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107 Cards in this Set
- Front
- Back
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Iron Deficiency Anemia
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microcytic hypochromic anemia caused by inadequate supplies of iron needed to synthesize hemoglobin, characterized by pallor, fatigue, and weakness. Laboratory diagnosis includes hgb, htc, transferrin, serum iron evaluation. Iron deficiency may be the result of an inadequate dietary supply, poor absorption in the digestive system,chronic bleeding. Replacement iron can be supplied by ferrous sulfate, preferably the oral form. The anemia should be corrected in 2 months, but therapy is continued for another 4 months to replace tissue stores.
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Thalassemia
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hemolytic hemoglobinopathy anemia characterized by microcytic, hypochromic, and short-lived red blood cells caused by deficient synthesis of hemoglobin polypeptide chains
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Cobalamin Deficiency
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Insidious onset
Nutritional deficiency of intrinsic factor Hereditary enzymatic defects of cobalamin utilization Cobalamin is absorbed in the distal ileum Gastric mucosa does not secrete intrinsic factor Pernicious anemia Seen in Scandinavians and African Americans |
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Thalassemia major (Cooley's anemia)
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homozygous form, evident in infancy, is recognized by anemia, fever, failure to thrive, and splenomegaly and is confirmed by characteristic changes in the red blood cells on microscopic examination. Frequent transfusions are necessary to maintain oxygen-carrying capacity of the blood. Red cells are rapidly destroyed, freeing large amounts of iron to be deposited in the skin, which becomes bronzed and freckled. The iron is also deposited in the heart, liver, and pancreas, which become fibrotic and dysfunctional. The spleen may become so enlarged that respiratory excursion is impeded and the abdominal organs are crowded. Headache, abdominal pain, fatigue, and anorexia often occur. No cure exists.
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thalassemia major manifestation
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Thalassemia major
Retarded developmental growth Retarded mental development Splenomegaly and hepatomegaly Jaundice |
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thalassemia major tx
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Blood transfusions
IV deferoxamine (Desferal) Splenectomy |
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Thalassemia minor manifestation
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Often asymptomatic
Mild to moderate anemia |
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thalassemia minor tx
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No treatment
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Folic Acid Deficiency causes
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Poor nutrition
Malabsorption syndromes Small bowel disorders Drugs - Impede absorption of folic acid Alcohol abuse Anorexia Hemodialysis -Lost during dialysis |
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Folic Acid Deficiency manifestation
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Occurs insidiously
GI Dyspepsia Smooth, beefy red tongue No neurological symptoms |
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Aplastic Anemia
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deficiency of all of the formed elements of blood (specifically red blood cells, white blood cells, and platelets), representing a failure of the cell-generating capacity of bone marrow. Neoplastic disease of bone marrow and destruction of bone marrow by exposure to toxic chemicals, ionizing radiation, or some antibiotics or other medications are common causes
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Acute Blood Loss/Chronic Blood Loss
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Signs and symptoms dependent upon amount of blood loss
Body needs 2-5 days to manufacture more RBCs RBCs, hemoglobin, and hematocrit are low |
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Hemolytic anemia (why do they become jaundiced?)
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Physical destruction of RBCs
Physical force Immune reactions Infectious agents and toxins |
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what is Sickle Cell Disease
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Inherited autosomal recessive disorder
Characterized by the presence of an abnormal form of hemoglobin Hemoblobin S Erythrocyte stiffens and elongates Decrease oxygen levels Affects more than 50,000 Americans |
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sickle cell manifestations
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Differ from individual to individual
Often anemic Prone to gallstones Pain Aching joints |
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sickle cell diagnosis
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Sickling test
Sickled S Hemoglobin Electrophoresis |
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sickle cell crisis
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Severe, painful, acute exacerbation of sickling
Severe capillary hypoxia occurs Tissue ischemia occurs Shock occurs |
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sickle cell causes
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Sickling episodes triggered by low oxygen tension in the blood
Viral or bacterial infections High altitude Emotional or physical stress Surgery Blood loss Dehydration |
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sickle cell complications
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As episodes of crisis are repeated
Heart become ischemic and enlarged Acute chest syndrome Pulmonary infarctions Retinal vessel obstruction Kidneys Spleen CVAs |
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sickle cell care
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Oxygen
Narcotics for pain control Hydration Bed rest Transfusion Prevent complications |
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Polycythemia
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Production and presence of increased numbers of RBCs
Secondary Polycythemia caused from chronic hypoxia stimulates erythropoietin production in the kidney, which in turn stimulates erythrocyte production |
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Polycythemia vera
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Polycythemia Vera
chromosomal mutation in a single stem cell develops in pts. who are 50 and older |
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Polycythemia Treatment
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Phlebotomy
desired hematocrit level is achieved Initially 300 to 500 ml of blood removed every other day then every 2 to 3 months Hydration therapy reduce blood’s viscosity Antiplatelet agents ASA |
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Polycythemia dx
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Elevated RBCs
Elevated Hemoglobin Elevated WBCs Elevated platelets |
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Thrombocytopenia
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Reduction of platelets below 15,000
Results in prolonged bleeding from minor trauma to spontaneous hemorrhaging Can occur following ingestion of food, herbs, drugs |
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Thrombocytopenia in Children
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Platelet count less than 150,000
Purpuric rash Normal bone marrow Absence of signs of other identifiable causes Acute Chronic Presence of thrombocytopenia for more than 6 months |
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Immune Thrombocytopenic Pupura(ITP)
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Autoimmune disease
Platelets are coated with antibodies Function normally When reaching spleen are destroyed Recognized as being foreign |
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ITP in Children
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Sudden onset of bruising and petechiae
Gums and mucous membrane bleeding Usually follows a virus illness |
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Care ITP
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Corticostersoids (prednisone)
Suppress phagocytic response of splenic macrophages Depress antibody formation High doses of IV immunoglobulin and anti-Rh (D) Compete with antiplatelet antibodies for macrophage receptors Splenectomy Platelet transfusion for life-threatening hemorrhage |
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Care ITP in Children
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Prevent intracranial bleeding
Monitoring platelet count Monitoring bleeding status IV or oral steroids Over 2-4 weeks IV immune globulin 1-2 days Splenectomy Chronic ITP |
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Thrombotic Thrombocytopenic Purpura (TTP)
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Uncommon syndrome
Manifestations Hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, renal abnormalities Enhanced agglutination of platelets Form microthrombi in arterioles and capillaries Precepitated by use of estrogen or pregnancy Bleeding and clotting occur simutaneously |
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Care TTP
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Treat the underlying disorder
If possible, remove causative agent Splenectomy Corticosteroids Dextran Vincristine |
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Heparin Induced Thrombocytopenia and Thrombosis Syndrome (HITTS)
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Known as white clot syndrome
Immune response to heparin Platelet aggregation occurs Decrease in circulating platelets Thrombocytopenia occurs Platelet thrombi form |
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Manifestations of HITTS
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Often asymptomatic
Bleeding Petechia Purpura Spontaneous hemorrhaging Platelet count less than 20,000 |
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Care: HITTS
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Heparin-Induced Thrombocytopenis and Thrombosis Syndrome
Plasmapheresis Protamine sulfate Thrombolytics Lepirudin (Refludan |
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Care ITP
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Immune Thrombocytopenic Purpura
Corticosteroids Immunoglobulins Danazol Immunosuppresives Splenectomy Platelet transfusions |
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Hemophilia and Von Willebrand Disease
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Sex linked recessive genetic disorder
Defective or deficient coagulation factor Hemophilia A Hemophilia B Von Willebrand’s disease |
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Hemophilia A
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Most common form
Classic hemophilia Factor VIII deficiency Seen in 1:5000-20,000 males Recessive sex-linked |
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Hemophilia B
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Christmas disease
Factor IX deficiency Seen in 1: 30,000-50,000 males Recessive sex-linked |
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Von Willebrand Disease
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Most common congenital bleeding disorder
Seen 1:100 Exists in mild to severe forms Deficiency in vWF Autosomal dominant |
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Diagnostics of Hemophilia and Von Willebrand disease
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Prothrombin time and thrombin time
Normal Platelet count Normal Partial thromboplastin time Prolonged Bleeding time Prolonged in von Willebrand’s Disease Normal in hemophilia A and B Factor assays Decreased factor VIII in Hemophilia A Decreased factor IX in Hemophilia B Decreased vWF in Von Willebrand Disease |
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Manifestations of Hemophilia and Von Willebrand Disease
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Slow, persistent, prolonged bleeding
Delayed bleeding after minor injuries Uncontrollable bleeding after dental surgeries or irritation of gingiva Epistaxis GI bleeding Hematuria Ecchymoses and subcutaneous hematomas Hemarthrosis |
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Treatment of Hemophilia and Von Willebrand Disease
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Prevent and treat bleeding
Replacement of blood and clotting factors Treatment of the complications DDAVP |
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Blood Component Therapy
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Packed RBCs
Severe anemia and blood loss Frozen RBCs Autotransfusions or rare donors Platelets Platelets less than 10,000-20,000 Fresh Frozen Plasma Bleeding due to clotting factors Albumin Hypovolemic shock and hypoalbuminemia Cryoprecipitates Replacement of clotting factors Especially factor VIII, Von Willebrand disease, and fibrinogen |
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Disseminated Intravascular Coagulation (DIC)
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Abnormally initiated and accelerated clotting
Uncontrollable hemorrhaging Profuse bleeding occurs Depletion of platelets and clotting factors Caused by an underlying disease or condition |
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Predisposing Conditions: DIC
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Acute DIC
Shock Septicemia Hemolytic processes OB conditions Malignancies Tissue damage Subacute DIC Malignant disease OB Chronic DIC Liver disease Systemic lupus erythematosus Localized malignancy |
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Causes of DIC in Children
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Trauma
Hypoxia Necrotizing enterocolitis Shcok Liver disease Overwhelming viral or bacterial infections Acute promyelocytic leukemia |
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Pathophysiology of DIC
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Event that causes activation of coagulation
Thrombi circulate in the bloodstream Thrombotic occlusion of microcirculation of all organs Fibrinolysis of the microcirculation Signs of microvascular thrombosis Circulating fibrin degradation products and consumption of platelets and coagulation proteins Signs of hemorrhage |
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Manifestations of DIC in Children
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Insidious onset
Excessive bruising and petechiae Oozing from puncture sites Oozing from sites of minor trauma Mild GI bleeding As disease progresses Purpuric rash Increased bleeding Hypoxemia Oliguria leading to renal failure Organ failure Intracranial hemorrhage |
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Manifestations of DIC
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Pallor, petechiae, purpura
Oozing of blood Bleeding from puncture sites Hematomas Tachypnea Tachycardia Hemoptysis GI bleeding Neurological changes Cyanosis, tissue necrosis |
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Diagnostics for DIC
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Prolonged prothrombin time
Prolonged partial thromboplastin time Prolonged activated partial thromboplastin time Decreased fibrinogen Decreased platelets Increased D-dimer |
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Treatment of DIC
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Identify and treat the underlying cause
Administer platelets Administer cryoprecipitate Administer fresh frozen plasma Heparin |
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Neutropenia
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Decrease in WBC count
Less than 500/ul Occurs with a variety of conditions and illnesses Most common cause is iatrogenic Common cause of infections |
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Leukemia
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General term
Group of malignant disorders affecting the blood and blood-forming tissues of the bone marrow, lymph system, and spleen Occurs in all age groups |
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Leukemia Etiology
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Result from a combination of factors including:
- Genetic factors - Environmental influences - Chromosomal changes - Chemical agents, chemotherapeutic agents, viruses, radiation and immunologic deficiencies |
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iatrogenic
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caused by treatment or diagnostic procedures. An iatrogenic disorder is a condition caused by medical personnel or procedures or through exposure to the environment of a health care facility
(Mosby, Mosby. Mosby's Dictionary of Medicine, Nursing & Health Professions, 7th Edition. Mosby, 102005.). <vbk:0-323-03562-0> |
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Leukemia Classifications
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Acute versus chronic
Acute Clonal proliferation of immature hematopoietic cells Malignant transformation of a single type of hematopoietic immature cell Cellular replication and expansion of the cell Chronic More mature forms of WBCs Gradual onset Type of WBC involved Type of leukocyte involved Myelogenous origin Lymphocytic origin |
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Leukemia causes
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Caused by bone marrow failure
Bone marrow overcrowding by abnormal cells Inadequate production of normal bone marrow elements Predisposed to anemia, thrombocytopenia, decrease in WBCs Leukemic cells infiltrate the pt’s. organs splenomegaly, hepatomegaly, lymphadenopathy, bone pain, and oral lesions |
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Acute Myelogenous Leukemia
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Increase in incidence with advancing age
60-70 years of age Occurs in 85% of adults Uncontrolled proliferation of myeloblasts, the precursors of granulocytes Onset abrupt and dramatic Serious infections and abnormal bleeding |
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Diagnostics of Acute Myelogenous Leukemia
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Decreased RBC, Hgb and Hct
Decreased platelets Decreased to increased WBCs with myeloblasts High LDH Hypercellular bone marrow with myeloblasts |
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Manifestations of Acute Myelogenous Leukemia
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Fatigue and weakness
Headache Mouth sores Anemia Bleeding Fever Infections |
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Acute Lymphocytic Leukemia
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Most common type found in children
Before age 14 Peak incidence seen 2-9 years of age Found in adults Immature leukocytes proliferate in the bone marrow Fever is often the first sign Bleeding is often present Leukemic meningitis often occurs |
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Diagnostics of Acute Lymphocytic Leukemia
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Decreased RBCs, Hgb, Hct
Decreased platelets Low, normal or increased WBCs High LDH Hypercellular bone marrow with lymphoblasts Presence of Philadelphia chromosome in one fourth of cases |
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Manifestations of Acute Lymphocytic Leukemia
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May appear abruptly
Fever Bleeding May be insidious Progressive weakness Fatigue Bone and/or joint pain Bleeding tendencies |
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Chronic Myelogenous Leukemia
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Found between the ages of 25-60
Peaks about 45 years of age Caused by excessive development of mature neoplastic granulocytes in the bone marrow that infiltrate the liver and spleen Chronic stable phase followed by the development of a more acute aggressive phase |
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Diagnostics of Chronic Myelogenous Leukemia
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Decreased RBC, Hgb, and Hct
Increased platelet count early in disease to decreased count later in disease Increased polymorphonuclear neutrophils Decreased leukocyte alkaline phosphatase Philadelphia chromosome |
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Manifestations of Chronic Myelogenous Leukemia - chronic
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Chronic stable phase
Often no symptoms Fever, fatigue Can last for several years Well controlled with treatment Progresses eventually to blastic phase |
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Manifestations of Chronic Myelogenous Leukemia - blastic
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Blastic phase
Refractory to treatment |
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Chronic Lymphocytic Leukemia
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Most common type
Occurs between 50-70 years of age Predominant in men Production and accumulation of functionally inactive but long-lived, mature-appearing leukocytes infiltrate the bone marrow, spleen, and liver Often no symptoms Detected during examination for unrelated condition |
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Diagnostics of Chronic Lymphocytic Leukemia
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Mild anemia and thrombocytopenia
Increased WBC Lymphocytes in bone marrow |
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Manifestations of Chronic Lymphocytic Leukemia
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Chronic fatigue
Anorexia Fever Splenomegaly Lymphadenopathy |
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Hairy Cell Leukemia
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Approximately 2% of all leukemias
Seen in males over age 40 Cells have a hairy appearance Chronic disease Lymphoproliferation predominantly involving B lymphocytes that infiltrate the bone marrow and spleen |
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Manifestations of Hairy Cell Leukemia
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Splenomegaly
Pancytopenia Infections Indolent disease requiring no therapy |
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Pancytopenia
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marked reduction in the number of red blood cells, white blood cells, and platelets.
(Mosby, Mosby. Mosby's Dictionary of Medicine, Nursing & Health Professions, 7th Edition. Mosby, 102005.). <vbk:0-323-03562-0> |
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Leukemia Collaborative Care
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Goal is to attain remission
Complete remission Partial remission Minimal residual disease Molecular remission |
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Leukemia Chemotherapy
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Decrease drug resistance
Minimize the drug toxicity Multiple drugs used with varying toxicities Interrupt cell growth at multiple points in the cell cycle |
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Induction therapy
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Bone marrow is depressed
Aggressive stage |
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Intensification therapy
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High dose therapy
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Consolidation therapy
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After remission achieved then
Maintenance therapy |
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Multi drug therapies
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Decrease drug resistance
Minimize the drug toxicity Multiple drugs with varying toxicities Interrupt cell growth Multiple points in the cell cycle |
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Bone Marrow and Stem Cell Transplantation
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Goal: totally eliminate leukemic cells from the body
Combination chemotherapy and radiation Once this has occurred the cells are infused from a donor Allogeneic Syngeneic Autologous Complications of allogeneic hematopoietic stem cell Graft versus host disease Relapse of leukemia Infection |
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Nursing Diagnoses leukemia
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Risk for infections (immunosuppressed)
Risk for injury (thrombocytopenia) Disturbed body image Ineffective coping Compromised family coping |
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Leukemia Nursing Goals
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Understand and cooperate with the treatment plan
Experience minimal side effects and complications from the disease and treatment Feel hopeful and supported during the periods of treatment, relapse, or remission |
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Lymphomas
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Malignant neoplasms
Originating in the bone marrow and lymphatic structures Proliferation of lymphocytes Two Major Types: Hodgkin’s Disease Non–Hodgkin’s Lymphoma |
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Hodgkin’s Disease
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Proliferation of abnormal giant, multinucleated cells
Reed-Sternberg cells Cells are located in lymph nodes Occurs most frequently between 15 to 35 years of age and above 50 years of age Cause is unknown |
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Hodgkin’s Disease causes
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Several key factors play a role in its development:
Epstein-Barr virus (EPV) Genetic predisposition Exposure to occupational toxins Prevalent in HIV infected individuals |
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Manifestations of Hodgkin’s Disease
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Onset usually insidious
Initial development enlargement of a single lymph node Cervical is the most common site, axillary, inguinal Nodes remain moveable and nontender Weight loss, fatigue, weakness, fever, chills, tachycardia, or night sweats Generalized pruritus without skin lesions may develop Pain upon ingestion of alcohol |
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Diagnostics of Hodgkin’s Disease
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Blood tests
decreased RBCs decreased WBCs Lymph node biopsy Reed-Sternberg cells Bone marrow examination and CT scan Staging of disease |
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Care of Hodgkin’s Disease
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Treatment depends on the nature and extent of the disease
Staging involves an A or B classification, Whether symptoms are present when the disease is found Roman numeral (I to IV) Location and extent of the disease |
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Reed-Sternberg cell
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one of a number of large, abnormal, multinucleated reticuloendothelial cells in the lymphatic system found in Hodgkin's disease. The number and proportion of Reed-Sternberg cells identified are the basis for the histopathologic classification of Hodgkin's disease.
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Treatment hodgkins
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Radiation therapy
Combination chemotherapy Radiation therapy and chemotherapy Intensive chemotherapy with bone marrow and stem cell transplantation treatment of choice for advanced stages (IIIB and IVB) |
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Non-Hodgkin’s Lymphoma
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Group of malignant neoplasms of the immune system affecting all ages
No hallmark feature Can originate outside the lymph nodes Majority have widely disseminated disease at the time of diagnosis The prognosis is generally not as good as that for Hodgkin’s disease Treatment involves radiation therapy and chemotherapy |
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Manifestations of Non-Hodgkin’s Lymphoma
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Painless lymph node enlargement
Symptoms are dependent upon spread of the disease |
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Multiple Myeloma
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Neoplastic plasma cells
Infiltrate the bone marrow Destroys the bone Develops slowly and insidiously Cause is unknown Radiation exposure Organic chemicals Herbicides and insecticides Genetics Viral infections |
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Manifestations of Multiple Myeloma
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Disease is advanced before symptoms occur
Major symptoms Pain in the pelvis, spine, and ribs Pain triggered by movement Diffuse osteoporosis Osteolytic lesions Vertebral destruction |
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Diagnostics of Multiple Myeloma
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Pancytopenia
Hypercalcemia Bence Jones protein in urine Elevated serum creatinine |
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Care of Multiple Myeloma
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Corticosteroids
Chemotherapy Hematopoietic stem cell transplantation Analgesics |
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Tumor Lysis Syndrome
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Tumor cells are lysed
Intracellular electrolytes are dumped into extracellular fluid Intracellular electrolytes different composition than extracellular electrolytes Kidneys overworked Need to excrete added electrolytes Leads to kidney failure Common Leukemias with very high WBCs Non-Hodgkin’s lymphomas Usually when extensive disease is present |
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Child With Cancer
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Reinforce teachings
Encourage parents to participate in cares Provide written and verbal instructions Teach signs and symptoms of infections and bleeding Emphasize when to contact physician versus seek immediate medical attention Make appropriate ancillary referrals Note community resources |
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Erythropoietin
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glycoprotein hormone synthesized mainly in the kidneys and released into the bloodstream in response to anoxia. The hormone acts to stimulate and to regulate the production of erythrocytes and thus increases the oxygen-carrying capacity of the blood.
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mcv
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The MCV is a measure of the average volume, or size, of a single RBC and is therefore used in classifying anemias.
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decreased mcv related anemias
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Iron-deficiency anemia,
Thalassemia,Anemia of chronic illness: These are the most common diseases associated with microcytosis. |
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decreased mch related anemias
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Microcytic anemia,Hypochromic anemia: The MCH is decreased if the size of the RBC is small or the hemoglobin is diminished.
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mch
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hgb in an RBC
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Reticulocyte counts
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The reticulocyte count is a test for determining bone marrow function and evaluating erythropoietic activity. This test is also useful in classifying anemias. A reticulocyte is an immature red blood cell (RBC) that can be readily identified under a microscope by staining the peripheral blood smear with Wright or Giemsa stain. It is an RBC that still has some microsomal and ribosomal material left in the cytoplasm. It sometimes takes a few days for that material to be cleared from the cell. Normally there are a small number of reticulocytes in the bloodstream.
The reticulocyte count gives an indication of RBC production by the bone marrow. Increased reticulocyte counts indicate the marrow is releasing an increased number of RBCs into the bloodstream, usually in response to anemia. A normal or low reticulocyte count in a patient with anemia indicates that the marrow response to the anemia by way of production of RBCs is inadequate and perhaps is contributing to or is the cause of the anemia (as in aplastic anemia, iron deficiency, vitamin B12 deficiency, depletion of iron stores). |
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Neutrophils
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Neutrophils are the most common PMN and are produced in 7 to 14 days and remain in the circulation for only 6 hours. The primary function of the neutrophil is phagocytosis (killing and digestion of bacterial microorganisms). Acute bacterial infections and trauma stimulate neutrophil production, resulting in an increased WBC coun
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shift to the left
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When neutrophil production is significantly stimulated, early immature forms of neutrophils often enter the circulation. These immature forms are called band or stab cells. This occurrence, referred to as a “shift to the left” in WBC production, is indicative of an ongoing acute bacterial infection.
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