Introduction to Cancer

8/9/2019 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


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


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


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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THANKYOU

Documents

Introduction to Cancer