Hematologic Diseases

Anatomy and Physiologic Overview

Hematologic system is composed of the blood and the organs that produce blood such as the reticuloendothelial system (RES) and bone marrow

Hematopoiesis Blood cell production done in the bone marrows (red), pelvis, ribs, epiphysis of the long bones Under normal conditions, the adult bone marrow produces about 175 billion erythrocytes, 70 billion neutrophils and 175 billion platelets. Erythropoiesis RBC production in the liver in utero (2-5 months) then in bone marrow o Needs iron, protein, pyridoxine (B6), cyanocobalamine (B12), folic acid, and copper Erythroblasts o Arise from the primitive myeloid stem cells in the bone marrow o Immature nucleated cell that gradually loses its nucleus o Cell is known as Reticulocyte at this stage Reticulocytes and other mature may be release prematurely into the circulation Erythropoietin o Stimulates the differentiation of the primitive myeloid stem cell into an erythroblast o A hormone produced primarily by the kidney o Level increased once the kidney detects low levels of O2 (e.g. anemia) Increased level of Erythropoietin stimulates marrow to increase production of erythrocytes Entire process take 5 days Iron Stores and Metabolism o The rate of absorption is regulated by the amount of iron already stored in the body and by the rate of RBC production o Additional amounts of Iron must be taken up by pregnant women to replace iron lost during menstruation o Stored as Ferritin o When required iron is release into the plasma, binds to transferrin and is transported into the membranes of the normoblasts (erythrocyte precursor cells) within the marrow, where it is incorporated into the haemoglobin o Men: 75 175 um/dL (13-31 umol/L) o Women: 65-165 ug/dL (11-29 umol/L) o Iron deficiency Bone marrow stores are rapidly depleted Haemoglobin synthesis = depressed Erythrocytes produced = small and low in Hemoglobin Indicated blood loss Vitamin B12 and Folic Acid Metabolism o Required for DNA synthesis o Both are derived from the diet o Folic Acid Absorbed in the proximal small intestine, but only small amount are stored in the body Folic Acid Deficiency stores within the body quickly become depleted o Vitamin B12 Strict vegetarians may ingest little Vit B12 because it is only found in foods of animal origin Combines with the intrinsic factor produced in the stomach Vitamin B12 factor complex absorbed in the distal ileum o Folic Acid and Vit B12 Deficiency Characterized by the production of abnormally large erythrocytes Megaloblasts Megaloblasts abnormal many are sequestered (trapped) while still in the bone marrow, their rate of release is decreased some actually die in the marrow before they can be release into the circulation Megaloblastic Anemia Reticuloendothilial system Mononuclear phagocyte system or macrophage (spleen, liver, lymphatic system, lungs)

BLOOD
Is a specialized organ in liquid form 55% of blood is composed of plasma 40-45% of blood is composed of RBC, WBC and Platelets Makes up 7-10% of the normal body weight Amounts to 5-6 L of volume What it carries: o Carries oxygen absorbed in the lungs o Carries nutrients absorbed in the GI tract o Carries hormones, antibodies and such o Carries waste products produced by cellular metabolism to the lungs, skin, liver and kidney where they will be eliminated Fibrinolytic System o Eventually dissolves clots (thrombi) formed within the blood vessels Hemostasis

o Balance between clot (thrombus) formation and clot dissolution CBC with differential o Hemoglobin makes up the mature erythrocytes contains Iron makes up 95% of cell mass large amount => good transport of O2 between lungs and tissues made up of four subunits (each containing a heme portion attached to a globin chain): Iron Present in the heme component Heme Has the ability to bind to O2 loosely and reversibly Oxygen Readily binds to haemoglobin in the lungs Carried as oxyhemoglobin in the arterial blood o A brighter than red haemoglobin = does not contain O2 Readily detaches from haemoglobin in the tissues, where O2 is needed for metabolism Venous blood Haemoglobin combines with H+ ions produced by cellular metabolism => buffers excessive acid Males 13-16 gm / dl Females 12-14 gm /dl o Hematocrit Males 42 50 % Female 40-48 %

RBC Erythrocytes
normal erythrocyte biconcave disk => large surface area that facilitates absorption and release of O2 molecules diameter of 8 um flexible => can pass easily through the capillaries membrane => very thin => gases such as O2 and CO2 can easily diffuse across it mature erythrocytes consists of haemoglobin no nuclei have many fewer metabolic enzymes than do most other cells marrow releases slightly immature forms of erythrocytes into the circulation => reticulocytes o normal response to an increase demand for erythrocytes Males 4.6 M 6.2 M per cu. Mm Females 4.2 M 5.4 m per cu. Mm Blood pH: 7.35 7.4 (slightly alkaline) Red Blood Cell Destruction Normal life span of an erythrocyte = 120 days Aged erythrocytes lose elasticity and become trapped in small blood vessels and the spleen removed from the blood by the RES, particularly in the liver and spleen As erythrocytes are being destroyed most of their haemoglobin is recycled Some are broken down to form Bilirubin and is secreted in the bile Divided into TWO CATEGORIES: Granulocytes o The presence of granules in the cytoplasm of the cell Neutrophils 60-70 % Most numerous Stain pink to violet hue Also called polymorphonuclear neutophils (PMNs, or polys) Also called Segmented neutrophils (segs) Eosinophils (with allergic rxn, parasitism) 1-4% Bright red in their cytoplasm Basophils (px who are septic or with leukemia, immatured type of WBC) 0-0.5 % Stain blue o Lymphocytes N: 5,000 10,000 cu. Mm 60% granulocytes 20-40% lymphocytes Monocytes (bacterial infection) 2-6 % Lymohocytes (virals, TB) 20-30 %

WBC Leukocytes

Platelets - Thrombocytes

200,000 350,000 cu.mm Thrombocytopenia Thrombocytosis Coagulation studies o PT Prothombin time(liver fnx; affected by vit K synthesis) N: 11-18 secs o PTT Partial Thromboplastin Time N: 50-80 secs (reflects deficiency in coagulation factor)

o Clotting time N: 5-10 minutes (req to produce fibrin) o Bleeding Time N: 30 secs 6 mins (degree which to will stop bleeding; reflects fnx of platelets) Miscellaneous Studies o Erythrocytes Sedementation Rate N: 0-20 mm/hr o Coombs Test indirect blood from mom, direct blood from the babys cord o Schillings Test Vit B12 in the gastro-intestinal system prep NPO x 8 hrs Radioactive Vit B12 given PO Vit B12 nonradioacitve given IM 2 hrs after urine collection for radioactive Vit B12 N: 15-40 % of oral dose excreted Urine and Stool o Hematuria Urine Macroscopic Microscopic Common cause: UTI, Stones o Urinalysis o Hematest o Hematoccult prep; no dark colored food x 24 hrs prior to test Fecal Occult Blood Testing Patient will undergo 3 days Iron free diet / meat free diet Radiologic o CXR o Scan o Lymphagiography Bone Marrow Aspiration and Biopsy o Preferred site iliac crest, sternum or tibia o Before: consent (invasive procedure), position exposing the site o After: pressure to site x 5 mins

Patient who has hematologic disorder are immunocompromised. Nursing Assessment: Pallor conjunctiva Jaundice (haemolytic) scleral palms of hands, soles of feet, yellowish coloring of the sclera o Indirect bilirubin Signs of bleeding such as petechiae, ecchymosis, hematoma, epistaxis Lymph nodes enlargement Limited join range of motion Splenomegaly or hepatomegaly Purpura o Low platelet and coagulation factor Hemarthrosis o Bleeding in the joint area o Hemarthosis blood aspirated o Hyorthrosis pus aspirated Physical Assessment Auscultate heart murmur, bruits Inspect above assessment Inspect above assessment Palpate lymph nodes, location, size, bones tenderness Percuss for splenomegaly, hepatomegaly Evaluate joint ROM and tenderness

BONE MARROW
Site of hematopoiesis / blood cell formation Usually limited to o Pelvis o Ribs o Sternum o Vertebrae One of the largest organs in the body o 4-5% of the total body weight Consists of o Cellular components (red marrow) o Fat (yellow marrow) Inc age = Dec red marrow #, replaced by the fat Extramedullary Hematopoiesis o The liver and the spleen resume the production of blood cells Higly vascular o Consists of the Stem Cell Have the ability to replicate itself => ensuring supply of stem cells throughout the life cycle Differentiation Process (Myeloid or Lymphoid System) Lymphoid System o Produces T or B Lymphocytes (WBC) Myeloid System o Produces RBCs, WBCs and Platelets o A defect in the myeloid system has a great effect throughout the body

ANEMIA
Classification According to Etiology Hypoproliferative Anemias o From dec. RBC production caused by a deficiency on cofactors required for erythropoiesis, bone marrow is supressed or is inadequately stimulated because of a lack of erythropoietin count Bleeding o From RBC loos (500 ml or <) o There is exposure of endothelial tissue Hemolytic o From increased destruction of RBCs which may occur because of an over over reactive RES or the bone marrow produces abnormal RBCs that are then destroyed by the RES (Reticulo Endothelial System) o No hemolysis with clotting o Hemolysis no clotting Definition A condition, in which the haemoglobin concentration is lower than normal, reflects fewer than normal RBCs within the circulation, which results to a diminished amount of oxygen delivered to body tissues. Not a disease in itself but a sign of an underlying disorder Most common manifestation of a hematologic disorder Basic underlying- tissue hypoxia Signs and Sxs depends upon severity and chronicity and age Clinical Manifestations Tissue Hypoxia o Underlying cause of all manifestations accompanying anemia o Common: Pallor Easy fatigability SOB shortness of breathing Dyspnea or exertion Tarry stools Weight loss Weakness Palpitations Hypotension on severe type of anema Anorexia Headache Dizziness Iron Deficiency Anemia o Palpitations, dizziness, easy fatigability o Cold sensitivity, pallow o Brittle nails, and hair o Plummer Vinsons Syndrome soreness and inflammation of mouth and tongue (stomatitis and glossitis) o Poor iron intake o Most common during 6 mons 2 years Developmental stage Adolescents Start of menarche puberty o May also be caused by chronic disease o Dx CBC Iron studies (serum iron, ferritin, transferrin) o Compute Total Saturation of Iron > 20 percent = Normal < 20 percent = IDA o Nursing management Oral iron route of choice; given after meals Liquid iron intake with straw because it stains Best absorbed with Vit C Stool becomes tarry and constipation may occur Parenteral Avoid tissue staining by using separate aspiration injection needles Z-Track method and deep IM Dietary Increase iron and roughage by eating meat and internal organs Vegetables Fiber Beans Raisins Blood transfusion Check for any previous hx of allergy When to verify serial number and blood type, must be done with another nurse Close monitoring of VS With consent Preventive Education

Especially in menstruating and pregnant women Bed Rest Reduce oxygen demand Megaloblastic Anemia o Anemias caused by deficiencies in Vit B12 and folic acid o Characterized by appearance of megalobalsts (abnormally large, primitive RBs) in blood and bone marrow Folic Acid Deficiency Folic Acid a vit necessary for nomal RBC prod, stored as folates o Deficiency occurs in people who rarely eat uncooked veggies (fresh) o Increased folic acid requirements Alcoholism Patient with chronic haemolytic anemias Pregnant women (spina bifida) o Management Eat source of folic acid Supplementation (5 mm / tablet) Fresh vegetables Vitamin B12 Deficiency Inadequate intake, can develop in strict vegetarians who consume no meat or dairy products o Intrinsic factor normally secreted by cells within the gastric mucosa and binds with dietary Vit B12 and travels with it to the ileum o PuD, gastric resections, ileum problems o Pernacious anemia Smooth, sore, red tongue and mild diarrhea (intestinal problem), extremely pale, parethesia, difficulty maintaining their balance because of damage to the spinal cord and also lost position sense o Typical manifestations of anemia Weakness Listlessness Fatigue o Vit B12 deficiency Neurologic manifestations o Management Increase dietary intake of Vit B 12 Animal proteins Eggs Dairy products Vit B12 injections weekly at first then monthly for maintenance Aplastic Anemia o Decrease in or damage to marrow stem cells, damage to the microenvironment within the marrow and replacement of the marrow with fat o Results in bone marrow aplasia (markedly reduced hematopoiesis) which results in anemia, leukopenia and thrombocytopenia o Infection and pregnancy can trigger it, or may be caused by certain medications, chemicals or radiation damage o Sulphonamides o Clinical Manifestations Pancytopenia Normocytic anemia Neutropenia Thrombocytopenia Increased susceptibility to infection Purpura Bleeding Retinal haemorrhage Dyspnea Fatigue o Management Bone marrow transplantation Common site: ileac crest Peripheral blood stem cell transplantation Immunosuppressive therapy (ATG / Cyclosporine) Asses for signs of Infections o Eliminate intake of raw fruits, vegetables, and raw meat, practice asepsis; reverse/protective isolation, limit visitors Bleeding o Avoid ASA admin.; use of soft bristled toothbrush, avoid anemias, avoid picking nose, avoid trauma, use electric razor Fatigue o Rest, avoid strenuous activity Anemia in Renal Disease o ESRD: Serum Creatinine > 3 mg/dl o Mild shortening of life span and deficiency in EPO o Iron deficiency sec to chronic blood loos from dialyzer (RRT) o Folic acid deficiency o HGB: 11-12 g/dl Anemia of Chronic Disease

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Normochromic Normocytic Anemia Chronic Inflammation Malignancy 6-8 weeks: Hgb 9 g/dL; Hct <29 % Normal cellularity of BM with normal Iron stores EPO low Mgt: treatment of underlying disease

NEUTROPENIA
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Neutrophils less than 2000/m Goal: preventing and limitn ginfection Based on severity and duration of neutropenia mgt: treat underlying cause (malignancy) corticosteroid: immunologic disorders o lymphoma Hodgkins Non-Hodgkins o most immunologic disorders are autoimmune Systemic Lupus Erythematosus (SLE) GM-CSF: decreased BM production o Granulocyte Macrophages Colony Stimulating Factor o Prevention of infection Nursing mgt: preventing and early recognition of signs and symptoms o Fatigue o Loss of appetite o Do not ellicit inflammatory response Causes of neutropenia (chart book) o Decreased production of neutrophils o Ineffective granulocytopoiesis Inability to produce granulocytes Megaloblastic anemia o Increased destruction of neutrophils Computation of the Absolute Neutrophil Count (ANC) ANC = [Total WBC count x (% neutrophils + % bands)] / 100 3 Normally, neutrophil count is > 2000/mm Neutrophenia Production o The most common/important: protecting patient against infection, recognizing early signs and symptoms = primary o Bleeding = secondary o Avoid rectal examination as possible o Thorough physical examination and history taking o Dietary DO NOT eat fresh o Patient is isolated = limit visitors; observe universal precaution o Hygiene Advise patient to change or take bath daily Change soiled diapers o IV site Observe infiltration o Dx studies CBC paying attention to absolute neutrophenic count

LEUKEMIA
Leucocytosis increased leukocytes in the circulation Leukaemia neoplastic proliferation of one particular cell type Acute form halted in blast phase, progress rapidly; with worst prognosis; immature = tend to be destroyed easily Chronic form evolved over periods of month, matured type; they skip apoptosis (program cell death) Classification According to stem cell line involved: o Lymphoid B Cells and T-Cells o Myeloid Macrophages Monocytes According to Onset o Acute Plastic phase o Chronic Matured type that escaped apoptosis Leukemia o Most common in childhood(3-5 years old) cancer; abnormal proliferation of WBC in blast form o Predisposing factors: Radiation Survivors of Hiroshima Benzol o Types of Leukemia Acute Lymphocytic Leukemia (ALL)

80-85% childhood leukemia o Most common luekemia in children Boys > girls (4 years) Bone pain, enlarged spleen and liver 95 % chance of obtaining remission with early diagnosis and treatment 75 % chance of survival over 5 years Initial induction therapy: steroids and vinca alkaloids Intensification / consolidation therapy: allogenic therapy o Immunosuppressant agent Dec. proliferation of immature cells Acute Non-Lyphocytic Leukemia (ANLL) Granulocytic and monocytic 60-80 percent will obtain remission with treatment 30-40% cure rate Chronic Lymphocytic Leukemia Older adults (72 years old) Derived from B lymphocytes (mature) Escaped apoptosis o B symptoms, lymphadenopathy, infection (anergy) Beta 2-microglobulin Mgt: fludarabine, cyclophosphamide, monoclonal antibody (chemo agents) o Patient = risk for infection (hematologic and exposure to treatment) Acute Myeloid Leukemia (AML) Results from a defect in hematopoietic stem cell that differentiates into all myeloid cells Most common nonlymphocytic leukemia Incidence rises with age (peak at age 60) Prognosis is highly variable 1-3 years with chemotheraphy; 2-5 months o Without chemo (induction GCSF consolidation = SE: Tumor Lysis hypercalemia, hyperurecemia and signs of RBC casts) o TX: allopurinol Clinical manifestations o Fever and infection (neutropenia) o Weakness and fatigue (anemia) o Bleeding tendencies (thrombocytopenia) o Pain from an enlarged spleen or liver (RES) splenomegaly and hepatomegaly o Hyperplasia of the gums o Bone pain Dx findings: o CBC Decrease mature leukocytes, erythrocytes and platelets Total leukocyte count can be low, normal or high o Bone Marrow Analysis Increase of immature blast cells (more than 30%) Medical Mgmt: o Bone Marrow Transplantation (BMT) Most effective Infusion of donor stem cell to initiate blood stem cell production Types Allogenic BMT Umbilical Cord blood Stem Cell Transplantation Autologous BMT Peripheral blood Stem Cell Transplantation o Autologous transplant Chronic Myeloid Leukemia Arises from mutation in myeloid stem cell Normal myeloid cells continue to be produced Preference for immature forms Marrow expands to cavities of long bones / extramedullary system Causes severe bone pain Translocation of Chromosome 22-0 (BCR-ABL) o Philadelphia Chromosome Uncommon in people < 20 years old Incidence increases with age (mean age 67 y/o) Mgt: tyrosine kinase inhibitor (Gleevac) Nursing Mgt: o Environment and staff Thorough hand hygiene Allow no one with infection No fresh flowers No fresh vegetables or uncooked meat Change water in containers every shift Ensure rooms is clean daily Patient o Avoid suppositories, enemas, rectal temperature taking May cause breakage or fissure in the mucosa o Practice deep breathing

Mobilize secretions Ambulate Prevent thrombosis o Prevent skin dryness Prevent proliferation of the skin o Use particulate filter mask Bleeding precautions o Use stool softeners or laxatives for constipation o Use smallest possible needle for venepuncture o No flossing of teeth o Use soft bristled toothbrush Common in patients in thrombocytopenic o

THROMBOCYTOPENIA
Causes Blood decrease characterized by an abnormally small number of platelets in the blood Common site of bleeding = CNS haemorrhage

Decreased production of platelets within the bone marrow o Leukemia, aplastic anemia, megaloblastic anemia o Chemotherapy, meds, alcohol o Myelodysplastic syndromes o Infections Toxins Septicaemia Viral infection Increased destruction of platelets o In the bloodstream (intravascular) Due to antibodies ITP (Idiopathic Thrombocytopenic Purpura) , Lupus erythematosus, malignant lymphoma, medications Due to Infecitons Bacterecemia Postviral infection o In the spleen or liver (extravascular) Hypersplenism / enlarged spleen sequestration of platelets in spleen Secondary to over productivity of RES Increased consumption of platelets o Disseminated intravascular coagulation o Determine platelet count Clinical Manifestations 3 Platelet count >50,000 / mm o Bleeding and petechiae usually do not occur o Excessive bleeding can follow surgery 3 Platelet count <20,000/mm o Petechiae o Nose and gingival bleeding o Excessive menstrual bleeding o Excessive bleeding after surgery or dental extractions 3 Platelet count < 5,000 / mm o Spontaneous, potentially fatal central nervous system or gastrointestinal haemorrhage (massive) Mgmt: Treatment of underlying disease Platelet transfusions FFP (Fresh Frozen Plasma) o Contains coagulant factors Splenectomy Pharmacologic Mgt: Vit K 10 mg, table or IV q 8 hrs Prednisone (immunosuppressive agent) Gamma Globulin(IVIg) Rh0 [D] Immune Globulin (WinRho) Nursing Mgt: Prevent complications o X aspirin, aspirin-containing meds o X intramascular injections o X rectal temp o X flossing, commercial mouthwash o X vigorous coughing or blowing Primary Thrombocythenia Increased in platelet >600,000/mm3 Abnormal size but prolonged life Same with polycythemia but does not progress to leukemia Asymptomatic until platelet exceed 1 million Bleeding Thrombosis Erythomyalgia Dx: BCB and Bone Marrow Analysis Affect M<F. Middle Age >65 y/o increases risk for thrombosis

Mgt: low dose ASA o Has antiplatelet activity Hyprocyurea, anagrelide, interferon alfa 2b o Anagralide more side effects Plateletpharesis o Like dialysis o Cannot be used for transfusion because they are already abnormal Health teaching about risk factors for thrombosis and side effects of medication Most common: GI symptoms Secondary Thrombocytosis Reactive elevation in platelet Secondary causes o Inflammation o Chronic disease o Iron deficiency o Malignancy o Chronic bleeding o Splenectomy Management: focused on the management of secondary causes

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

Not a disease May be triggered by sepsis, trauma, cancer (especially prostate and acute promyelocytic leukemia), shock, abruption placentae, toxins or allergic reactions Life threatening Pathophysiology o Normal hemostatic mechanisms are altered so that a massive amount of tiny clots forms in the microcirculation o As platelets and clotting factor are consumed to form microthrombi, coagulation fails o Result of excessive clotting is bleeding First to decrease : platelets Circulatory hypotension Medical mgt: o Most important management is treating the underlying cause o Secondary Goal: Correct secondary effects of tissue ischemia by improving oxygenation, replacing fluids, correcting electrolyte imbalances, and administering vasopressor medications (epinephrine drip, levophen drip) o Heparin Infusion For patient with massive clotting To prevent further clot formation Every 6 hours APTP

DISORCERS ASSOCIATED WITH THE LYPMHATIC SYSTEM HODGKINS DISEASE A relatively rare malignant B lymphocyte cell disease of the lymph system that has an impressive cure rate More common in men Chronic immunosuppressive therapy Has two peaks of incidence Hodgkins Lymphoma o Proliferation of Reed-Sternberg cells in a single lymph node then travel to other lymph o Cause by Epstein Barr Virus o Progression Stage 1: single Lymph Node Stage 2: 2 or more lymph nodes on the same side of the diaphragm or in an extra lymphatic organ; GOOD PROGNOSIS Stage 3: both sides of diaphragm Stage 4: disease disseminates, spreads to other extralymphatic organs like spleen; POOR PROGNOSIS Unicentric in origin Epstein Barr Virus REED STERNBERG CELL o Malignant cell Clinical manifestations o Painless enlargement of one or more lymph node (neck) o Pruritus o Cough o Pulmonary effusion, jaundice, abdominal pain, bone pain o Herpes zoster infection o B Symptoms Fever without chills Drenching swears Weight loss >10% o Mild anemia o Absent / decreased reaction to sensitivity tests Could not manifest the usual signs and symptoms of inflammation Medical Management

Staging laparotomy then radiation therapy Obtain biopsy specimen of retroperitoneal lymph nodes and both lobes of liver and remove spleen Chemotherapy = 80% effective (doxorubicin, bleomycin, vinblastine) Radiation therapy still very useful to extensive adenopathy Late Manifestations o Hepatomegaly o Splenomegaly o Difficulty in breathing o Facial edema Superior vena cava syndrome Blood vessels is being occluded by lymph adenopathies o Blood can no longer go the R side of heart o Enlargement of the lower extremities

NON-HODGKINS DISEASE Poor prognosis Heterogeneous group of cancers Originate from the neoplastic growth of lymphoid tissues Lymphoid tissues involved are largely infiltrated with malignant cells Spread if malignant cells is unpredictable Extranodal tissue May involve B Lymphocutes and T Lymphocytes Higher the age, the higher the incidence of NHL Etiologic Factor o Unknown o Immunodeficiencies o Viral infection o Incidence is high among white individuals o Exposure to dyes, pesticides and solvent Pathophy o NHL arises when some lymphocytes begin to divide uncontrollably and grow in a n abnormal way, or when the cells do not die as new lymphocytes Clinical Manifestations o Symptoms may be absent or very minor Early stage o Lymphadenopathy Stage III or IV o B Symptoms Drenching night sweats Recurrent fever Unintentional weight loss >10% Management o Radiation o Chemotherapy MULTIPLE MYELOMA Abnormal proliferation of plasma cells Immature and malignant and invade the bone marrow, lymph nodes and live, spleen and kidneys Leads to bone destruction throughout the body Causes o Environmental o Genetic Bone demineralization occurs and large amounts of Ca are lost urine in blood and urine- renal calculi- renal failure o Lesions: bone lytic lesions Resulting to pathologic fractures o Abnormal proliferations of plasma cells Bence Hones CHON in Urine Increase Bun Creatinine Increased Calcium Risk factors o Familial tendency o Radiation therapy o Exposure to chemicals Clinical Manifestations o Backache or bone pain o Sudden pathologic fracture o Diffuse osteoporosis o Hypercalcemia o Anemia Diagnostic Tests o Bone marrow biopsy o Blood and urine examination BUN crea o (+) Bence Jones Protein Management o Combination therapy: steroid/melphalan

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Bone marrow transplant Reduce calcium level: bisphosphonates Encourage activity The more sedentary, the more immobilize the Ca

THROMBOTIC DISORDER Decreasing clotting inhibitors within the circulation Altered hepatic function Lack of hepatic function Tortuous or atherosclerotic vessels Malignancy o Hypercoagulable states Fibrino Lysis Therapies o Splenectomy Anemia o Therapeutic Apheresis: Separation o Therapeutic Phlebectomy: polycythemia, hemochromatosis (excessive copper and iron in the blood) o Blood component therapy Whole blood plasma and formed elements Packed RBC RBC Prioprecipitate clotting FFP all Complications of blood transfusion o Febrile non haemolytic reaction o Acute haemolytic reaction o Allergic reaction o Circulatory overload o Bacterial contamination o Transfusion related to lung injury o Delayed haemolytic reaction