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staging

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staging Clinico_pathological staging is important for: 1.It gives estimate of prognosis. 2.It is useful in planning of treatment. 3.It is useful in comparison of ... – PowerPoint PPT presentation

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Title: staging


1
staging
  • Clinico_pathological staging is important for
  • 1.It gives estimate of prognosis.
  • 2.It is useful in planning of treatment.
  • 3.It is useful in comparison of outcome from
    different centers.

Histological diagnoses is done by biopsy
Types of biopsies 1.Incisional biopsy removal
of a small portion of a tumour by.. a.
Endoscopic biopsies b. core-needle biopsy by
tru-cut needle. c. fine-needle aspiration
biopsy 2.Excisional biopsy the whole tumour is
removed with the draining lymph node
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TNM staging system
  • T size of primary tumour.
  • N extent of spread to regional L.N.
  • M presence or absence of distant metastases.

Histological grading
It assesses the degree of differentiation a.
well-differentiated (good prognosis) b.
moderately differentiated (bad prognosis) c.
poorly differentiated (worst prognosis)
Screening for cancer
Is the detection of disease in an asymptomatic
population to improve outcomes by early diagnosis
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Criteria for screening
  • The disease a. recognizable at early stage b.
    treatment at early stage is beneficial. C. common
    disease.
  • 2.The test a. sensitive and specific. b.
    acceptable by people. c. safe and inexpensive.
  • 3.The program a. Adequate further diagnostic
    tools. b. beneficial treatment is available. c.
    benefit more than physical and psychological
    harm.
  • E.g.. Breast and colorectal cancer.

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The multi disciplinary team in cancer treatment
  • 1. surgery the main aim of cancer surgery is
    local control of tumour, surgery can be a.
    diagnostic. b. curative. c. palliative. d.
    preventive. e.reconstructive .
  • A. diagnostic surgery , e.g. obtaining tissue for
    diagnosis like in laparoscopy.
  • B. curative surgery removal of the primary
    tumour and as much as possible of the surrounding
    tissue and L.N .
  • C. palliative surgery like in inoperable
    carcinoma of head of pancreas , we anastamose the
    G.B to jejunum to alleviate .obst. Jaundice.
  • D. preventive surgery like in F.A.P. treated by
    pan procto-colectomy .
  • E. reconstructive surgery to restore the
    continuity of G.I.T.

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2.Radiotherapy
  • Is the use of mega voltage x-ray or gamma rays
    which generates energy more than 1.1 million
    volt.
  • Its advantages
  • 1.it can treat deeply seated tumours.
  • 2.it causes minimal skin reaction.
  • 3.absorption of radiation is similar in all
    tissues.

Molecular effects of ionising radiation
ionising radiation interacts with tissue by tow
ways 1.direct action primary ionisation of
macromolecules. 2.indirect action by production
of reactive species from breakdown of water which
then causes damage to macromolecules (moving an
electron from H2O to form H2O this is called
free radical which causes most of the damage to
the DNA. The biological effect of radiation is
enhanced by oxygen which reacts with the free
radical. Radiation dosage is prescribed by Gray
which is the absorption of 1. joule (J) of
energy by one Kg of tissue.
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Radiobiology (the four Rs)
  • 1.Repair after radiation damage there are two
    patterns of repair
  • A. sublethal damage repair (SLD) takes 4-6 hrs
    after afraction of radiotherapy then the cell
    will be repaired . This happens to the normal
    cells.
  • B. potentially lethal damage (PLD) happens after
    4-6 hrs of radiation. Cells will not be repaired
    (killed). This happens to cancer cells.
  • 2.repopulation ,after killing cancer cells by
    radiotherapy in growth fraction this gives
    stimuli to cells inclonogenic fraction to start
    and repopulate tumour , so , tumour will shrink.
  • 3.redistribution cells G2 or M are more
    sensitive to radiotherapy than cells in late S
    phase. This will synchronise the cells.
  • 4.reoxygenation hypoxic cells are
    radio-resistant . So, every time we use
    radiothearpy oxygenated cells are killed. And the
    portion of hypoxic cells becomes oxygenated ,
    this takes 24 hrs.
  • These four factors provides the reason for
    fractionation of radiotherapy.

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Tumour factors determining the success of
radiotherapy
  • 1.radio sensitivity tumours are variable In
    their sensitivity to radiotherapy e.g. seminoma
    and lymphoma are more sensitive than soft tissue
    sarcoma.
  • 2. tumour volume the larger the tumour is the
    higher proportion of cells that are hypoxic or
    anoxic . So more resistant to R.T.
  • 3.the site of the tumour tumours which lie
    adjacent to organs which are easily damaged by
    R.T are difficult to treat.

Complications of R.T
It arises from inevitable damage to normal tissue
adjacent to the tumour . The most sensitive
tissues are 1.bone marrow . 2.gonads.
3.eyes. 4.mucosa of GIT. 5.lungs. 6.kidneys. 7.li
ver.
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Treatment planning
  • Aims
  • 1.maximum required dose is reached to the Tu.
  • 2.minimal dose to nearby organs.
  • To do so, we have to know
  • A. the volume that needs to be treated.
  • B. the required dose to kill the Tu.
  • C. the arrangement of RT. fields

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Volume of Tu.
  • 1.gross Tu. Volume (GTV) is the actual Tu.
    Volume.
  • 2.clinical target volume (CTV) Tu.
    microscopical Tu. Cells around Tu.
  • 3.planning target volume (PTV) is the above
    extra margine to allow for variation in shape and
    position of Tu.
  • 4.treatment volume (TV) is the practical volume
    treated by the machine.
  • 5.irradiated volume is all the above plus small
    margine due to scatter of R.T.

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Dosage of R.T
  • Is the over all dose in Grays divided by the over
    all time of treatment
  • 1.normal fractionation is Five fraction per week
    .
  • 2.hypo fractionation is fewer than four fractions
    per week.
  • 3. hyper fractionation two fractions per day
    ten fractions per week.

Field arrangement
1. single field is used for palliation. 2.parall
el opposed fields is used for head and neck
Tu. 3.multiple field for deeply seated TU. Like
prostate . U. Bladder .
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3.chemotherapy
  • Classification of C.T agents are
  • 1.alkylating agents .e.g. cyclophos phamide and
    melphalan.
  • Action it binds to protein or DNA and inhibit
    their function.
  • (non cycle specific)
  • 2.anti-metabolites , e.g. 5-fluorouracil and
    methotrexate .
  • Action they inhibit DNA synthesis leading to
    cell death. They work through the (S phase )
    (cycle specific).
  • 3.vinca alkaloids , e.g. vinicristine
    ,vinblastine.
  • Action arrest cell in mitosis (act at M) (cycle
    specific).
  • 4.anti-biotics , e.g. adriamycin , bleomycin .
  • Action binds to double stranded DNA preventing
    its replication (non- cycle specific).

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C.T drug resistance
  • 1.interinsic resistance the TU. from the start
    is resistant to C.T by its own nature , e.g. lipo
    - sarcoma.
  • 2.acquired resistance it arises after several
    exposures to the drug due to selection of
    resistant cells by destruction of sensitive cells.

Why C.T must be given intermittently and in
combination and over apro-longed period
Each time C.T is used growth fraction (G.F) is
killed , by time clonogenic fraction (C.F) will
transfer to be ( G.F) and TU. Shrinks . This
needs C.T to be given intermittently and over
apro-longe period and in combination to overcome
drug resistance
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Combination C.T
  • How to choose combination C.T
  • 1.each drug must be active against the TU. If
    used alone.
  • 2.drugs must not be similar in toxicities.
  • 3.they must have different mechanisms of action.
  • 4. they must be used close to their maximum
    tolerable dose.

Response to C.T
1.cure H.D ,acute childhood leukaemia , chorio
carcinoma , E.sarcoma , willms TU. 2.improved
survival overian CA. , breast CA. , M.M
. 3.non-responsive CA. malignmant melanoma
thyroid carcinoma , R.C.C.
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Complications of C.T
  • A. mild nausea, vomiting , mucositis ,
    alopecia.
  • B. moderate leucopenia , thrombocytopenia.
  • C. sever cardiac toxicity , (ADM) , lung
    fibrosis (bleomycin) , nephro toxicity
    (cisplatin) , second cancer formation.
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