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Year 4 - Oncology > Haematology > Flashcards

Haematology Flashcards

1
Q

What is multiple myeloma?

A
  • Multiple myeloma (MM) is a haematological malignancy characterised by plasma cell proliferation.
  • It arises due to genetic mutations which occur as B-lymphocytes differentiate into mature plasma cells. MM is the second most common haematological malignancy.
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2
Q

What are some of the features of clinical presentation of myeloma?

A
  • CRABBI
  • Calcium: Hypercalcaemia occurs as a result of increased osteoclast activity within the bones
    • This leads to constipation, nausea, anorexia and confusion
  • Renal: Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules -> renal damage -> dehydration and increasing thirst
    • Other causes of renal impairment in myeloma include amyloidosis, nephrocalcinosis, nephrolithiasis
  • Anaemia: Bone marrow crowding suppresses erythropoiesis -> anaemia
    • This causes fatigue and pallor
  • Bleeding: bone marrow crowding also results in thrombocytopenia which puts patients at increased risk of bleeding and bruising
  • Bones: Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions
    • Presents as pain (especially in the back) and increases the risk of fragility fractures
  • Infection: a reduction in the production of normal immunoglobulins results in increased susceptibility to infection
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3
Q

How is myeloma ixd?

A
  • Bloods: anaemia (FBC) and thrombocytopenia (FBC); raised U&E and raised calcium
  • Peripheral blood film: rouleaux formation
  • BLIP
    • Bence Jones protein (raised concentrations of monoclonal IgA/IgG proteins in the urine)
    • Serum free light chain
    • Serum IgG
    • Serum protein electrophoresis
  • Bone marrow aspiration + trephine biopsy: confirms the diagnosis if the number of plasma cells is significantly raised
  • Gold standard: Whole-body MRI (or CT if MRI is not suitable) is used to survey the skeleton for bone lesions
  • Xray: ‘rain-drop’ skull. Dark spots seen on X-ray which due to bone lysis.
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4
Q

How is symptomatic myeloma diagnosed?

A
  • Monoclonal plasma cells in the bone marrow >10%
  • Monoclonal protein within the serum/urine (as determined by electrophoresis)
  • Evidence of end-organ damage e.g. hypercalcaemia, elevated creatinine, anaemia or lytic bone lesions/fractures
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5
Q

How is asymptomatic myeloma + MGUS defined?

A

Assymptomatic myeloma

  1. Serum paraprotein >30 g/L
  2. +/- Clonal plasma cells >10% on bone marrow biopsy
  3. NO myeloma-related organ or tissue impairment

Mx: no treatment initially. Watch and wait approach was adopted

MGUS

  1. Serum paraprotein <30 g/L
  2. Clonal plasma cells <10% on bone marrow biopsy
  3. NO myeloma-related organ or tissue impairment

Mx: MGUS therefore usually requires no treatment.

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6
Q

How is myeloma mxd?

A
  • <65 - autologous stem cell transplant
    • Induction therapy consists of Bortezomib + Dexamethasone
  • > 65 - generally unsuitable for autologous stem cell transplantation*
    • Induction therapy consists of Thalidomide + an Alkylating agent + Dexamethasone
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7
Q

How are the sx of myeloma mxd?

A
  • Pain: treat with analgesia
  • Pathological fracture: Zoledronic acid
  • Infection: patients receive annual influenza vaccinations
  • Immunoglobulin replacement therapy.
  • VTE prophylaxis
  • Fatigue/ anaemia: treat all possible underlying causes. If symptoms persist consider an EPO analogue.
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8
Q

What are the signs of waldenstroms macroglobulinaemia?

A
  • monoclonal IgM paraproteinaemia
  • systemic upset: weight loss, lethargy
  • hyperviscosity syndrome e.g. visual disturbance
  • the pentameric configuration of IgM increases serum viscosity
  • hepatosplenomegaly
  • lymphadenopathy
  • cryoglobulinaemia e.g. Raynaud’s
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9
Q

What is Waldenstrom’s macroglobulinaemia?

A
  • Waldenstrom’s macroglobulinaemia is an uncommon condition seen in older men.
  • It is a lymphoplasmacytoid malignancy characterised by the secretion of a monoclonal IgM paraprotein
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10
Q

How is Waldenstrom’s macroglobulinaemia Ixd?

A
  • Raised ESR, IgM (serum electrophoresis)
  • +ve urine sulfosalicylic acid test
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11
Q

What are the complications of Waldenstrom’s macroglobulinaemia?

A
  • Free light chains accumulate and block renal tubules -> cause cast aggregates -> inflammation + obstruction
  • Blood hyperviscosity
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12
Q

What are some of the complications of radio/chemoteh

A
  • Radiotherapy: SE: ↑ risk of second malignancies—solid tumours (especially lung and breast, also melanoma, sarcoma, stomach and thyroid cancers), ischaemic heart disease, hypothyroidism, and lung fibrosis due to the radiation field.
  • Chemotherapy: SE: myelosuppression, nausea, alopecia, infection. non-Hodgkin’s lymphoma, and infertility may be due to both chemo- and radiotherapy
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13
Q

How is Waldenstrom’s macroglobulinaemia mxd?

A
  • No cure
  • Tx: plasmapheresis, chemo (chlorambucil, fludarabine), immunotherapy
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14
Q

From what cell does Hodgkin lymphoma (HL) arise?

A

B lymphocytes

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15
Q

Name and describe two cell types present in Hodgkin lymphoma (HL).

A
  • Large, multi-nucleated giant cells called ‘Reed-Sternberg’ cells
  • Large, mono-nucleated cells called malignant ‘Hodgkin cells’.
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16
Q

Name the 4 subtypes of Classical Hodgkin lymphoma (HL).

A
  • Nodular Sclerosis - most common
  • Mixed Cellularity
  • Lymphocyte-rich
  • Lymphocyte-depleted
17
Q

What are some RFs for HL?

A

An affected sibling; EBV, SLE; post-transplantation, smoking, FH, NHL, HIV

18
Q

What are some sx of HL?

A
  • Lymphadenopathy: enlarged, non-tender, ‘rubbery’ superficial lymph nodes (60–70% cervical, also axillary or inguinal). Node size may fluctuate, and they can become matted.
  • B type sx: Fever, weight loss, night sweats, pruritus, and lethargy.
  • Possible alcohol-induced lymph node pain
  • Mediastinal lymph node involvement: can cause mass effect, eg bronchial or SVCO or direct extension, eg causing pleural effusions.
19
Q

What are some of the signs of HL?

A
  • Lymphadenopathy
  • Cachexia
  • Anaemia
  • Spleno- or hepatomegaly.
  • SVCO
  • Paraneoplastic syndromes such as cerebellar degeneration, neuropathy or Guillain-Barré syndrome
20
Q

What Ix are used for HL?

A
  • Bloods: FBC, film, ESR, LFR, LDH, urate, Ca2+. ↑ESR or ↓Hb indicate a worse prognosis. LDH↑ as it is released during cell turnover.
  • Tissue diagnosis: Lymph node excision biopsy
    • ​Image-guided needle biopsy
    • Laparotomy
    • Mediastinoscopy may be needed.
  • Imaging: CXR, Gold standard: CT/PET of thorax, abdo, and pelvis.
  • Immunocytochemistry: CD15 and CD30 antigens are positively expressed on Reed-Sternberg cells
21
Q

What staging system is used for HL? (+NHL?

A
  • ## Ann Arbor system: Done by imaging ± marrow biopsy if b symptoms, or stage iii–iv disease
  • ## 1.Confined to single lymph node region.
  • ## 2.Involvement of two or more nodal areas on the same side of the diaphragm.
  • Involvement of nodes on both sides of the diaphragm.
  • Spread beyond the lymph nodes, eg liver or bone marrow.
22
Q

How is NHL/HL mxd?

A
  • Stages I-a and II-a: Radiotherapy + short courses of chemotherapy for (eg with ≤3 areas involved)
  • Stages II-a>: Longer courses of chemotherapy >3 areas involved through to iv-b.
    • ‘ABVD: Adriamycin, (doxorubicin), Bleomycin, Vinblastine, Dacarbazine cures ~80% of patients. ​
  • Relapsed disease: high-dose chemotherapy followed by autologous stem cell transplantation.
23
Q

What are the RF for NHL?

A
  • Elderly
  • Caucasians
  • History of viral infection (specifically Epstein-Barr virus)
  • Family history
  • Certain chemical agents (pesticides, solvents)
  • History of chemotherapy or radiotherapy
  • Immunodeficiency (transplant, HIV, diabetes mellitus)
  • Autoimmune disease (SLE, Sjogren’s, coeliac disease)
24
Q

What are the sx of NHL?

A
  • Painless lymphadenopathy (non-tender, rubbery, asymmetrical)
  • Constitutional/B symptoms (fever, weight loss, night sweats, lethargy)
  • Extranodal Disease - gastric (dyspepsia, dysphagia, weight loss, abdominal pain), bone marrow (pancytopenia, bone pain), lungs, skin, central nervous system (nerve palsies)
25
Q

How can you differentiate HL from NHL?

A
  • Lymphadenopathy in Hodgkin’s lymphoma can experience alcohol-induced pain in the node
  • ‘B’ symptoms typically occur earlier in Hodgkin’s lymphoma and later in non-Hodgkin’s lymphoma
  • Extra-nodal disease is much more common in NHL than in HL
26
Q

What ix are used for NHL?

A
  • Blood: FBC, UE, LFT, ↑LDH: worse prognosis, reflecting ↑cell turnover.
  • Marrow and node biopsy for classification (complex, based on the who system of high- or low-grade).
  • Staging: Ann Arbor system (CT± PET of chest, abdomen, pelvis.
  • Cytology of any effusion: LP for CSF cytology if CNS signs
27
Q

How does mx differ for high grade vs low grade NHL?

A
  • Low-grade lymphomas: indolent, often incurable and widely disseminated.
    • Include: follicular lymphoma, marginal zone lymphoma/malt, lymphocytic lymphoma (closely related to CLL and treated similarly), lymphoplasmacytoid lymphoma (produces IgM = Waldenström’s macroglobulinaemia
  • High-grade lymphomas: more aggressive, but often curable. There is often rapidly enlarging lymphadenopathy with systemic symptoms.
    • Include: Burkitt’s lymphoma (childhood disease with characteristic jaw lymphadenopathy) lymphoblastic lymphomas (like all), diffuse large b-cell lymphoma
28
Q

What is polycythaemia vera?

A
  • Myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in red cell volume, often accompanied by overproduction of neutrophils and platelets.
  • Mutation in JAK2 is present in approximately 95% of patients with polycythaemia vera
  • Peaks in the sixth decade.
29
Q

What are some of the signs and sx of polycythaemia vera?

A
  • hyperviscosity
  • pruritus, typically after a hot bath
  • splenomegaly
  • haemorrhage (secondary to abnormal platelet function)
  • plethoric appearance
  • hypertension in a third of patients
  • low ESR
30
Q

What ix are used for polycythaemia?

A
  • FBC/film (raised haematocrit; neutrophils, basophils, platelets raised in half of patients)
  • JAK2 mutation
  • Serum ferritin
  • UE, LFTs
  • If JAK2 mutations is -ve:
    • red cell mass
    • arterial oxygen saturation
    • abdominal ultrasound
    • serum EPO level
    • bone marrow aspirate + trephine
    • cytogenetic analysis
    • erythroid burst-forming unit (BFU-E) culture
31
Q

How is polycythaemia mxd?

A
  • aspirin: reduces the risk of thrombotic events
  • venesection: to keep the haemoglobin in the normal range
  • chemotherapy: hydroxyurea + phosphorus-32 therapy

Year 4 - Oncology (2 decks)

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