neoplastic disruptions alterations in cell function & differentiation pp
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Transcript of neoplastic disruptions alterations in cell function & differentiation pp
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Alterations in Cell Alterations in Cell Function and Function and
DifferentiationDifferentiationManagement of Neoplastic Disruptions
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I. Epidemiology of cancerI. 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
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A. Cancer incidence and A. Cancer incidence and prevalence by site and sex prevalence by site and sex
Men Prostate Lung/Bronchus Colon/Rectum Urinary Tract Melanoma
Women Breast Lung /Bronchus Colon/Rectum Uterus Ovary
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Leading Leading Cancer Site Cancer Site PercentagesPercentages
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Estimated mortality Estimated mortality
Men Lung/Bronchus Prostate Colon/rectum Pancreas Non-Hodgkin’s
lymphoma
Women Lung/Bronchus Breast Colon/rectum Pancreas Ovary
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II. Host defense mechanisms inII. Host defense mechanisms in control of cancer/neoplasia 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
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B. Immunological defense B. Immunological defense against CAagainst 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
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Macrophage functioning in response Macrophage functioning in response to malignant target cellsto malignant target cells
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2. How cancerous cells evade2. How cancerous cells evade immune system 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
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Tumor associated antigens on Tumor associated antigens on surface of malignant cellssurface of malignant cells
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Blocking Antibodies Preventing T-Blocking Antibodies Preventing T-Cell from Destroying Malignant CellCell from Destroying Malignant Cell
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III. Normal vs. abnormal cellIII. Normal vs. abnormal cell growth and reproduction 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
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Phases of normal cell cyclePhases 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
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Cell CycleCell Cycle
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B. Cell proliferationB. 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
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C. Cell differentiationC. 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
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Normal Cellular DifferentiationNormal Cellular Differentiation
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IV.IV. Characteristics of Benign andCharacteristics of Benign andMalignant NeoplasmsMalignant Neoplasms
A. Terminology
1. Tumor
2. Neoplasia
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B. Benign NeoplasmsB. 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
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C. Malignant NeoplasmsC. 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
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Benign vs. MalignantBenign vs. Malignant
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1. Cancer cell characteristics1. 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
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2. Invasion and metastasis2. Invasion and metastasis
Cancer spreads by: Direct invasion and extension
Seeding of cancer cells in body cavities
Metastatic spread through blood or lymph pathways
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MetastasisMetastasis
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Process of metastasisProcess of metastasis
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Sites of bloodborne metastasesSites of bloodborne metastases
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Metastasis to the brainMetastasis to the brain
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Metastasis to the boneMetastasis to the bone
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3. Tumor growth3. 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.
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V. Carcinogenesis and majorV. Carcinogenesis and major risk factors 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
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a. Oncogenea. 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 cellsOnly one single altered gene copy can cause an overgrowth
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b. Proto-oncogeneb. 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…?
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c. Anti-oncogene/Suppressor genec. 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
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Stages in Development of a Malignant NeoplasmStages in Development of a Malignant Neoplasm
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2. Cancer cell transformation2. 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 2nd step of
carcinogenesis
Physical/chemical/biological agents, ex. virus, can cause cancer
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b. Promotion – 2nd stepUnregulated accelerated growth in already initiated cells by various chemical and growth factorsCharacterized by reversible proliferation of altered cell if promoter substance removed
2. Cancer cell transformation2. Cancer cell transformation
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c. Progression – 3rd stepCellular changes formed during initiation and promotion assume increased malignant behaviorCells divide in uncoordinated fashion, invade and destroy neighboring tissue
2. Cancer cell transformation2. Cancer cell transformation
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Process of Cancer DevelopmentProcess of Cancer Development
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Initiation, Promotion and ProgressionInitiation, Promotion and Progression
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B. Risk factors B. Risk factors
1. Heredity Predisposition to approx. 50 types of cancer
has been observed in families 10% of cancers have strong genetic link
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2. Hormones2. Hormones
Thought to drive cell division Women – breast, ovary, endometrium Men – prostate, testis
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3. Immunologic mechanisms3. 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
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4. Chemical carcinogens4. Chemical carcinogens
Cigarette smoke Workplace carcinogens Air pollution Diet Alcohol
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5. Radiation5. Radiation
Ultraviolet exposure
Ionizing radiation exposure
Electromagnetic field exposure
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6. Oncogenic viruses6. Oncogenic viruses
Incorporate themselves into genetic structure of cell
Alter future generations of cell Human papillomavirus (HPV) Epstein-Barr virus (EBV)
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VI. Prevention and early VI. Prevention and early detection of cancer detection of cancer
Primary Prevention
Secondary Prevention
Tertiary Prevention
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A. Preventive measuresA. Preventive measures
Important role for RN Must have knowledge and skills to educate
community about: health-related behaviors risk factors screening and detection methods
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1. Patient education1. 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
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Seven Warning Signs of CancerSeven Warning Signs of Cancer
C A U T I O N – nagging cough/hoarseness See Lewis Table 16-8
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B. Screening procedures forB. Screening procedures for different types of cancer sites different types of cancer sites
SBE for breast cancer Rectal exams for prostate cancer Sigmoidoscopy/colonoscopy Occult blood for colon cancer
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VII. Ways of classifying cancerVII. Ways of classifying cancer
Tumors are classified on basis of: cell type tissue of origin benign or malignant degree of differentiation anatomic site function
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A. By anatomic siteA. 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
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B. Histological Analysis B. Histological Analysis ( (““GradingGrading””))
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
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Mutation of a Cell LineMutation of a Cell Line
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C. Extent of disease (C. Extent of disease (““StagingStaging””))
Describes location and pattern of spread of tumor TNM most common:
Tumor (primary) Node Metastasis
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Clinical StagingClinical Staging
0 - CA in situ I - tumor limited to tissue or organ II - limited local spread III - extensive local and regional spread IV - metastasis
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VIII. Major treatment options in VIII. Major treatment options in
cancer treatment 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
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Goals of cancer treatmentGoals of cancer treatment
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A. SurgeryA. 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
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Goals of surgeryGoals of surgery
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B. RadiationB. 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
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Types of RadiationTypes 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
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Linear accelerator treatment for Linear accelerator treatment for head and neck cancerhead and neck cancer
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Wet desquamation from RT
Dry desquamation from RT
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C. ChemotherapyC. 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
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Goals of chemotherapyGoals of chemotherapy
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1. Classifications1. 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
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Action Sites of CCS [Antineoplastic] DrugsAction Sites of CCS [Antineoplastic] Drugs
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Action Sites of Non–Cell Cycle–Specific Action Sites of Non–Cell Cycle–Specific Antineoplastic Agents Antineoplastic Agents
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2. Examples2. Examples
See Table 16-9 “Classifications of Chemotherapy Drugs” in Lewis
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Chemotherapy/survival relationshipChemotherapy/survival relationship
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3. Routes of administration3. 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
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PICC Line placementPICC Line placement
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Tunneled Central LineTunneled Central Line
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Huber needle access of implanted portHuber needle access of implanted port
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4. Extravasations4. 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
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5. Toxicity and side effects5. 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
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5. Toxicity and side effects (cont.)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 functionSome choose to bank their gametes.
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6. Nursing consideration for6. Nursing consideration forpatients on chemotherapypatients 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
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D. Hormonal therapyD. Hormonal therapy
Used for cancers that are responsive to or dependent on hormones for growth: breast prostate adrenal glands endometrium
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E. BiotherapyE. 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
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Biologic Response ModifiersBiologic Response Modifiers
Changes person’s biologic response to cancer Cytokines: IFNs, ILs that bind Monoclonal antibodies: produced by B-cells Hematopoietic growth factors: epogen?
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F. Targeted therapyF. Targeted therapy
Drugs that target processes of cancer cells specifically
Leave normal cells unharmed
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G. Bone marrow and peripheralG. Bone marrow and peripheral blood stem cell transplantation blood stem cell transplantation
High dose chemo and radiation therapy used to ablate or suppress bone marrow
Self or donor stem cells transplanted
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Stem cell transplantStem cell transplant