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Year 3 OSCE > Case 20- Haematological Malignancy > Flashcards

Case 20- Haematological Malignancy Flashcards

1
Q

Leukaemia

A

Cancer of stem cells in the bone marrow

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2
Q

Pathophysiology

A

Excessive production of one cell line leads to suppression of other cell lines causing underproduction of other cell types- results in pancytopenia (combination of anaemia, leukopenia, thrombocytopenia)

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3
Q

ALL CELLMATES HAVE COMMON AMBITIONS

A

Under 5 and over 45- ALL
Over 55- CLL
Over 65- CML
Over 75- AML

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4
Q

Presentation of leukaemia

A

Fatigue, fever (night sweats), failure to thrive children), pallor (anaemia), petechiae and abnormal bruising, abnormal bleeding, lymphadenopathy, hepatosplenomegaly, bone pain, frequent infections

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5
Q

Petechiae

A

Bleeding under the skin caused by thrombocytopenia. Differentials;

Leukaemia
Meningococcal septicaemia
Vasculitis
HSP
ITP
Non accidental injury

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6
Q

Investigations for leukaemia

A

1) FBC, blood film, LDH (raised)
2) Bone marrow biopsy- main investigation
3) CXR- mediastinal lymphadenopathy
4) Lymph node biopsy- assess lymph node involvement
5) CT MRI PET- staging and assessing other tumours

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7
Q

Bone marrow biopsy

A

Aspiration- take a few cells in a liquid sample (examines straight away)

Trephine- solid core sample of the bone marrow. Superior assessment (few days of preparation before examination)

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8
Q

Acute lymphoblastic leukaemia

A

Usually B lymphocytes- acute proliferation
Most common childhood malignancy (2-5 yrs)
Associated with Down’s syndrome
Blast cells on blood film

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9
Q

Chronic lymphocytic leukaemia

A

Chronic proliferation of the B lymphocytes
Warm autoimmune haemolytic anaemia
Can form high grade lymphoma- Richter’s transformation
Smear/ smudge cells on a film
Most common leukaemia in adults overall
High risk of infections

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10
Q

Chronic myeloid leukaemia

A

Philadelphia chromosome (t(9:22))
3 phases- chronic (5 year asymptomatic phase),accelerated, blast phase (often the fatal phase)
Increased granulocytes (at different stages of maturation ie. bands) and or thrombocytosis

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11
Q

Acute myeloid leukaemia

A

Can transform from a myeloproliferative disorder like PCRV or myelofibrosis
High proportion of blast cells- have rods inside them called Auer rods

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12
Q

Management of leukaemia

A

1) Discuss in MDT- refer to haematology and oncology
2) Chemotherapy, steroids, radiotherapy
3) Bone marrow transplant

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13
Q

Lymphoma

A

Affects the lymphocytes inside the lymphatic system (cancerous cells proliferate within the lymph nodes and cause lymphadenopathy)

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14
Q

Risk factors for Hodgkin’s lymphoma

A

HIV/ EBV
Rheumatoid arthritis and sarcoidosis
Family history

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15
Q

Presentation of Hodgkin’s lymphoma

A

Lymphadenopathy- neck, groin, axilla (non tender and rubbery, unilateral and spreading)
Pain on drinking alcohol (for Hodgkin’s)
B symptoms- fever, weight loss, night sweats
LDH raised

Others;
Fatigue, itching, cough, SOB, abdominal pain, recurrent infections

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16
Q

Investigations s for Hodgkin’s lymphoma

A

FBC, UE, LFT, coagulation profile, Ca (metastasis), LDH (raised) ESR, HIV test (risk for NHL), blood film
Excisional Lymph node biopsy- reed stern berg cells/mirror image nuclei (large B cells with multiple nuclei and nucleoli)
CT MRI PET scans- stage lymphoma

NB- reed sternberg (large cells with a bilobed nucleus and prominent eosinophilic inclusion-like nucleoli)

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17
Q

Management of Hodgkin’s lymphoma

A

Chemotherapy and radiotherapy- can be cured
Flu pneumococcal vaccines

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18
Q

Non Hodgkin’s lymphoma

A

Many different types (Burkitts, MALT lymphoma (H pylori), diffuse large B cell lymphoma).

Risk factors- HIV/ EBV/ H pylori/ Hep B or C/ trichloroethylene (several industrial processes)/ FH

Similar presentation to Hodgkin’s so can on,y be differentiated on biopsy

Chemo, radio, stem cell transplantation, monoclonal antibodies

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19
Q

Myeloma

A

Cancer of the plasma cells (B lymphocytes that produce antibodies). Found in the bone marrow

They produce immunoglobulins (antibodies)- heavy chains and light chains. IgG often produced in abundance in myeloma. The antibody produced by all the cancerous cells is identical so is referred to as a monoclonal paraprotein

Bence Jones protein found in the urine of myeloma patients- light chain of the immunoglobulin

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20
Q

Multiple myeloma

A

Myeloma that affects multiple areas of the body

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21
Q

MGUS (Monoclonal gammopathy of undetermined significance)

A

Excess of a single type of antibody or component, without features of myeloma or cancer

Very rarely progresses to myeloma

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22
Q

Anaemia

A

Cancerous plasma cells invade the bone marrow and suppress other cell lines- get anaemia, neutropenia and thrombocytopenia

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23
Q

Myeloma bone disease

A

Increased osteoclast activity and suppressed osteoblasts activity

Patchy imbalance between the 2 cell types leads to osteolytic lesions throughout the body (can get pathological fractures)

Get hypercalacemia due to the increased bone turnover

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24
Q

Myeloma renal disease

A

High levels of immunoglobulins attack the tubules
Hypercalacemia impairs renal function
Dehydration
Medications like bisphisphanates can be harmful to the kidneys

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25
Hyperviscosity
More proteins in the blood- therefore it is more viscous Causes many issues- easy bruising, easy bleeding, loss of sight (vascular disease of the eye), purple discolouration of the extremities, heart failure, stroke
26
Way to remember features of myeloma
CRABBI Calcium Renal failure (light chains deposited in tubules, also get nephrolothiasis and amyloidosis) Anaemia (normocytic, normochromic) Bone lesions/ pain (osteoporosis) Bleeding (thrombocytopenia) Infection
27
Myeloma investigations
Bloods- FBC (anaemia and thrombocytopenia), bone profile (Ca (raised)), ESR (raised), plasma viscosity (raised), LFT (metastasis), UE (urea and creatinine raised), serum protein electrophoresis (free light chains) Urinalysis and electrophoresis- renal disease and bence Jones protein (urine electrophoresis) Bone marrow aspiration and trephine biopsy Imaging- asses bone lesions (MRI CT DEXA scan) NB- MRI now first line scan BLIP- bence Jones, serum free light chains, immunoglobulins and proteins
28
Management of myeloma
1) MDT- oncology and haematology 2) Chemotherapy 3) Stem cell transplantation 4) Bone complications- bisphisphanates, radiotherapy, orthopaedic surgery to stabilise bones NB- non curable. Takes a relapsing and remitting course
29
TTP- thrombotic thrombocytopenic purpura
A type of thrombotic microangiography- platelets occlude the microvasculature
30
Risks for TTP
Pregnancy, cancer, HIV, SLE, clopidogrel, quinine, oestrogen Xs
31
Sx of TTP
Fever, neurological abnormalities, thrombocytopenia (petechiae/ purpura), microangiopathic haemolytic anaemia (fatigue/ jaundice), impaired renal function (haematuria/ proteinuria/ oliguria/ anuria)
32
Investigations for TTP
Bloods- FBC, peripheral smear (schistocytes), UE (creatinine increased, AKI)
33
HUS- Haemolytic Uraemic Syndrome
A thrombotic microangiography in which microthrombi (platelets) form and occlude the microvasculature NB- often affects children and is caused by the shiga toxin of E. coli
34
Sx of HUS
Usually a diarrhoeal illness (bloody) precedes the onset of HUS Sx in many children; Thrombocytopenia- petechiae Micronagiographic haemolytic anaemia- fatigue, jaundice Impaired renal function- hameaturia, proteinuria, oliguria, anuria
35
Treatment of TTP
Plasma exchange therapy Steroids
36
ITP- Immune Thrombocytopenic Purpura
Diagnosis of exclusion in isolated thrombocytopenia A) primary- viral infection causes an autoimmune reaction B) secondary- lymphoma, leukaemia, SLE, HIV
37
Sx of ITP
Commonly asymptomatic Features can include easy bruising, petechiae, haematuria, bleeding, malaena NB- adults are usually treated with steroids
38
Most common childhood malignancy
ALL
39
Specific management of CML
Imatinib (inhibitor of tyrosine kinase)
40
CLL features in investigation
Lymphocytosis Anaemia Smudge cells Immunophenotyping Uncontrolled proliferation of small, mature lymphocytes in the bone marrow, lymph nodes (resulting in lymphadenopathy) and spleen (resulting in splenomegaly).
41
Implications of CLL
Anaemia Hypogammaglobulinaemia (recurrent infections) Warm autoimmune haemolytic anaemia) Richters transformation (transformation to a high grade lymphoma)
42
Richters transformation features
Patient deteriorates very quickly and becomes unwell Other features; Lymph node swelling Fever without infection Weight loss Night sweats Nausea Abdominal pain
43
Burrkitts lymphoma
High grade B cell neoplasm Endemic form- maxilla or mandible (EBV) Sporadic form- abdominal tumours t(8:14) Starry sky appearance on microscopy
44
Management of burkitts lymphoma
Chemotherapy, but can cause tumour lysis syndrome Treat with rasburicase first
45
Complications of tumour lysis syndrome
Hyperkalaemia Hyperphosphataemia Hypocalcaemia Hyperuricaemia Acute renal failure
46
What malignancy can H pylori predispose somebody to?
Gastric lymphoma (MALT)
47
Nodular sclerosing Hodgkin’s lymphoma
Most common Good prognosis Common in women Lacunar cells
48
Mixed cellularity Hodgkin’s lymphoma
20% Good prognosis Large number of reed stern berg cells
49
Lymphocyte predominant Hodgkin’s lymphoma
Best prognosis
50
Lymphocyte depleted Hodgkin’s lymphoma
Worst prognosis
51
Poor prognosis in Hodgkin’s lymphoma
B symptoms -weight loss (>10% in 6 months) -fever (>38) -night sweats
52
Ann Arbor staging of lymphoma (NHL and HL)
I- single lymph node II- 2 or more lymph nodes/regions on the same side of the diaphragm III- nodes on both sides of the diaphragm IV- spreads beyond’s the lymph nodes A- no systemic symptoms other than pruritus B- B symptoms present
53
MGUS
A cause of paraproteinaemia that is often mistaken for multiple myeloma
54
Features of MGUS
Asymptomatic No bone pain or increased infections 10-30% have a demyelinating neuropathy
55
Differentiating MGUS and myeloma
Normal immune function Lower levels of paraproteins Stable levels of paraproteins No clinical features of myeloma eg, lyric lesions or renal disease Normal beta 2 micorglobulin levels
56
Myelodysplastic syndrome
Pre-leukaemia, may progress to AML Presents with bone marrow failure (anaemia, neutropenia, thrombocytopenia)
57
Myelofibrosis
Myeloproliferative disorder Hyperplasia of megakaryocytes Haematopoiesis occurs in the liver and spleen
58
Features of Myelofibrosis
Anaemia eg. Elderly person with fatigue Massive Splenomegaly B symptoms- weight loss, night sweats, fever etc.
59
Laboratory findings of Myelofibrosis
Anameia Tear drop poikilocytes on blood film Unobtainable bone marrow biopsy (dry tap)- trephine biopsy needed High urate and LDH
60
Rain drop. Vs pepper pot skull
Multiple myeloma- rain drop Pepper pot skull- hyperparathyroidism
61
Differentiating HL and NHL
Alcohol induced pain in HL B symptoms occur earlier in HL Extra nodal disease is more common in NHL eg. Gastric (dyspepsia, dysphagia, abdominal pain), bone marrow (pain, pancytopenia), lung, skin, CNS (nerve palsies)
62
Prophylaxis of TLS
IV allopurinol or IV rasburicase
63
Complication of TLS
AKI Arrhythmia
64
Diagnosis of clinical tumour lysis syndrome
Laboratory TLS + increased creatinine, or cardiac arrhythmia (even sudden death), or seizure
65
Waldenstroms macroglobulinaemia (lymphoplasmocytic leukaemia)
Paraproteinaemia Weight loss, lethargy Hyper-viscosity Hepatosplenomegaly Lymphadenopathy Cryoglobulinaemia (raynauds)
66
What medication can be used to treat chronic neutropenia
filgrastim (or perfilgrastim)
67
What medication can be used to treat chronic neutropenia
filgrastim (or perfilgrastim)
68
Management of ITP (adult)
1) first-line treatment is oral prednisolone 2) pooled normal human immunoglobulin (IVIG) may also be used it raises the platelet count quicker than steroids, therefore may be used if active bleeding or an urgent invasive procedure is required splenectomy is now less commonly used
69
Investigations for HUS
FBC UE blood film stool sample- shiga toxin
70
Management of HUS
treatment is supportive e.g. Fluids, blood transfusion and dialysis if required there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients

Year 3 OSCE (61 decks)

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