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Alterations in Cell
  Function and
 Differentiation
Management of Neoplastic Disruptions
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
A. Cancer incidence and
     prevalence by site and sex
Men               Women
 Prostate         Breast

 Lung/Bronchus    Lung /Bronchus

 Colon/Rectum     Colon/Rectum

 Urinary Tract    Uterus

 Melanoma         Ovary
Leading
Cancer Site
Percentages
Estimated mortality
Men                Women
 Lung/Bronchus     Lung/Bronchus

 Prostate          Breast

 Colon/rectum      Colon/rectum

 Pancreas          Pancreas

 Non-Hodgkin’s     Ovary

  lymphoma
II. Host defense mechanisms in
        control of cancer/neoplasia
A. 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
B. Immunological defense
           against CA
1. Immune surveillance mechanisms
Cytoxic T cells - kill tumor cells
Natural Killer cells - directly lyse tumor cells
Monocytes/Macrophages - important in
  detection of CA cells. Secret cytokines
B cells – produce antibodies that bind to and kill
  tumor cells
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 as being different from
    self cells
   Closely resemble cells they originate from
   Process where cancer cells evade immune
    system is called immunologic escape
Tumor associated antigens on
 surface of malignant cells
Blocking Antibodies Preventing T-
Cell from Destroying Malignant Cell
III. Normal vs. abnormal cell
          growth and reproduction
A. Review of normal cell cycle
Reproduction of both healthy and malignant
   cells follow cell cycle pattern
Time required for one tissue cell to divide and
   reproduce into 2 identical cells
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
Cell Cycle
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
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
Normal Cellular Differentiation
IV. Characteristics of Benign and
            Malignant Neoplasms
A.    Terminology
      1. Tumor



      2. Neoplasia
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
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
Benign vs. Malignant
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
neoplastic disruptions   alterations in cell function & differentiation pp
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
Metastasis
Process of metastasis
Sites of bloodborne metastases
neoplastic disruptions   alterations in cell function & differentiation pp
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 actively dividing or moving
          through cell cycle
         Duration of cell cycle
         Number of cells being lost compared with number
          of cells being produced

In blood cancers ex. leukemia, the cancer is rapidly dividing as it mimics
normal life-cycle of surrounding cells EXCEPT scheduled death.
The cancer cells persist.
V. Carcinogenesis and major
            risk factors
A. Carcinogenesis
1. 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
a. Oncogene
    Cancer causing gene – altered gene
    Gene that promotes autonomous cell growth in
     cancer cells
    Mutations of normal growth-regulating genes



Oncogenesis: mechanism by which normal cells mutate into cancer cells
Only one single altered gene copy can cause an overgrowth
b. Proto-oncogene
   Normal growth-promoting gene thought to be
    active when appropriate growth-promoting
    signals reach cell
   “On switch” for cellular growth




If there’s a mutation in the proto-oncogene, then the cell is released from…?
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
Stages in Development of a Malignant Neoplasm
2. Cancer cell transformation
a. 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
2. Cancer cell transformation
b. Promotion – 2nd step
Unregulated accelerated growth in already

initiated cells by various chemical and growth
factors
Characterized by reversible proliferation of

altered cell if promoter substance removed
2. Cancer cell transformation
c. Progression – 3rd step
Cellular changes formed during initiation and

promotion assume increased malignant behavior
Cells divide in uncoordinated fashion, invade

and destroy neighboring tissue
Process of Cancer Development
Initiation, Promotion and Progression
B. Risk factors
1.   Heredity
    Predisposition to approx. 50 types of cancer
     has been observed in families
    10% of cancers have strong genetic link
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:
       People with immunodeficiency disease
       Organ transplant pts taking immunosuppressant
        drugs
       Elderly
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
   Human papillomavirus (HPV)
   Epstein-Barr virus (EBV)
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:
        health-related behaviors
        risk factors
       screening and detection methods
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
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 cancer
   Sigmoidoscopy/colonoscopy
   Occult blood for colon cancer
VII. Ways of classifying cancer
Tumors are classified on basis of:
 cell type

 tissue of origin

 benign or malignant

 degree of differentiation

 anatomic site

 function
A. By anatomic site
Epithelial tissue - carcinomas
Connective tissue - sarcomas
Lymphatic tissue - lymphomas
Glial cells of the CNS - gliomas
Blood forming organs (mainly bone marrow)-
  leukemias
B. Histological Analysis
               (“Grading”)
Grade I: cells differ slightly from normal cells and
 are well differentiated
Grade II: cells are more abnormal and moderately
 differentiated
Grade III: cells are very abnormal (severe
 hyperplasia) and poorly differentiated
Grade IV: cells are immature and primitive and
 undifferentiated, no resemblance to tissue of
 origin
Mutation of a Cell Line
C. Extent of disease (“Staging”)
   Describes location and pattern of spread of tumor
   TNM most common:
       Tumor (primary)
       Node
       Metastasis
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
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
Goals of cancer treatment
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
Goals of surgery
B. Radiation
Used to interrupt cellular growth. Can:
 immediately kill cells

 delay or halt cell cycle progression

 cause damage in nucleus that causes cell death

  after replication
Types of Radiation
1.   External radiation - source placed outside the
     body
     “Lethal tumor dose”: will eradicate 95% of tumor while
     preserving normal tissue


2.   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
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
    some aspect of cell division
   More rapidly dividing cells more susceptible
   Normal cells die too
Goals of chemotherapy
1. Classifications
a. Cell cycle specific
 Destroys cells in specific phases of cell cycle

b. Cell cycle non-specific
 Act independently of cell cycle phases

 Often combine with cell-cycle specific to

  increase number of cells killed
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 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
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
        circulation.
   Can cause tissue necrosis and damage to
    underlying tendons, nerves, and blood vessels
   Treatment - stop drug immediately and apply
    ice. Notify MD
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
5. Toxicity and side effects (cont.)
GI system - N & V most common; stomatitis
Hematopoietic system - depressed bone marrow function
       anemia, thrombocytopenia, etc.
Renal system - damage by direct effects during excretion or
  accumulation of end products after cell lysis
Hair loss (alopecia) - hair cells are rapidly dividing
Cardiopulmonary 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.
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
D. Hormonal therapy
   Used for cancers that are responsive to or
    dependent on hormones for growth:
       breast
       prostate
       adrenal glands
       endometrium
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
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?
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
    ablate or suppress bone marrow
   Self or donor stem cells transplanted
Stem cell transplant

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neoplastic disruptions alterations in cell function & differentiation pp

  • 1. Alterations in Cell Function and Differentiation Management of Neoplastic Disruptions
  • 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. A. Cancer incidence and prevalence by site and sex Men Women  Prostate  Breast  Lung/Bronchus  Lung /Bronchus  Colon/Rectum  Colon/Rectum  Urinary Tract  Uterus  Melanoma  Ovary
  • 5. Estimated mortality Men Women  Lung/Bronchus  Lung/Bronchus  Prostate  Breast  Colon/rectum  Colon/rectum  Pancreas  Pancreas  Non-Hodgkin’s  Ovary lymphoma
  • 6. II. Host defense mechanisms in control of cancer/neoplasia A. 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. B. Immunological defense against CA 1. Immune surveillance mechanisms Cytoxic T cells - kill tumor cells Natural Killer cells - directly lyse tumor cells Monocytes/Macrophages - important in detection of CA cells. Secret cytokines B cells – produce antibodies that bind to and kill tumor cells
  • 8. Macrophage functioning in response to malignant target cells
  • 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. Tumor associated antigens on surface of malignant cells
  • 11. Blocking Antibodies Preventing T- Cell from Destroying Malignant Cell
  • 12. III. Normal vs. abnormal cell growth and reproduction A. Review of normal cell cycle Reproduction of both healthy and malignant cells follow cell cycle pattern Time required for one tissue cell to divide and reproduce into 2 identical cells
  • 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
  • 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. 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
  • 18. IV. Characteristics of Benign and Malignant Neoplasms A. Terminology 1. Tumor 2. Neoplasia
  • 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. 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
  • 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
  • 24. 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
  • 27. Sites of bloodborne metastases
  • 31. 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 produced In blood cancers ex. leukemia, the cancer is rapidly dividing as it mimics normal life-cycle of surrounding cells EXCEPT scheduled death. The cancer cells persist.
  • 32. V. Carcinogenesis and major risk factors A. Carcinogenesis 1. 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
  • 33. a. Oncogene  Cancer causing gene – altered gene  Gene that promotes autonomous cell growth in cancer cells  Mutations of normal growth-regulating genes Oncogenesis: mechanism by which normal cells mutate into cancer cells Only one single altered gene copy can cause an overgrowth
  • 34. b. Proto-oncogene  Normal growth-promoting gene thought to be active when appropriate growth-promoting signals reach cell  “On switch” for cellular growth If there’s a mutation in the proto-oncogene, then the cell is released from…?
  • 35. 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
  • 36. Stages in Development of a Malignant Neoplasm
  • 37. 2. Cancer cell transformation a. 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
  • 38. 2. Cancer cell transformation b. Promotion – 2nd step Unregulated accelerated growth in already initiated cells by various chemical and growth factors Characterized by reversible proliferation of altered cell if promoter substance removed
  • 39. 2. Cancer cell transformation c. Progression – 3rd step Cellular changes formed during initiation and promotion assume increased malignant behavior Cells divide in uncoordinated fashion, invade and destroy neighboring tissue
  • 40. Process of Cancer Development
  • 42. B. Risk factors 1. Heredity  Predisposition to approx. 50 types of cancer has been observed in families  10% of cancers have strong genetic link
  • 43. 2. Hormones  Thought to drive cell division  Women – breast, ovary, endometrium  Men – prostate, testis
  • 44. 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
  • 45. 4. Chemical carcinogens  Cigarette smoke  Workplace carcinogens  Air pollution  Diet  Alcohol
  • 46. 5. Radiation  Ultraviolet exposure  Ionizing radiation exposure  Electromagnetic field exposure
  • 47. 6. Oncogenic viruses  Incorporate themselves into genetic structure of cell  Alter future generations of cell  Human papillomavirus (HPV)  Epstein-Barr virus (EBV)
  • 48. VI. Prevention and early detection of cancer  Primary Prevention  Secondary Prevention  Tertiary Prevention
  • 49. 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
  • 50. 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
  • 51. Seven Warning Signs of Cancer  C  A  U  T  I  O  N – nagging cough/hoarseness  See Lewis Table 16-8
  • 52. 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
  • 53. VII. Ways of classifying cancer Tumors are classified on basis of:  cell type  tissue of origin  benign or malignant  degree of differentiation  anatomic site  function
  • 54. A. By anatomic site Epithelial tissue - carcinomas Connective tissue - sarcomas Lymphatic tissue - lymphomas Glial cells of the CNS - gliomas Blood forming organs (mainly bone marrow)- leukemias
  • 55. B. Histological Analysis (“Grading”) Grade I: cells differ slightly from normal cells and are well differentiated Grade II: cells are more abnormal and moderately differentiated Grade III: cells are very abnormal (severe hyperplasia) and poorly differentiated Grade IV: cells are immature and primitive and undifferentiated, no resemblance to tissue of origin
  • 56. Mutation of a Cell Line
  • 57. C. Extent of disease (“Staging”)  Describes location and pattern of spread of tumor  TNM most common:  Tumor (primary)  Node  Metastasis
  • 58. 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
  • 59. 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
  • 60. Goals of cancer treatment
  • 61. 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
  • 63. B. Radiation Used to interrupt cellular growth. Can:  immediately kill cells  delay or halt cell cycle progression  cause damage in nucleus that causes cell death after replication
  • 64. Types of Radiation 1. External radiation - source placed outside the body “Lethal tumor dose”: will eradicate 95% of tumor while preserving normal tissue 2. 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
  • 65. Linear accelerator treatment for head and neck cancer
  • 66. Wet desquamation from RT  Dry desquamation from RT
  • 67. 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
  • 69. 1. Classifications a. Cell cycle specific  Destroys cells in specific phases of cell cycle b. Cell cycle non-specific  Act independently of cell cycle phases  Often combine with cell-cycle specific to increase number of cells killed
  • 70. Action Sites of CCS [Antineoplastic] Drugs
  • 71. Action Sites of Non–Cell Cycle–Specific Antineoplastic Agents
  • 72. 2. Examples  See Table 16-9 “Classifications of Chemotherapy Drugs” in Lewis
  • 74. 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
  • 77. Huber needle access of implanted port
  • 78. 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
  • 79. 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
  • 80. 5. Toxicity and side effects (cont.) GI system - N & V most common; stomatitis Hematopoietic system - depressed bone marrow function  anemia, thrombocytopenia, etc. Renal system - damage by direct effects during excretion or accumulation of end products after cell lysis Hair loss (alopecia) - hair cells are rapidly dividing Cardiopulmonary 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.
  • 81. 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
  • 82. D. Hormonal therapy  Used for cancers that are responsive to or dependent on hormones for growth:  breast  prostate  adrenal glands  endometrium
  • 83. 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
  • 84. 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?
  • 85. F. Targeted therapy  Drugs that target processes of cancer cells specifically  Leave normal cells unharmed
  • 86. 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

Editor's Notes

  1. Reappearance of oncofetal Ags thought to be result of…
  2. Immunocompromised individuals are at higher risk for cancer development
  3. TS: cannot find tumor NX: regional lymph nodes unable to be assessed
  4. Cure, control, or palliation
  5. 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.
  6. Limiting! Ex. Only targets cancer cells in M-phase (only a 1 hour window)  multiple drugs used at once
  7. Created by Unregisterd version of Xtreme Compressor
  8. Vesicant solutions can be administered this way
  9. The closer the entry point to the heart, the higher the risk of infection
  10. Huber needle: the only type of needle that can be used because it won’t core out a portion of the diaphragm
  11. Fatigue alone accounts for 80% of symptoms
  12. A premenopausal woman might receive androgens with chemo whereas a postmenopausal woman may receive estrogen.
  13. Reverse isolation