3.Classify cancer.
4. Pathophysiologyof cancer cells/theory of pathogenesis
5. Grading and Staging and TNM CLASSIFICATION SYSTEM
6. 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.
4.
DESCRIPTION:
- A neoplasicdisorder that can involve all body organs
characterized by:
a. Uncontrolled growth and spread of abnormal cells
b. Proliferation: rapid reproduction by cell division
c. Invasion: growth of primary tumor into surrounding
tissue
d. 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.
5.
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.
6.
Lymphomas: neoplasms thatoriginate 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.
7.
Sarcomas: neoplasms thatoriginate 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.
9.
5 STAGES:
1.) Gap/Growthphase (G1) – time after formation of cell, RNA,
CHON synthesis
2.) Synthesis (S) phase – DNA replication
3.) Gap/Growth phase (G2) – continued RNA & CHON synthesis
4.) 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
11.
- 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.
12.
e. Neoplasia: refersto abnormal cell growth; maybe
benign or malignant.
Benign: harmless, not infiltrative of other tissues
Malignant: always harmful, may spread or metastasize to
tissues sometimes far removed from the site of origin.
CHARACTERISITIC OF A PROLIFERATIVE CELL/TUMOR
NEOPLASTIC CELLS NEOPLASTIC TUMORS
Appear larger than normal
w/ 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.
13.
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
14.
PATHOPHYSIOLOGY OF CANCERCELLS:
CARCINOGENESIS
Involves 3 process:
1. Initiation : carcinogens changes the DNA of the cell
causing cell mutation
2. Promotion: repeated exposure to carcinogen resulting to
expression of cellular abnormality or genetic mutation
3. Progression: the expressed ability to invade and
metastasize.
15.
Cell alteration
mutation ofprotooncogene 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)
16.
Theory of Pathogenesis
1.Transform by unknown mechanism on exposure to
certain etiologic agents including:
Virus: (EBV, HSV II, HPV,CMV,Hepa B) - oncovirus
Chemical: 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.
17.
- Increased riskfor 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.
18.
GRADING AND STAGING
GRADING:
GradeI: 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
19.
STAGING
Stage 0: carcinomain situ
Stage 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 METASTASIS
BREAST CA: bone, lung
LUNG CA: brain
COLORECTAL CA: liver
PROSTATE CA: bone, spine
BRAIN TUMORS: CNS
20.
TNM CLASSIFICATION SYSTEM
Green,F., et al. 6th
edition. AJCC Cancer Staging Manual
SYMBOL 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
21.
PRIMARY TUMOR (T)
TxPrimary 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
25.
C A UT I O N UP
C – hange in bowel/bladder habits
A – ny sore that does not heal
U – nusual bleeding or discharge
T – hickening or lump in breast or elsewhere
I – ndigestion
O – bvious change in wart or mole
N – agging cough or hoarseness
U –nusual anemia
P - ain
26.
Cellular growthcharacteristics
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:
27.
Difference Between Benignand malignant
BENIGN MALIGNANT
Cell
characteristics
Well- differentiated
cells that resemble
normal cells of the
tissue from which
the tumor originated
Cells are
undifferentiated
Often 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
28.
BENIGN MALIGNANT
Rate ofgrowth 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
29.
BENIGN MALIGNANT
Tissue
destruction
Does notusually
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
30.
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
MARKER CLINICAL SIGNIFICANCE
Alphafetoprotein (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
33.
General Cancer SignsAnd
Symptoms
1.Weight loss
2.Fever
3.Fatigue
4.Pain
5.Changes in skin
34.
Specific Cancer Signsand 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
1. Acquisition ofknowledge 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
37.
Smoking damagesnearly 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
38.
Control foodportions 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.
39.
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
40.
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.
1. Biopsy: surgicalincision 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
47.
Interventions:
- OPD setting– prepare pt w/doc’s order – obtain Inform
consent.
2. BMA – if hematolymphoid malignancy is suspected.
3. Chest radiograph
4. CBC
5. CT scan: computed tomography
6. Cytological studies: Pap smear
7. Liver function test: ALT/AST
8. MRI
9. Presence of oncofetal Ag such as CEA & AFP
10. Protoscopic examination: Guaiac for occult blood
11. Radiographic studies: mammogram
12. Radioisotope scans: liver, brain, bone, lung
substances that mayprotect 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
52.
for healthyeyes is found in green leafy vegetables
such as:
3. Lycopene
• Tomatoes
• watermelon
• guava
• papaya
• apricots
• pink
grapefruit
• blood
• collard greens
• Spinach
• kale
2. Lutein
6. VitaminC (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 oils
also found in: Mangos, Nuts, & broccoli
56.
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.
57.
S/E of surgery:
1.Loss of function of a specific body part
2. Reduced function as a result of organ loss
3. Scarring or disfigurement
4. Grieving about altered body image or imposed change
in lifestyle.
58.
- Assignment: Saturday.June 18, 2011
Read on radiation therapy, bone marrow transplantation.
Quiz on the discussed topics.