild-moderate form to microcytic anemia ii. (major) a severe microcytic hypochronic anemia they be fatal and this disorder cause hemolysis iii. Found in people of Mideteranian, African and Southeast Asia origin iv. The condition is thought to be response to malaria ETIOLOGY: 10% prevalence rate in this geographical area. Those with inherit with beta genes (hemozygotes) which result a profound a life threatening anemia PATHOPHYSIOLOGY: Are antosomal recessive genetic disorder associated with mutation in globulin genes The globulin proteins, vital for synthesis Hgb is composed of (2) alpha and (2) beta polypeptide chains known as alpha globulin and beta globulin Hemolysis result from an imbalance in the alpha and beta which are normally paired, the excess impaired and beta globulin chain, which aggravates and form precipitate that damage the RBC membrane, if the RBC damage will lead to vascular disease.

MEGOBLASTIC ANEMIA
A group of disorders caused by impaired DNA synthesis resulting in defective RBCs, these anemia share morphology of megaloblast (large abnormal and premature RBCs in the blood and bone marrow) there are caused by deficiency of Vit. B12 (Cobalamin) and Folic Acid Common Features include the ff: a. Leukopenia - # of RBC b. Thrombocytopenia - # of platelets c. Oral ,GI, Neurological Manifestations d. A favorable response to injection of either Vit. B12 or Folic Acid.

CLINICAL MANIFESTATION: Individuals has also alpha Thalassemias may have very mild and artificially asymptomatic Individual with Thalassemias major are Dx early in life because the lack of Hgb because which apparent. Affected children appear N at birth (because fetal Hgb certain no beta globins) however in first few months switches of life has Hgb synthesis to fetal to adult for manifestation of severe anemia begins to appear. The children has also pain, failure to thrive frequent infection, diarrhea, spleenomegaly, hepatomegaly, jaundice from RBC hemolysis and bone hyperplasia. Fetal Dx from special type of Thalassemias can be made through amniocentesis, molecular a mutation is present, Dx after 8 weeks of gestation. OUTCOME MANAGEMENT: Thalassemias (minor): doesnt refuse Tx (Major) provide adequate N Hgb for erythropoiesis and to alleviate the effect of Fe overload.