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 Staging  Prognostic assessment  Formulation of a treatment plan (either curative or palliative)

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Presentation on theme: " Staging  Prognostic assessment  Formulation of a treatment plan (either curative or palliative)"— Presentation transcript:

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2  Staging  Prognostic assessment  Formulation of a treatment plan (either curative or palliative)

3  = to determine all sites of disease  Use a combination of Anatomical imaging (CT or MRI) Functional isotope scanning ( 18 fluorodeoxyglucose positron-emission tomography[ 18 FDG PET] and gallium-67 scanning) Bone marrow examination Lumbar puncture Further tissue biopsies (occasionally)

4  Provides prognostic information  Allows treatments to be tailored to patient (disease extent, sites of involvement)  Allows determination of sites to be examined later to document remission  Anatomical imaging identifies pathological sites  size, appearance  Functional imaging identifies disease within normal- sized lymph nodes or within sites that have a lack of contrast between normal and diseased areas (eg spleen, liver)  Staging is most commonly performed using the Ann Arbor system

5  Stage I  A single lymph node region (I) or  A single extra-lymphatic organ or site (IE)  Stage II  2+ lymph node regions (same side of the diaphragm) (II) or  Localised involvement of an extralymphatic organ or site & 1+ lymph node regions (same side of the diaphragm )(IIE).  Stage III  Involvement of lymph node regions on both sides of the diaphragm (III),  May be accompanied by localised involvement of an extralymphatic organ or site (IIIE) or by involvement of the spleen (IIIS) or both (IIISE)  Stage IV  Diffuse or disseminated involvement of one or more extralymphatic organs or tissues +associated lymph node enlargement  Systemic symptoms  The stages are further subclassified into A and B categories. The B designation is given to patients with unexplained loss of more than 10% of body weight in the six months before diagnosis, unexplained fever with temperatures above 38°C, or drenching night sweats

6  Determine if the aim is cure, prolongation of life or palliation  Multidisciplinary team: haematologists; medical oncologists; radiological oncologists; anatomical pathologists; surgeons; allied health; GP

7  Chemotherapy  systemic control  Radiotherapy  high quality local disease control  Surgery  Alone or in combination  Don’t forget CAMs!

8  Common regimes include combinations of Cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP), and fludarabine with cyclophosphamide (FC) For highly aggressive disease, alternating regimens of up to 10 chemotherapy agents may be used  Recent: monoclonal antibodies and non-cytotoxic small-molecule antineoplastic agents Several monoclonal antibodies (directed at proteins expressed on the surface of lymphoma cells)  eg. anti- CD20 monoclonal antibody rituximab (commonly used in combination with multi-agent chemotherapy in managing non-Hodgkin lymphoma and is also finding a role in ‘maintenance’ therapy after the completion of induction chemotherapy)

9  Immediate complications Nausea, vomiting, ulceration of GIT mucosa Alopecia Anaemia, thrombocytopenia  easily treated Neutropenia  more complicated, but can be decreased with G-CSF Infections  febrile neutropenia can be fatal if not treated immediately  Long-term complications Psychosocial Second malignancies (due to chemo/radiotherapy) Thyroid, hepatic and/or renal dysfunction Infertility

10  = metabolic disturbances seen after initiation of cancer treatment.  most common with bulky, rapidly proliferating, and treatment-responsive tumors (eg. acute leukaemia, high-grade NHL)  Rapid killing of neoplastic cells  release of intracellular ions and metabolic byproducts  inundates renal elimination and cellular buffering mechanisms  hyperuricemia, hyperkalaemia, hyperphosphatemia, hypocalcemia, acute renal failure  Can also cause cardiac arrhythmias &/or metabolic acidosis  Principles of management Identification of high-risk patients  begin prophylaxis Early recognition of metabolic and renal complications  supportive care

11  Symptoms: nausea, vomiting, lethargy, oedema, fluid overload, congestive heart failure, cardiac dysrhythmias, seizures, muscle cramps, tetany, syncope, and sudden death  Use prophylactic measures in people at risk (eg. If they already show some mild metabolic disturbances)  Delay in recognition and initiation of treatment of tumor lysis syndrome can be life-threatening  treat ASAP  Surveillance: ECG, renal surveillance, fluid status, vital signs, BUN, creatinine, uric acid, K+, Ca2+, PO4-, LDH

12  Choices:  High-intensity salvage regimens Possibly autologous or allogeneic stem cell transplantation  Standard-intensity regimens for relapsed indolent disease  Purely symptomatic management

13  More chemo  more killing of BM stem cells  dec rbc, wbc and platelets  Types of transplants:  Autologous = use stem cells initially from the patient Are treated with chemotherapy to remove any malignant cells  Allogeneic = use stem cells or bone marrow from a matched donor

14  Prognosis varies widely  Limited-stage Hodgkin lymphoma: >90% chance of cure  High-grade non-Hodgkin lymphoma: >60%  Indolent non-Hodgkin lymphomas: not curable, Treated five year survival: exceeds 70%  Prognostic scoring systems allow risk stratification at the outset of therapy Best known & validated is the International Prognostic Index (IPI) for aggressive non-Hodgkin lymphoma  Incorporates the patient’s age, general health, disease stage, number of extranodal disease sites and disease activity (measured by LDH)

15  Two major goals: Detecting relapsed or recurrent disease Monitoring for late effects of therapy  The GP must monitor other aspects of the patient’s health  The specialist team should conduct regular reviews (even during remission)  Consider their psychosocial wellbeing as they may focus on the possibility of the cancer recurring  can lead to anxiety and depression


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