Hemo/Oncology Flashcards

1
Q

Myelodysplastic Syndrome (MDS)

A
  • Pre-leukemia
  • Problem w/ common myeloid progenitor cells
  • Pancytopenias
  • 33% transform to AML
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2
Q

Incidence of MDS

A
  • Median age 65-70
  • M>F
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3
Q

S/S of MDS

A
  • Symptoms of cytopenias
  • Splenomegaly
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4
Q

What are the goals of MDS Management?

A
  • Control symptoms
  • Improve quality of life
  • Prevent progression to AML
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5
Q

How is MDS managed?

A
  • Supportive Care
    • Blood transfusions
    • Erythropoietin
  • Chemotherapy
    • Decitabine
    • 5-azacytidine
  • Stem Cell Transplant (BMT)
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6
Q

Types of Leukemias

A
  • Acute Lymphoblastic Leukemia (ALL)
  • Acute Myelogenous Leukemia (AML)
  • Chronic Lymphoblastic Leukemia (CLL)
  • Chronic Myelogenous Leukemia (CML) – Philadelphia Chromosome – 95%
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7
Q

Acute Myelogenous Leukemias

A
  • Acute (fast & immature)
    • Prolonged cell division →
      • Maturation failure
      • Too many immature WBC
      • Crowd out bone marrow and “spill” into circulation
        • Blast crisis
    • Accounts for ≈ 1.2% of all new cancer cases
    • ≈ 1.8% of all cancer deaths
    • Five year survival ≈ 26.6%
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8
Q

Chronic Myelogenous Leukemias

A
  • Chronic (slow & mature)
    • Myeloproliferative disorder
      • Too many mature WBS
    • Philadelphia Chromosome
      • bcr-abl: a gene made by the Philadelphia Chromosome
    • Accounts for ≈ 0.5% of all new cancer cases
    • ≈ 0.2% of all cancer deaths
    • Five year survival ≈ 65.1%
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9
Q

Acute Lymphocytic Leukemia

A
  • Most common type of leukemia in young children
    • Accounts for ≈ 0.4% of all new cancer cases
    • ≈ 0.2% of all cancer deaths
    • Five year survival ≈ 68.1%
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10
Q

Chronic Lymphocytic Leukemia

A
  • Most common chronic adult leukemia
    • Accounts for ≈ 1.1% of all new cancer cases
    • ≈ 0.8% of all cancer deaths
    • Five year survival ≈ 82.6%
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11
Q

Laboratory & Diagnostics Findings of Leukemia

A
  • CBC w/ differential
    • ↑↑↑ WBC
    • Blast %
  • Peripheral blood smear
    • Presence of blasts
    • Presence of malignant cells
  • Bone Marrow Biopsy
    • Posterior Iliac Crest
    • Elevated blast %
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12
Q

Leukemia Management

A
  • Dependent of type of Leukemia
  • Chemotherapy Purpose?
    • Clean out marrow
    • Achieve remission?
  • Relapse? Refractory?
    • Bone marrow transplant
  • Splenectomy
  • *Antibiotics*
  • Serial monitoring for life
  • Neupogen or Neulasta to regenerate BM after ablation
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13
Q

Chemotherapy Classes

A

Alkylating Agents

Antimetabolite Agents

Others

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14
Q

Alkylating Agents

A
  • Alkylating Agents 1: Nitrogen Mustards
    • Alkylates and crosslinks DNA
    • Ex: cyclophosphamide, ifosfamide, melphalan
  • Alkylating Agents 2: Nitrosoureas
    • Alkylates and crosslinks DNA
    • Ex: lomustine, carmustine, streptozocin
  • Alkylating Agents 3: Platinum Analogs
    • Binds and crosslinks DNA
    • Ex: cisplatin, carboplatin, oxaliplatin
  • Alkylating Agents 4: Other
    • Alkylates and crosslinks DNA
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15
Q

Antimetabolite Agents

A
  • Antimetabolite Agents 1: Folate Analogs
    • Inhibits lymphocyte proliferation
    • Ex: methotrexate, pemetrexed, pralatrexate
  • Antimetabolite Agents 2: Purine Analogs
    • Inhibits DNA synthesis
    • Ex: clofarabine, cladribine, fludarabine, mercaptopurine, thioguanine, pentostatin
  • Antimetabolite Agents 3: Pyrimidine Analogs
    • Induces DNA hypomethylation – restores cellular control
    • Ex: cytarabine, decitabine, fluorouracil, gemcitabine, azacitidine,
  • Antimetabolite Agents 4: Other
    • Inhibits ribonucleotide reductase, immediately inhibiting DNA synthesis
    • Ex: hydroxyurea
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16
Q

Other Chemo Classes

A
  • Kinase Inhibitors
    • Ex: imatinib (Gleevec), ibrutinib (Imbruvica)
  • Differentiating Agents
    • Ex: arsenic trioxide (used in APL)
  • Antitumor Antibiotic (Anthracyclines) – think cardiotoxicity!!!
    • Doxorubicin
  • Antitumor Antibiotics (Others)
    • mitoxantrone, bleomycin
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17
Q

Combination therapy

A
  • Given in divided doses per cycle
  • Treatment is measured in similar fashion:
    • “P.R. is a 73 year old ♂ with relapsed/refractory AML, currently on C2D15 of vidaza/busulfan/arsenic.”
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18
Q

Potential Nursing Dx for Leukemias

A
  • Pain r/t overactive bone marrow AEB leukocytosis
  • Altered Immunity r/t effects of chemotherapy AEB leukopenia
  • Risk for injury r/t tumor lysis syndrome AEB declining renal function, hyperkalemia, hyperphosphatemia, and uric academia
  • Risk for injury r/t fatigue and other chemotherapeutic effects
  • Risk for Infection r/t deficient immunity AEB leukopenia
  • Pain r/t stimulated bone marrow
  • Knowledge Deficit
  • Impaired Family Coping
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19
Q

Nursing Interventions

A
  • Coordinate care to reduce traffic in and out of room
  • Provide safe environment, reduce risk for falls, call button w/in reach, bedside toileting, adequate lighting
  • Encourage deep breathing and UOB and/or use of incentive spirometer
  • Auscultate breath sounds
  • Examine skin for breakdown
  • Encourage good oral care
  • Prohibit live plants/flowers
  • Restrict fresh fruits and only allow fruits with thick skin
  • Change IV tubing according to hospital policy
  • Change central line dressings according to hospital policy
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20
Q

Lymphomas

A

Hodgkin’s Lymphoma

and

Non-Hodgkin’s Lymphoma

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21
Q

Stages of Lymphoma

A
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22
Q

Stage I Lymphoma

A
  • Disease is localized to single lymph node or group of nodes
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23
Q

Stage II Lymphoma

A
  • Multiple lymph nodes or groups of nodes
  • Confined to 1 side of diaphragm
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24
Q

Stage III Lymphoma

A
  • Spleen involvement and/or
  • Lymph nodes on both sides of diaphragm
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25
Q

Stage IV Lymphoma

A
  • Liver or bone marrow involvement
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26
Q

Hodgkin’s Lymphoma

A
  • Aka Hodgkin’s disease
  • malignat condition charachterized by proliferation abnormal gian, multinucleated ccells, called Reed-Sternberg cells, which are located in lymph nodees
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27
Q

Hodgkins Lymphoma I & P

A
  • M>F, Bi-modal age onset:
    • avg age: 28
    • Less common peak: 55
  • Accounts for ≈ 0.5% all new cancer cases
  • ≈ 0.2% of all cancer-related deaths
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28
Q

Hodgkin’s Lymphoma adenopathy

A
  • Cervical & Mediastinal
  • Spreads in a predictable fashion
  • Uncommonly found outside of lymph nodes (4%)
  • Reed sternberg cells
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29
Q

Non-Hodgkin’s Lymphoma

A

heterogeneous group of malignant neoplasms of primarily B-, T-, or natural killer (NK) cell origin affecting all ages

Classifications

  • B-cell
  • T- cell
  • Natural Killer (NK)
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30
Q

B- Cell Lymphomas

A

about 85%

  • Follicular B Cell
  • Mantle Cell
  • Marginal Zone
  • Interfollicular
  • Burkitt’s - most highly aggressive
  • Diffuse Large B Cell - most common aggressive lymphoma
  • Primary Effusion
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31
Q

T Cell NHLs

A

About 15%

  • Anaplastic Large Cell
  • T-cell Lymphoma
32
Q

Lymphoma treatment and side effects

A
  • XRT
    • Sperm banking?
    • Night sweats
    • Compromised skin
    • Diarrhea
    • Pain
  • Chemotherapy
    • N/V/D
  • BMT
  • Treatment begins after radiographic exams and initial staging are complete!
33
Q

Potential nursing dx for lymphomas

A
  • Risk for ineffective breathing pattern r/t enlarged mediastinal nodes and/or radiation treatment to neck/chest
  • Acute pain r/t injury of chemotherapy and/or radiation therapy
  • Anxiety r/t new diagnosis
  • Risk for Infection r/t potential bone marrow depression due to effects of chemotherapy
  • Risk for Infection r/t compromised skin during radiation
  • Fatigue r/t effects of cancer, chemotherapy, and radiation therapy
  • Knowledge deficit
34
Q

Nursing interventions for Lymphomas

A
  • Assess and monitor respiratory rate, depth, and rhythm
  • Note for signs of respiratory distress including use of accessory muscles, nasal flaring, and cyanosis
  • Instruct and assist with deep-breathing techniques
  • Encourage involvement of ADLs as tolerated
  • Assess and monitor skin for signs of break down or infection related to radiation treatments
  • Assess for pain and provide pain relief with relaxation techniques, and medication, as ordered
  • Provide a quiet environment
  • Provide therapeutic communication to patient and family regarding treatment and disease process
35
Q

Tumor Lysis Syndrome (TLS)

A
  • Metabolic disorders
    • Destruction of cells
    • Leukemia & Lymphoma
    • ↑K+, ↑PO4-, ↓Ca++
    • Hyperuricemia
      • (↑ C5H4N4O3)
    • Hyperuricosuria
    • Acute Renal Failure (ARF)
      • Acute uric acid nephropathy
  • Commonly
    • Poorly differentiated lymphomas
      • Burkett’s Lymphoma
    • ALL, AML
    • Melanomas (rarely)
36
Q

Tumor Lysis Syndrome (TLS) prevention

A
  • Allopurinol (IV or PO)
  • Rasburicase
  • Sevelamer
  • Alkalinizing Urine
    • NaCO3 or Diamox
37
Q

TLS treatment

A
  • Rasburicase, Loop diuretics, fluids
  • HD - hemofiltration dialysis
  • CVVHD continuous veno-venous hemofiltration dialysis
38
Q

Cairo-Bishop Definition

A
  • Lab TLS (2 or more, 3 days before or 7 days after Tx)
    • Uric acid > 8mg/dL
    • K+ > 6mEq/L
    • PO4- > 4.5mg/dL
    • Ca++ < 7mg/dL
    • OR 25% ↑
  • Clinical TLS (Lab TLS + 1 or more of the following)
    • ↑ Cr (1.5x upper normal)
    • Cardiac arrhythmia
    • Seizure
39
Q

Superior Vena Cava Syndrome

A
  • Approximately 90% are caused by malignancy compressing the SVC
    • Facial swelling
    • Upper extremity swelling
    • JVD
  • Positive Pemberton’s Sign
    • When patient raises both arms simultaneously:
      • Facial flushing
      • JVD
      • Stridor
40
Q

Superior Vena Cava Syndrome Diagnostics

A
  • CXR
  • CT
41
Q

SVCS treatment

A
  • Referral
  • Treat the cause
    • Chemotherapy
    • XRT
    • surgery
42
Q

Thrombocytopenias

A
  • Disseminated Intravascular Coagulopathy - DIC
  • Thrombotic Thrombocytopenic Purpura (TTP)
  • Idiopathic Thrombocytopenic Purpura (ITP)
43
Q
  • Disseminated Intravascular Coagulopathy (DIC)
A
  • Pathologic activation of clotting cascade
  • Numerous small clots (microemboli) consume platelets and clotting factors
  • Normal clotting inhibited due to lack of platelets and clotting factors leading to bleeding
  • Microemboli clog up microcirculation leading to end organ failure
44
Q

DIC S/S

A
  • Hemorrhage (oral, nasal, venipuncture sites, abnormal pupils)
  • Bruising
  • Renal Failure
  • Gangrene
45
Q

DIC Lab Values

A
  • Thrombocytopenia
  • ↓ Fibrinogen
  • ↑ PT, PTT, INR
46
Q

DIC treatment

A
  • Must treat the underlying cause
  • Heparin gtt
  • Platelet transfusions
  • Cryoprecipitate
  • Fresh Frozen Plasma
  • Tissue Plasminogen Activator (tPA)
47
Q

Nursing DX for DIC

A
  • Fluid volume deficit r/t blood loss
  • Risk for injury r/t microemboli
  • Impaired family coping
  • Knowledge deficit
48
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A
  • Like DIC – many microscopic thrombosis cause end organ failure
  • Anti-ADAMTS13 (AA13) enzymes
  • Schistocyte formation
    • Shear stress from RBC
  • Plasmapheresis to reduce number of AA13
49
Q

Idiopathic Thrombocytopenic Purpura (ITP)

A
  • Unknown reason for low platelet count and bruising
  • Platelet antibodies?
50
Q

ITP S/S

A
  • Bruising
  • Abnormal pupillary reactions
  • AMS
51
Q

ITP treatment

A
  • Platelet transfusion
    • Effective?
      • Monitor count prior to and 1 hour after transfusion
    • Ineffective?
      • Anti-rheumatic drugs
      • Methotrexate
      • Rituximab
      • IV Immunoglobulins
      • Repeat transfusion
  • Corticosteroids
  • Splenectomy
    • Origin of antibodies
52
Q

Bleeding precautions (thrombocytopenias)

A
  • Use soft toothbrush
  • Electric Razor
  • Avoid ASA
  • Examine urine for Blood
    • Medical emergency
  • Examine stool
    • Black tarry stools
    • Medical emergency
53
Q

Nursing DX for thrombocytopenias

A
  • Risk for injury
  • Impaired skin integrity
  • Knowledge deficit
  • Risk for bleeding
54
Q

Supporative care for MDS

A

Blood transfustions & Erythropoietin

55
Q

Chemotherapy for MDS

A

Decitabine & 5-azacytidine

56
Q

Other than supportive care and chemortherapy, how else is MDS managed

A

Stem Cell Transplant (BMT)

57
Q

How do Nitrogen Mustards & Nitrosoureas work?

A

Alkylates and crosslinks DNA

58
Q

How do Platinutm Analogs work?

A

Binds and crosslinks DNA

59
Q

How do other alkylating agents work?

A

Alkylates and crosslinks DNA

60
Q

Examples of Nitrogen Mustards

A

Cyclophospamide, ifosfamide, melphalan

61
Q

Examples of Nitrosoureas drugs?

A

lomustine, carmustine, streptozocin

62
Q

Exampleas of Platinum Analogs?

A

cisplatin, carboplatin, oxaliplatin

63
Q

How do Folate Analogs work?

A

Inhibits lymphocyte proliferation

64
Q

Examples of Folate Analogs?

A

methotrexate, pemtred, pralatrexate

65
Q

How do Purine Analogs work?

A

Inhibits DNA synthesis

66
Q

Examples of Purine Anaglogs?

A

clofarabine, cladribine, fludaramine, mercaptopurine, thiguanine, pentostatin

67
Q

How do Pyrimidine Analogs work?

A

Induces DNA hypotheylation - restores cellular control

68
Q

Examples of Pyrimidine Analogs?

A

cytarabine, decitabine, fluorouracil, gecitabine, azacitidine

69
Q

How do other antimetabolite agents work?

A

Inhibits ribonucleotide reductase, immediately inhibiting DNA synthesis

70
Q

Example of other antimetabolite agents?

A

hydroxyurea

71
Q

Examples of Kinase Inhibitors/

A

imatinib (Gleevec), ibrutinib (Imbruvica)

72
Q

Differentiating agents examples

A

arsenic trioxide (used in APL)

73
Q

Antitumor Antibiotic (Anthracyclines

A

think cardiotoxicity!!!: Doxorubicin

74
Q

Other antitumber antibiotics

A

mitoxantrone, bleomycin

75
Q

How is combination therapy given?

A

in divided doses per cycle