Introduction to Cancer
Transcript of Introduction to Cancer
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ONCOLOGY NURSING
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CANCER TERMINOLOGY
Anaplastic :- tumor cells are completely
undifferentiated and bear no resemblance
to cells of tissues of their origin.
Hyperplasia :- an increase in the number of
normal cells in a normal arrangement in a
tissue or organ; usually leads to increase
in the size or part and an increase in
functional activity.
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CANCER TERMINOLOGY
Metaplasia :- the replacement of one type of fully
differentiated cell by another fully differentiated cell in
another parts of the body where the second cell type does
not normally occur.
Dysplasia :- an alteration in the size ,shape, and organization
of differentiated cells; cells lose their regularity and show
variability in size and shape, usually in response to an
irritant; cells may revert to normal when the irritant is
removed but may transform to a neoplasia.
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CANCER TERMINOLOGY
Metastasis :- the ability of neoplastic cells to spread from the
original site of the tumor to distant organs ,spreading as the
same cell type as the original neoplastic tissue.
Carcinoma :- A form of cancer that is composed of epithelial
cells that tend to infiltrate surrounding tissues and may
eventually spread to distant sites .
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CANCER TERMINOLOGY
Oncogenes :- cancer genes that are altered versions of
normal genes.
Proto- oncogenes :- repressed oncogenes existing in
normal cells which can be activated by many differentfactors and cause the host cells to become malignant.
Tumor : usually synonymous with neoplasm.
Neoplasm :- the word neoplasm is derive from Greek wordneos , new ,and plasis ,molding. Thus, neoplasm is defined
as an abnormal new growth or formation ,of tissue that
serves no useful purpose and may harm the host organism.
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ETIOLOGY-MULTISTEP PROCESS OF
CARCINOGENESIS
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ETIOLOGY
Viruses
Chemical agents
tar,soot,asphalt ,aniline dyes ,hydrocarbons, crude
paraffin oil, fuel oil, nickel. Physical agents
Radiation (uv radiations and ionizing radiations) and asbestos
Drugs and hormones
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RISK FACTORS OF CANCER
ENDOGENOUS
1. Age
cancer incidence increase with age.
2.Genetic heritage
some cancers exhibit a clear inheritance pattern.
3.Hormonal factors
Donot act as primary carcinogens, but appear to
influence the process of carcinogenesis.
4.Immunologic factors
malignant cells are antigenically different & should be
recognized & destroyed by an intact immune system.
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EXTERNAL RISK FACTORS
DRUGS &CHEMICAL
RADIATIONS
TOBACCO
NUTRITION :-
DIET HIGH IN FAT AND CALORIES
SEXUAL PRACTICES
EARLY ONSET SEX & MULTIPLE PARTNERS .
VIRUSES
PSYCHOSOCIAL FACTORS
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CLASSIFICATION OF CANCER
Tumor can be classified according to :-
Anatomic site
Histology (grading )
Extend of disease (staging)Purposes of classification :-
1. To communicate the status of the cancer to all members
of health team.
2. Assist in determining the most effective treatment plan.3. Evaluation of treatment .
4. Compare like groups for statistical purposes.
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ANATOMIC SITE CLASSIFICATION
CARCINOMA originating from embryonal ectoderm (skin &
glands ) and endoderm (mucus membranes linings of the
respiratory tract ,gastrointestinal tract ,and genitourinary
tracts)
SARCOMAS originating from embryonal mesoderm
(connective tissue,muscle,bone,and fat)
LYMPHOMAS & LEUKEMIAS originating from the
hematopoietic system.
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HISTOLOGIC CLASSIFICATION
GRADE I : cells differ slightly from the normal cells (mild
dysplasia ) & are well differentiated.
GRADE II : cells are more abnormal (moderate dysplasia )&moderately differentiated.
GRADE III :cells are very abnormal (severe dysplasia ) &
poorly differentiated.
GRADE IV : cells are immature & primitive ( anaplasia ) and
undifferentiated ;origin of cells is difficult to identify.
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CLINICAL STAGING :-extend & spread of
disease .
STAGE 0 : cancer in situ
STAGEI : tumor limited to the tissues of origin; localized
tumor growth
STAGEII : limited local spread
STAGEIII : extensive local & regional spread
STAGEIV : metastasis
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TNM CLASSIFICATION SYSTEM
It involves three parameters :-
Tumor size and invasiveness (T)
Presence and absence of regional spread to the lymph
nodes(N) Metastasis to distant organ sites .(M)
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MANAGEMENT OF CANCER
Complete eradication of malignant disease
(CURE )
Prolonged survival & containment of cancer cell
growth
( CONTROL)
Relief of symptoms associated with the disease
(PALLIATION )
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MULTIPLE MODALITIES IN CANCER
TREATMENT
Surgery
Radiation therapy
Chemotherapy
Biologic response modifiers
(BRM ) therapy.
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SURGERY Surgical removal of the entire cancer remains
the ideal and most frequently used treatment.
Types of surgery :-
Diagnostic surgery
Prophylactic
PalliativeReconstructive
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DIAGNOSTIC SURGERY
Such as biopsy to obtain tissue samples
for analysis of cells suspected to be
malignant.
Types of biopsy :-
Excisional biopsy
Incisional biopsy
Needle aspiration biopsy
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PROPHYLLATIC SURGERY :-
it involves removing non vital tissues or organs that are likelyto develop cancer e.g. colectomy,mastectomy,oophorectomy.
PALLATIVE SURGERY :-
when cure is not possible ,the goals of the treatment are to
make the patients as comfortable as possible and to promote
satisfying & productive life as long as possible.
RECONSTRUCTIVE SURGERY :-
it may follow curative & radical surgery and carried out in ann
attempt to improve function or obtain a more desirable
cosmetic effect
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RADIATION THERAPY
In this ,ionizing radiations are used to interrupt
cellular growth.
Two types of ionizing radiations i.e.
electromagnetic rays (x ray & gamma rays ) andparticles ( electrons ,beta
particles,protons,neutrons and Alfa particles ) can
lead to tissue disruption .
A radiosensitive tumor is one that can be
destroyed by a dose of radiation that still allows
for cell regeneration in the normal tissue
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Mechanism of action
Radiation therapy works by damaging the DNA of
cells.
The damage is caused by a photon, electron,
proton, neutron, or ion beam directly or indirectlyionizing the atoms which make up the DNA chain.
Indirect ionization happens as a result of the
ionization of water, forming free radicals, notably
hydroxyl radicals, which then damage the DNA. In the most common forms of radiation therapy,
most of the radiation effect is through free radicals
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Mechanism of action
cells have mechanisms for repairing DNA damage,
breaking the DNA on both strands proves to be the most
significant technique in modifying cell characteristics.
Because cancer cells generally are undifferentiated andstem cell-like, they reproduce more, and have a
diminished ability to repair sub-lethal damage compared
to most healthy differentiated cells.
The DNA damage is inherited through cell division,
accumulating damage to the cancer cells, causing them todie or reproduce more slowly.
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Dose
The amount of radiation used in radiation therapy is
measured in gray (Gy), and varies depending on the type
and stage of cancer being treated. For curative cases, the
typical dose for a solid epithelial tumor ranges from 60 to
80 Gy, while lymphomas are treated with 20 to 40 Gy.
Preventative (adjuvant) doses are typically around 45 - 60
Gy in 1.8 - 2 Gy fractions (for Breast, Head and Neck
cancers respectively.)
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Many other factors are considered by radiation oncologists
when selecting a dose, including whether the patient is
receiving chemotherapy, patient comorbidities, whether
radiation therapy is being administered before or after
surgery, and the degree of success of surgery.
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The placement of brachytherapy
sources
can be temporary or permanent
permanent brachytherapy, the sources are surgically
sealed within the body and left there, even after all of the
radiation has been given off. The remaining material (inwhich the radioactive isotopes were sealed) does not cause
any discomfort or harm to the patient. Permanent
brachytherapy is a type of low-dose-rate brachytherapy.
temporary brachytherapy, tubes (catheters) or other
carriers are used to deliver the radiation sources, and boththe carriers and the radiation sources are removed after
treatment. Temporary brachytherapy can be either low-dose-
rate or high-dose-rate treatment.
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Systemic radiation therapy
In systemic radiation therapy, a patient swallows or
receives an injection of a radioactive substance, such as
radioactive iodine or a radioactive substance bound to a
monoclonal antibody.
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External-beam radiation therapy
External-beam radiation therapy is most often
delivered in the form of photon beams (either x-
rays or gamma rays) .
A photon is the basic unit of light and other forms ofelectromagnetic radiation.
It can be thought of as a bundle of energy.
The amount of energy in a photon can vary.
For example, the photons in gamma rays have
the highest energy, followed by the photons in x-
rays.
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DRUG THERAPY
Alkylating agents
Nitrosoureas
Platinum drug
Antimetabolites Antitumor antibiotics
Mitotic inhibitors
Topoisomerase inhibitors
Corticosteroids
Hormone therapy
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ALKYLATING AGENTS
Cell cycle phase non specific agents
Damage DNA by causing breaks in the
double stranded helix. if repaired does not
occur cell will die immediately (cytocidal ),orwhen they attempt to divide (cytostatic )
Examples:- nitrogen mustard ;-
cyclophosphamide ,thiotepa
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NITROSOUREAS
Cell cycle phase- non specific agents
like alkylating agents ,break DNA helix
,interfering with DNA replication;cross
blood brain barrier.Example :- carmustine,lomustine
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PLATINUM DRUGS
Cell cycle phase non specific
Binds to DNA & RNA ,miscoding
information and /or inhibiting DNA
replication ,and cells die.
Examples:- cisplatin,carboplatin
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ANTIMETABOLITES
CELL CYCLE PHASE SPECIFIC AGENTS
Mimics naturally occurring substances ,thus interfering
with enzyme function or DNA synthesis. Primarily acts
during S phase .purines & pyrimidines are building blocks
of nucleic acids needed for DNA & RNA synthesis.
Interferes with purine metabolism-mercaptopurine
Interferes with pyrimidine metabolism -5- flouro uracil
Interferes with folic acid metabolism-methotrexate
Interferes with DNA synthesis hydroxyurea.
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ANTI TUMOR ANTIBIOTICS
Cell cycle phase non specific agents
Binds directly to DNA,thus inhibiting the
synthesis of DNA and interfering with
transcription ofRNA .
Example :- doxarubicin,mitomycin
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MITOTIC INHIBITORS
Cell cycle phase specific agents
Taxanes antimicrotubule agents that
interfers with mitosis .Acts during G 2
phase & mitosis to stabilize
microtubules ,thus inhibiting cell
division.example:- pacliaxel
Vinca alkaloids :- acts in M phase to
inhibit mitosis. Ex.
Vincristine,vinblastine
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TOPOISOMERASEINHIBITORS
Cell cycle phase specific agents
Inhibits the normal enzyme
topoisomerase that function to make
reversible breaks & repairs in DNA that
allows for flexibility of DNA in
replication .
Ex. etoposide
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CORTICOSTERIOD
Cell cycle phase non specific agents
Disrupts the cell memgrane and inhibits
synthesis of protien;decreased circulating
lymphocytes;inhibit mitosis;depress
immune system;increase sense of well
being.
Ex. Cortisone,methylprednisolone.
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HORMONAL THERAPY
Cell cycle phase non specific agents
Antiestrogen :- selectively attach to estrogen receptors,
causing down regulation of them and inhibiting tumor
growth ;also known as SERMs ( selective estrogen receptor
modulators ) ex. Tamoxifen
Estrogen :- interfers with hormone receptors and proteins
ex. Estradiol.
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Miscellaneous
Inhibits protien synthesis ex. L-
asparaginase.
Causes changes in DNA in leukemia cells
and degrades the fusionn protien ex.
Arsenic trioxide.
Suppresses mitosis at interphase ;appears
to alter preformed DNA,RNA ,& protien.
Ex. Procarbazine.
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Chemotherapy can produce many side
effects, such as:
Anemia, low red blood cell count
Low white blood cell count (this increases
risk for infection)
Hair loss, or thinning hair
Bleeding or bruising (due to low platelet
count)
Dry skin, or rashes
Fatigue
Diarrhea, constipation
Nausea or vomiting
Muscle and nerve
problems
Lung problems and
difficulty breathing;
coughing excessively
Fertility and sexualityproblems
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NURSING RESPONSIBILITIES
RADIATION THERAPY
CHEMOTHERAPY
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PROBLEM ETIOLOGY NURSING MANAGEMENT
GI SYSTEM :-
Stomatitis,mucositis
,esophagitis
Epithelial cells are destroyed
by the chemotherapy or
radiation therapy
Inflammation & ulceration
occurs due to rapid cell
destruction
Assess oral mucosa daily
Be aware that eating ,talking
and swallowing may be
difficult.
Encourage pt to use artificial
saliva to manage dryness(radiations)
Discourage use of irritants
Apply topical anesthetics
Nausea ,vomiting Release of intracellular
breakdown products
stimulates vomiting centre inthe brain.
GI lining destroyed
Teach pt to eat & drink
,when no nauseated.
Administer antiemeticUse diversional activities
Anorexia Release of TNF & IL from
macrophages has appetite
suppresor effect
Monitor weight
Encourage pt to eat small
frequent meals,high
protein,high calric
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Diarrhoea Denuding of epithelial
lining of intestines.
Side effect of
chemotherapy
Radiations toabdomen,pelvis,lumbosac
ral area
Give antidiarrheoal agents as
needed.
Encourage low fibre,low residue
diet.
Encourage fluid intake ,atlrast 3litres
Constipation
Hepatotoxicit
y
Decrease intestinal motility
related to autonomic
nervous system dysfunction
Caused by neurotoxiceffects of plant
alkaloids(vincristine,
vinblastine)
Toxic effects from
chemotherapy drugs(usually transient and
resolves when drug is
stopped)
Instruct patient to
Take stool softeners as needed
Eat high-fiber foods
Increase fluid intake
Monitor liver function tests
HEMATOLO B M it h l bi d h t it
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HEMATOLO
GIC SYSTEM
Anemia
Bone marrow
depressed secondary to
therapy.
Malignant infiltration of
bone marrow by cancer
Monitor hemoglobin and hematocrit
levels
Administer iron suppliments and
erythropoietin.
Encourage intake of foods that promoteRBC production
Leukopenia Depression of bone
marrow secondary to
chemotherapy or radiationtherapy
Infection most frequent
cause of morbidity and
death in cancer patients
Respiratory and
genitourinary system
usual sites of infection
Monitor WBC count especially neutrophils
Teach patients to report temperature
elevation & other manifestations of infection.Teach pt to avoid large crowds& people
with infection.
Administer WBC growth factors
Thrombo-
cyotopenia
Bone marrow depressed
,sec. to chemotherapy.
Malignant infiltration ofbone marrow that crowds
Observe S/S of bleeding(petec
hiae,ecchymosis ).
Monitor platelet count.
INTEGUMENTARY Destruction of hair Suggest ways to cope with hair loss
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INTEGUMENTARY
SYSTEM:-
ALOPECIA
Destruction of hair
follicles by
chemotherapy or
radiation to scalp.
Hair loss usually
temporary withchemotherapy
,usually permanent in
response to
radiations.
Suggest ways to cope with hair loss
.
Cut long hair before the therapy.
Avoid use of electric hair razor .
Discuss impact of hair loss on self
image.
Skin changes from
dry to moist
desquamation
Radiation damage to
skin
Chemotherapy
induced skin
damages
Hyperpigmentation
Telangietasis
Photosenstivity
Acneiform eruptions
Acral erythema
Alert pt to potential skin changes .
Encourage pt to avoid sun exposure .
Implement symptomatic management
as needed .
Application of lotion .
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=
Respiratory system : Radiation pneumonitis
develops 2-3 mo after
start of treatment
After 6-12 mon ,fibrosis
occurs & is evident on xray
Monitor for dry ,hacking
cough,fever and exertional
dyspnea.
Cardiovascular system :-
myocarditis
Inflammation secondary to
radiation injury.
Complication when chest
wall is irridiated ,may occur
to 1 yr after treatment .
Monitor ofr clinical
manifestations of these
disorders
Monitor heart with ECG
Drug therapy may bemodified ,if s/s of
deteriorating cardiac
enzymes present .
Hyperuricemia Increased uric acid levels
due to chemotherapy
induced cell destruction
Monitor uric acid levels.
Allopurinol may be given as
prophylactic management.Encourage fluid intake .
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