RBC, WBC, and Coagulation Disorders Flashcards

1
Q

Anemia

A

Lower than normal hemoglobin concentration and reduced number of erythrocytes.

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2
Q

Causes of Anemia

A
  • Inherited Hemolytic Anemia: Sickle cell disease, thalassemia.
  • Red Blood Cell Membrane Abnormality: Acanthocytosis, hereditary elliptocytosis, hereditary spherocytosis, stomatocytosis.
  • Enzyme Deficiencies: Glucose-6-phosphate dehydrogenase deficiency.
  • Acquired Hemolytic Anemia: Antibody-related (autoimmune hemolytic anemia, isoantibody/transfusion reaction, cold agglutinin disease), not antibody-related (disseminated intravascular coagulation, hypersplenism, infection, liver disease, mechanical heart valve, microangiopathic hemolytic anemia, paroxysmal nocturnal hemoglobinuria, toxins, trauma, uremia).
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3
Q

Symptoms of anemia

A

Symptoms of anemia depend on factors like severity, rapidity of development, duration, metabolic requirements, and the presence of other conditions. Common manifestations include weakness, fatigue, pallor of the skin and mucous membranes, jaundice, angular cheilitis, brittle nails, and pica. Complications may include heart failure, paresthesias, and confusion.

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4
Q

Anemia assessment findings

A
  • Laboratory Tests: Hemoglobin, hematocrit, reticulocyte count, RBC indices (MCV, RDW), iron studies, serum vitamin B12, folate levels, haptoglobin, erythropoietin levels, complete blood count (CBC).
  • Additional Studies: Bone marrow aspiration, colonoscopy, upper endoscopy to identify underlying conditions causing anemia.
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5
Q

Anemia nursing interventions

A
  • Managing Fatigue: Assist in prioritizing activities, establishing a balance between activity and rest, and addressing conditions contributing to fatigue.
  • Maintaining Adequate Nutrition: Encourage a well-balanced diet, educate on the interference of alcohol with essential nutrients, and provide dietary supplements as prescribed.
  • Managing Activity Intolerance: Monitor vital signs, pulse oximetry, adjust medications, and ensure appropriate fluid replacement.
  • Promoting Effective Management of Prescribed Therapy: Educate patients on the purpose, administration, and potential side effects of prescribed medications. Support adherence to treatment plans and collaborate to address barriers.
  • Monitoring and Managing Potential Complications: Assess for signs and symptoms of heart failure, perform neurologic assessments for megaloblastic anemias, and intervene promptly.
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6
Q

Iron deficiency Anemia

A

Iron deficiency anemia occurs when the intake of dietary iron is insufficient for hemoglobin synthesis. The body can store about one fourth to one third of its iron requirements, and anemia develops when these stores are depleted. Functional iron deficiency can occur when iron delivered to erythroid precursors is inadequate.

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7
Q

Iron deficiency causes

A
  • Inadequate dietary iron intake.
  • Blood loss, especially gastrointestinal bleeding, which is a common cause in men and postmenopausal women.
  • Conditions such as ulcers, gastritis, tumors, inflammatory bowel disease, menorrhagia (excessive menstrual bleeding), and pregnancy with inadequate iron intake.
  • Chronic alcohol abuse, use of aspirin, steroids, or nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Iron malabsorption, as seen after gastrectomy, bariatric surgery, celiac disease, and inflammatory bowel diseases.
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8
Q

Iron deficiency assessment findings

A
  • Symptoms of anemia (weakness, fatigue).
  • Severe or prolonged cases may show a smooth, red tongue; brittle and ridged nails; and angular cheilosis.
  • Signs may subside after iron replacement therapy.
  • Relevant history may include multiple pregnancies, GI bleeding, and pica.
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9
Q

Iron deficiency nursing interventions

A
  • Preventive education for menstruating women and pregnant women.
  • Encourage iron-rich foods with vitamin C for better absorption.
  • Assist in selecting a healthy diet; provide nutritional counseling if needed.
  • Instruct on the importance of continuing therapy until iron stores are replenished.
  • Oral iron is best absorbed on an empty stomach; instruct patients on proper administration to minimize side effects.
  • Educate on potential side effects and ways to manage them.
  • Liquid iron may stain teeth; precautions can be taken.
  • IV supplementation may be used in specific cases; nurses should be aware of the formulation and potential risks.
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10
Q

Iron deficiency tests ordered

A
  • Definitive diagnosis through bone marrow aspiration (rarely done); stained aspirate reveals low or absent iron levels.
  • Commonly diagnosed through laboratory tests: low serum ferritin levels, low serum iron, elevated total iron-binding capacity (TIBC), and small erythrocytes (decreased mean corpuscular volume - MCV).
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11
Q

Vitamin b12 defiency

A

Anemias associated with vitamin B12 deficiency result in megaloblastic changes in bone marrow and peripheral blood due to the crucial role of B12 in normal DNA synthesis. Megaloblastic red blood cells, along with abnormal nonlymphoid leukocytes and platelets, are produced. Bone marrow analysis shows hyperplasia, with large and irregular precursor erythroid and myeloid cells. Many abnormal cells are destroyed within the bone marrow, leading to insufficient mature cells entering the peripheral blood. Pancytopenia may develop over time.

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12
Q

Vitamin B12 deficiency causes

A

Vitamin B12 deficiency can result from:
- Inadequate dietary intake (rare, especially in vegans).
- Impaired absorption from the GI tract, common in older adults, inflammatory bowel disease, GI surgeries (ileal resection, bariatric surgery, gastrectomy), and the use of certain medications (metformin, histamine blockers, antacids, proton pump inhibitors).
- Absence of intrinsic factor, leading to pernicious anemia; intrinsic factor is necessary for vitamin B12 absorption and is typically secreted by cells in the gastric mucosa.

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13
Q

Vitamin b12 deficiency assessment findings

A
  • Symptoms are gradual due to compensatory mechanisms; weakness, listlessness, and fatigue may not be apparent initially.
  • Neurological manifestations specific to vitamin B12 deficiency include a smooth, sore, red tongue, mild diarrhea, confusion, paresthesias (numbness, tingling), difficulty maintaining balance, and loss of position sense (proprioception).
  • Pallor, mild jaundice, and a pale-yellow skin color may be observed, especially in patients with light skin.
  • Progressive neurologic symptoms with spontaneous partial remissions and exacerbations.
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14
Q

Vitamin B12 deficiency Nursing interventions

A
  • Assessment includes inspection of skin, tongue, and mucous membranes for signs of megaloblastic anemia.
  • Neurologic assessment for complications, including gait, coordination, and position sense.
  • Referral to physical and occupational therapy for assistive devices and safety concerns.
  • Instruction on soft bland foods for those with mouth and tongue soreness.
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15
Q

Vitamin B12 deficiency tests ordered

A
  • Serum levels of vitamin B12 are analyzed.
  • Elevated methylmalonic acid and homocysteine levels are more sensitive indicators of vitamin B12 deficiency.
  • Intrinsic factor antibody test to determine the presence of pernicious anemia.
  • Neurologic assessment includes tests of position, vibration sense, cognitive function, gait, and stability.
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16
Q

Folic acid deficiency anemia

A

Folic acid deficiency, like vitamin B12 deficiency, leads to megaloblastic changes in bone marrow and peripheral blood due to the essential role of folic acid in normal DNA synthesis. This results in abnormally large erythrocytes (megaloblastic red blood cells) and abnormal nonlymphoid leukocytes and platelets. Bone marrow analysis shows hyperplasia, with precursor erythroid and myeloid cells being large and irregular. Insufficient mature cells enter the peripheral blood, and over time, pancytopenia may develop.

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17
Q

Folic acid deficiency anemia causes

A

Folic acid deficiency can result from:
- Inadequate dietary intake, especially in individuals with a diet deficient in green vegetables and liver.
- Alcohol ingestion, which increases folic acid requirements and is common in those with alcohol abuse disorder.
- Conditions such as liver disease, chronic hemolytic anemias, and pregnancy, where erythrocyte production is increased.
- Small bowel diseases like celiac disease that interfere with normal folic acid absorption.

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18
Q

Folic acid deficiency anemia assessment findings

A
  • Symptoms are similar to vitamin B12 deficiency, and both anemias may coexist.
  • Gradual onset and progression, allowing the body to compensate until severe anemia.
  • Pallor, mild jaundice, and a pale-yellow skin color may be observed, especially in patients with light skin.
  • Neurological manifestations specific to vitamin B12 deficiency do not occur with folic acid deficiency.
  • Symptoms are similar to vitamin B12 deficiency, and both anemias may coexist.
  • Gradual onset and progression, allowing the body to compensate until severe anemia.
  • Pallor, mild jaundice, and a pale-yellow skin color may be observed, especially in patients with light skin.
  • Neurological manifestations specific to vitamin B12 deficiency do not occur with folic acid deficiency.
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19
Q

Folic acid deficiency anemia nursing interventions

A
  • Assessment includes inspection of the skin, tongue, and mucous membranes for signs of megaloblastic anemia.
  • Mild jaundice may be evident, especially in the sclera with natural lighting.
  • Vitiligo and premature graying of the hair are common in those with folic acid deficiency.
  • Careful neurologic assessment is important to identify complications.
  • Safety concerns regarding impaired gait, coordination, and position sense.
  • Physical and occupational therapy referrals may be needed for assistive devices.
  • Instruction on choosing soft bland foods for those with mouth and tongue soreness.
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20
Q

Folic acid deficiency anemia labs ordered

A
  • Serum levels of both folic acid and vitamin B12 are analyzed.
  • Measurement of the amount of folate within red blood cells is a more sensitive test to determine true folate deficiency.
  • Elevated homocysteine levels may be present in folic acid deficiency.
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21
Q

Aplastic anemia

A

Aplastic anemia is a rare disease characterized by a decrease in or damage to bone marrow stem cells, damage to the bone marrow microenvironment, and replacement of marrow with fat. Stem cell damage is mediated by the body’s T cells, leading to an attack on the bone marrow, resulting in aplasia and markedly reduced hematopoiesis. This condition leads to severe anemia, significant neutropenia, and thrombocytopenia.

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22
Q

Aplastic anemia causes

A
  • Can be acquired, congenital (rare), or idiopathic (without an apparent cause).
  • Associated with certain medications, chemicals (benzene, benzene derivatives), and radiation damage.
  • Certain toxic materials like inorganic arsenic, glycol ethers, plutonium, and radon.
  • Nonviral hepatitis may be a precipitating factor in about 10% of cases.
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23
Q

Aplastic anemia assessment findings

A
  • Insidious onset with complications from bone marrow failure.
  • Symptoms include fatigue, pallor, dyspnea, and purpura (bruising) due to thrombocytopenia.
  • Lymphadenopathy and splenomegaly may occur.
  • Retinal hemorrhages are common.
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24
Q

Aplastic anemia nursing interventions

A
  • Thorough assessment for signs of infection and bleeding.
  • Monitoring for side effects of therapy, including hypersensitivity reactions during ATG administration.
  • Monitoring long-term effects of cyclosporine therapy.
  • Patient education on drug–drug interactions and the importance of not stopping immunosuppressive therapy abruptly.
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25
Q

Aplastic anemia tests ordered

A
  • CBC reveals pancytopenia (lower-than-normal counts of erythrocytes, neutrophils, and platelets).
  • Neutrophil counts less than 1,500/mm³, hemoglobin less than 10 g/dL, and platelet counts less than 50,000/mm³.
  • Bone marrow biopsy typically shows an extremely hypoplastic or aplastic bone marrow, often replaced with fat.
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26
Q

Polycythemia Vera

A

Polycythemia vera is the most common of the three Philadelphia chromosome-negative myeloproliferative disorders. It is characterized by hypercellular bone marrow, leading to elevated counts of erythrocytes, leukocytes, and platelets in the peripheral blood. Erythrocyte elevation predominates, and hematocrit can exceed 60% in some cases.

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27
Q

Polycythemia vera causes

A

The exact cause is not mentioned in the passage, but it is associated with a mutation of the JAK2 gene.

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28
Q

Polycythemia Vera assessment findings

A
  • Variable symptoms; some patients may be asymptomatic at initial diagnosis.
  • Symptoms related to erythrocytosis: neurologic symptoms (headache, dizziness, vision changes), abdominal symptoms (early satiety, abdominal discomfort/pain), cardiovascular symptoms (ruddy complexion, angina, claudication, dyspnea, hypertension, thrombophlebitis), constitutional symptoms (fatigue, night sweats).
  • Pruritus, erythromelalgia (burning, painful sensation, erythema in fingers or toes).
  • Elevated uric acid leading to gout and renal stone formation.
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29
Q

Polycythemia Vera nursing interventions

A
  • Management of fatigue includes pharmacologic agents and nonpharmacologic treatments.
  • Pruritus management includes antihistamines, emollient lotion, SSRIs, interferon-alfa, and narrow band ultraviolet B phototherapy.
  • Thrombosis and bleeding risk assessments, lifestyle modifications, and education about signs and symptoms are crucial.
  • Avoidance of iron supplements is emphasized to prevent further stimulation of RBC production.
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30
Q

Polycythemia Vera labs ordered

A
  • Diagnosis based on clinical symptoms, laboratory findings, and the presence of a mutation of the JAK2 gene.
  • Assessment includes palpation of the spleen, history of thrombotic events, blood transfusions, or medications associated with causing erythrocytosis.
  • Patients with the JAK2 mutation who do not meet the criteria for a diagnosis of polycythemia vera may have “masked polycythemia vera,” which has a poorer overall rate of survival.
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31
Q

Neutropenia

A

Neutropenia is defined as a neutrophil count less than 2,000/mm3. It results from either decreased production of neutrophils or increased destruction of cells. Neutrophils play a crucial role in preventing and limiting bacterial infections.

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32
Q

Neutropenia causes

A
  1. Decreased Production of Neutrophils:
    • Aplastic anemia (due to medications or toxins)
    • Chemotherapy
    • Metastatic cancer, lymphoma, leukemia
    • Myelodysplastic syndromes
    • Radiation therapy
  2. Ineffective Granulocytopoiesis:
    • Megaloblastic anemia
  3. Increased Destruction of Neutrophils:
    • Bacterial infections
    • Hypersplenism
    • Immunologic disorders (e.g., systemic lupus erythematosus)
    • Medication-induced (formation of antibodies to medication)
33
Q

Neutropenia assessment findings

A
  • No definite symptoms until the patient develops an infection.
  • Routine CBC with differential can reveal neutropenia before infection onset.

Risk Factors for Infection:
- Severity of neutropenia: Risk increases with decreasing neutrophil count.
- Duration of neutropenia: Longer duration leads to an increased infection risk.
- Nutritional status, deconditioning, lymphocytopenia, invasive procedures, hypogammaglobinemia, poor hygiene, poor dentition, mucositis, antibiotic therapy, and certain medications increase infection risk.

34
Q

Neutropenia nursing interventions

A
  • Assess severity of neutropenia and risk factors for infection.
  • Patient education on self-care plan and when to seek medical attention.
  • Regular blood draws for CBC with differential based on suspected duration and severity of neutropenia.
  • Assess ANC (Absolute Neutrophil Count) to determine the severity of neutropenia.
35
Q

Leukemia

A

Leukemia is characterized by unregulated proliferation of leukocytes in the bone marrow. In acute forms or late stages of chronic forms, the excessive leukemic cell proliferation leaves little room for normal cell production. Extramedullary hematopoiesis can occur in the liver and spleen. Acute forms may involve infiltration of leukemic cells in other organs, such as the meninges, lymph nodes, gums, and skin.

36
Q

leukemia causes

A

The cause of leukemia is not fully known, but risk factors include exposure to radiation or chemicals, certain genetic disorders, and viral infections. Bone marrow damage from pelvic radiation or certain chemotherapy drugs can cause acute leukemia, often years after treatment for another malignancy.

37
Q

Leukemia assessment findings

A
  • Fatigue, weakness, pallor: Due to anemia from decreased red blood cells.
  • Bruising, bleeding: Due to thrombocytopenia from decreased platelets.
  • Frequent infections: Due to neutropenia from decreased normal white blood cells.
  • Bone pain: Resulting from the invasion of leukemic cells into bone marrow.
  • Enlarged lymph nodes: Reflecting infiltration by leukemic cells.
  • Unexplained weight loss: Common in leukemia.
38
Q

Leukemia nursing interventions

A
  • Monitor for signs and symptoms of leukemia, such as fatigue, weakness, pallor, bruising, bleeding, frequent infections, bone pain, enlarged lymph nodes, and unexplained weight loss.
  • Provide emotional support and education to patients and families about the disease, treatment options, and potential complications.
  • Administer and monitor responses to chemotherapy and other treatments.
  • Implement measures to prevent and manage complications, including infection control practices.
  • Assess and manage pain and discomfort associated with the disease and treatments.
  • Monitor for potential complications such as bleeding, infection, and organ infiltration.
  • Collaborate with the healthcare team to address the psychological and social impact of leukemia on patients and families.
39
Q

Leukemia tests ordered

A
  • Complete Blood Count (CBC): To assess levels of different blood cells, including leukocytes.
  • Bone Marrow Aspiration and Biopsy: To confirm the diagnosis, identify the type of leukemia, and assess the extent of bone marrow involvement.
  • Cytogenetic Testing: To detect chromosomal abnormalities associated with specific types of leukemia.
  • Lumbar Puncture: If central nervous system involvement is suspected, this test may be performed to analyze cerebrospinal fluid.
  • Imaging Studies: Such as X-rays, CT scans, or MRIs may be done to detect organ infiltration.
40
Q

Acute myelin leukemia

A

Acute Myeloid Leukemia (AML) originates from genetic mutations in myeloid hematopoietic stem cells (HSC), leading to the clonal development of abnormal blast cells. These blast cells proliferate excessively, crowding out normal bone marrow production and impairing the development of myeloid cells, including monocytes, granulocytes (neutrophils, basophils, eosinophils), erythrocytes, and platelets.

41
Q

Acute myeloid leukemia causes

A

The exact cause of AML is unclear, but known risk factors include increasing age, male gender, exposure to chemicals (e.g., benzene, pesticides), ionizing radiation, prior treatment with certain chemotherapeutic drugs, tobacco smoking, other blood disorders, and specific genetic disorders (e.g., Down syndrome, Trisomy 8, or Fanconi anemia).

42
Q

Acute myeloid leukemia assessment findings

A
  • Nonspecific initial complaints, gradually worsening over time.
  • Symptoms due to neutropenia: Fever and infection.
  • Symptoms related to anemia: Pallor, fatigue, weakness, dyspnea on exertion, dizziness.
  • Symptoms reflective of thrombocytopenia: Ecchymoses, petechiae, epistaxis, gingival bleeding.
  • Proliferation of leukemic cells within organs leads to additional symptoms: Pain from an enlarged liver or spleen, hyperplasia of the gums, bone pain.
  • Petechiae or ecchymoses on the skin; occasionally, leukemic infiltrates may be visible.
  • Leukemic cells can infiltrate the gingiva or synovial spaces of joints.
  • Lymphadenopathy (enlargement of lymph nodes) or splenomegaly (enlargement of the spleen) is rare.
  • Fevers may occur and are not always due to infection.
43
Q

Acute myeloid leukemia nursing interventions

A
  • Monitor for signs and symptoms of AML and associated complications.
  • Provide emotional support and education to patients and families about the disease, treatment options, and potential complications.
  • Administer and monitor responses to chemotherapy and other treatments.
  • Implement measures to prevent and manage complications, including infection control practices.
  • Assess and manage pain and discomfort associated with the disease and treatments.
  • Collaborate with the healthcare team to address the psychological and social impact of AML on patients and families.
  • Support patients during induction therapy, addressing severe side effects such as neutropenia, anemia, thrombocytopenia, infections, and mucositis.
  • Facilitate the patient’s transition to consolidation therapy and subsequent treatment phases.
  • Monitor for complications such as bleeding, infection, tumor lysis syndrome, and gastrointestinal problems.
  • Provide supportive care, including blood product transfusions, antimicrobial therapy, and measures to prevent complications.
44
Q

Acute myeloid leukemia lab orders

A
  • Complete Blood Count (CBC): Decrease in erythrocytes and platelets; percentage of normal cells is usually vastly decreased.
  • Bone Marrow Analysis: Shows an excess (more than 20%) of blast cells, confirming the diagnosis.
  • Cytogenetic Testing: Classifies AML into different subgroups based on cytogenetics, histology, morphology, and genetic mutations.
  • Lumbar Puncture: If central nervous system involvement is suspected.
  • Imaging Studies: Such as X-rays, CT scans, or MRIs may be done to detect organ infiltration.
45
Q

Chronic myeloid leukemia

A

Chronic Myeloid Leukemia (CML) arises from a mutation in the myeloid stem cell, leading to uncontrolled proliferation of cells. This results from a chromosomal translocation, the Philadelphia chromosome, where a fusion gene (BCR-ABL) is formed. The abnormal BCR-ABL gene signals cells to produce excessive leukocytes, converting normal cells into leukemic cells. This leads to a wide spectrum of cell types in the blood, from blast forms to mature neutrophils. The marrow expands into long bone cavities, and extramedullary hematopoiesis occurs in the liver and spleen, causing painful enlargement.

46
Q

Chronic myeloid causes

A

CML results from a specific chromosomal translocation where a section of DNA is shifted from chromosome 22 to chromosome 9, forming the abnormal BCR-ABL fusion gene. Risk factors include increasing age, male gender, a history of smoking, and exposure to high doses of radiation.

47
Q

Chronic myeloid assessment findings

A
  • Chronic Phase: Few symptoms, leukocytosis detected incidentally, rare complications.
  • Accelerated Phase: Worsening blood counts, new chromosomal changes, symptoms like fatigue, anemia, splenomegaly, dyspnea, bone pain, fevers, and weight loss.
  • Blast Crisis: Advanced phase resembling acute leukemia (AML), leukocytosis exceeding 100,000/mm³, dyspnea, confusion, enlarged, tender spleen and liver, malaise, anorexia, weight loss. Lymphadenopathy indicates late disease and poor prognosis.
48
Q

Chronic myeloma leukemia nursing intervention

A
  • Patient Education: Educate patients about the disease, treatment options, and potential complications, emphasizing the importance of adherence to oral tyrosine kinase inhibitors (TKIs).
  • Medication Management: Monitor and manage side effects of TKIs, such as fatigue, asthenia, pruritus, headache, skin rash, and oropharyngeal pain.
  • Adherence Support: Assess and address factors influencing medication adherence, including forgetfulness and delays in drug administration.
  • Monitoring: Regularly monitor patients for adverse signs and symptoms of therapy, including changes in urinary output, ECG abnormalities, and myelosuppression.
  • Symptom Management: Assist patients in managing symptoms such as fatigue, pain, and other discomforts associated with the disease and its treatment.
  • Emotional Support: Provide emotional support to patients dealing with the chronic nature of CML and potential challenges associated with long-term treatment.
  • Coordination of Care: Collaborate with the healthcare team to ensure comprehensive care and timely adjustments to the treatment plan based on patient response.
  • Safety Measures: Educate patients on safety measures related to drug interactions, handling of medications, and reporting adverse effects promptly.
49
Q

Chronic myeloma leukemia lab orders

A
  • Complete Blood Count (CBC): To detect leukocytosis and changes in blood counts.
  • Bone Marrow Analysis: Identifies the presence of blast cells and confirms the diagnosis.
  • Cytogenetic Testing: Identifies the Philadelphia chromosome and confirms the presence of BCR-ABL fusion gene.
  • Imaging Studies: Such as X-rays, CT scans, or MRIs to detect organ enlargement and extramedullary hematopoiesis.
50
Q

Acute lymphocytic leukemia

A

Acute Lymphocytic Leukemia (ALL) results from the uncontrolled proliferation of immature cells (lymphoblasts) derived from the lymphoid stem cell. In approximately 75% of cases, the precursor to the B lymphocyte is the cell of origin, while T-lymphocyte ALL occurs in about 25% of cases. The BCR-ABL translocation is found in 20% of ALL blast cells. This uncontrolled proliferation leads to an inhibition of normal hematopoiesis, reducing the numbers of granulocytes, erythrocytes, and platelets. ALL commonly infiltrates organs, causing pain from enlarged liver or spleen, bone pain, and central nervous system (CNS) involvement with symptoms like cranial nerve palsies, headache, and vomiting.

51
Q

Acute lymphocytic leukemia causes

A

The exact cause of ALL is not specified in the passage. However, risk factors include age (75-80% of cases in children, median age at diagnosis 15 years), male gender predominance, prior exposure to chemotherapy or radiation therapy, and specific genetic conditions (e.g., Down syndrome, neurofibromatosis, Klinefelter syndrome, and Fanconi anemia).

52
Q

Acute lymphatic leukemia assessment findings

A
  • Nonspecific Manifestations: Clinical manifestations may be nonspecific, and some patients may have no symptoms initially.
  • Incidental Finding: The disease is commonly found incidentally with routine laboratory studies or physical exams for another condition.
  • Leukocyte Counts: At diagnosis, leukocyte counts may be either higher or lower than normal, with a high proportion of immature lymphoblasts.
  • Organ Involvement: Manifestations of leukemic cell infiltration into organs, including pain from an enlarged liver or spleen, bone pain, and frequent CNS involvement with symptoms such as cranial nerve palsies, headache, and vomiting.
53
Q

Acute lymphocytic leukemia nursing interventions

A
  • Patient Education: Provide information about the disease, treatment options, and potential complications to promote understanding and collaboration in care.
  • Medication Management: Support patients in managing unique adverse effects of treatment, such as infection susceptibility, avascular necrosis, thrombosis risk, and hepatic toxicity.
  • Adherence Support: Assess and address factors affecting medication adherence, including the complexity of treatment plans.
  • Monitoring: Regularly monitor for treatment-related complications, infections, and signs of relapse.
  • Emotional Support: Offer emotional support due to the complexity of treatment and potential adverse effects.
  • Coordination of Care: Collaborate with the healthcare team for comprehensive care, especially in the administration of complex treatment protocols.
  • HSCT Education: If applicable, educate patients about the potential benefits, risks, and complications associated with hematopoietic stem cell transplantation (HSCT).
  • CAR-T Therapy Education: If applicable, provide information about Chimeric Antigen Receptor T-cell (CAR-T) therapy, its process, and potential outcomes.
54
Q

Acute lymphocytic leukemia test orders

A
  • Complete Blood Count (CBC): Detects abnormal leukocyte counts and immature lymphoblasts.
  • Bone Marrow Analysis: Identifies the presence of blast cells, confirms the diagnosis, and provides information on genetic markers.
  • Cytogenetic Testing: Identifies specific chromosomal translocations, such as the BCR-ABL translocation.
  • Imaging Studies: May be used to assess organ enlargement, especially of the liver and spleen.
  • Special Testing after Remission: Immunophenotyping, immunoglobulin gene rearrangements, T-cell receptor genes, and molecular testing to detect minimal residual disease and assess prognosis.
55
Q

Chronic lymphocytic leukemia

A

Chronic Lymphocytic Leukemia (CLL) is characterized by a malignant clone of B lymphocytes. These cells, which are fully mature, escape apoptosis (programmed cell death), leading to their excessive accumulation in the bone marrow, blood, and lymphoid tissues. The disease is associated with a progressive accumulation of leukemic cells in these locations.

56
Q

Chronic lymphocytic leukemia causes

A
  1. Familial Predisposition: A strong familial predisposition exists with CLL, with a 10% occurrence in individuals with a first- or second-degree relative with the same diagnosis.
  2. Agent Orange Exposure: Veterans of the Vietnam War exposed to Agent Orange may be at risk for CLL. Dioxin in Agent Orange has been found to be carcinogenic, and there is evidence linking it to CLL.
57
Q

Chronic lymphocytic leukemia assessment findings

A
  1. Lymphocytosis: An increased lymphocyte count is always present.
  2. Lymphadenopathy: Common, severe, and sometimes painful accumulation of lymphocytes in lymph nodes.
  3. Splenomegaly: Enlargement of the spleen may occur.
  4. B Symptoms: Constitutional symptoms such as fever, drenching night sweats, and unintentional weight loss over six months are associated with worse prognoses.
  5. Autoimmune Complications: Autoimmune hemolytic anemia or idiopathic thrombocytopenic purpura may occur.
58
Q

Chronic lymphocytic leukemia nursing interventions

A
  1. Infection Prevention: Due to reduced immunoglobulin levels, nursing interventions focus on reducing the risk of infections. IV treatment with immunoglobulin (IVIG) may be given to select patients with recurrent infections.
  2. Vaccination: Patients with CLL should receive pneumonia and flu vaccinations to reduce the risk of infections. Live vaccines should be avoided.
  3. Monitoring and Periodic Assessment: Ongoing periodic assessment of complete blood count (CBC), blood chemistries, electrocardiogram (ECG), blood pressure, and bowel habits is crucial for patients on various treatment modalities, including targeted therapies and immunotherapy.
  4. Patient Education: Educate patients on the risks associated with CLL, the importance of vaccinations, and the need for regular monitoring and follow-up.
  5. Symptom Management: Nursing interventions focus on controlling bothersome symptoms, such as drenching night sweats and painful lymphadenopathy, particularly in patients with impaired physical status.
59
Q

Chronic lymphocytic leukemia tests ordered

A
  1. Immunophenotyping: Critical for diagnosis, it identifies the presence of a malignant clone of B cells and gauges prognosis.
  2. Cytogenetic and Molecular Analyses: Techniques such as fluorescence in situ hybridization (FISH) are used to guide prognosis and therapy.
  3. Beta-2 Microglobulin Measurement: Elevated levels correlate with a more advanced clinical stage and poorer prognosis.
60
Q

Hodgkin lymphoma

A

Hodgkin Lymphoma (HL) originates as a unicentric disease, initiating in a single node and spreading along the lymphatic system. The pathologic hallmark is the Reed–Sternberg cell, a gigantic tumor cell of immature lymphoid origin arising from B lymphocytes.

61
Q

Hodgkin lymphoma causes

A
  1. Unknown Cause: The specific cause of Hodgkin lymphoma is unknown.
  2. Risk Factors:
    • Age: Two peak incidences at ages 15-34 and after 60.
    • Viral Infections: Epstein–Barr virus, HIV, or human herpesvirus 8 (HHV8).
    • Family History.
    • Exposure to Cytotoxic Agents.
    • Long-term Immunosuppressive Therapy.
    • Agent Orange Exposure (in veterans).
62
Q

Hodgkin lymphoma assessment findings

A
  1. Lymphadenopathy: Usually begins as an enlargement of one or more lymph nodes on one side of the neck, typically painless and firm.
  2. Mediastinal Mass: May be seen on chest x-ray; can cause dyspnea if large enough to compress the trachea.
  3. B Symptoms: Indicative of more advanced disease; present in about 40% of patients and used in determining stage and prognosis.
  4. Organ Involvement: Clinical manifestations from compression of organs, leading to symptoms such as cough, jaundice, abdominal pain, or bone pain.
  5. Pruritus: Common and distressing symptom.
  6. Fatigue, Decreased Appetite, Splenomegaly: Other common symptoms.
  7. Impaired Cellular Immunity: Absent or decreased reaction to skin sensitivity tests, increased susceptibility to infections, particularly herpes zoster.
63
Q

Hodgkin lymphoma nursing interventions

A
  1. Infection Prevention: Due to impaired cellular immunity, focus on preventing infections, especially herpes zoster.
  2. Symptom Management: Address distressing symptoms such as pruritus, fatigue, and pain.
  3. Education on Risk Reduction: Inform patients about factors increasing the risk of second cancers, such as tobacco and alcohol use, and provide strategies for risk reduction.
  4. Screening for Late Effects: Regular screening for late effects of treatment, including secondary malignancies and cardiovascular disease.
  5. Patient Education: Provide information on self-care strategies, disease management, and potential long-term complications associated with chemotherapy.
64
Q

Hodgkin lymphoma lab ordered

A
  • CBC with differential.
    • Serum electrolytes, BUN, and creatinine.
    • ESR.
    • Liver and renal function studies.
    • Immunohistochemistry and cytogenetic evaluation.
    • HIV testing.
    • Hepatitis B and C testing
65
Q

Non Hodgkin lymphoma

A

Non-Hodgkin Lymphomas (NHL) are a heterogeneous group of cancers originating from neoplastic growth in lymphoid tissue. Unlike Hodgkin lymphoma, NHL involves largely infiltrated lymphoid tissues, with unpredictable spread, often affecting multiple nodes and extranodal tissues. The neoplastic cells arise from a single clone of lymphocytes, and morphological variations can occur.

66
Q

Non Hodgkin lymphoma causes

A
  • Unknown Etiology: No common etiologic factor has been identified.
  • Risk Factors:
    • Immune deficiencies or autoimmune disorders.
    • Prior cancer treatment.
    • Organ transplant recipient.
    • History of viral infections (Epstein–Barr virus, HIV, HHV8).
    • Exposure to herbicides, pesticides, solvents, dyes, and defoliating agents like Agent Orange.
67
Q

Non Hodgkin lymphoma assessment findings

A
  1. Lymphadenopathy: Painless swelling in lymph nodes in the neck, axillary region, or groin.
  2. Symptoms: Highly variable, depending on the type and stage of lymphoma. Indolent disease may be asymptomatic, while aggressive forms can cause B symptoms (see Chart 30-1).
  3. Organ Compromise: Enlarged lymph nodes can compress organs, leading to symptoms like cough, shortness of breath, chest pain, abdominal pain, nausea, early satiety, weight loss, acute kidney injury, or bowel obstruction.
  4. CNS Involvement: Symptoms may include confusion, motor weakness, poor motor coordination, visual and speech changes (progressive multifocal leukoencephalopathy).
68
Q

Non Hodgkin lymphoma nursing interventions

A
  1. Infection Prevention: Due to myelosuppression and defective immune response, focus on minimizing infection risks and educating patients on infection signs.
  2. Symptom Management: Address symptoms related to specific organ compromise, such as pain, respiratory distress, or gastrointestinal issues.
  3. Patient Education: Educate patients on minimizing infection risks, recognizing signs of infection, and the importance of contacting healthcare providers if symptoms develop.
  4. Fatigue Management: Assist patients in managing fatigue, a common side effect of both chemotherapy and radiation therapy.
  5. Regular Follow-up and Screening: Emphasize the importance of regular follow-up appointments and screening for signs and symptoms of secondary malignancies.
  6. Health Behavior Recommendations: Encourage adherence to health behavior recommendations for cancer survivors, including smoking cessation, maintaining a normal body weight, good nutrition habits, and regular exercise.
69
Q

Non Hodgkin lymphoma tests ordered

A
  1. Incisional or Excisional Lymph Node Biopsy: Immunophenotyping and cytogenetic analysis.
  2. Flow Cytometry: Determines specific antigen on malignant cells.
  3. Fluorescence In Situ Hybridization (FISH): Analyzes DNA and RNA for chromosomal abnormalities.
  4. Laboratory Studies: Similar to Hodgkin lymphoma, including CBC with differential, serum electrolytes, BUN, creatinine, testing for viruses (Epstein–Barr, HHV8, hepatitis B), and other relevant tests.
  5. Imaging: CT scans of the chest, abdomen, and pelvis; PET scan; MUGA or ECG (if anthracycline-based regimen planned); and bone marrow biopsy and aspirate if marrow involvement is suspected.
70
Q

Multiple myeloma

A

Multiple myeloma is a malignant disease originating from the most mature form of B lymphocytes, known as plasma cells. In this condition, malignant plasma cells produce a nonfunctional immunoglobulin called the monoclonal protein or M protein. This abnormal protein, along with substances that stimulate angiogenesis, leads to the growth of clusters of plasma cells. Multiple myeloma may evolve from a premalignant stage called monoclonal gammopathy of undetermined significance (MGUS). Patients with MGUS have the M protein but typically do not exhibit symptoms of multiple myeloma.

The disease can result in bone destruction and marrow failure. Additionally, plasmacytomas, infiltrations of malignant plasma cells into other tissues, can occur, affecting areas such as the sinuses, spinal cord, and soft tissues.

71
Q

Multiple myeloma causes

A

The specific etiology of multiple myeloma is unknown, but certain risk factors increase its occurrence. These risk factors include age (more common in individuals over 70), African American ethnicity, exposure to radiation, petroleum products, benzenes, and Agent Orange, family history, male gender, and conditions like monoclonal gammopathy of undetermined significance (MGUS) or plasmacytoma.

72
Q

Multiple myeloma assessment findings

A
  1. CRAB Features (Classic Manifestations):
    • HyperCalcemia
    • Renal dysfunction
    • Anemia
    • Bone destruction
  2. Bone-related Manifestations:
    • Bone pain, typically in the back or ribs, increasing with movement and decreasing with rest.
    • Vertebral collapse, fractures, kyphosis, and spinal cord compression in severe cases.
  3. Renal Dysfunction:
    • Present in 33% of patients at diagnosis, with potential causes including myeloma kidney, hypercalcemia, amyloid deposits, and hyperviscosity.
  4. Anemia:
    • Due to reduced space for erythrocyte production in the bone marrow.
  5. Other Complications:
    • Risk of infection, hyperviscosity, neurologic complications (spinal cord compression, peripheral neuropathy), and venous thromboembolism (VTE)
73
Q

Multiple myeloma nursing interventions

A
  1. Pain Management:
    • Use NSAIDs for mild pain or in combination with opioid analgesics.
    • Monitor renal function closely due to potential NSAID-related complications.
  2. Hypercalcemia Management:
    • Assess for signs and symptoms of hypercalcemia, such as polyuria, nausea, constipation, anorexia, confusion, and decreased renal function.
    • Administer aggressive hydration.
    • Consider bisphosphonates and corticosteroids for hypercalcemia treatment.
  3. Infection Prevention:
    • Educate patients on methods to prevent infections.
    • Monitor for signs of infection and promptly intervene.
    • Consider infection prophylaxis with antiviral agents and antibiotics.
  4. Emotional/Psychological Support:
    • Assess and provide emotional/psychological support to cope with the diagnosis and treatment.
    • Educate patients about effective coping skills.
74
Q

Multiple myeloma tests ordered

A
  1. CBC with Differential:
    • Evaluates blood cell counts, as multiple myeloma can affect erythrocytes, leukocytes, and platelets.
  2. BUN, Serum Creatinine, Creatinine Clearance:
    • Assesses renal function, which is often compromised in multiple myeloma.
  3. Serum Electrolytes (Calcium and Albumin):
    • Monitors electrolyte levels, especially calcium, which may be elevated due to bone resorption.
  4. LDH and Beta-2 Microglobulin:
    • Measure the degree of tumor burden.
  5. Serum Protein Electrophoresis or Free Light Chain Assay:
    • Detects the presence of M protein, a key marker in multiple myeloma.
  6. Cytogenetic Studies:
    • Examines chromosomal abnormalities associated with multiple myeloma.
  7. Radiographic Evaluation (CT Scan, MRI, PET Scan):
    • Determines the presence of lytic bone lesions.
  8. Bone Marrow Aspiration and Biopsy:
    • Evaluates bone marrow plasma cell abnormalities.
75
Q

Immune thrombocytopenia purpura

A

Immune Thrombocytopenic Purpura (ITP) is an acquired immune disorder characterized by thrombocytopenia resulting from pathologic antiplatelet antibodies, impaired production of megakaryocytes, and T-cell–mediated destruction of platelets. Primary ITP occurs in isolation, while secondary ITP is associated with other disorders, including autoimmune diseases, viral infections, and certain drugs. Antiplatelet antibodies develop and bind to the patient’s platelets, leading to their destruction by the reticuloendothelial system (RES) and tissue macrophages. The body compensates by increasing platelet production in the bone marrow.

76
Q

Immune thrombocytopenic purpura causes

A

Primary ITP is idiopathic, while secondary ITP is associated with autoimmune diseases, viral infections (hepatitis C, HIV), drugs (cephalosporins, sulfonamides, furosemide), and other immune dysregulation syndromes.

77
Q

Immune thrombocytopenic purpura assessment findings

A

ITP is often asymptomatic, but common signs include easy bruising, heavy menses, and petechiae on the extremities or trunk. Severe thrombocytopenia increases the risk of life-threatening bleeding, especially from mucosal surfaces.

Assessment Findings:
1. Low platelet count (less than 100,000/mm3).
2. Easy bruising, heavy menses, and petechiae.
3. Wet purpura (bleeding from mucosal surfaces) indicates a greater risk of life-threatening bleeding.
4. Severe thrombocytopenia (platelet count less than 20,000/mm3), prior minor bleeding episodes, and advanced age increase the risk of severe bleeding.

78
Q

Immune thrombocytopenic purpura nursing intervention

A
  1. Thorough assessment of lifestyle for bleeding risks.
  2. Medication history, including OTC medications, herbs, and supplements.
  3. Monitor for sulfa-containing medications and those interfering with platelet function.
  4. Assess for recent viral illness and symptoms of intracranial bleeding.
  5. Neurologic assessment for patients with wet purpura and low platelet counts.
  6. Avoid injections, rectal medications, and rectal temperature measurements.
  7. Assess fatigue levels and provide support and coping strategies.
  8. Educate patients on signs of exacerbation, medication details, monitoring, and follow-up.
  9. Instruct patients to avoid agents interfering with platelet function and adopt preventive measures for bleeding risks.
  10. Provide counseling on the risks associated with long-term corticosteroid use and the need for monitoring and potential interventions.
79
Q

Immune thrombocytopenic purpura tests ordered

A
  1. Platelet count: A platelet count less than 100,000/mm3 is the primary criterion for diagnosis.
  2. History and physical examination: To exclude other causes of thrombocytopenia and identify sites of bleeding.
  3. Testing for hepatitis C and HIV: To rule out viral infections as potential causes.
  4. Bone marrow aspirate: May reveal an increased number of megakaryocytes.
  5. Assess for H. pylori infection: Treatment to eradicate the infection may improve platelet count.