hematological

Question Answer
YELLOW MARROW Found in long bonesComposed of fat cells
RED MARROW Site of hematopoiesisRBCsWBCsPlateletsSite of hematopoiesis
BONE MARROW Highly vascularContains stem cells
Myeloid- ErythrocytesLeukocytesPlatelets
Lymphoid= T lymphocytesB lymphocytes
RBC’S 3.6-5.4 million/mm3
CLINICAL SIGNS & SYMPTOMS of Anemia Skin pallor, mucous membranes, conjunctiva, nail bedsHeart and respiratory rate increasesTissue hypoxia leading to angina, fatigue, dyspnea on exertion, night cramps (heart failure)Cerebral hypoxia leading to HA, dizziness, and dim vision
DIAGNOSTIC TESTS for Anemia CBCIron level and iron-binding capacitySerum ferritinSickle cell testHemoglobin electrophoresisSchilling test- B12Bone marrow examination
Hemoglobin Women 12 – 16 g/dlMen 13.5 – 18 g/dl
Hematocrit Women 38% – 47%Men 40% – 54%
RBCs 4.5 – 6
WBCs 4000 – 11,000
Platelets 150,000 – 400,000
IRON METABOLISM Obtained from food & supplementsAbsorbed in duodenum, jejunumPresent in heme (Hgb in RBC)Stored as ferritinRecycled after phagocytosis of old RBCs
VITAMIN B12 AND FOLIC ACID Required for DNA synthesisAcquired through dietB12 combines with intrinsic factor from stomach and absorbed in ileumEffects of decreased absorption not apparent for 2-4 yearsAbnormal cells- megaloblasts- may lead to megaloblastic anemia
IRON DEFICIENCY ANEMIA Usually r/t chronic bleeding; menstruation, elderly; lack of dietary intake brittle, spoon-shaped nails, cheilosis smooth sore tongue, picaTreatment includes increased dietary intake of iron-rich foods and oral or parenteral iron supplements
Sources of iron (heme)- beef, chicken, egg yolks, clams, oysters, pork, turkey, vealBran, brown rice, dried beans, dried fruits, greens, oatmeal
Drugs for Iron replacement Ferrous sulfate ( Feosol)Ferrous gluconate ( Fertinic)Iron dextran injection (Imferon)
Nursing responsibilities related to Iron replacement Drugs – Assess for drug rx: antacids, allopurinol, Vit EGive with OJ to increase absorption Use straw to prevent teeth stainingMonitor for toxicity: nausea, diarrhea, constipationTeaching do not give w/ milk); stools may be dark; increase fiber
VITAMIN B12 DEFICIENCY Usually d/t decreased intake or poorly absorbed; Leads to increased # immature RBC’s
Failure to absorb-B-12 leads to Pernicious Anemia
Pernicious Anemia S&S Develops d/t lack of intrinsic factorS&S develop gradually; pallor, jaundice, weakness; sore beefy red tongue; paraesthesias; proprioception
VITAMIN B12 DEFICIENCY Drugs- Cyanocobalamin- oral or injection
Nursing responsibilities for Cyanocobalamin B-12 Drugs Drug interactions: cimetidine, colchicine, timed-release K+Do not mix with any other drug in syringeIM or deep subcut.Burning sensation at injection siteMay need to be taken for life
FOLIC ACID DEFICIENCY Required for DNA synthesis and maturation of RBC’sCells will be fragile and immatureUsually d/t inadequate intake; elderly, alcoholics, drug addiction alcohol suppresses folate metabolismAt risk pop.: TPN, pregnancy, hemodialysis, chemo agents
FOLIC ACID DEFICIENCY S&S Pallor, weakness, fatigue, SOB, palpitationsGlossitis, cheilosis, diarrheaNO NEUROLOGIC S&S- helps to differentiate from B12 – Folic acid supplements- green leafy veggies; broccoli, organ meats, eggs, asparagus, milk
Nursing responsibilities for Folic Acid Deficiency Assess for Rx interactions: corticosteroids, BCP, sulfonamidesDo not mix in syringe with other meds
HEMOLYTIC ANEMIAS Premature lysis of RBC’sHemopoietic activity increases in marrow
Causes of Hemolytic Anemias Intrinsic- problems w/I RBC structureExtrinsic- drugs, chemicals, toxins, infections, burns, mechanical damage ( prosthetic heart valves)
THALASSEMIA Inherited disorder of hemoglobin synthesisProduces “target cells”Affect Mediterranean, Asians, africans, african-american4 genes responsible
S&S of Thalassemia Splenomegaly, bronze skin, bone marrow hyperplasiaAnemia, heart failure, fx of long bones; accumulation of iron in heart, liver, pancreasTreated with transfusions
ACQUIRED HEMOLYTIC ANEMIA Caused by factors outside of RBCMechanical traumaAutoimmune InfectionsTransfusion rxDrugs, toxins, chemical agents, venoms
S&S of Acquired Hemoltic Anemia vary; spleen enlarged, jaundice, pathologic fx of long bonesTachycardia, pallor
APLASTIC ANEMIA Bone marrow fails to produce all 3 types of blood cellsbone marrow replaced with fatMany times cause unknown- Radiation exposureChemicalsChemoDrugs Infections such as mono
S&S of Aplastic Anemia vary, insideousFatiguePallorProgressive weaknessExertional dyspneaHATachycardia and heart failureRemove cause and tx with transfusionsBone marrow transplant
POLYCYTHEMIA ERYTHROCYTOSIS Too many cells in blood- RBC’sHCT > 55% males; > 50% femalesClassified as primary or secondaryPrimary – polycythemia vera
POLYCYTHEMIA VERA Rare; Jewish ancestryProliferation of myeloid stem cellsCause unknownElevated erythrocytesCan last over long period of timeSpleen takes over and enlargesBone marrow becomes fibrolytic and reduces production
S&S of Plycythemia Vera Ruddy complexion-plethora SplenomegalyHead ache, dizziness, fatigue, wt. loss, night sweatsIncreased blood viscosity- angina, claudication, DVT’sElevated B/PElevated uric acid- gout, renal stonesGeneralized pruritus- itching
SECONDARY POLYCYTHEMIA Increased RBC’s d/t excess erythopoietin or prolonged hypoxiaMost common formResults from kidney disease or tumorsChronic hypoxia results fro high altitude, chronic heart and lung diseaseSimilar S&S; no splenomegaly
POLYCYTHEMIA PV: low erythropoietinSP: high erythropoietinSP: focus on cause of disorderPeriodic phlebotomy- 300-500 mlAntihistamines to relieve pruritisChemo agents- hydroxyurea (PV)PREVENTIONHydration, prevent blood stasis, monitor for thrombosis
PLATELET AND COAGULATION DISORDERS Disorders affect hemostasis- control of bleedingComplex interactions between platelets and clotting mechanisms
PLATELETS Thrombocytes- no cell nucleus, cannot replicateProduce substances for clottingFormed in bone marrow- thrombopoietinLive up to 10 days150,00-400,000Excess: thrombocytosisDeficit: thrombocytopenia
THROMBOCYTOPENIA Platelet count < 100,000May lead to bleeding/hemorrhagePetechiae Purpura Often mucous membranes of mouth, nose, GIResults from:Decreased productionIncreased sequestration in spleenAccelerated destruction
IMMUNE THROMBOCYTOPENIA Auto-immune with accelerated destructionAffects young adults; women>men; acute and chronicPetechia, purpura on chest, arms, neck; epistaxis, hematuria, wt loss, fever, HA
Purpura THROMBOCYTOPENIA Rare; thrombi occlude arterioles and capillaries; heart, lungs, liver, kidneys, brainPlatelet aggregation is key feature
Dx tests for THROMBOCYTOPENIA CBC; platelets, antinuclear antibodies (ANA)Serologic- hepatitis, HICV; bone marrow
Medication for Thrombocytopenia Oral glucocorticoids (prednisone)
Treatment for Thrombocytopenia Platelet transfusions; 1 unit = 30-60 ml of concentrate; increase of 100,000 /unitPlasmaphoresis- remove client’s plasma and replace with FFP( fresh frozen plasma)Surgery- remove spleen- site of platelet destruction
THROMBOCYTOPENIA Nursing Care bleedingassess for bleeding (early ID)Apply pressure; avoid straining, picking, blowing use soft bristle brushRinse mouth with saline q 2-4 hr; use petroleum jelly for moisture; avoid alcohol based mouthwashesCool liquids; avoid trauma
DISSEMINATED INTRAVASCULAR COAGUALTION- DIC Widespread intravascular clotting and bleedingLife-threateningSyndrome; Sepsis
HEMOPHILIA Group of heredity diseases that lead to persistent and sometimes severe bleedingResults from deficiencies of clotting factors Form platelet plug but clotting deficit does not allow stable fibrin clot leads to hemarthrosis- blood in joints
Hemophilia A- most common, VIII, mother to son, varying degrees
Hemophilia B (christmas), IX, clinically identical to A
Von Willebrand’s disease- most common, (vW), associated with VIII, men and women =
S&S HEMOPHILIA Hemarthrosis; bruising, oral and GI bleeding, hematuria, epistaxis, pain
Medication treatment of Hemophilia Clotting factors- FFP, cryoprecipitates, concentratesFFP replaces all Factor VIII (A)- heat treated to reduce risk of transmitting diseasesDesmopressin acetate (DDAVP)- causes release of VIIIFactor IX- IV
WHITE BLOOD CELL AND LYMPHOID TISSUE DISORDERS White blood cells (WBC’s, leukocytes)- defense against microorganisms5,000-10,000Leukocytosis-excessLeukopenia-deficiencyOriginate from stem cells in bone marrowTypes:GranulocytesAgranulocytes
Neutrophils- segs, 60-70% of WBC’s-phagocytes First to arrive at site of injuryIncrease during inflammationLifespan of 10 hours, constantly replaces
Eosinophils 1-3%, found in intestinal and lung tissueIncrease during allergic rx or parasite infections
Basophils- 1%; contain heparin, histamineIncrease during inflammation and allergic rx
Agranulocytes- enter blood before maturation
Monocytes- largest, 3-8%, phagocytotic; form macrophagesDispose of foreign waste, inflammation, active part of immune response
Lymphocytes – 20-30%; mature into B and T cellsB cells-humoral immune and antibodiesT cells- cell-mediated immunity process
LEUKONPENIA Neutropenia- majority of WBC; affected most often; <1500cellsCongenital vs acquiredSecondary to prolonged infectionHematologicStarvationAutoimmune (rheumatoid arthritis)Agranulocytosis- severe, <200 cells,
LEUKONPENIA Neutrophis play impt role in immune responseOpportunistic infections develop- BacterialFungalRespiratory
S&S of Leukopenia malaise, chills, fever, weaknessAdminister hematopoietic growth factorsPrimary nursing responsibility is protection
INFECTIOUS MONONUCLEOSIS Invasion B cells lymphoid Epstein-Barr virusyoung, self-limiting, present saliva4-8 weeks, insidious HA,malaise, fever, sore throat, lymph enlargement, B –cells produce antibodies, T-cells attack; dead B-cells and increased # lead to swelling
INFECTIOUS MONONUCLEOSIS WBC’s normal to low early, then elevated 4-6 weeks; platelets elevatedRecovery in 2-3 weeks, lethargy for up to 3 monthsBed rest, analgesics
MULTIPLE MYELOMA Malignancy in plasma cells multiply uncontrollably and infiltrate bone marrow, lymph, spleen, tissues Plasma cells are B-cells that produce antibodies increased blood viscosity and can damage kidney tubulesBone can pathologic fxDevelops slowly
S&S of Multiple Myeloma Bone painHypercalcemiaNeurologic dysfunctionRecurrent infectionsRenal failureChronic progression
Diagnosis of Multiple Myeloma X-rays, bone marrow exam, CBC, urinanalysis, biopsy of bone

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