Prepared by: Anna Marie M. Montalban, RN, US-RN
1. Description of cancer2. Definition of terms:- Apoptosis- Benign- Carcinogen- Carcinoma- Hospice- Lymphomas- Leukemia or myeloma- Malignant- Metastasis- Nadir- Neoplasm- Sarcoma- Tumor markers- Undifferentiated cells
3.Classify cancer.4. Pathophysiology of cancer cells/theory of pathogenesis5. Grading and Staging and TNM CLASSIFICATION SYSTEM6. Elaborate the seven warning signs of cancer .7. Identify the risk factors.8. Identify common tumor markers.9. Identify diagnostic tests.10. Differentiate benign from malignant neoplasms.11. Differentiate proliferative patterns from characteristics of a
normal cells.
DESCRIPTION:- A neoplasic disorder that can involve all body
organs characterized by:a. Uncontrolled growth and spread of abnormal cellsb. Proliferation: rapid reproduction by cell divisionc. Invasion: growth of primary tumor into
surrounding tissued. Metastasis: spread or transfer of cancer cells from
one organ or part to another not directly connected.
- Result from a process of altered cell growth and differentiation which is uncoordinated and lacks normal regulatory controls over cell growth and division.
DEFINITION OF TERMS:apoptosis: program & controlled cell destruction w/c eliminates damaged, improperly produced & worn out cells w/out harming the other areas. A normal process of cell deletion & renewal.
- carcinogen: a physical, chemical, or biological stressor that causes neoplastic changes in normal cells.
- carcinoma: a new growth or malignant tumor that originates from epithelial cells, the skin, GIT, lungs , uterus, breast and other organs.
- differentiation: a process which normal body cells have individual characteristics allowing them to perform different body functions.
- Hospice: a concept of care for terminally ill clients that includes the idea of intensive caring rather than intensive care. The family and the client are the focus of nursing care and the goal is to relieve pain and facilitate the optimal quality of life.
Lymphomas: neoplasms that originate from the lymphoid organs.
Leukemia or myelomas: neoplasms that originates from blood forming organs.
Malignant: term for growth that metastasize and grow; cancerous lesions that are disordered, uncontrolled and chaotic proliferation of cells.
Metastasis: the transfer of disease from organ or part to another not directly connected w/it.
Nadir: the period of time during w/c an antineoplastic med has its most profound effects on the B.M.
Neoplasm: a new growth, w/c maybe benign or malignant.
Protooncogenes: a normal gene that can become an oncogene d/t mutation or increased expression.
Oncogene: a gene that has the potential to cause CA; protooncogenes which is converted via mutation/chromosomal arrangement.
Sarcomas: neoplasms that originate from muscle, bone, fat, lymph system, or connective tissues.
Tumor markers: specific bodily subs. that seem to indicate tumor progression or regression.
Undifferentiated cells: cells that have lost the capacity for specialized functions.
5 STAGES:1.) Gap/Growth phase (G1) – time after formation of cell, RNA,
CHON synthesis2.) Synthesis (S) phase – DNA replication3.) Gap/Growth phase (G2) – continued RNA & CHON synthesis4.) Mitosis: cell division: PMAT- Prophase: chromatin coil shortens forming 2 pairs of
chromatids, centrioles move to opposite end forming a mitotic spindle
- Metaphase: chromosomes cluster & align midway between spindle poles
- Anaphase: centromeres divide, divided chromosomes moves to opposite side of the spindle poles.
- Telophase: chromosome uncoil & become chromatin, nuclear envelope and nucleoli appear at each daughter cell
5.) Go – cells not yet destined to replicate, ceases at this stage
- Benign & malignant cells display diff. characteristics of cellular growth, degree of differentiation (anaplasia) that determines cells malignant potential.
a. hyperplasia: “ increase in the number of cells in a tissue”; maybe normal/abnormal cellular response.
b. Metaplasia: refers to conversion of 1 type of cell in a tissue to another type not normal for that tissue – it results from an outside stimulus affecting parent stem cells and maybe reversible or progress to dysplasia.
c. Dysplasia: refers to change in size, shape or arrangement of normal cells into bizarre cells – may precede an irreversible neoplastic change.
d. Anaplasia: involves a change in the structure of cells & their orientation to one another, Cx by loss of differentiation returning to a more primitive form.
e. Neoplasia: refers to abnormal cell growth; maybe benign or malignant.
Benign: harmless, not infiltrative of other tissuesMalignant: always harmful, may spread or
metastasize to tissues sometimes far removed from the site of origin.
CHARACTERISITIC OF A PROLIFERATIVE CELL/TUMORNEOPLASTIC CELLS NEOPLASTIC TUMORS
Appear larger than normalw/ bigger nuclei
Disorganized, irregular nests or sheets or neoplastic cells
Exhibit uncontrolled proliferation w/no contact inhibition.
Contain high % of proliferating cells
Serve no homeostatic function.
Some have the ability to metastasize – spread from the original site to distant organs.
a.) Solid tumors: associated w/the organs from w/c they develop, e.g breast or lung CA.
b.) Hematological CA: originates from blood cell forming tissues e.g. leukemia, lymphoma
RISK FACTORS:-tobacco-alcohol-diet-reproductive and sexual behavior-occupation-pollution-industrial products-medicines-infectious agents-endogenous hormone-genetics
PATHOPHYSIOLOGY OF CANCER CELLS: CARCINOGENESIS
Involves 3 process:1. Initiation : carcinogens changes the DNA of
the cell causing cell mutation2. Promotion: repeated exposure to carcinogen
resulting to expression of cellular abnormality or genetic mutation
3. Progression: the expressed ability to invade and metastasize.
Cell alterationmutation of protooncogene inactivate tumor(activate cell proliferation suppressing gene& differentiation)
Activate oncogene cell lose control/differentiation
unregulated cell growth
malignant neoplasm
Epithelial lining of the Hematopoietic
Mammary ducts/lobules E.L. of the stem cells(breast CA) major bronchi (Leukemia) (lung CA)
Theory of Pathogenesis1. Transform by unknown mechanism on exposure to
certain etiologic agents including:Virus: (EBV, HSV II, HPV,CMV,Hepa B) - oncovirusChemical: cobalt, tar, asphalt, aniline dyes,
hydrocarbons in cigarette smoke, air pollutants from industry, fuel oils
Physical stressors: excessive exposure to sunlight or radiation, diet: high fat & low fiber diets, high animal fat intake, preservatives, additives, nitrates
Genetic: abnormal chromosome patterns – Burkitt’s lymphoma, AML/CML, skin CA or familial predispositions e.g breast, colorectal, stomach & lung CA
2. Dev’t of CA is often closely linked to immune system failure as evidenced by:
-increased incidence of malignancy in organ transplant recipients who receive immunosuppressive therapy.
- Increased risk for dev’t of 2nd malignancies in pt receiving long term chemo to treat 1st malignancy.
3. CA occurrence typically reflects a combination of genetic inheritance, host mechanism, and envt’l influences contribute 80-90% of all CA.
Predisposing factors Precipitating factors
CA begins at molecular stage, begins mutation & damage of 1 or more genomes.
Abnormal cells forms a clone & begins to proliferate abnormally.
Abnormal cells infiltrate to tissues, gain access to lymph & blood vessels causing an access to other areas in the body.
GRADING AND STAGINGGRADING:Grade I: Cells differ slightly from normal cells and
are well differentiated (mild dysplasia).Grade II: cells are more abnormal and are
moderately differentiated(moderate dysplasia).Grade III: cells are very abnormal and are poorly
differentiated (severe dysplasia)Grade IV: cells are immature (anaplasia) &
undifferentiated
STAGINGStage 0: carcinoma in situStage I: tumor limited to the tissue of origin,
localized tumor growth (in primary site but has not spread)
Stage II: Limited local spread (spread to nearby area but still in primary site)
Stage III: Extensive local and regional spread (spread throughout nearby area)
Stage IV: Metastasis (spread to close or distant organs)
COMMON SITES OF METASTASISBREAST CA: bone, lungLUNG CA: brainCOLORECTAL CA: liverPROSTATE CA: bone, spineBRAIN TUMORS: CNS
TNM CLASSIFICATION SYSTEM Green, F., et al. 6th edition. AJCC Cancer Staging
ManualSYMBOL INTERPRETATION
T The extent of the primary tumor
N The absence or presence and extent of regional lymph node metastasis
M The absence or presence of distant metastasis
THE USE OF NUMERICAL SUBSETS OF TNM COMPONENTS INDICATES THE PROGRESSIVE
EXTENT OF THE MALIGNANT DISEASE.
T PRIMARY TUMOR
N REGIONAL LYMPH NODE
M DISTANT METASTASIS
PRIMARY TUMOR (T)
Tx Primary tumor cannot be assessed.
T0 No evidence of primary tumor.
Tis Carcinoma in Situ
T1, T2, T3, T4 Increasing size and/or local extent of the primary tumor
REGIONAL LYMPH NODES (N)
Nx Regional Lymph nodes cannot be assessed.
N0 No regional lymph node metastasis.
N1, N2, N3 Increasing involvement of regional lymph nodes
DISTANT METASTASIS (M)
Mx Distant metastasis cannot be assessed.
M0 No distant metastasis
M1 Distant metastasis
C A U T I O N UPC – hange in bowel/bladder habitsA – ny sore that does not healU – nusual bleeding or dischargeT – hickening or lump in breast or
elsewhereI – ndigestionO – bvious change in wart or moleN – agging cough or hoarsenessU –nusual anemiaP - ain
Cellular growth characteristics Method of growth Rate of growth Ability to metastasize or spread General effects Destruction of tissue Ability to cause death
Benign and Malignant cells DIFFERS in:
Difference Between Benign and malignant
BENIGN MALIGNANT
Cell characteristics
Well- differentiated cells that resemble normal cells of the tissue from which the tumor originated
Cells are undifferentiatedOften bear little resemblance to the normal cells of the tissue from which they arise
Mode of growth Tumor grows by expansion and does not infiltrate the surrounding tissues; usually encapsulated
Grows at the periphery and sends out processes that infiltrate and destroy the surrounding tissues
BENIGN MALIGNANT
Rate of growth slow Variable; depends on level of differentiation (the more anaplastic the tumor the faster its growth
Metastasis Does not spread by metastasis
Gains access to the blood and lymphatic channels and metastasize to other areas of the body
BENIGN MALIGNANT
General effects
Usually localized phenomenon that does not cause generalized effects unless its location interferes with vital functions
Often causes generalized effects, such as anemia, weakness, and wt. loss
BENIGN MALIGNANT
Tissue destruction
Does not usually cause tissue damage unless its location interferes with blood flow
Often causes extensive tissue damage as the tumor outgrows its blood supply or encroaches on blood flow to the area; may also produce substances that cause cell damage
Ability to cause death
Does not usually cause death unless its location interferes with vital functions
Usually causes death unless growth can be controlled
Adeno glandular tissue (with glands) Angio blood vessels(arteries, veins, capillaries)
Basal cell epithelium,mainly sun exposed areas embryonal gonads fibro fibrous tissue (ligaments & tendons) lympho lymphoid tissue (tonsils, peyer’s,lymph
nodes Melano pigmented cells of epithelium Myo muscle tissue (heart)
osteo bone squamous epithelium cell
Tissue of origin
Oligodendroglioma – dendrites
Meningioma – meninges
Medulloblastoma – medulla
Epindydomas - ependymal cells
Astrocytoma - astrocytes
Cellular origin
MARKER CLINICAL SIGNIFICANCE
Alpha fetoprotein (AFP) Testicle cancer
Carcinoembryonic antigen (CEA) Colon cancer
Prostate specific antigen (PSA) Prostate cancer
CA 15-3 Breast cancer
CA 125 Ovarian cancer
HCG Gestational trophoblastic disease
General Cancer Signs And Symptoms
1.Weight loss
2.Fever
3.Fatigue
4.Pain
5.Changes in skin
Specific Cancer Signs and Symptoms
1. Changes in bowel habits and bladder fnx
2. Sores that do not heal
3. Unusual bleeding or discharge
4. Thickening or lump in breast or other parts of the body
5. Ingestion or trouble swallowing
6. Recent change in wart or mole
7. Nagging cough or hoarseness
DETECTION and PREVENTION of CANCER
1.Acquisition of knowledge and skills to educate client, community and society about cancer risk
2.Assisting patients to avoid known carcinogenic substances
3.Involvement in the adopting dietary and various lifestyle changes
4.Use of teaching and counseling skills to encourage patients to participate in cancer prevention programs and promotion of healthy lifestyles
PRIMARY PREVENTION
SECONDARY PREVENTION
1.Cancer screening programs
Smoking damages nearly every organ in the human body, is linked to at least 10 different cancers, and accounts for some 30% of all cancer deaths Quit smoking!
A sunburn will fade, but damage to deeper layers of skin
Finding a shade, wearing hats, sunglasses, and clothing—are needed to shield your skin from the sun. Sunscreen alone is not enough protection.
Eating right, being active, and maintaining a healthy weight are important ways to reduce your risk of cancer—as well as heart disease and diabetes
PREVENTION OF CANCER
Control food portions for a great start for weight loss. Use low-fat cooking methods like roasting, baking, broiling, steaming, or poaching. Choose foods that are rich in anti-oxidants. Minimal amount of oil please…
Find activities to fit your lifestyle and ideas for raising active kids as well as staying motivated yourself.
Incorporate fitness into your lifestyle. Motivate yourself.
a.) Early detection: SCREENING TEST- 7 early warning signs of cancer: C A U T I O N UP- BSE: perform 7-10 days after menses;
postmenopausal /hysterectomy clients should select “specific day” of the month.TSE:
- Papanicolaou’s test (Pap) smear test: cytologic analysis of a sample scrape from the cervix & other tissues – cervical neoplasia.
- Stools for occult blood – guiac test- Sigmoidoscopy ( using flexible scope to examine the
rectum & sigmoid colon), colonoscopy (fiberoptic endoscopy study in the lining of the large intestine).
- Mammography
b.) Primary prevention: b.1) focuses on reducing risk factors –
external/internal environment that increases the susceptibility of the pt for CA dev’t.
b.2) General factors that influences CA incidence & mortality:
-sex, age, geographic location, socioeconomic status
-ethnic/cultural background, personal habits, occupation and personal/family health histories.
BREAST SELF
EXAMINATION
- Cervical CA: early age @ 1st intercourse, multiple sexual partners, HPV infection (condyloma/warts),smoking
DIAGNOSTIC EXAMS
1. Blood and urine tests
2. Alkaline phosphates - increase in osteogenic carcinoma
3. Calcium - elevated in multiple myeloma bone metastases
4. Sodium - decreased in bronchogenic carcinoma
5. Potassium - decreased in extensive liver carcinoma
6. Serum Gastrin - measures gastric secretions
7. Neutrophilic leukocytosis – tumors
8. Eosinophilic leukocytosis – brain tumors, Hodgkin’s disease
9. Lymocytosis – chronic lymphocytotic anemia
Laboratory exams
1. Biopsy: surgical incision of a small piece of tissue for microscopic examination, provides histological proof of malignancy.
Types:- needle: aspiration of cells- Incisional: removal of a wedge of suspected tissue
from a larger mass- Exicisional: complete removal of the entire lesion- Staging: multiple needle or incisional biopsies in
tissues where metastasis is suspected.Tissue Examination:- Following excision: frozen section or permanent
paraffin section. FROZEN SECTION: quick, takes minutes – diagnosis (+)PARAFFIN SECTION: takes about 24 hours – clearer
details
Interventions:- OPD setting – prepare pt w/doc’s order – obtain
Inform consent.2. BMA – if hematolymphoid malignancy is
suspected.3. Chest radiograph4. CBC5. CT scan: computed tomography6. Cytological studies: Pap smear7. Liver function test: ALT/AST8. MRI9. Presence of oncofetal Ag such as CEA & AFP10. Protoscopic examination: Guaiac for occult blood11. Radiographic studies: mammogram12. Radioisotope scans: liver, brain, bone, lung
Magnetic Resonance Imaging (MRI) scan
PREVENTION OF CANCER USING
ANTI-OXIDANTS
substances that may protect cells from the damage caused by unstable molecules known as free radicals.
Antioxidants
1.Beta-carotene
• sweet potatoes• carrots• cantaloupe• squash• apricots• pumpkin• mangos
Some green leafy vegetables like:
• collard greens• spinach• kale
for healthy eyes is found in green leafy vegetables such as:
3. Lycopene
• Tomatoes• watermelon• guava• papaya
• apricots• pink grapefruit• blood
• collard greens• Spinach• kale
2. Lutein
4. Selenium ( mineral)
a component of antioxidant enzymes. Plant foods like:
• rice & wheat• Brazil nuts contain selenium.
5. Vitamin A • Liver• sweet potatoes• Carrots• Milk• egg yolks• mozzarella cheese.
6. Vitamin C (ascorbic acid) • fruits and vegetables • Cereals• Beef• poultry and fish.
7. Vitamin E (alpha-tocopherol) in many oils including:
• wheat germ• Safflower• corn and soybean oilsalso found in: Mangos, Nuts, & broccoli
a.) Prophylactic surgery: perform w/existing premalignant condition or known family hx predisposing the person to CA dev’t.
b.) Curative surgery: all gross & microscopic tumor is removed or destroyed.
c.) control (cytoreductive): a “debulking” procedure consist of removing part of the tumor thus decreasing the number of CA cells, increasing the chance of other therapies.
d.) Palliative: improve quality of life during survival time;
Done to reduce pain, relieve airway, GIT or urinary tract obstruction; relieve pressure on the brain or spinal cord, prevent hemorrhage, remove infected or ulcerated tumors or drain abscess.
e.) reconstructive or rehabilitative: improve quality of life
by restoring maximal fxn & appearance.
S/E of surgery:1. Loss of function of a specific body part2. Reduced function as a result of organ loss3. Scarring or disfigurement4. Grieving about altered body image or imposed
change in lifestyle.
- Assignment: Saturday. June 18, 2011
Read on radiation therapy, bone marrow transplantation.
Quiz on the discussed topics.
Magnetic Resonance Imaging (MRI) scan
Oligodendroglioma – dendrites
Meningioma – meninges
Medulloblastoma – medulla
Epindydomas - ependymal cells
Astrocytoma - astrocytes
Cellular origin