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Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
Multiple myeloma
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Multiple myeloma

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  • 1. Multiple Myeloma
  • 2.
    • What is multiple myeloma?
  • 3.
    • It is a malignant disease of the plasma cells of bone marrow.
    • Remains an incurable disease .
  • 4.
    • What is the most common monoclonal protein found in MM?
  • 5.
    • IgG (55%)
    • IgA (20%)
    • In approximately 20% there is no paraproteinaemia, only light chains in the urine.(BJP)
  • 6.
    • What are the risk factors for MM?
  • 7.
    • Age >60.
    • Exposure to pesticides.
    • Radiation
    • Benzene
    • ? Presence of IL-6 and HHV8 (Kaposi’s sarcoma Herpes Virus)
  • 8.
    • What are the clinical features of MM?
  • 9.
    • Disease of elderly.
    • Median age >60
    • More common in black Africans.
    • Bone destruction
    • Renal failure
    • Bone marrow infiltration
  • 10.
    • May be symptomatic or asymptomatic.
    • Symptomatic myeloma characterized by presence of ROTI and CRAB.
    • Myeloma R elated O rgan or T issue I mpairment.
    • C alcium levels increased
    • R enal failure
    • A nemia
    • B one lesion
  • 11.
    • What is the cause for renal failure in MM?
  • 12.
    • Deposition of light chains in the tubules (most common).
    • Also:
    • hypercalcaemia, hyperuricaemia, use of NSAIDs (rarely) and deposition of amyloid.
  • 13.
    • What is the consequence of bone marrow infiltration with plasma cells?
  • 14.
    • anaemia
    • neutropenia
    • Thrombocytopenia
    • Production of paraproteins.
  • 15.
    • What is the consequence of bone destruction in MM?
  • 16.
    • Fracture of long bones
    • Vertebral collapse
    • Hypercalcemia
  • 17.
    • What is the cause of spinal cord compression in MM?
  • 18.
    • Due to soft tissue plasmacytomas
  • 19.
    • In terms of cytogenetics which one has a better prognosis?
    • Hypodiploidy (<45 chromosomes) or
    • Hyperdiploidy (>50 chromosomes)?
  • 20.
    • Hyperdiploidy.
  • 21.
    • In MM which bone activity is increased?
    • Osteoblast or osteoclast?
  • 22.
    • Increased osteoclastic activity.
    • That is why biphosphonates is useful in MM because it inhibits osteoclastic activity.
  • 23.
    • Why do patients with MM get recurrent infections?
  • 24.
    • Because there is a reduction in the normal immunoglobulin levels ( immuneparesis ), contributing to the tendency for patients with myeloma to have recurrent infections.
  • 25.
    • What are the lab findings in MM?
  • 26.
    • FBC- normal or low.
    • ESR, CRP-almost always raised.
    • Blood film- Rouleaux formation , macrocytosis.
    • U&Es, Cr-renal failure
    • Serum B2 microglobulin >2.5mg/L.
    • Raised LDH
    • Serum calcium- normal or raised.
    • Serum ALP-normal
    • Total protein-normal or raised.
    • Serum albumin- normal or low.
    • SPE - monoclonal band.
    • Serum free light chain assay
    • Uric acid-normal or raised
    • 24-hour urine electrophoresis and immunofixation is used for assessment of light-chain excretion.
    • Bone marrow aspirate or trephine shows characteristic infiltration by plasma cells .Amyloid may be found.
  • 27.
    • What are the imaging studies used to diagnose MM?
  • 28.
    • Skeletal survey-lytic lesion. easily seen in skull.
    • CT, MRI and PET are used in plasmacytomas (bone or soft tissue deposits).
    • Sestamibi- picks up bone dx missed on skeletal survey.
    • MRI spine- may show imminent compression/collapse.
  • 29.
    • Myeloma affecting the skull. Note the rounded lytic translucencies produced by infiltration of the skull with myeloma cells.
  • 30.
    • What are the stages of MM?
  • 31.  
  • 32.
    • How do you diagnose MM?
  • 33.
    • Two out of three diagnostic features should be present:
    • paraproteinaemia or Bence Jones protein
    • radiological evidence of lytic bone lesions
    • an increase in bone marrow plasma cells.
  • 34.
    • What is the treatment for MM?
  • 35.
    • supportive care
    • chemotherapy
    • Autologous or allogeneic stem cell transplantation.
  • 36.
    • What is the supportive therapy?
  • 37.
    • Treat the anemia-erythropoetin helps.
    • Treat the infection
    • Radiotherapy/sytemic chemo/high dose dex for bone pain.
    • Kyphoplasty and vertebroplasty for treating vertebral fractures.
    • Biphosphonates (pamidronate/zoledronic acid)- beware of osteonecrosis of the jaw.
  • 38.
    • What are the chemo options?
    • For Elderly?
    • For Younger patients?
  • 39. For elderly
    • If not fit for transplant, treat with Melphalan + Prednisone + Thalidomide (MPT).
    • Beware:
    • Melphalan +prednisone = stem cell toxicity.
    • (only use in non-transplant candidate)
    • Melphalan-nephrotoxic.
  • 40. For younger patients
    • High-dose dexamethasone based induction .
    • Followed by high-dose melphalan with peripheral blood stem cell rescue (autotransplantation)
    • Stem cell transplant- improves survival but not curative .
    • CR in 40%.
    • median survival increasing to 6 years.
  • 41.
    • What agents to use for relapse myeloma?
  • 42.
    • Thalidomide (immunomodulatory derivatives)
    • Lenalidomide + dexamethasone.
    • (the above combination is more effective than high-dose dexamethasone alone in relapsed or refractory multiple myeloma-NEJM)
    • Bortezomib (proteosome inhibitor)- higher incidence of herpes zoster.
    • 78% improvement in median time to progression with Bortezomib.
    • Choice based on side effect profile.
  • 43.
    • What are the prognostic markers of MM?
  • 44. Bad prognosis if…
    • Raised B2-microglobulin >4.
    • Low serum albumin <3g/dl.
    • Cytogenetics – ch13 deletion, hypodiploidy, T(4:14)
    • Raised LDH, CRP, Cr.
    • Low platelet <150 and Hb<100.
    • Bone marrow plasma cell percentage ≥ 50%
    • Age >70.
  • 45.
    • What features would make you suspect MGUS?
  • 46. MGUS
    • Monoclonal Gammapathy of Undetermined Significance.
    • Asymptomatic patient. Advanced age.
    • Presence of low serum M-protein <3 g/dL
    • No evidence of myeloma.
    • Minimal infiltrate of bone marrow (<10%)
    • IgG most common (70%).
    • BJP negative (69%)
    • Overall risk of progression= 1% per year.
    • No treatment is required.
  • 47.
    • What is the most important risk factor for progression of MGUS to plasma cell cancer?
  • 48.
    • M band size . The bigger, the worse.
    • IgM or IgA monoclonal protein has increased risk.
  • 49.
    • If a patient is found to have high levels of IgM paraprotein?
    • What is the most likely diagnosis?
  • 50.
    • Waldenstrom Macroglobulinemia.
  • 51.
    • What are the side effects of Thalidomide?
  • 52.
    • Constipation
    • Somnelence.
    • Painful neuropathy- major side effect.

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