Alterations in Cell  Function and DifferentiationManagement of Neoplastic Disruptions
I. Epidemiology of cancer   Uncontrolled and unregulated growth of cells   Can occur in any age and ethnicity   2nd mos...
A. Cancer incidence and     prevalence by site and sexMen               Women Prostate         Breast Lung/Bronchus   ...
LeadingCancer SitePercentages
Estimated mortalityMen                Women Lung/Bronchus     Lung/Bronchus Prostate          Breast Colon/rectum    ...
II. Host defense mechanisms in        control of cancer/neoplasiaA. Tumor antigens - Tumor-associated antigens (TAAs)     ...
B. Immunological defense           against CA1. Immune surveillance mechanismsCytoxic T cells - kill tumor cellsNatural Ki...
Macrophage functioning in response     to malignant target cells
2. How cancerous cells evade            immune system   Depends on ability of immune system to    recognize cancer cells ...
Tumor associated antigens on surface of malignant cells
Blocking Antibodies Preventing T-Cell from Destroying Malignant Cell
III. Normal vs. abnormal cell          growth and reproductionA. Review of normal cell cycleReproduction of both healthy a...
Phases of normal cell cycle   G1 phase – post mitotic phase. Relatively    dormant - some RNA & protein synthesis   S ph...
Cell Cycle
B. Cell proliferation   Cells divide and reproduce   Regulated so number of cells dividing = to    number dying or being...
C. Cell differentiation   Cells transformed into different and more    specialized cell types   Adult cell achieves spec...
Normal Cellular Differentiation
IV. Characteristics of Benign and            Malignant NeoplasmsA.    Terminology      1. Tumor      2. Neoplasia
B. Benign Neoplasms   Well differentiated cells that cluster together in    single mass   Resemble cells of tissue of or...
C. Malignant Neoplasms   Less well differentiated cells   Able to break loose, enter circulation or lymph    system, and...
Benign vs. Malignant
1. Cancer cell characteristics   Cells fail to undergo normal cell proliferation    and differentiation   Anaplasia – te...
2. Invasion and metastasis   Cancer spreads by:       Direct invasion and extension       Seeding of cancer cells in bo...
Metastasis
Process of metastasis
Sites of bloodborne metastases
Metastasis to the brain
Metastasis to the bone
3. Tumor growth     Rate of tissue growth in normal and cancerous      cells depends on:         Number of cells activel...
V. Carcinogenesis and major            risk factorsA. Carcinogenesis1. Terms important in carcinogenesis  Two mutational ...
a. Oncogene    Cancer causing gene – altered gene    Gene that promotes autonomous cell growth in     cancer cells    M...
b. Proto-oncogene   Normal growth-promoting gene thought to be    active when appropriate growth-promoting    signals rea...
c. Anti-oncogene/Suppressor gene   Gene that inhibits proliferation of cells   Genetic signal that normally inhibits    ...
Stages in Development of a Malignant Neoplasm
2. Cancer cell transformationa. Initiation – 1st Step Exposure of cells to appropriate doses of  carcinogenic agent - mak...
2. Cancer cell transformationb. Promotion – 2nd stepUnregulated accelerated growth in alreadyinitiated cells by various c...
2. Cancer cell transformationc. Progression – 3rd stepCellular changes formed during initiation andpromotion assume incre...
Process of Cancer Development
Initiation, Promotion and Progression
B. Risk factors1.   Heredity    Predisposition to approx. 50 types of cancer     has been observed in families    10% of...
2. Hormones   Thought to drive cell division   Women – breast, ovary, endometrium   Men – prostate, testis
3. Immunologic mechanisms   Cancer associated with impairment or decline    in immune system. See increase in:       Peo...
4. Chemical carcinogens   Cigarette smoke   Workplace carcinogens   Air pollution   Diet   Alcohol
5. Radiation   Ultraviolet exposure   Ionizing radiation exposure   Electromagnetic field exposure
6. Oncogenic viruses   Incorporate themselves into genetic structure    of cell   Alter future generations of cell   Hu...
VI. Prevention and early            detection of cancer   Primary Prevention   Secondary Prevention   Tertiary Prevention
A. Preventive measures   Important role for RN   Must have knowledge and skills to educate    community about:        h...
1. Patient education   Numerous factors influence degree of    knowledge people have about CA risk factors    and health ...
Seven Warning Signs of Cancer   C   A   U   T   I   O   N – nagging cough/hoarseness   See Lewis Table 16-8
B. Screening procedures for      different types of cancer sites   SBE for breast cancer   Rectal exams for prostate can...
VII. Ways of classifying cancerTumors are classified on basis of: cell type tissue of origin benign or malignant degre...
A. By anatomic siteEpithelial tissue - carcinomasConnective tissue - sarcomasLymphatic tissue - lymphomasGlial cells of th...
B. Histological Analysis               (“Grading”)Grade I: cells differ slightly from normal cells and are well differenti...
Mutation of a Cell Line
C. Extent of disease (“Staging”)   Describes location and pattern of spread of tumor   TNM most common:       Tumor (pr...
Clinical Staging   0 - CA in situ   I - tumor limited to tissue or organ   II - limited local spread   III - extensive...
VIII. Major treatment options in                 cancer treatment   Goals - Cure, Control, Palliation   Used to be consi...
Goals of cancer treatment
A. Surgery   Approx 90% treated surgically   Main benefit - removal of tumor with minimal    damage to other body cells...
Goals of surgery
B. RadiationUsed to interrupt cellular growth. Can: immediately kill cells delay or halt cell cycle progression cause d...
Types of Radiation1.   External radiation - source placed outside the     body     “Lethal tumor dose”: will eradicate 95%...
Linear accelerator treatment for     head and neck cancer
   Wet desquamation    from RT   Dry desquamation    from RT
C. Chemotherapy   Systemic administration of anticancer    chemicals   Most agents are cytotoxic - interfere with    som...
Goals of chemotherapy
1. Classificationsa. Cell cycle specific Destroys cells in specific phases of cell cycleb. Cell cycle non-specific Act i...
Action Sites of CCS [Antineoplastic] Drugs
Action Sites of Non–Cell Cycle–Specific        Antineoplastic Agents
2. Examples   See Table 16-9 “Classifications of    Chemotherapy Drugs” in Lewis
Chemotherapy/survival relationship
3. Routes of administration   Topical, Oral, IM, IV, SQ, Arterial,    Intercavity, Intrathecal routes   Depends on type ...
PICC Line placement
Tunneled Central Line
Huber needle access of implanted port
4. Extravasations   “Escape of fluids into the surrounding tissue”       Such as in IV infiltration. Apply ice to slow  ...
5. Toxicity and side effects   Can be acute or chronic   Cells with rapid growth rates are very    susceptible to damage...
5. Toxicity and side effects (cont.)GI system - N & V most common; stomatitisHematopoietic system - depressed bone marrow ...
6. Nursing consideration for           patients on chemotherapy   Fluid and electrolytes   Infection and bleeding      ...
D. Hormonal therapy   Used for cancers that are responsive to or    dependent on hormones for growth:       breast     ...
E. Biotherapy   Active Immunotherapy – acts as nonspecific    stimulant of immune system   Passive Immunotherapy – trans...
Biologic Response Modifiers   Changes person’s biologic response to cancer       Cytokines: IFNs, ILs that bind       M...
F. Targeted therapy   Drugs that target processes of cancer cells    specifically   Leave normal cells unharmed
G. Bone marrow and peripheral      blood stem cell transplantation   High dose chemo and radiation therapy used to    abl...
Stem cell transplant
neoplastic disruptions   alterations in cell function & differentiation pp
neoplastic disruptions   alterations in cell function & differentiation pp
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  • Reappearance of oncofetal Ags thought to be result of…
  • Immunocompromised individuals are at higher risk for cancer development
  • TS: cannot find tumor NX: regional lymph nodes unable to be assessed
  • Cure, control, or palliation
  • Rapidly dividing cells are more susceptible to radiation damage because there’s less time to repair DNA mutations. Daughter cells inherit mutated DNA. The downside is that radiation isn’t limited to targeting cancer cells, but also normal cells.
  • Limiting! Ex. Only targets cancer cells in M-phase (only a 1 hour window)  multiple drugs used at once
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  • Fatigue alone accounts for 80% of symptoms
  • A premenopausal woman might receive androgens with chemo whereas a postmenopausal woman may receive estrogen.
  • Reverse isolation
  • neoplastic disruptions alterations in cell function & differentiation pp

    1. 1. Alterations in Cell Function and DifferentiationManagement of Neoplastic Disruptions
    2. 2. I. Epidemiology of cancer Uncontrolled and unregulated growth of cells Can occur in any age and ethnicity 2nd most common cause of death in US  1/5 deaths from cancer  Over 50% under age 65
    3. 3. A. Cancer incidence and prevalence by site and sexMen Women Prostate  Breast Lung/Bronchus  Lung /Bronchus Colon/Rectum  Colon/Rectum Urinary Tract  Uterus Melanoma  Ovary
    4. 4. LeadingCancer SitePercentages
    5. 5. Estimated mortalityMen Women Lung/Bronchus  Lung/Bronchus Prostate  Breast Colon/rectum  Colon/rectum Pancreas  Pancreas Non-Hodgkin’s  Ovary lymphoma
    6. 6. II. Host defense mechanisms in control of cancer/neoplasiaA. Tumor antigens - Tumor-associated antigens (TAAs) result of malignant transformations - Oncofetal antigen: found on surface & inside of cells as well as fetal cells. - CEA: carcinogen embryonic antigen found in cancer cells of GI tract - AFP: alpha-fetoprotein found in hepatocytes
    7. 7. B. Immunological defense against CA1. Immune surveillance mechanismsCytoxic T cells - kill tumor cellsNatural Killer cells - directly lyse tumor cellsMonocytes/Macrophages - important in detection of CA cells. Secret cytokinesB cells – produce antibodies that bind to and kill tumor cells
    8. 8. Macrophage functioning in response to malignant target cells
    9. 9. 2. How cancerous cells evade immune system Depends on ability of immune system to recognize cancer cells as being different from self cells Closely resemble cells they originate from Process where cancer cells evade immune system is called immunologic escape
    10. 10. Tumor associated antigens on surface of malignant cells
    11. 11. Blocking Antibodies Preventing T-Cell from Destroying Malignant Cell
    12. 12. III. Normal vs. abnormal cell growth and reproductionA. Review of normal cell cycleReproduction of both healthy and malignant cells follow cell cycle patternTime required for one tissue cell to divide and reproduce into 2 identical cells
    13. 13. Phases of normal cell cycle G1 phase – post mitotic phase. Relatively dormant - some RNA & protein synthesis S phase - DNA synthesis occurs G 2 phase – pre mitotic phase. Some RNA & protein synthesis M Phase - cell division occurs G o Phase - resting phase
    14. 14. Cell Cycle
    15. 15. B. Cell proliferation Cells divide and reproduce Regulated so number of cells dividing = to number dying or being shed Cell types fit into 3 large groups:  Well differentiated neurons, skeletal and cardiac muscle cells  Parent or progenitor cells  Undifferentiated stem cells
    16. 16. C. Cell differentiation Cells transformed into different and more specialized cell types Adult cell achieves specific set of structural, functional, and life expectancy characteristics Orderly process
    17. 17. Normal Cellular Differentiation
    18. 18. IV. Characteristics of Benign and Malignant NeoplasmsA. Terminology 1. Tumor 2. Neoplasia
    19. 19. B. Benign Neoplasms Well differentiated cells that cluster together in single mass Resemble cells of tissue of origin Slow, progressive rate of growth Expands, but unable to metastasize Usually enclosed in fibrous capsule
    20. 20. C. Malignant Neoplasms Less well differentiated cells Able to break loose, enter circulation or lymph system, and form secondary malignant tumors at other sites Grow rapidly, spread widely Potential to kill regardless of original location
    21. 21. Benign vs. Malignant
    22. 22. 1. Cancer cell characteristics Cells fail to undergo normal cell proliferation and differentiation Anaplasia – term used to describe lack of cell differentiation in cancerous tissue Cancer cells do not function properly and do not die according to time frame of normal cells
    23. 23. 2. Invasion and metastasis Cancer spreads by:  Direct invasion and extension  Seeding of cancer cells in body cavities  Metastatic spread through blood or lymph pathways
    24. 24. Metastasis
    25. 25. Process of metastasis
    26. 26. Sites of bloodborne metastases
    27. 27. Metastasis to the brain
    28. 28. Metastasis to the bone
    29. 29. 3. Tumor growth  Rate of tissue growth in normal and cancerous cells depends on:  Number of cells actively dividing or moving through cell cycle  Duration of cell cycle  Number of cells being lost compared with number of cells being producedIn blood cancers ex. leukemia, the cancer is rapidly dividing as it mimicsnormal life-cycle of surrounding cells EXCEPT scheduled death.The cancer cells persist.
    30. 30. V. Carcinogenesis and major risk factorsA. Carcinogenesis1. Terms important in carcinogenesis Two mutational routes that result in uncontrolled cell proliferation are characteristic of cancer:  stimulation of gene causing hyperactivity  inhibition of gene causing inactivity
    31. 31. a. Oncogene  Cancer causing gene – altered gene  Gene that promotes autonomous cell growth in cancer cells  Mutations of normal growth-regulating genesOncogenesis: mechanism by which normal cells mutate into cancer cellsOnly one single altered gene copy can cause an overgrowth
    32. 32. b. Proto-oncogene Normal growth-promoting gene thought to be active when appropriate growth-promoting signals reach cell “On switch” for cellular growthIf there’s a mutation in the proto-oncogene, then the cell is released from…?
    33. 33. c. Anti-oncogene/Suppressor gene Gene that inhibits proliferation of cells Genetic signal that normally inhibits proliferation is removed – causes unregulated growth “Turns off” or regulates unneeded cellular proliferation
    34. 34. Stages in Development of a Malignant Neoplasm
    35. 35. 2. Cancer cell transformationa. Initiation – 1st Step Exposure of cells to appropriate doses of carcinogenic agent - makes them susceptible to malignant transformation Irreversible alteration in cell’s genetic structure Not usually significant to cells until 2 nd step of carcinogenesis Physical/chemical/biological agents, ex. virus, can cause cancer
    36. 36. 2. Cancer cell transformationb. Promotion – 2nd stepUnregulated accelerated growth in alreadyinitiated cells by various chemical and growthfactorsCharacterized by reversible proliferation ofaltered cell if promoter substance removed
    37. 37. 2. Cancer cell transformationc. Progression – 3rd stepCellular changes formed during initiation andpromotion assume increased malignant behaviorCells divide in uncoordinated fashion, invadeand destroy neighboring tissue
    38. 38. Process of Cancer Development
    39. 39. Initiation, Promotion and Progression
    40. 40. B. Risk factors1. Heredity Predisposition to approx. 50 types of cancer has been observed in families 10% of cancers have strong genetic link
    41. 41. 2. Hormones Thought to drive cell division Women – breast, ovary, endometrium Men – prostate, testis
    42. 42. 3. Immunologic mechanisms Cancer associated with impairment or decline in immune system. See increase in:  People with immunodeficiency disease  Organ transplant pts taking immunosuppressant drugs  Elderly
    43. 43. 4. Chemical carcinogens Cigarette smoke Workplace carcinogens Air pollution Diet Alcohol
    44. 44. 5. Radiation Ultraviolet exposure Ionizing radiation exposure Electromagnetic field exposure
    45. 45. 6. Oncogenic viruses Incorporate themselves into genetic structure of cell Alter future generations of cell Human papillomavirus (HPV) Epstein-Barr virus (EBV)
    46. 46. VI. Prevention and early detection of cancer Primary Prevention Secondary Prevention Tertiary Prevention
    47. 47. A. Preventive measures Important role for RN Must have knowledge and skills to educate community about:  health-related behaviors  risk factors  screening and detection methods
    48. 48. 1. Patient education Numerous factors influence degree of knowledge people have about CA risk factors and health promoting behaviors: race cultural influences level of education income age
    49. 49. Seven Warning Signs of Cancer C A U T I O N – nagging cough/hoarseness See Lewis Table 16-8
    50. 50. B. Screening procedures for different types of cancer sites SBE for breast cancer Rectal exams for prostate cancer Sigmoidoscopy/colonoscopy Occult blood for colon cancer
    51. 51. VII. Ways of classifying cancerTumors are classified on basis of: cell type tissue of origin benign or malignant degree of differentiation anatomic site function
    52. 52. A. By anatomic siteEpithelial tissue - carcinomasConnective tissue - sarcomasLymphatic tissue - lymphomasGlial cells of the CNS - gliomasBlood forming organs (mainly bone marrow)- leukemias
    53. 53. B. Histological Analysis (“Grading”)Grade I: cells differ slightly from normal cells and are well differentiatedGrade II: cells are more abnormal and moderately differentiatedGrade III: cells are very abnormal (severe hyperplasia) and poorly differentiatedGrade IV: cells are immature and primitive and undifferentiated, no resemblance to tissue of origin
    54. 54. Mutation of a Cell Line
    55. 55. C. Extent of disease (“Staging”) Describes location and pattern of spread of tumor TNM most common:  Tumor (primary)  Node  Metastasis
    56. 56. Clinical Staging 0 - CA in situ I - tumor limited to tissue or organ II - limited local spread III - extensive local and regional spread IV - metastasis
    57. 57. VIII. Major treatment options in cancer treatment Goals - Cure, Control, Palliation Used to be considered cured if no cancer recurrence for 5 years after treatment Widespread invasions associated with poor prognosis Choice of Rx depends on staging - more metastasis = more aggressive approach
    58. 58. Goals of cancer treatment
    59. 59. A. Surgery Approx 90% treated surgically Main benefit - removal of tumor with minimal damage to other body cells Surgery involves risk Usually followed by radiation or chemotherapy
    60. 60. Goals of surgery
    61. 61. B. RadiationUsed to interrupt cellular growth. Can: immediately kill cells delay or halt cell cycle progression cause damage in nucleus that causes cell death after replication
    62. 62. Types of Radiation1. External radiation - source placed outside the body “Lethal tumor dose”: will eradicate 95% of tumor while preserving normal tissue2. Internal radiation/Brachytherapy - source placed close to or directly in the tumor site Seeds, beads, needle, catheter, etc. Brachytherapy: limits radiation to duration of treatment? Time, Distance, Shielding
    63. 63. Linear accelerator treatment for head and neck cancer
    64. 64.  Wet desquamation from RT Dry desquamation from RT
    65. 65. C. Chemotherapy Systemic administration of anticancer chemicals Most agents are cytotoxic - interfere with some aspect of cell division More rapidly dividing cells more susceptible Normal cells die too
    66. 66. Goals of chemotherapy
    67. 67. 1. Classificationsa. Cell cycle specific Destroys cells in specific phases of cell cycleb. Cell cycle non-specific Act independently of cell cycle phases Often combine with cell-cycle specific to increase number of cells killed
    68. 68. Action Sites of CCS [Antineoplastic] Drugs
    69. 69. Action Sites of Non–Cell Cycle–Specific Antineoplastic Agents
    70. 70. 2. Examples See Table 16-9 “Classifications of Chemotherapy Drugs” in Lewis
    71. 71. Chemotherapy/survival relationship
    72. 72. 3. Routes of administration Topical, Oral, IM, IV, SQ, Arterial, Intercavity, Intrathecal routes Depends on type of drug, required dose, and type, location, and extent of tumor Patients frequently have central lines placed for chemotherapy due to the frequency of treatment and vesicant (caustic) nature of the medications
    73. 73. PICC Line placement
    74. 74. Tunneled Central Line
    75. 75. Huber needle access of implanted port
    76. 76. 4. Extravasations “Escape of fluids into the surrounding tissue”  Such as in IV infiltration. Apply ice to slow circulation. Can cause tissue necrosis and damage to underlying tendons, nerves, and blood vessels Treatment - stop drug immediately and apply ice. Notify MD
    77. 77. 5. Toxicity and side effects Can be acute or chronic Cells with rapid growth rates are very susceptible to damage Various body systems may be affected
    78. 78. 5. Toxicity and side effects (cont.)GI system - N & V most common; stomatitisHematopoietic system - depressed bone marrow function  anemia, thrombocytopenia, etc.Renal system - damage by direct effects during excretion or accumulation of end products after cell lysisHair loss (alopecia) - hair cells are rapidly dividingCardiopulmonary system - can cause cumulative cardiac toxicities. Toxic effects on lung function. Sometimes necessitates transplant.Reproductive system - affects testicular & ovarian function Some choose to bank their gametes.
    79. 79. 6. Nursing consideration for patients on chemotherapy Fluid and electrolytes Infection and bleeding  thrombocytopenia, leukopenia Skin Problems Hair Loss Nutritional Concerns  d/t stomatitis, anorexia, N/V Chemotherapy administration Self protection
    80. 80. D. Hormonal therapy Used for cancers that are responsive to or dependent on hormones for growth:  breast  prostate  adrenal glands  endometrium
    81. 81. E. Biotherapy Active Immunotherapy – acts as nonspecific stimulant of immune system Passive Immunotherapy – transfer of cultured immune cells into person with cancer  Sensitized NK cell  T lymphocytes  Cytokines
    82. 82. Biologic Response Modifiers Changes person’s biologic response to cancer  Cytokines: IFNs, ILs that bind  Monoclonal antibodies: produced by B-cells  Hematopoietic growth factors: epogen?
    83. 83. F. Targeted therapy Drugs that target processes of cancer cells specifically Leave normal cells unharmed
    84. 84. G. Bone marrow and peripheral blood stem cell transplantation High dose chemo and radiation therapy used to ablate or suppress bone marrow Self or donor stem cells transplanted
    85. 85. Stem cell transplant

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