1. MEDICAL SURGICAL
NURING
PRESENTED BY
MRS HEENA MEHTA
S.Y.M.SC NURSING
IVALUATION BY
MR.P.YONATANSIR
ASSOCIATE PROFESSER
J G NURSING COLLEGE

4. • INTRODUCTION OF CHEMOTHERAPY
• The use of chemicals to treat cancer first
began in the early 1940.The modern
chemotherapy begun in 1948 with
introduction of nitrogen mustard. Since
that time Scientiests continued to search
for medication to treat neoplasm.
• , such as a virus or other microorganism.

5. • DEFINITION OF CHEMOTHERAPY
• The treatment of cancer using specific
chemical agents ordrugs that are selectively
destructive to malignant cells andtissues.
• The treatment of disease using chemical
agents or drugsthat are selectively
toxic to the causative agent of thedisease, s
uch as a virus or other microorganism.

6. OBLECTIVES OF THECHEMOTHERAPY
• *The main objective in treating patients with
chemotherapy is
• to maximize the death of malignant tumor
cells.
• * To cure the client with cancer.
• * To control the tumor growth when cure is not
possible.
• *To extend the lifespan and improve the quality
of life of client with cancer.

7. HOW CHEMOTHERAPY WORKS
• it is helpful to understand the normal
life cycle of a cell, or the cell cycle.
• All living tissue is made up of cells.
Cells grow and reproduce to replace
cells lost through injury or normal
“wear and tear.”

8. • The cell cycle is a series of steps that both
normal cells and cancer cells go through
in order to form new cells.
• This discussion is somewhat technical, but
it can help you understand how doctors
predict which drugs are likely to work well
together and how doctors decide how
often doses of each drug should be given

9. • The cell cycle has 5 phases which are
labeled below using letters and numbers.
Since cell reproduction happens over and
over, the cell cycle is shown as a circle. All
the steps lead back to the resting phase
(G0), which is the starting point.
• After a cell reproduces, the 2 new cells
are identical. Each of the 2 cells made
from the first cell can go through this cell
cycle again when new cells are needed.

11. • The Cell Cycle
• G0 phase (resting stage): The cell has
not yet started to divide. Cells spend much
of their lives in this phase. Depending on
the type of cell, G0 can last from a few
hours to a few years. When the cell gets a
signal to reproduce, it moves into the G1
phase.
• G1 phase: During this phase, the cell
starts making more proteins and growing
larger, so the new cells will be of normal
size. This phase lasts about 18 to 30

12. • S phase: In the S phase, the
chromosomes containing the genetic
code (DNA) are copied so that both of
the new cells formed will have
matching strands of DNA. The S
phase lasts about 18 to 20 hours.
• G2 phase: In the G2 phase, the cell
checks the DNA and gets ready to
start splitting into 2 cells. This phase
lasts from 2 to 10 hours

13. • M phase (mitosis): In this phase,
which lasts only 30 to 60 minutes, the
cell actually splits into 2 new cells.
• This cell cycle is important because
many chemotherapy drugs work only
on cells that are actively reproducing
(not cells that are in the resting phase,
G0). Some drugs specifically attack
cells in a particular phase of the cell
cycle (the M or S phases, for
example.

14. CHEMOTHERAPY DRUGS

15. • Chemotherapy drugs act
through a variety of
mechanism but, essentially,
kill cells by:
• Limiting DNA synthesis and
expression- By interfering
with synthesis of buiding
blocks for nucleic acid.

16. • Cross- linking polymer
DNA-Damaging the DNA
template and cross-link
the twostands of the
double helix , preventing
replication.

17. • DNA double stand breaks- Bind
selectively with DNA, producing
complexes that block DNA
replication andformation of DNA
dependent RNA.
• Preventing formation of mitotic
apparatus- Prevent chromosome
segregation at mitosisby producing
metaphase arrest.

18. CLASSIFICATION OF CHEMOTHERAAPY
• Chemotherapeutics agents are broadly
classified as:
• Cell cycle-specific Drugs: Those
chemotherapeutic agents that destroy
cells in specific phases of the cell cycle .
Most affect cells in the S-phase by
interfering with DNA and RNA synthesis.

19. • Cell cyle non specific Drugs:
• Those chemotherapeutic
agents that act independently
of the cell cycle phase are
termed cell cycle non- specific
drugs. These drugs usually
have a prolonged effect on cell
, leading to cellular damage or
death.

20. • Chemotherapeutic agents
also classifiedaccording
tovarious chemical groups
eachwith a different
mechanism of action. These
include

21. 1-Alkylating agents-
• Alkylating agents are so named
because of their ability to alkylate
many nucleophilic functional groups
under conditions present in cells.
They impair cell function by forming
covalent bonds with the amino,
carboxyl, sulfhydryl, and phosphate
groups in biologically important
molecules.
• Cisplatin and carboplatin, as well
as oxaliplatin, is alkylating agents.

22. Polyfunctional Alkylating Drugs:
Mechanism of Action
• Alkyl group transfer
–Major interaction: Alkylation of
DNA
• Primary DNA alkylation site:
N7 position of guanine
• interaction may involve single
strands or both strands .

23. –Other interactions: these
drugs react with carboxyl,
sulfhydryl, amino, hydroxyl,
and phosphate groups of
other cellular constituents
–These drugs usually form a
reactive intermediate –
ethylene ammonium ion.

24. • Polyfunctional Alkylating
Drug Resistance
-Increased ability to repair
DNA defects
-Decreased cellular
permeability to the drug
-Increased glutathione
synthesis

25. • Injection site damage (vesicant
effects) and systemic toxicity.
• Toxicity:
– dose related
– primarily affecting rapidly dividing
cells
• bone marrow
• GI tract
–nausea and vomiting within less
than an hour-- with
mechlorethamine, carmustine
(BCNU) or cyclophosphamide

26. –Emetic effects: CNS
»reduced by pre-
treatment with
phenothiazines or
cannabinoids.
•gonads

27. – Major Toxicity: bone marrow suppression
• dose-related suppression of myelopoiesis:
primary effects on
–megakaryocytes
–platelets
–granulocytes
• Bone marrow suppression is worse when
alkylating agents are combined with other
myelosuppressive drugs and/or radiation (dose
reduction required)

28. • Oral Route of
Administration:cycloph
osphamide (Cytoxan),
melphalan (Alkeran),
chlorambucil
(Leukeran), busulfan
(Myleran), lomustine
(CCNU,CeeNU)

29. • Nitrosoureas:
– not cross reactive ( with
respect to tumor resistance)
with other alkylating drugs.
–Nonenzymatic by
transformation required to
activate compounds.
–Highly lipid- soluble-- crosses
the blood-brain barrier (BBB)

30. • useful in treating brain tumors
–Act by cross-linking: DNA
alkylation
–More effective against cells in
plateau phase than cells in
exponential growth phase
–Major route of
elimination:urinary excretion
–Steptozocin:
• sugar-containing nitrosourea

31. Other Alkylating Drugs
• Procarbazine (Matulane)
– Methylhydrazine derivative
– Active in Hodgkin's disease
(combination therapy)
– Teratogenic, mutagenic,
leukemogenic.
– Side effects:
• nausea, vomiting,
myelosuppression
• hemolytic anemia
• pulmonary effects

32. • Dacarbazine (DTIC)
–Clinical use:
• Melanoma
• Hodgkin's disease
• soft tissue sarcoma
–Synthetic drug; requires
activation by liver
microsomal system.
• Parenteral administration

33. – Side effects:
• nausea, vomiting, myelosuppression
• Altretamine (Hexalen)
– Clinical use:
• alkylating agent-resistant: ovarian
carcinoma
– Activated by biotransformation
(demethylation)
– Side effects:
• nausea, vomiting, central and
peripheral nervous system
neuropathies.
• relatively mild myelosuppressive
effects.

34. • Cisplatin (Platinol)
– Clinical use:
• Genitourinary cancers
–testicular
–ovarian
–bladder
• In combination with bleomycin
and vinblastine: curative
treatment for
nonseminomatous testicular
cancer

35. Alkylating Agent Toxicity: Summary
• IV mechlorethamine,
cyclophosphamide, carmustine:
Nausea and Vomiting (common)
• Oral cyclophosphamide: Nausea
and Vomiting (less frequently)
• Most Important Toxic Effect:Bone
marrow suppression, leukopenia,
thrombocytopenia

36. –secondary to
myelosuppression --
• severe infection
• septicemia
–hemorrhage
• Cyclophosphamide
(Cytoxan):alopecia,
hemorrhagic cystitis (may be
avoided by adequate
hydration)

37. 2- Anti-metabolites –
• Anti-metabolites masquerade
as purines ((azathioprine, mercaptopurine))
or pyrimidines—which become the building
blocks of DNA. They prevent these substances
from becoming incorporated in to DNA during
the "S" phase (of the cell cycle), stopping normal
development and division. They also affect RNA
synthesis. Due to their efficiency, these drugs are
the most widely used cytostatics

38. -Tumor resistance to methotrexate:
• decreased drug transport into the
cell
• altered dihydrofolate reductase
enzyme -- lower affinity for
methotrexate
• decreased polyglutamate
formation
• quantitative increase in
dihydrofolate reductase enzyme
concentration in the cell (gene
amplification, increased message)

39. – Adverse effects:
• Bone marrow suppression
• Dermatologic
• GI mucosa
• Adverse effects reversed by
leucovorin (citrovorum factor)
–Leucovorin "rescue" may be used
in cases of over dosage or in high-
dose methotrexate protocols
– Other uses:
• Treatment of rheumatoid arthritis
• In combination with a prostaglandin:
induces abortion

40. • Purine Antagonists
– 6-Thiopurines (Mercaptopurine [6-MP];
Thioguanine [6-TG])
– Mercaptopurine (Purinethol)
• Mechanism of Action:Activation by
hypoxanthine-guanine phosphoribosyl
transferase (HGPRT) to form 6-thioinosinic
acid which inhibits enzymes involved in purine
metabolism. (thioguanylic acid and 6-
methylmercaptopurine ribotide (MMPR) also
active)
• Clinical Use:
– childhood acute leukemia
– the analog, azathioprine (Imuran)--
immunosuppressive agent.

41. – Thioguanine
• purine nucleotide pathway enzyme-inhibitor
– decreased intracellular concentration of
guanine nucleotides
– inhibition of glycoprotein synthesis
– Mechanism of Action: inhibits DNA/RNA
synthesis
• Clinical Use:
– Synergistic with cytarabine in
treating adult acute leukemia.
– Drug resistance
• Decreased HGPRT activity
• In acute leukemia -- increased alkaline
phosphatase, which dephosphorylates
thiopurines nucleotides

42. – Adverse Effects:
• Both mercaptopurine and thioguanine,
given orally, are excreted in the urine.
– 6-MP is converted to an inactive
metabolite, 6-thioruric acid, by xanthine
oxidase .6-TG: requires deamination
before metabolism by xanthine oxidase.
– In cancer (hematologic) chemotherapy,
allopurinol is used to inhibit xanthine
oxidase, to prevent hyperuricemia
associated with tumor cell lysis
{xanthine oxidase inhibition blocks
purine degradation -- purines (more
soluble) are excreted instead of uric
acid (less soluble)}

43. use of allopurinol thus
blocks acute gout and
nephrotoxicity.
However, the combination
of allopurinol and 6-
mercaptopurine, because
of xanthine oxidase
inhibition, can lead to
mercaptopurine toxicity;
This interaction does not
occur with 6-TG.

44. -Fludarabine phosphate
• parenteral administration;
renal excretion
• dephosphorylated to active
form:
• Mechanism of Action:DNA
synthesis inhibition
• Clinical Use:
–lymphoproliferative disease
• Adverse Effect:dose-limiting --
myelosuppression.

45. – Cladribine: (Leustatin)
• phosphorylated by deoxycytidine
kinase
–incorporated into DNA
–Mechanism of Action: increased
strand breaks (inhibition of
repair mechanisms)
• Clinical Use:
–Hairy cell leukemia
• Adverse Effects:
–Transient severe
myelosuppression; possibly
associated with infection.

46. – Pentostatin:
• irreversible inhibitor adenosine deaminase
– results in toxic accumulation of
deoxyadenosine nucleotides (especially in
lymphocytes)
• Adverse Effects:
– immunosuppression (T cell mediated
immunity)
– myelosuppression
– kidney function impairment
– CNS toxicity
– liver toxicity
• Pyrimidine Antagonists:
– Flurouracil (5-FU), normally given by IV
administration (oral absorption erratic)

47. • Biotransformed to ribosyl- and deoxyribosyl-
derivatives.
– Mechanism of Action:
» One derivative, 5-fluoro-2'-deoxyuridine 5'-
phosphate (FdUMP), inhibits thymidylate
synthase and its cofactor,a tetrahydrofolate
derivative, resulting in inhibition of
thymidine nucleotide synthesis.
» Another derivative, 5-fluorouridine
triphosphate is incorporated into RNA,
interfering with RNA function.
» Cytotoxicity:effects on both RNA and DNA
• Clinical Use: Systemically -- adenocarcinomas;
Topically: skin cancer
• Floxuridine (FUDR): similar to 5-FU, used for
hepatic artery infusion.
•

48. • Major Toxicity: myelosuppression, mucositis
– Cytarabine (ara-C) IV administration
• Mechanism of Action:S phase-specific antimetabolite
– Biotransformed to active forms: ara-CTP, competitive inhibitor of DNA
polymerase.
» Blocks DNA synthesis; no effect on RNA or protein synthesis
– cytarabine incorporated into RNA and DNA -- interfering with chain
elongation

49. • Clearance: deamination (inactive
form)
• S phase specificity: highly
schedule-dependent
• Clinical Use: almost exclusively for
acute myelogenous leukemia
• Adverse Effects:
–nausea
–alopecia
–stomatitis
– severe myelosuppression

50. – Azacitidine (IV administration):
• Mechanism of Action: active
derivatives inhibit orotidylate
decarboxylase -- reducing
pyrimidine nucleotide synthesis;
azacitidine -- incorporated into DNA
and RNA; inhibits DNA, RNA, and
protein synthesis.
• Investigational drug -- second-line
agent in treatment of acute
leukemia
• Adverse Effect: myelosuppression.

51. 3- Plant alkaloids and terpenoids .
• hese alkaloids are derived from plants and
block cell division by
preventing microtubule function.
Microtubules are vital for cell division, and,
without them, cell division cannot occur. The
main examples are vinca
alkaloids and taxanes.

52. • Vinblastine -- (Velban)
– Mechanism of action: microtubule depolymerization
• Mitotic arrest at metaphase; interferes with chromosome
segregation
– Clinical Use::
• Systemic treatment of Hodgkin's disease
• Lymphomas
– Adverse Effects:
• nausea
• vomiting
• alopecia
• bone marrow suppression

53. • Vincristine -- (Oncovin)
– Mechanism of action: microtubule depolymerization
• Mitotic arrest at metaphase; interferes with chromosome
segregation
– Clinical Use::
• In combination with prednisone: induction of remission in
children with acute leukemia
• useful in treating some other rapidly proliferating neoplasms
– Adverse Effects:
• significant frequency of neurotoxic reactions
• occasional: bone marrow depression

54. • Podophyllotoxins (etoposide {VP-
16}and teniposide {VM-26})
– Etoposide and teniposide:
structurally similar
–Mechanism of action: Block cell
cycle: in late S-G2 phase
• inhibition of topoisomerase II --
DNA damage
–IV administration
–Urinary excretion; some in bile

55. – Clinical Use:
• Etoposide (VP-16,VePe-sid):
–monocytic leukemia
–testicular cancer
–oat cell lung carcinoma
• Teniposide (Vumon): lymphomas
– Adverse Effects:
• nausea
• vomiting
• alopecia
• significant hematopoietic
toxicity and lymphoid toxicity

56. • Camptothecins (topotecan and irinotecan )
– Mechanism of action: interfere with
activity of topoisomerase I (cuts and
religates single stranded DNA. DNA is
damaged
– Clinical Uses:
• Topotecan: metastatic ovarian cancer --
including cisplatin-resistant forms (as
effective as paclitaxel)
• Adverse Effects: Topotecan --
–Primary
»neutropenia
»thrombocytopenia
»anemia

57. –Other
»nausea
»nominee
»alopecia
• Irinotecan:prodrug-metabolized active topoisomerase
I inhibitor
–Used in management of colon and rectal cancer,
including tumors not responding to 5-FU
–Adverse Effects: Irinotecan --
»Most common: diarrhea
»also common: nausea, vomiting
• Dose limiting adverse effect: myelosuppression

58. • Taxanes (Paclitaxel (Taxol) and Docetaxel
(Taxotere))
–Paclitaxel (Taxol): derivative of the
Western Yew
–Mitotic spindle inhibitor: enhances
tubulin polymerization
–Clinical Uses:
• Ovarian
• Advanced breast cancer

59. –Dose-limiting Adverse Effects:
•neutropenia
•thrombocytopenia
•peripheral neuropathy
–Docetaxel (Taxotere):Used in
advanced breast cancer
•Adverse Effects:bone marrow
suppression

60. 4- Topoisomerase inhibitors-
• Topoisomerases are enzymes our
cells use to break the DNA bonds
before copying and repair of
breaks after copying.
Topoisomerase inhibitors
interfere with DNA repair causing
the cancer cell to die because
damaged DNA cannot be
translated into proteins, such as
transport and digestive proteins

61. • Topoisomerase inhibitors are cell
cycle specific, that is, they only
kill cells that are in a particular
phase of cell division and
generally do not have any effect
on other cells. Examples of
Topoisomerase inhibitors are
Etoposide and Topotecan.

62. • Topoisomerase inhibitors are agents
designed to interfere with the action
of topoisomerase enzymes (topoisomeras
e I and II), which are enzymes that control
the changes
in DNA structureby catalyzing the
breaking and rejoining of
the phosphodiester backbone of DNA
strands during the normal cell cycle.

63. • In recent years, topoisomerases have
become popular targets
for cancer chemotherapy treatments.
It is thought that topoisomerase
inhibitors block the ligation step of
the cell cycle, generating single and
double stranded breaks that harm
the integrity of the genome.
Introduction of these breaks
subsequently lead to apoptosis and
cell death.

64. • Classification
• Topoisomerase inhibitors are
often divided according to which
type of enzyme it inhibits.
• Topoisomerase
I inhibitors: irinotecan, topotecan,
camptothecin and lamellarin D all
target type IB topoisomerases,

65. • Topoisomerase
II inhibitors: etoposide (VP-
16), teniposide, doxorubicin, d
aunorubicin, mitoxantrone, am
sacrine, ellipticines, aurintricar
boxylic acid, and HU-331, a
quinolone synthesized
from cannabidiol.

66. • Numerous plant derived natural
phenols (ex. EGCG, genistein, querc
etin, resveratrol) possess strong
topoisomerase inhibitory
properties affecting both types of
enzymes. They may express
function of phytoalexins -
compounds produced by plants to
combat vermin and pests.

67. • Use of topoisomerase inhibitors for
antineoplastic treatments may lead
to secondary neoplasms because of DNA
damaging properties of the compounds. Also
plant derived polyphenols shows signs of
carcinogenity, especially in feuses and
neonates who do not detoxify the compounds
sufficiently.An association between high
intake of tea (containing polyphenols) during
pregnancy and elevated risk of childhood
malignant central nervous system (CNS)
tumours has been found.

68. 5- Cytotoxic antibiotics-
• It is bind directly toDNA , thusinhibite
the synthesis of DNA and interfering
with transcpition of RNA.
• actinomycin ,anthracyclines,doxorubi
cin
• Daunorubicin,valrubicin ,epirubicin
are example of antibiotics.

69. Anticancer Drugs: Antibiotics
• Clinically useful anticancer
antibiotics: derived from
Streptomyces
• These antibiotics act by:
– DNA intercalation, blocking synthesis of
DNA and RNA
• Anthracyclines: Doxorubicin
(Adriamycin, Rubex, Doxil) and
Daunorubicin (DaunoXome)
– IV administration; hepatic metabolism;
biliary excretion; some urinary excretion;
enterohepatic recirculation.

70. • Among the most useful anticancer
antibiotics
– Mechanism of action:
• DNA intercalation -- blocking synthesis
of DNA and RNA; DNA strands scission -
- by affecting topoisomerase II
• Altering membrane fluidity and ion
transport
• Semiquinone free radical an oxygen
radical generation (may be responsible
for myocardial damage)

71. – Doxorubicin (Adriamycin, Rubex, Doxil)--
very important anticancer agent --
• Carcinomas-Doxorubicin
• breast carcinoma
• ovarian carcinoma
• thyroid carcinoma
• endometrial carcinoma
• testicular carcinoma
• lung carcinoma
• Sarcomas-Doxorubicin
• Ewing's sarcoma
• osteosarcoma
• rhabdomyosarcomas
•

72. • Hematologic Cancers-Doxorubicin
• acute leukemia
• multiple myeloma
• Hodgkin's disease
• non-Hodgkin's lymphoma
• Adjuvant therapy in: osteogenic sarcoma and breast
cancer
• Generally used in combination protocols with:
– cyclophosphamide (Cytoxan)
– cisplatin (Platinol)
– nitrosoureas

73. • Major Use: Acute Leukemia
• Daunorubicin: limited utility-- limited efficacy in
treating solid tumors.
• Idarubicin: approved for acute myeloid leukemia
– Idarubicin in combination with cytarabine: more active
than daunorubicin in inducing complete remission in
acute myelogenous leukemia.
• Adverse Effects:
– Bone marrow depression (short duration)
– Cumulative, dose-related, possibly irreversible
cardiotoxicity.
– Total, severe alopecia

74. • Dactinomycin (Cosmegen)
– IV administration; 50 percent remains
unmetabolized.
– Mechanism of action: intercalation
between guanine-cytosine base pairs
• inhibits DNA-dependent RNA synthesis
• blocks protein synthesis
– Clinical Uses:
• dactinomycin in combination with
vincristine (Oncovin)and surgery (may
include radiotherapy) in treatment of
Wilms' tumor
• dactinomycin with methotrexate:
maybe curative for localized or
disseminated gestational
choriocarcinoma.

75. Adverse Effects:
Major dose limiting toxicity: bone
marrow suppression (all blood elements
affected -- particularly platelets and
leukocytes)
occasional severe thrombocytopenia
nausea
vomiting
diarrhea
oral ulcers
Dactinomycin: immunosuppressive
(patient should not receive live virus
vaccines)
alopecia/skin abnormalities
interaction with radiation ("radiation
recall")

76. • Plicamycin (Mithramycin)
• Mechanism of action:binds to DNA --
interrupts DNA-directed RNA synthesis
–Also decreases plasma calcium
(independent tumor cell action;acts on
osteoclasts)
• Clinical Uses:
–some efficacy in testicular cancer that is
unresponsive to standard treatment:
–especially useful in managing severe
hypercalcemia associated with cancer

77. • Adverse Effects:
–nausea
–vomiting
–thrombocytopenia
–leukopenia
–hypocalcemia
–liver toxicity
–bleeding disorders

78. • Mitomycin: (Mutamycin)
– Mechanism of action:
• metabolic activation to produce a DNA
alkylating agent.
• Solid tumor hypoxic stem cells may be more
sensitive to the action of mitomycin.
• Best available drug, in combination with x-rays,
to kill hypoxic tumor cells.
– Clinical Use:
• in combination chemotherapy {with vincristine
and bleomycin}: squamous sell carcinoma of
the cervix

79. • adenocarcinoma of the stomach, pancreas, and lung
{along with flurouracil and doxorubicin}
• second-line drug: metastatic colon cancer
• topical intravesical treatment of small bladder
papillomas.
– Adverse Effects:
• severe myelosuppression, especially after repeated
doses, suggest action on hematopoietic stem cells.
• Vomiting
• anorexia
• occasional nephrotoxicity
• occasional interstitial pneumonitis

80. • Bleomycin (Blenoxane)
• Mechanism of Action:binds to DNA --
produces single- and double-strand
breaks (free radical formation)
– Cell cycle specific: arrests division in G2
– Synergistic effects with vinblastine and
cisplatin (curative protocol for testicular
cancer)
• Clinical Uses:
– Testicular cancer
– Squamous cell carcinoma: head, neck,
cervix, skin, penis, and rectum

81. –combination treatment: lymphoma
–intracavity treatment: malignant effusions
in ovarian breast cancer
• Adverse Effects:
–Anaphylactoid reaction (potentially fatal)
–Fever
–anorexia, blistering, hyperkeratosis (palms)
–pulmonary fibrosis (uncommon)
• No significant myelosuppression

82. 6-Nitrosourceas-
•It is like alkylating
agents,break DNA
helix.

83. • Structural Features
• Nitrosourea
• Mechanism of Action
• Hydrolysis of Nitrosourea group produces two
active species
• Alkylating Agents with Nitro group provides
crosslinking in DNA for Chemotherapy
• Carbamoylating agent O=C=N-R causing toxic
effects of blocking DNA Polymerase and DNA
Repair enzymes by binding to nucleophilic sites on
proteins

84. • Toxicity
• Carbamoylating agent
• Carcinogenic
• Mutanogenic
• Infertility
• Bone marrow depression

85. Agent Structure Details
Indications
Brain Tumor
Hodgkins
Lymphoma
Side Effects
Lomustine
Delayed
Myelosuppressi
on
Pulmonary
Toxicity

86. Indications
Pancreatic
Cancer (Beta Cells)
Side Effects
GLUT-2 Transporter
Substrate, leading to
Streptozocin lower
levels of Insulin and a
form of Type
II Diabetes
Renal Toxicity
Drug interactions
Doxorubicin
Not a GLUT-2
Ethylchloride
Transporter Substrate
Chlorozotocin instead of methyl on
Otherwise Per
nitrosourea
Streptozocin

87. 7-Mitotic inhibitors-
• Anti microtubule agent
that interefere with mitosis
act during the late G2 phse
and mitosis to stabilize
microtubules, thus
inhibiting cell division

88. Use of mitotic inhibitors in
cytogenetics
• Cytogenetics, the study
of chromosomal material by analysis
of G-Banded chromosomes, uses
mitotic inhibitors extensively. In order
to prepare a slide for cytogenetic
study, a mitotic inhibitor is added to
the cells being studied.

89. • Specific agents
• Taxanes
• Taxanes are complex terpenes produced by the
plants of the genus Taxus (yews). Originally derived
from the Pacific yew tree, they are now synthesized
artificially. Their principal mechanism is the
disruption of the cell's microtubule function by
stabilizing microtubule formation. Microtubules are
essential to mitotic reproduction, so through the
inactivation of the microtubule function of a cell,
taxanes inhibit the cell's division.

90. • Paclitaxel—used to
treat lung
cancer, ovarian
cancer, breast cancer,
and advanced forms
of Kaposi's sarcoma. [5]
• Docetaxel—used to treat
breast, ovarian, and non-
small cell lung cancer

91. • Vinca alkaloids
• Vinca
alkaloids are amines produced
by the hallucinogenic
plant Catharanthus
roseus (Madagascar
Periwinkle). Vinca alkaloids
inhibit microtubulepolymerizat
ion, thereby inhibiting mitosis.

92. • Vinblastine—used to treat leukaemia, Hodgkin's
lymphoma, non-small cell lung cancer, breast
cancer and testicular cancer. It is also a component
in a large number of chemotherapy regimens.[8]
• Vincristine—used to treat lymphoma, breast cancer,
lung cancer, and acute lymphoblastic leukemia.[8]
• Vindesine—used to treat leukaemia,
lymphoma, melanoma, breast cancer, and lung
cancer.[8]
• Vinorelbine—used to treat breast cancer and non-
small-cell lung cancer

93. • Colchicine
• Colchicine is an alkaloid derived
from the autumn crocus
(Colchicum autumnale). It inhibits
mitosis by inhibiting microtubule
polymerization. While colchicine is
not used to treat cancer in
humans, it is commonly used to
treat acute attacks of gout

94. • Podophyllotoxin
• Podophyllotoxin and Podophyllin,
derived from the may apple plant, are
used to treat viral skin infections.
• Griseofulvin
• Griseofulvin, derived from a
Penicillium mold, is an antifungal
drug.

95. • A mitotic inhibitor is a drug that
inhibits mitosis, or cell division. These
drugs disrupt microtubules, which are
structures that pull the cell apart when it
divides. Mitotic inhibitors are used
in cancer treatment, because cancer cells
are able to grow and eventually spread
through the body (metastasize) through
continuous mitotic division and so are
more sensitive to inhibition of mitosis
than normal cells

96. 8-Corticosteroids-
• Discrupt the cell membrain
and inhibit synthesis of
protein,decrease circulting
lymphocytes, inhibit
mitosis.

97. • Discrupt the cell membrain and
inhibit synthesis of protein,decrease
circulting lymphocytes, inhibit
mitosis.
• Pharmacologic doses of steroid
inhibited growth of various tumor
systems. Tissue culture studies
confirmed that lymphoid cells were
the most sensitive to glucocorticoids,
and responded to treatment with

98. • ribonucleic acid (RNA), and protein
synthesis. Studies of proliferating human
leukemic lymphoblasts supported the
hypothesis that glucocorticoids have
preferential lymphocytolytic effects. The
mechanism of action was initially thought
to be caused by impaired energy use via
decreased glucose transport and/or
phosphorylation; it was later discovered
that glucocorticoids induce apoptosis, or
programmed cell death, in certain

99. • Corticosteroids can be used to kill
lymphoma, leukemia and multiple
myeloma cells and may also be used
to ease the side effects of other
chemotherapy drugs. In addition to
their chemotherapy action,
corticosteroids also help reduce
nausea, vomiting and allergic
reactions caused by cancer treatment

100. 9-Hormone therapy-
•Selectively attach to
estrogen receptors,
cuasing downregulation
of them and inhibiting
tumor growth

101. Anticancer Agents: Hormones
• Introduction
• Breast and prostatic cancer: palliation with sex
hormone therapy
• Adrenal corticosteroid treatment-- useful in:
– acute leukemia
– myeloma
– lymphomas
– other hematologic cancers

102. • Pharmacological effects:
–Steroid hormones bind to steroid
receptors:
–Efficacy of steroid treatment depends
on specific receptor presence on
malignant cell surface.
• Clinical Use:Treatment of:
–female and male breast cancer
–prostatic cancer
–endometrial cancer of uterus

103. • Adverse Effects:
–Fluid retention (secondary to Na-retaining
properties)
–Androgens-masculinization (long-term use)
–Estrogens-feminization (long-term use)
–Adrenocortical steroids:
• hypertension
• diabetes
• enhanced susceptibility to infection
• cushingoid appearance

104. • Estrogen and Androgen Inhibitors:
(Tamoxifen and Flutamide)
• Tamoxifen: Breast cancer treatment
–Oral administration.
–Activity against progesterone-
resistant endometrial neoplasm
–Chemopreventive:women -- high-
risk for breast cancer

105. – Mechanism of Action:
• Competitive partial agonist-inhibitor of
estrogen
• Binds to estrogen-sensitive tissues (receptors
present)
• Best antiestrogen effect requires minimal
endogenous estrogen presence {estradiol has a
much higher affinity for the estrogen receptor
than tamoxifen's affinity for the estrogen
receptor}
• Suppresses serum levels of insulin-like growth
factor-1; and up-regulates local TGF-beta
production. These properties may explain

106. – Adverse Effects:
• Generally mild
• Most frequent: hot flashes
• Occasionally: fluid retention, nausea
– Clinical Use:
• Advanced breast cancer
– Most likely to be effective if:
» lack endogenous estrogens
{oophorectomy; postmenopausal}
» Presence of cytoplasmic estrogen
receptor;presence of cytoplasmic
progesterone receptorColeman
• Prolongs survival {surgical adjuvant therapy}
in postmenopausal women with estrogen
receptor-positive breast cancer.

107. • Flutamide (Eulexin): prostatic cancer
–Antagonizes remaining androgenic
effects after orchiectomy or leuprolide
treatment
• Gonadotropin-Releasing Hormone
Agonists (Leuprolide and Goserelin
(Zoladex))
• Leuprolide and goserelin: synthetic
peptide analogues of gonadotropin-
releasing hormone (GnRH, LHRH)

108. – Mechanism of Action: Analogues more potent --
behave as GnRH agonists.
• pituitary effects: when given continuously -- initial
stimulation then inhibition of follicle-stimulating hormone
and leutinizing hormone.
• Clinical Use: treating metastatic prostate
carcinoma
• Comparing leuprolide with diethylstilbestrol
(DES):
– Similar suppression of androgens synthesis and
serum prostatic acid phosphatase .

109. – Adverse Effects: Leuprolide less frequently
causes:
• nausea
• vomiting
• edema
• thromboembolism
• painful gynecomastia
–Leuprolide and goserelin: medication more
costly, the more cost-effective given
reduced frequency of complications.

110. • Aromatase Inhibitors (Aminoglutethimide
and Anastrozole (Arimidex))
• Aminoglutethimide:
–Mechanisms of action: Reduction in
estrogen concentration
• Aminoglutethimide: inhibitor of
adrenal steroid synthesis ( blocks
conversion of cholesterol to
pregnenolone {first-step})

111. • Aminoglutethimide inhibits extra-adrenal
estradiol and estrone synthesis.
• Aminoglutethimide inhibits an aromatase
enzyme {catalyzes conversion of
androstenedione to estrone}
–This conversion may occur in fat.
– Clinical Use:
• Metastatic breast cancer (tumors contain
estrogen or progesterone receptors)
–Aminoglutethimide is administered with
adrenalreplacement doses of
hydrocortisone to ensure avoidance of
adrenal insufficiency.

112. » Hydrocortisone is used in preference to
dexamethasone, because dexamethasone
increases the degradation of aminoglutethimide.
• Aminoglutethimide in combination with
hydrocortisone: Second-Line Therapy for women
treated with tamoxifen (aminoglutethimide causes
more adverse side effects than tamoxifen)
• Anastrozole (Arimidex): new, selective,
nonsteroidal aromatase inhibitor.
– appears to have no effect on glucocorticoid
or mineralocorticoid synthesis
– Clinical Use:
• Treatment of advanced estrogen-or
progesterone-receptor positive non--
tamoxifen responsive breast cancer

113. 10-Miscellneous-
• Inhibite the protein synthesis,
enzymes derived from the yeast
Enwinia used to deplete the
supply of asparagines for leukemic
cells that are dependent on
exogenous source of this amino
acid

114. Miscellaneous Anticancer Drugs
• Amsacrine:
– Hepatic metabolism
– Mechanism of Action:
• DNA intercalation: produces single-and double-strand breaks
• interaction with topoisomerase II-DNA complexes
– Clinical Uses:
• Anthracyclines- and cytarabine-resistant acute myelogenous
leukemia
• Advanced ovarian cancer
• Lymphomas

115. – Adverse Effects:
• Does-limiting hepatic toxicity
• Cardiac arrest has been noted with amsacrine infusion
• Asparaginase (El-spar):
– Mechanism of action: depletion of serum asparagine
{forming aspartic acid and ammonia}
• Decreased blood levels of asparagine and glutamine inhibit
protein synthesis in those neoplastic cells that express
decreased levels of asparagine synthase.
• Most normal cells express sufficient levels of asparagine
synthase to avoid toxicity.

116. • Hydroxyurea:
– Mechanism of action:
• Inhibits ribonucleotide reductase; depletes
deoxyribonucleoside triphosphate pools
• Acts at S phase.
– Clinical Uses:
• Melanoma [secondary role]
• Chronic myelogenous leukemia [secondary role]
– Adverse Effects:
• Bone marrow suppression
• nausea
• vomiting
• diarrhea

117. • Mitoxantrone (Novantrone):
– Mechanism of action:
• Induces DNA strand breaks
• Inhibits RNA and DNA synthesis
– Clinical Uses:
• Refractory acute leukemia
• Pediatric and adult acute myelogenous leukemia
• non-Hodgkin's lymphoma's
• breast cancer
– Adverse Effects:
• Dose-limiting: leukopenia
• mild nausea
• vomiting
• stomatitis
• alopecia
• some cardiotoxicity {arrhythmias}

118. • Mitotane (Lysodren):
– Clinical Use:Single indication-- adrenal
carcinoma
• Reduces excessive steroid secretion
– Adverse Effects:
• diarrhea
• mental depression
• skin eruption
• anorexia
• nausea
• somnolence
• dermatitis

119. • Retinoic acid Derivatives:
– Clinical Uses:
• Remissions -- acute promyelocytic
leukemia
• 13-cis-Retinoic acid:
chemopreventive -- second primary
tumors in patients with hand and
neck squamous cell carcinoma.
– Adverse Effects:
• skeletal effects
• hepatic effects
• teratogenic effects
• mucocutaneous effects

120. • Bone Marrow Growth Factors (sargramostim
and filgrastim):
–Reduces neutropenic sepsis and other
complications of chemotherapy
–Filgrastim shortens neutropenic state
following induction chemotherapy for acute
nonlymphocytic leukemia.
• Amifostine
• Cytoprotective from effects of chemotherapy

121. CONCEPT IN CHEMOTHERAPY
• ADJUVANT CHEMOTHERAPY-
• Adjuvant chemotherapy is the utilization of
antineoplastics agents in additionto surgery
orradiotherapy. The rationale is to destroy cancer
cells left behind in the operative field or
disseminated through the blood stream to
metastaticlocation.

122. • NEOADJUVANT CHEMOTHERAPY
• It refers to the initial use of chemotherapy to
reduce the bulk and lower the stage of atumor,
making it amenable to cure with subsequent
localtherapy.
• COMBINATION CHEMOTHERAPY
• It refers to the use of cytotoxic drugs in
combination. It isconsistently superior to single
agent therapy.

123. ADMINISTRATION OF
CHEMOTHERAPY
• Depending on clinical setting , chemotherapy may
be administered by the physician,staffnurse or
specialized team ember,such as the oncology
clinical nurse specialist or intravenous therapist.

124. ROUTE OF ADMINISTRATION
• 1-Oral
• This rout is normally used for cyclophosphamide,
capecitabine drugs.
• 2-Intramuscular
• This rout is normally used for Bleomycin drug.
• 3-Intravenous-
• This rout is normally used for Daxarubicine,
vincristine,cisplatin, 5-fu drugs.

125. • 4- Intracavitary(pleural,peritoneal) –
• This rout is normally used for radioisotopes ,
alklying agents, methotrexate.
• 5-Intrathecal
• For mithotraxate and cytarabine.
• 6-Intraartical-
• For DTIC,5-fu, Methotraxate.
• 7-Perfusion
• For alkylating agents

126. • 8-Continuous infusion-
• For 5-fu,methotraxate and cytarabine.
• 9-Subcutaneous-
• For cytarabine
• 10-Topical
• For 5-fu crem.

127. TOXIC EFFCT OF CHEMOTHERAPY
• Toxicity associated with
chemotherapy can be acue or
chronic. Cell with rapid growth
rates(e.g epithelium, bone marrow,
hair follicles,and sperm) are very
susceptible to damage from these
agents. Varius body system may also
be affected by these drugs

128. GASTROINTESTINAL SYSTEM
• Nausea and voming
• Anorexia
• Taste alteration
• Weight loss
• Oral mucositis
• Diarrhea
• Constipation

129. HEMATOPIETIC SYSTEM
• Leukopenia
• Anemia
• Thrombocytopeniautropenia
• Neutopenia
• Increase risk of infection and
bleeding

130. INTEGUMETARY SYSTEM
• Alopesia
• Skinreaction such as Red
patches(erythema),urticaria,
• hyper pigmentation in the nailbeds,
• mouth or gums or
teeth,Photosensitivity

131. REPRODUCTIVE SYSTEM
• Testicular and ovarian function
impairedso result
Azoospermia,oligospermia and sterility in
male and
• Amenorrhea,menopausal manifestations
and
• sterility in female with increase risk of
abortion and fetal malformation.
• In second and third trimester result low

132. IMMUNE SYSTEM
•Risk for fatal infection
•Stomatitis,enteritis,gingi
vitis and more infection
•Fatique
•Hair loss

133. Damage to specific organs may occur,
with resultant symptoms:
• Cardiotoxicity (heart damage)
• Hepatotoxicity (liver damage)
• Nephrotoxicity (kidney damage)
• Ototoxicity (damage to the inner ear),
producing vertigo
• Encephalopathy (brain dysfunction)

134. Chemotherapy regimens
Example of uses, and other
Name Components
notes
Adriamycin
ABVD (doxorubicin), bleomycin, vin Hodgkin's lymphoma
blastine, dacarbazine
Adriamycin
AC (doxorubicin), cyclophospha Breast cancer
mide
Bleomycin, etoposide,
Adriamycin
(doxorubicin), cyclophospha
BEACOPP Hodgkin's lymphoma
mide, Oncovin
(vincristine), procarbazine,pre
dnisone
Bleomycin, etoposide, Testicular cancer, germ cell
BEP
platinum agent (cisplatin) tumors
Cyclophosphamide,
CA Adriamycin (doxorubicin) Breast cancer
(same as AC)

135. Cyclophosphamide,
Adriamycin
CAF Breast cancer
(doxorubicin), fluorouracil
(5-FU)
Cyclophosphamide,
CAV Adriamycin Lung cancer
(doxorubicin), vincristine
Cyclophosphamide, BCNU
CBV (carmustine), VP-16 Lymphoma
(etoposide)
Chlorambucil, vincristine
(Oncovin), procarbazine, pre
ChlVPP/EVA dnisone, etoposide, vinblasti Hodgkin's lymphoma
ne, Adriamycin
(doxorubicin)
Cyclophosphamide,
hydroxydoxorubicin
CHOP Non-Hodgkin lymphoma
(doxorubicin), vincristine
(Oncovin), prednisone

136. Non-Hodgkin
Cyclophosphamide,
lymphoma in patients
Oncovin
COP or CVP with history
(vincristine), predniso
ofcardiovascular
ne
disease
Cyclophosphamide, met
CMF hotrexate, fluorouracil ( Breast cancer
5-FU)
Cyclophosphamide,
Oncovin Non-Hodgkin
COPP
(vincristine), procarbazi lymphoma
ne, prednisone
Epirubicin, cyclophosph
EC Breast cancer
amide
Gastric
Epirubicin, cisplatin, flu

137. Etoposide, prednisone,
Oncovin, cyclophosph
EPOCH amide, Lymphomas
and hydroxydaunorub
icin
Fluorouracil (5-
FEC FU), epirubicin, cyclop Breast cancer
hosphamide
Fluorouracil (5-FU),
FL (Also known as
leucovorin (folinic Colorectal cancer
Mayo)
acid)
Fluorouracil (5-FU),
FOLFOX leucovorin (folinic Colorectal cancer
acid), oxaliplatin
Fluorouracil (5-FU),

138. High-risk progressive or
ICE-R ICE + rituximab
recurrent lymphomas
Methotrexate, bleomycin,
Adriamycin
m-BACOD (doxorubicin), cyclophospham Non-Hodgkin lymphoma
ide, Oncovin
(vincristine), dexamethasone
Methotrexate, leucovorin
(folinic acid), Adriamycin
(doxorubicin), cyclophosphamid
MACOP-B Non-Hodgkin lymphoma
e, Oncovin
(vincristine),prednisone, bleomy
cin
Mechlorethamine, Oncovin
MOPP (vincristine), procarbazine, pred Hodgkin's lymphoma
nisone
methotrexate, vinblastine, adria
MVAC Advanced bladder cancer[2]
mycin, cisplatin
Procarbazine, CCNU
PCV Brain tumors

139. Prednisone, doxorubicin (a
driamycin), cyclophospha
mide, etoposide, cytarabine
ProMACE-CytaBOM Non-Hodgkin lymphoma
, bleomycin, Oncovin
(vincristine),methotrexate,
leucovorin
Rituximab, fludarabine, cycl B cell non-Hodgkin
R-FCM
ophosphamide, mitoxantrone lymphoma
Doxorubicin, mechlorethami
ne, bleomycin, vinblastine, v
Stanford V Hodgkin's lymphoma
incristine, etoposide, prednis
one
Thal/Dex Thalidomide, dexamethasone Multiple myeloma
Paclitaxel, ifosfamide, Testicular cancer, germ cell
TIP
platinum agent cisplatin tumors in salvage therapy
Vincristine, Actinomycin, Cy
VAC Rhabdomyosarcoma
clophosphamide

140. Vincristine,
Adriamycin
VAD Multiple myeloma
(doxorubicin), dexa
methasone
Hodgkin's
Vincristine and
VAMP lymphoma, leukemi
others
a, multiple myeloma
Vincristine,
Adriamycin
(doxorubicin), predn Hodgkin's
VAPEC-B
isone, etoposide, cyc lymphoma
lophosphamide, bleo
mycin

141. Care of the patient with chemotherapy
• Before care
• During care
• After care

142. RADIOTHERAPY
• introduction
• More than 60% of all clients with
cancer receive radiation therapy
at some point during the course of
their disease Radiation therapy
may be used as a primary,adjuvant
or palliative treatment modality.

143. • RT is the only treatment used and
aims to achieve local cure of the
cancer.
• e.g. early stage Hodkin’s disease,
skincancer and carcinoma of
cervix.

144. HISTORICAL BACKGROUND
• X-rays were discovered in 1885 by the
German physicist,Wilhelm Conrad
Roentgen, alsocalled the father of
diagnostic radiology.
• Parallel to the discovery of X-rays,
Becquerel discovered radioactivity in
1898.
• During the early 1900s,radiobiological
experiments were conducted.

145. TYPES OF RADIATION
• ionizing radiation
• non-ionizing radiation
• Photons (x-rays and gamma
rays),
• Particle radiation

146. METHOD OF RADIATION
• EXTERNAL RADIATION THERAPY
• INTERNAL RADIATION THERAPY
• A-SEALED SOURCE RADIOTHERAPY
• B-UNSEALED SOURCE RADIATION
THERAPY
• MULTI-FIELD THERAPT
• CONFORMAL RADIATION

147. EXTERNAL RADIATIN THERAPY-

148. A-Conformal radiotherapy

149. • Conformal radiotherapy is a common type of
external beam radiotherapy. It is also called
3D conformal radiotherapy (3D CRT).
Conformal radiotherapy uses the same types
of radiotherapy machine as standard beam
external radiotherapy. But the radiotherapists
put metal blocks in the path of the radiation
beam. The blocks change the shape of the
beam so that it ‘conforms’ more closely to the
shape of the tumour.

150. B-Intensity modulated radiotherapy

151. • Intensity modulated radiation therapy
(IMRT) uses hundreds of tiny devices
called collimators to shape the
radiotherapy area. The collimators also
vary the intensity of the beams during
each dose of treatment. The radiotherapy
beams are aimed at the tumour from
different directions. The collimators can
move during treatment so that the
machine gives very precise doses to a
cancer or to specific areas within the

152. C-Image guided radiotherapy

153. • In image guided radiotherapy
(IGRT) CT, MRI, or PET scans
are taken regularly during the
treatment. The scans are
processed by computers to
show changes in the size and
position of the tumour.

154. D-Tomotherapy

155. • Part of the tomotherapy
machine can rotate completely
around the patient to take CT
scans and give radiotherapy to
a very localised area.

156. E-Stereotactic radiotherapy and
radiosurgery

158. • Stereotactic radiotherapy gives
radiotherapy in fewer sessions,
using smaller radiation fields and
higher doses than 3D conformal
radiotherapy. A single treatment
of this type is sometimes called
radiosurgery, Gamma Knife or
Cyberknife

159. F- Proton therapy

160. • One of the newer ways of
giving radiotherapy uses a
different type of radiation
beam called a proton
beam. Protons collect
energy as they slow down
and travel through the
body. They then release
this energy at their target
point – the tumour.

161. G-Electron beam radiotherapy

162. • Electron beams cannot
travel very far through
body tissue. This type of
radiotherapy is used to
treatskin cancers or
tumours very close to the
surface of the body.

163. • External radiation therapy may
help relieve the problems
caused by the tumors.
Treatment may be done to the
following body areas:

164. • Head and neck
• Chest:
• Arms and legs:
• Bones
• Abdomen:
• Pelvic area

165. 2-INTERNAL RADIATION THERAPY

166. • Internal radiotherapy is used mainly to treat
cancers in the head and neck area,
the cervix, womb, prostate or the skin.
• Treatment is given in one of two ways:
• Brachytherapy - putting solid radioactive material
(the source) close to or inside the tumour for a
limited period of time.
• Radioisotope treatment - by using a radioactive
liquid, which is given either as a drink or as an
injection into a vein

167. Brachytherapy

168. Radioisotope therapy

169. A-SEALED SOURCE RADIOTHERAPY

170. • brachytherapy /brachy·ther·a·
py/ (-ther´ah-pe) treatment
with ionizing radiation whose
source is applied to the surface
of the body or within the body
a short distance from the area
being treated

171. • Surface Applicator or "Mould"
brachytherapy.
• Interstitial brachytherapy.
• Intracavitary brachytherapy places
the sources inside a pre-existing
body cavity.

172. .B-UNSEALED SOURCE RADIATION
THERAPY

173. •Unsealed source
radiotherapy relates to
the use of soluble forms
of radioactivesubstances
which are administered to
the body
by injection or ingestion.

174. • 1 Iodine
• 2 Other unsealed
sources
• 3 Experimental antibody
based methods - alpha
emitters

175. Iodine

176. •
• For example, iodine is an element selectively
taken up by the thyroid gland in healthy
people. Thyroid disease (both benign
conditions like thyrotoxicosis and malignant
conditions like papillarythyroid cancer) can be
treated with radioactive iodine (iodine-131)
which is then concentrated into the thyroid.
Iodine-131
produces beta and gamma radiation.

177. Other unsealed sources
Isotope Use Description
131I-MIBG
for the treatment
of phaeochromocytoma andn
(metaiodobenzylguanidine) euroblastoma
the main place of use
of phosphorus is the bone
32P for overactive bone marrow marrow
89Sr 153Sm
for secondary cancer in the strontium and samarium beh
& bones ave just like calcium

178. strontium and
for secondary samarium beh
89Sr cancer in the ave just like
& 153Sm bones calcium
radiosynovecto
my in
90Y the knee joint

179. Experimental antibody based
methods - alpha emitters
• ITU work is being done on
Alpha-Immunotherapy, this
is an experimental method

180. MULTI-FIELD THERAPY
• In the planning of X-ray
therapy the aim is to
deliver a lethal dose to the
lesion without doing
significant harm to healthy
tissue

181. CONFORMAL RADIATION T
• Three-Dimensional Conformal Radiation
Therapy (3D-CRT)
• Tumors are not regular; they
come in different shapes and
sizes. Three-dimensional
conformal radiation therapy, or
3D-CRT,

182. Common side effects of radiation
therapy
• skin problems
• fatigue from lack of sleep;
• Diarrhea
• Nausea and vomiting
• Dry mouth
• Trouble swallowing
• Swelling
• Hair loss
• Sexual problems
• Urinary and bladder changes

183. Site-specific side effects
• Head and neck
• Chest.
• Stomach and abdomen
• Pelvis.

184. Nursing care of the patient
• Before care
• During care
• After care