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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
Q

Hyperviscosity

A

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

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26
Q

Way to remember features of myeloma

A

CRABBI

Calcium
Renal failure (light chains deposited in tubules, also get nephrolothiasis and amyloidosis)
Anaemia (normocytic, normochromic)
Bone lesions/ pain (osteoporosis)
Bleeding (thrombocytopenia)
Infection

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27
Q

Myeloma investigations

A

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

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28
Q

Management of myeloma

A

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

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29
Q

TTP- thrombotic thrombocytopenic purpura

A

A type of thrombotic microangiography- platelets occlude the microvasculature

30
Q

Risks for TTP

A

Pregnancy, cancer, HIV, SLE, clopidogrel, quinine, oestrogen Xs

31
Q

Sx of TTP

A

Fever, neurological abnormalities, thrombocytopenia (petechiae/ purpura), microangiopathic haemolytic anaemia (fatigue/ jaundice), impaired renal function (haematuria/ proteinuria/ oliguria/ anuria)

32
Q

Investigations for TTP

A

Bloods- FBC, peripheral smear (schistocytes), UE (creatinine increased, AKI)

33
Q

HUS- Haemolytic Uraemic Syndrome

A

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
Q

Sx of HUS

A

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
Q

Treatment of TTP

A

Plasma exchange therapy
Steroids

36
Q

ITP- Immune Thrombocytopenic Purpura

A

Diagnosis of exclusion in isolated thrombocytopenia

A) primary- viral infection causes an autoimmune reaction
B) secondary- lymphoma, leukaemia, SLE, HIV

37
Q

Sx of ITP

A

Commonly asymptomatic

Features can include easy bruising, petechiae, haematuria, bleeding, malaena

NB- adults are usually treated with steroids

38
Q

Most common childhood malignancy

A

ALL

39
Q

Specific management of CML

A

Imatinib (inhibitor of tyrosine kinase)

40
Q

CLL features in investigation

A

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
Q

Implications of CLL

A

Anaemia
Hypogammaglobulinaemia (recurrent infections)
Warm autoimmune haemolytic anaemia)
Richters transformation (transformation to a high grade lymphoma)

42
Q

Richters transformation features

A

Patient deteriorates very quickly and becomes unwell

Other features;
Lymph node swelling
Fever without infection
Weight loss
Night sweats
Nausea
Abdominal pain

43
Q

Burrkitts lymphoma

A

High grade B cell neoplasm
Endemic form- maxilla or mandible (EBV)
Sporadic form- abdominal tumours
t(8:14)
Starry sky appearance on microscopy

44
Q

Management of burkitts lymphoma

A

Chemotherapy, but can cause tumour lysis syndrome
Treat with rasburicase first

45
Q

Complications of tumour lysis syndrome

A

Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia
Hyperuricaemia
Acute renal failure

46
Q

What malignancy can H pylori predispose somebody to?

A

Gastric lymphoma (MALT)

47
Q

Nodular sclerosing Hodgkin’s lymphoma

A

Most common
Good prognosis
Common in women
Lacunar cells

48
Q

Mixed cellularity Hodgkin’s lymphoma

A

20%
Good prognosis
Large number of reed stern berg cells

49
Q

Lymphocyte predominant Hodgkin’s lymphoma

A

Best prognosis

50
Q

Lymphocyte depleted Hodgkin’s lymphoma

A

Worst prognosis

51
Q

Poor prognosis in Hodgkin’s lymphoma

A

B symptoms
-weight loss (>10% in 6 months)
-fever (>38)
-night sweats

52
Q

Ann Arbor staging of lymphoma (NHL and HL)

A

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
Q

MGUS

A

A cause of paraproteinaemia that is often mistaken for multiple myeloma

54
Q

Features of MGUS

A

Asymptomatic
No bone pain or increased infections
10-30% have a demyelinating neuropathy

55
Q

Differentiating MGUS and myeloma

A

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
Q

Myelodysplastic syndrome

A

Pre-leukaemia, may progress to AML

Presents with bone marrow failure (anaemia, neutropenia, thrombocytopenia)

57
Q

Myelofibrosis

A

Myeloproliferative disorder
Hyperplasia of megakaryocytes
Haematopoiesis occurs in the liver and spleen

58
Q

Features of Myelofibrosis

A

Anaemia eg. Elderly person with fatigue
Massive Splenomegaly
B symptoms- weight loss, night sweats, fever etc.

59
Q

Laboratory findings of Myelofibrosis

A

Anameia
Tear drop poikilocytes on blood film
Unobtainable bone marrow biopsy (dry tap)- trephine biopsy needed
High urate and LDH

60
Q

Rain drop. Vs pepper pot skull

A

Multiple myeloma- rain drop

Pepper pot skull- hyperparathyroidism

61
Q

Differentiating HL and NHL

A

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
Q

Prophylaxis of TLS

A

IV allopurinol or IV rasburicase

63
Q

Complication of TLS

A

AKI
Arrhythmia

64
Q

Diagnosis of clinical tumour lysis syndrome

A

Laboratory TLS + increased creatinine, or cardiac arrhythmia (even sudden death), or seizure

65
Q

Waldenstroms macroglobulinaemia (lymphoplasmocytic leukaemia)

A

Paraproteinaemia
Weight loss, lethargy
Hyper-viscosity
Hepatosplenomegaly
Lymphadenopathy
Cryoglobulinaemia (raynauds)

66
Q

What medication can be used to treat chronic neutropenia

A

filgrastim (or perfilgrastim)

67
Q

What medication can be used to treat chronic neutropenia

A

filgrastim (or perfilgrastim)

68
Q

Management of ITP (adult)

A

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
Q

Investigations for HUS

A

FBC UE blood film
stool sample- shiga toxin

70
Q

Management of HUS

A

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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