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year 4 CDM 2 > Case 15: Lymphoma > Flashcards

Case 15: Lymphoma Flashcards

1
Q

Hodgkin’s lymphoma

A
  • A rare haematological cancer due to uncontrolled proliferation of B-lymphocytes which build up in the lymph node, spleen or bone marrow
  • Bimodal age range of 20-30 and >80, affects males more
  • Differentiated from Non-Hodgkin’s lymphoma due to histology of multinucleated lymphocytes called Reed-Sternberg cells
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2
Q

Hodgkin’s lymphoma risk factors

A
  • EBV: precedes Hodgkin’s lymphoma by 4 years
  • Immunosuppression: organ transplantation, Immunosuppressant therapy, HIV
  • Autoimmune conditions: RA, SLE and sarcoidosis
  • Family history
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3
Q

The 2 types of Hodgkin’s lymphoma

A
  • Classical Hodgkin’s lymphoma (95%)
  • Nodular lymphocyte predominant Hodgkins lymphoma: more commonly affects males, not associated with EBV. Absence of Reed-Sternberg (RS) cells and characterised by LP (’popcorn’) cells. Presents with peripheral adenopathy and affects the mesenteric lymph nodes
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4
Q

The 4 subtypes of classical Hodgkin’s lymphoma

A
  • Nodular sclerosing
  • Mixed cellularity
  • Lymphocyte
  • Lymphocyte depleted
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5
Q

Hodgkin’s lymphoma clinical features

A
  • Lymphadenopathy: painless, asymmetrical with cervical node or mediastinal involvement
  • Fever, night sweat, unintentional night sweats
  • Abdo pain, Pruritus
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6
Q

Hodgkin’s lymphoma investigations

A
  • FBC: normocytic anaemic and eosinophilia
  • LDH raised
  • Lymph node biopsy: Reed-Sternberg cells are diagnostic (owl’s eye appearance)
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7
Q

Hodgkin’s lymphoma management

A
  • chemotherapy:
    • ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine): considered the standard regime
    • BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone): alternative regime with better remission rates but higher toxicity
  • radiotherapy
  • combined modality therapy (CMT): chemotherapy followed by radiotherapy
  • hematopoietic cell transplantation: used for relapsed or refractory classic Hodgkin lymphoma
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8
Q

Complications of Hodgkin’s Lymphoma

A
  • Most patients achieve long term survival
  • Risk of secondary malignancy: for example solid tumours like breast and lung
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9
Q

Non-Hodgkin’s lymphoma

A
  • Malignant accumulation of lymphocytes which accumulate in the lymph node or other organs.
  • Most cases involve B cell proliferation
  • Affects B and T cells
  • Non- Hodgkin’s lymphoma (more common) is any other type of lymphoma which is not Hodgkins
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10
Q

Non Hodgkin’s Lymphoma risk factors

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)
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11
Q

Non-Hodgkin’s Lymphoma symptoms

A
  • Painless lymphadenopathy: non-tender, rubbery, asymmetrical
  • 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)
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12
Q

What organs/systems are affected in non-Hodgkin’s lymphoma

A
  • gut (e.g. gastric MALT lymphoma)
  • skin (e.g. T cell lymphoma)
  • oropharynx (e.g. MALT lymphoma)
  • nervous system (e.g. Waldenstrom’s)
  • bone
  • lung
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13
Q

Difference in symptoms between Hodgkin’s and non-Hodgkin’s lymphoma

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 non-Hodgkin’s lymphoma than in Hodgkin’s lymphoma
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14
Q

Non-Hodgkin’s Lymphoma investigations

A
  • Excisional Lymph node biopsy: first line
  • CT or PET CT chest, abdomen and pelvis (staging)
  • HIV
  • FBC (normocytic anaemia), ESR, LDH, Blood film, beta 2 microglobulin (prognostic)
  • Protein electrophoresis: IgM monoclonal paraprotein (Waldenstorms)
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15
Q

Non Hodgkins Lymphoma management

A
  • Either watchful waiting, Chemotherapy or radiotherapy
  • Rituximab is used in combo with conventional chemo regimes (i.e. CHOP) for a variety of NHL types
  • Flu/pneumococcal vaccine
  • If neutropenic may need antibiotic prophylaxis
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16
Q

Treatment for low and high grade Non-Hodgkin’s lymphoma

A
  • Low grade: treatment may not be needed if asymptomatic. Consider chemo, radiotherapy or H.pylori eradication for gastric MALT lymphoma
  • Chemo: Alpha interferon and rituximab (if CD20+)
  • High grade: chemotherapy and autologous or allogenic stem cell transplant if refractory
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17
Q

Complications of Non-Hodgkin’s Lymphoma

A
  • Bone marrow infiltration causing anaemia, neutropenia or thrombocytopenia
  • Superior vena cava obstruction
  • Metastasis
  • Spinal cord compression
  • Complications related to treatment e.g. Side effects of chemotherapy
  • Low grade NHL has better prognosis, High grade has a worse prognosis but higher cure
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18
Q

Low grade non-Hodgkins lymphoma types

A
  • follicular lymphoma (CD20+) (second most common)
  • marginal zone lymphoma e.g. MALT lymphoma
  • lymphocytic lymphoma
  • Waldenstrom’s macroglobulinaemia
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19
Q

High grade non Hodgkin lymphoma types

A
  • diffuse large B cell lymphoma (CD20+) - DLBCL (most common)
  • mantle cell lymphoma
  • peripheral T cell lymphoma
  • Burkitt lymphoma
  • lymphoblastic lymphoma
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20
Q

Non-Hodgkins lymphoma Burkitt

A
  • Risk of tumour lysis after chemo. Give urate oxidase before chemo to prevent risk
  • Types: endemic (African), sporadic
  • Presents with jaw lymphadenopathy (more common in children)
  • Associated with EBV
  • On microscope shows starry night appearance (lymphocyte sheets interspersed with macrophages containing dead tumour cells)
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21
Q

Non-Hodgkin’s lymphoma: MALT lymphoma and Waldenstrom’s Macroglobulinaemia

A

MALT lymphoma
- Associated with H.pylori
- Good prognosis 80% respond to H.oylori medication

Waldenstrom’s Macroglobulinaemia: characterised by by monoclonal IgM paraprotein and older men

22
Q

MGUS (Monoclonal gammopathy of undetermined significance)

A
  • Pre-malignant phase before Multiple myeloma
  • Its a benign paraproteinemia (relatively common)
  • Its usually asymptomatic with demyelinating neuropathy in some
  • 50% develop myeloma after 15 years
23
Q

What features differentiate MGUS from myeloma

A
  • normal immune function
  • normal beta 2 microglobulin
  • lower level of paraproteinaemia
  • stable level of paraproteinaemia
  • no clinical features of myeloma e.g. lytic lesions or renal disease
24
Q

Hyperviscosity syndrome

A
  • What is it: increase in plasma viscosity due to elevated paraproteins, RBC or WBC
  • Causes: Myeloma, Waldenstorm’s macroglobulinaemia, PV, Leukaemia
25
Q

Presentation and management of Hyperviscosity syndrome

A
  • Classic triad of
  • neuro symptoms (impaired cognition, headache, seizures)
  • visual changes due to retinopathy
  • mucosal bleeding
  • Treatment: Plasmapheresis
26
Q

Multiple Myeloma

A
  • Haematological malignancy due to a genetic mutation in B cell differentiation resulting in excess plasma cells.
  • Second most common haematological malignancy. Genetic factors
  • More common in males, Afro-Caribbean, 60-70.
  • Jobs associated: Radiation, farming, meta chemical, combustion fuel
27
Q

Multiple Myeloma characteristics

A
  • Monoclonal proteins (functionally useless antibody) in serum and/or urine. In the urine known as Bence Jones protein
  • Lytic bone lesions (destruction of bone)
  • Excess plasma cells in the bone marrow
  • Cancerous plasma cells release light chains and immunoglobulin (paraprotein/monoclonal band/ M protein) into the serum
28
Q

Multiple Myeloma Clinical features: CRABBI

A
  • Calcium: Hypercalcaemia- due to increased osteoclastic bone resorption ( bone destruction) caused by local cytokines released by the myeloma cells. Plasma cells infiltrate the bone marrow
  • Renal damage
  • Anaemia: bone marrow crowding suppresses erythropoiesis
  • Bones: lytic bone lesions causes pain (in the back) and pathological fractures
  • Infections: S.pneumoniae, Hi.influenzae, VZV
29
Q

Renal impairment in Myeloma patients

A
  • Bence Jones nephropathy: Monoclonal production of immunoglobulins cause light chain deposition in the renal tubules. Causes cast formation in the ascending loop of Henle and nephron destruction. Casts are made from Bence Jones protein and Tamm Horsfall glycoproteins
  • Other mechanisms: Amyloidosis, nephrocalcinosis (deposition of calcium in renal tubules), Nephrolithiasis (kidney stones)
30
Q

Treatment of renal impairment in Myeloma patients

A
  • Prevention: high fluid intake (3L a day), bring down the calcium, RRT
  • Avoid nephrotoxic drugs: NSAID, aminoglycosides
  • Careful monitoring
  • Treat infection
  • Bring down the calcium
31
Q

Multiple Myeloma bone problems

A
  • Hypercalcaemia (confusion, N+V, abdo pain), Fractures, Spinal cord compression
  • TNF, IL1 and IL6 cytokines stimulate osteoclasts in myeloma
  • Treatment: IV fluids, steroids, Bisphosphonates (no effect on disease directly but prevent fractures and hypercalcaemia and increase survival)
  • Radiotherapy and/or surgical stabilisation if fractures occur
32
Q

Multiple myeloma other features

A
  • Amyloidosis i.e. Macroglossia, Carpal tunnel syndrome, Neuropathy, Hyper viscosity.
  • Infection: less production of normal antibodies
  • Bleeding: bone marrow crowding causes thrombocytopaenia
33
Q

Multiple Myeloma: investigations

A
  • Bloods: FBC (normocytic anaemia), U&E, bone profile (hypercalcaemia), ESR
  • Peripheral blood film: Rouleaux formation (stacked RBC)
  • Protein electrophoresis: Raised concentration of IgA/IgG proteins in the serum. In the urine Bence Jones proteins
  • Bone marrow aspiration: confirms diagnosis if plasma cells are raised (>10%)
34
Q

Multiple Myeloma: Imaging

A
  • Whole body MRI
  • X-ray: ‘rain drop skull.’ Random pattern of dark spots
  • Wedge compression fracture of vertebrae
35
Q

Diagnostic criteria for multiple Myeloma

A
  • Clonal bone marrow plasma cells ≥10% or biopsy-proven plasmacytoma.
  • One or more myeloma-defining event
36
Q

Multiple Myeloma: Myeloma defining event

A
  • > 60% plasma cells in bone marrow
  • Involved:uninvolved light chain ratio ≥100
  • > 2 focal lesions on MRI (>5mm)
  • Hypercalcaemia
  • Renal insufficiency. >177 Creatinine
  • Anaemia
  • 1 or more lytic bone lesion on X-ray, CT or PET (>5mm)
37
Q

Multiple Myeloma treatment- induction therapy

A
  • targeted drugs (such as thalidomide, lenalidomide, bortezomib, daratumumab)
  • chemotherapy (such as cyclophosphamide or melphalan)
  • steroids (such as prednisolone or dexamethasone)
38
Q

Multiple Myeloma management

A
  • Incurable
  • Chemo alone if unsuitable for transplant (frail, >65, comorbidities)
  • Autologous haematopoietic cell transplantation with chemotherapy: Only used if young and healthy as high risk of graft versus host disease
39
Q

Multiple Myeloma disease progression

A
  • Non curable may have relapsing events where you offer 2nd or 3rd line therapy. Eventually becomes refractor to treatment and disease progresses causing death
  • Median survival time: 3-4
  • Need to control their renal function, bone disease and active disease
  • Poor Prognostic factors: high Serum Beta-2 microglobulin, cytogenetics, high LDH, age, peripheral blood plasma cells (increased cancerous cells), low albumin
40
Q

Multiple Myeloma managing symptoms

A
  • Pain: analgesia
  • Pathological fracture: Bisphosphonates for bone disease
  • Infection: annual influenza vaccine, Immunoglobulin replacement therapy, prophylactic antibiotics
  • Venous thromboembolism prophylaxis
  • Fatigue: erythropoietin analogue
41
Q

Multiple myeloma complications

A
  • hyperviscosity syndrome
  • spinal cord compression
  • death due to kidney failure or infection
42
Q

Revised International Staging System (R-ISS)

A
  • An improved prognostic staging model for multiple myeloma.
  • Combines ISS stage, high-risk cytogenetics, and lactate dehydrogenase (LDH) levels.
  • The R-ISS classifies patients into three risk categories: 1 is the best, 3rd is the worst
  • ISS staging system just considers albumin and Beta-2-microglobulin
43
Q

ISS staging of Myeloma

A
  • Stage 1: beta 2 microglobulin <3.5, albumin >3.5. Survival 62 months
  • Stage 3: Beta 2 microglobulin >5.5. Survival 29 months
44
Q

Causes of Thrombocytosis

A
  • Raised platelets
  • Post surgery
  • Infection/Inflammation- acute or chronic
  • Bleeding
  • Iron deficiency
  • Malignancy
  • Rebound post-chemotherapy
  • Hyposplenism/asplenia
45
Q

Thrombocytosis investigations

A
  • Inflammatory markers e.g. CRP
  • Ferritin
  • If acute and clear cause then repeat once stimulus is over (can be a lag)
  • Check blood film if persistent
  • Normally no need for aspirin if reactive thrombocytosis
46
Q

Thrombocytosis: when to investigate further

A
  • Investigate further if persistent, no secondary cause, Splenomegaly, Unprovoked thrombosis
  • Possible Haematological causes: Myeloproliferative neoplasm (ET, PV, PMF, CML), any malignancy
47
Q

Types of Myeloproliferative Neoplasms

A
  • Essential thrombocythaemia (ET)
  • Polycythaemia vera (PV)
  • Primary myelofibrosis (PMF)
  • Chronic myeloid leukaemia (CML)
48
Q

Myelofibrosis i.e. Myeloproliferative neoplasm blood film

A
  • Teardrop-shapedred blood cells
  • Anisocytosis(varying sizes of red blood cells)
  • Blasts(immature red and white cells)
49
Q

Essential Thrombocythemia (ET)

A
  • Clonal bone marrow disorder- type of cancer where the bone marrow produces too many platelets (>600)
  • Usually >50 years
  • Due to acquired mutation on JAK2, MPL or CALR genes
  • Continuously activates signal pathway causing platelet overproduction
  • Mostly picked up incidentally but can have thrombosis (arterial and venous), migraine, bleeding (haemorrhage), erythromelalgia (burning pain- fingers or toes), itch
  • Confirmed by bone marrow biopsy
50
Q

Essential Thrombocythemia management

A
  • Aspirin 75mg for all
  • Manage cardiovascular risk factor i.e. BP, diabetes and Cholesterol
  • If high risk factors (>60 years, >1500 platelets, previous thrombotic event, other cardiovascular risk factors)- Cytoreduction (Chemotherapy)
  • Cytoreduction- Hydroxycarbamide (reduces thrombotic events). Other options to add: interferon alpha (for younger patient), anagrelide, busulfan
  • Prognosis is good- risk of transformation to MF (Myelofibrosis) or acute leukaemia
  • Anagrelide is a specialist platelet lowering agent

year 4 CDM 2 (39 decks)

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