DISORDERS ASSOCIATED WITH ERYTHOCYTES ANEMIA A disorder characterized by RBC and hemoglobin and hematocrit levels below normal

vels below normal range ; anemia also exhibit increased RBC DESTRUCTION (hemolytic anemia) Causes delivery of insufficient amounts of oxygen to tissues and cells Erythrocytes are classified according to size, shape and color Hemoglobin content is expressed as normochromic or hypochromic anemia RBC size is usually expressed as macrocytic, microcytic or normocytic Anemias may be divided into those that are the result of Blood loss (hemorrhage) Impaired production of RBCs (bone marrow depression) Increased destruction of RBCs ( hemolysis) Nutritional deficiencies (long term iron deficiency) Marrow failure is linked to a disease process, toxic exposure, tumor and unknown causes A decrease in RBC production or destruction results in a lower number of circulating blood cells Bone marrow hematopoietic function manifests the inability to produce the needed quantity Loss of oxygen carrying element in the blood results in a supply/demand imbalance in vital organs Peripheral circulation compensates by shunting blood to vital organs, causing hypoxic status in other areas of the body Rapid hematopoietic effort causes blood cell irregularities (immature RBCs) and inability to produce RBCs with a resultant decrease of RBC count When pt. has anemia the problem is low Hgb and O2

Clinical Manifestations Most adults do not experience symptoms, until the Hemoglobin is less than 8g/dL The OLDER adult experience symptoms when the Hemoglobin is less than 10g/dL SIGN AND SYMPTOMS arise from decreased oxygen carrying capacity : ANOREXIA CARDIAC DILATION DISORIENTATION DIZZINESS DYSPEPSIA (UPSET STOMACH OR INDIGESTION) DYSPNEA EXERTIONAL DYSPNEA FATIGUE HEADACHE INSOMNIA PALLOR ( MUCOUS MEMBRANES AND SKIN) PALPITATION SOB SYSTOLIC MURMUR TACHYCARDIA

VERTIGO MEDICAL MANAGEMENT

Depends on the cause May correct or lessen the anemic condition Treatment is often specific to particular anemia

NURSING DIAGNOSIS Ineffective tissue perfusion (cardiovascular), related to reduction of cellular components necessary for delivery of oxygen to the cells Monitor changes in V/S and mental alertness Monitor cardiac rhythms Monitor Hgb, hematocrit and RBCs Assess baseline arterial blood gases (ABGs) and electrolytes Note presence/ degree of dyspnea, cyanosis, hemoptysis Impaired gas exchange, r/t RBC, hemoglobin and hematocrit deficit Evaluate ability to manage ADLs, r/t OXYGEN decrease Assess activity response , dyspnea and HR Observe for cyanosis, hypoxia Maintain bed rest as necessary and provide range of motion Monitor O2 sat. Administer O2 Activity intolerance , r/t O2 deficit, secondary to decreased hemoglobin and hematocrit Plan optimum rest Assist in identifying intolerance Assess ability to perform ADLs Assess potential for injury caused by mobility impairment Teach performing at own rate of ability, to reduce energy expenditure Monitor HgB and hematocrit levels

HYPOVOLEMIC ANEMIA (BLOOD LOSS ANEMIA) Abnormally low circulating blood volume due to blood loss Secondary anemia 500 ml can be tolerated Blood loss of 1000 ml or more in an adult can be SEVERE! Can cause decreased cardiac output r/t internal and external hemorrhage caused by surgical procedure, GI bleeding , menorrhagia ( heavy menstrual and prolonged period), trauma or severe burns Loss of blood decreased the amount of circulating fluid and hemoglobin and decreases the amount of oxygen carried to the tissues of the body Average adult total blood volume: 6000 mg Can tolerate loss up to 500ml If the loss is 1000 ml, hypovolemic shock may occur

The rapidity of blood loss is r/t severity and number of signs and symptoms Do not do CPR, pumping will just pop the blood outside RBC and hematocrit levels drop to half the normal range

CLINICAL MANIFESTATIONS S/SX of hypovolemia & hypoxemia: Weakness Stupor Irritability Pale Cool Moist skin Hypotension Tachycardia (rapid, weak, thready pulse) Hypothermia Hemoglobin less than 10g/100ml Hematocrit less than 40% Vitamin b12 deficiency Internal hemorrhage causes PAIN because of tissue distention , organ displacement and nerve compression Pain may be localized or referred Decreased RBC, HEMOGLOBIN levels may not be evident after severe blood loss Severity of patients S/Sx correlates with the severity of BLOOD LOSS

MEDICAL MANAGEMENT For massive hemorrhage, need to CONTROL the bleeding Treat for shock: oxygen elevate lower extremities, keep WARM replace the volume of circulating fluid with blood transfusion (packed RBCs) , plasma ,* dextran (volume expander or blood derivative) or other IV therapy (lactated ringer) Oxygen therapy is ordered to restore decreased available oxygen Caused by decreased Hgb in the blood Patient may need supplemental IRON; b/c the availability of iron affects the marrow production of erythrocytes

NURSING INTERVENTION Monitor blood and fluid restoration and identify blood loss sites to control bleeding Patients should be kept flat and warm V/S frequent intervals I & O measured, with careful monitoring of urine output for oliguria caused by decreased renal perfusion

PERNICIOUS ANEMIA

Absence of intrinsic factor Intrinsic factor is essential for the absorption of vitamin B12 Deficiency of vitamin B12 affects growth and maturity of all body cells Vitamin B12 also related to NERVE MYELINATION (connective fat covered a bunch of neurons) May cause progressive demyelination and degeneration of nerves and white matter electrical impulse will jump instead if traveling smoothly, there may be electrical conduction problem in the brain Capable of great injury, destruction or DEATH Result of metabolic defect: absence of glycoprotein intrinsic factor secreted by gastric mucosa Intrinsic secretion fails b/c of gastric mucosal atrophy Pernicious anemia is an AUTOIMMUNE disease The gastric atrophy results in the destruction parietal cells PROGRESSIVE, MEGALOBLASTIC,MACROCYTIC anemia affecting older adults The intrinsic factor, is essential for absorption of vitamin B12 (cyanocobalamin) This vitamin is r/t nerve and myelination and if it is absent, progressive demyelination and degeneration of nerves and white matter occur

CLINICAL MANIFESTATIONS: Extreme weakness Dyspnea Fever Hypoxia Weight loss Jaundice (destruction of RBCs) : slight icterus; the end of RBC are Bilirubin(deposited in the kidney, urine is dark yellow) responsible for turning skins yellow skin color may appear pale lemon yellow b/c of excessive destruction of the RBCs, causes the bile pigments to increase in the blood serum; Edema of the legs occur Pallor GI complaints: constipation & diarrhea DYSPHAGIA SORE BURNING TONGUE ( SMOOTH & ERYTHAMATOUS) NEUROLOGICAL SYMPTOMS: Tingling of the hands& feet Disorientation Personality changes and behavior problems Partial or TOTAL PARALYSIS MEDICAL MANAGEMENT VIT. B12 ( cyanocobalmin) injections (1000 units) Folic acid supplements, iron replacement are ordered RBC transfusion

 NURSING DIGNOSIS

If the anemia is severe,pt. may be transfused with packed red blood cells The standard treatment : 1000 units of vit. B12, administered IM for 2 wks Daily for 1 week Weekly for 1 month Monthly for life Diet: high in protein, vitamins and minerals All gastric bypass pt. have to be in vit. B12 Sensitive to cold , additional lightweight, warm blankets may be needed Conserve energy to prevent injury

Risk for injury r/t sensory and motor losses, alteration in mental status Imbalanced nutrition: less than body requirements r/t sore mouth and tongue, diarrhea and constipation

APLASTIC ANEMIA Clinical manifestations Pancytopenic Repeated infections with high fever Dyspnea Decrease bone marrow function Aplasia ( failure of a normal process of cell generation and development) Congenital and acquired Congenital: primary Caused by chromosomal alterations 30% of aplastic anemia that appear in childhood are inherited Acquired: Viral invasion, medications, chemicals, radiation, chemotherapy certain strong antibiotic can cause aplastic anemia Related to exposure to viral invasion, medication, chemicals, radiation or chemotherapy in which the hematopoietic tissue is replaced by fatty marrow, causing a defect in RBC production 70% of acquired aplastic anemia are idiopathic (unknown) Immune mediated disease Depression of erythrocyte production results in lowered hemoglobin and RBCs Leukopenia and thrombocytopenia develop Usually pancytopenic (a lot of drop in number) All 3 major blood elements (red,white cells and platelets) from the bone marrow are absent or reduce Incidence of aplastic Anemia is low

Palpitations Bleeding tendencies: petechiae, echymoses, bleeding gums, epistaxis GI and GU bleeding

MEDICAL MANAGEMENT Identify and remove cause Bone marrow suppression is expected w. certain antineoplastic medications or radiations therapy Lab values monitored to maintain control Blood transfusions avoided, prevent iron overloading and develop antibodies to tissue antigens Platelet transfusions that are human lymphocyte antigen (HLA) matched are used to treat serious bleeding in a thrombocytopenic pt. Blood transfusion avoided to minimize the risk of rejection for a bone marrow transplant candidate Splenectomy: Required in pts. With hypersplenism when that is the cause of destruction of normal platelets Surgical excision of the spleen may be performed to treat blood dyscrasias w/ incidence of splenomegaly, to treat trauma to the spleen or to remove dead spleen Pt. is observed for infection or inflammation Complications: hemorrhage, shock, paralytic ileus Parental therapy maintained Nasogastric Suction used if paralytic ileus develops Movement and positioning to prevent infection or postoperative pneumonia Steroids and Androgens: Are sometimes used to stimulate the bone marrow Immunosuppressive therapy with antithymocyte globulin and cyclosporine has become an important therapy for pts. Who are not candidates for bone marrow transplantation Bone marrow transplantation : Treatment of choice in pt. younger than the age of 50 who have a compatible donor Granulocyte macrophage colony stimulating factor is used in biologic response modifier treatment for aplastic anemia Indicated in certain conditions: Immunodeficiency, cancer, leukemia and recurrent aplastic anemia A matched donor and recipient are essential to avoid rejection or complications Pt. place on reserve isolation (neutropenic precautions) with monitoring for fever or infection Medication therapy may include immunosuppresants, antibiotics and antianxiety agents Used in hematological malignancies following large doses of chemotherapy or radiation That can be administered b.c of toxicity to the bone marrow Obtained by multiple marrow aspirations under general or spinal anesthesia Yielding 500 to 800 ml of marrow Shortly after chemotherapy, patient receives donated marrow through an IV catheter The infusion of marrow is called rescue process

Marrow travels through the blood stream to the bone marrow, where it begins to manufacture new leukocytes , erythrocytes and thrombocytes The infused marrow repopulates the marrow of the patient after several weeks Medications: cyclosporine (immunosuppressant) and chemotherapy (prevent graft versus host complications)

Nursing Interventions Nursing Diagnosis Activity intolerance, r/t inadequate tissue oxygenation Risk for infection, r/t increased susceptibility Pts who have aplastic anemia are highly susceptible to infection Strict aseptic technique Meticulous care for dressing changes and IV site care Prevent skin and mucous membrane integrity, avoid IM injections! Administration of rectal medications or rectal temp. Protective device: egg crate mattress In case of thrombocytopenia: Assess for bleeding and trauma Pt. urine and stool should be monitored for occult or gross blood

IRON DEFICIENCY ANEMIA RBCs contain decreased levels of hemoglobin Excessive iron loss : caused by chronic bleeding , intestinal ,uterine, gastric malnourished=iron deficiency anemia Vegetarians at risk Most common cause is excessive iron loss In adults most common cause is chronic intestinal or uterine bleeding! Can also be caused by bleeding from gastric or duodenal ulcers , esophageal varices, hiatal hernias, colonic diverticula and tumors The major sources of chronic blood loss are from the GI and GU system GI bleeding is often not apparent and may exist for a considerable time before the problem is identified Loss of 50 to 75ml of blood from upper GI is required for stools to appear black or melenic The color results from the iron in the RBCs Menstrual blood losses and blood losses r/t pregnancy are common causes of iron deficiency anemia in young adult women Commonly it results in malabsorption of iron caused by diseases such as celiac disease and sprue Subtotal gastrectomy may lead to iron deficiency caused by ACHLORHYDRIA ( loss of hydrochloric acid) Occult bleeding and decreased iron postgastrectomy diets

CAUSES OF IDA: Iron deficiency may develop from inadequate dietary intake ,malabsorption , blood loss or hemolysis (breakdown of red blood cells) Daily iron intake from food and dietary supplements is adequate to meet the needs of men and older women , may be inadequate for those individuals who have higher iron needs (menstruating pregnant women) Malabsorption of iron may occur after certain types of GI surgery and in malabsorption syndromes Iron absorption occurs in the duodenum. Malabsorption of iron may involve disease of the duodenum in which absorption surface is altered or destroyed Blood loss is major cause of iron deficiency in adults The major sources of chronic blood loss are from GI and GU Common causes of GI blood loss: Peptic ulcers Gastritis Esophagitis Diverticulitis Hemorrhoids Neoplasms Average monthly menstrual blood loss is about 45 mL causes the loss of 22mg of iron

CLINICAL MANIFESTATIONS: PALLOR FATIGUE ,WEAKNESS SOB ANGINA: S/SX OF HF GLOSSITITS : BURNING TONGUE PAGOPHAGIA HEADACHE PARESTHESIA

MEDICAL MANAGEMENT Iron Salts such as, Ferrous sulfate 900 mg daily Oral or injection (Z TRACK) Hematocrit level should rise 5% to 15% in 3 weeks and the Hgb level to 2 to 5g/dL

Ascorbic acid, enhance iron absorption Diet high in iron Too much iron can lead to constipation Food Source of iron: ORGAN MEATS FISH

POULTRY EGGS GREEN LEAFY VEGETABLES WHOLE GRAINS : LEGUMES AND NUTS DRIED BEANS DRIED FRUITS: APRICOTS, DATES, FIGS, PRUNES AND RAISINS SHELLFISH

NURSING NTERVENTIONS: Medication therapy for iron replacement Assist to plan periods of rest when fatigue is present Diarrhea or nausea is significant, but black tarry stools are not (expected with iron therapy)

SICKLE CELL ANEMIA Most common genetic disorder Predominantly in African Americans Abnormal,cresent shape RBC containing Hgb A defective Hgb molecule Severe, chronic ,incurable condition (Disease)HOMOZYGOUS: having two identical genes inherited from each parent for a given hereditary characteristic An episode of acute sickling of erythrocytes , which causes occlusion and ischemia in distal blood vessels Sickling indicates clumping or aggregation of these misshapen RBCs which lodge in small blood vessels (Trait) Sickle cell trait is HETEROZYGOUS: having two different gene The indvi has Hg-S and Hg-A in the RBCs Tissue hypoxia and ischemia may occur, causing pain and edema as a result of inflammation Destruction of fragile RBCs inhibits oxygen carrying formation

CLINICAL MANIFESTATIONS: PRECIPITATING FACTORS: DEHYDRATION CHANGE IN OXYGEN TENSION IN THE BODY( high elevation) blood becomes thicker Such as infection,overexertion,weather changes (cold), ingestion alcohol and smoking LOSS OF APPETITE IRRITABILITY WEAKNESS ABDOMINAL ENLARGEMENT (pooling of blood in the liver, spleen, other organs may accompany JAUNDIE) JOINT AND BACK PAIN EDEMA OF EXTRMITIES

destroyed RBCs are being deposited Usually the pt. is asymptomatic for the first 10-12 weeks of age, at which time most of the fetal Hgb has been replaced by Hbs Complications include multisystem failure, infarctions, hemorrhage and retinal damage leading to BLINDNESS MEDICAL MANAGEMENT:

No specific treatment for the disease Alleviate symptoms: Oxygen( control hypoxia and sickling) Rest Fluids Analgesics(treat pain) Parental morphine and hydromorphone are preferred opioid analgesics for acute sickle cel crisis pain Bone marrow transplant For example: chronic leg ulcers may be treated w/bed rest, antibiotics, warm saline soaks, mechanical or enzyme debridement and dressings