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Dermatology & Haematology > Haematological malignancy > Flashcards

Haematological malignancy Flashcards

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1
Q

What is polycythaemia?

A

An abnormally increased concentration of haemoglobin in the blood

Can be primary or secondary

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2
Q

What are the causes of polycythaemia?

A

Primary
- Polycythaemia ruba vera

Secondary

  • High altitude
  • Chronic lung disease
  • Cyanotic heart disease
  • Ectopic EPO
  • HCC
  • Burns
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3
Q

Pathophysiology of polycythaemia rubra vera?

A

Haematological malignancy

A mutation in a single haemopoietic stem cell resulting in myeloproliferation of RBCs, neutrophils, platelets

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4
Q

Clinical presentation of polycythaemia rubra vera?

A

Incidental finding on bloods

Thrombosis: stroke, MI, DVT, PE

Pruritus (with heat)
Erythromelalgia

Splenomegaly

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5
Q

When do patients often present with polycythaemia rubra vera?

A

Over 50 years

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6
Q

Investigations of polycythaemia rubra vera?

What would they show?

A

FBC:

  • raised Hb, WCC, platelets
  • low ferritin

Bone marrow biopsy: hypercellular

CT/MRI: splenomegaly

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7
Q

Which blood tests would help you differentiate between primary and secondary polycythaemia?

A

FBC:

  • Primary: raised Hb, WCC, platelets
  • Secondary: just raised Hb

Serum EPO:

  • Primary: low (trying to compensate for the excess cells)
  • Secondary: high (something is causing raised EPO levels, ectopic, or poor perfusion)
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8
Q

Management of polycythaemia rubra vera?

A

Thromboprophylaxis
Venesection
Anti-histamines
Hydroxyurea

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9
Q

What is myelofibrosis/

A

A rare bone marrow cancer

Proliferation of an abnormal clone of haemopoietic stem cells in the bone marrow resulting in fibrosis, replacement of bone marrow with scar tissue

There is also myeloid metaplasia

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10
Q

What is myeloid metaplasia?

A

Extramedullary haemopoiesis

In the spleen, liver and more

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11
Q

What causes myelofibrosis?

A

Primary: just happens

Secondary: to polycythaemia, leukaemias, lymphomas, multiple myeloma, infection (HIV, TB), radiation

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12
Q

Clinical features of myelofibrosis?

A

Anaemia

Leukopenia or leukocytosis (opportunistic infection)

Thrombocytopenia or thrombocytosis (bleeding tendency)

Constitutional: malaise, night sweats, low grade fever, weight loss

Extramedullary haemopoiesis:

  • hepatosplenomegaly
  • spinal cord compression, focal neurological deficit
  • ascites
  • haematuria

Progressive marrow failure, dyspnoea, abdo pain, bone pain

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13
Q

Investigations of myelofibrosis? What would they show?

A

FBC: anaemia, thrombocytopenia (or osis), leukopenia (or cytosis)
Signs of DIC

Peripheral blood film: teardrop poikilocytosis

Bone marrow biopsy: fibrosis

MRI: to look at marrow

Cytogenetic studies: especially looking for JAK mutations

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14
Q

Management of myelofibrosis?

A

Allogenic stem cell transplant is only chance at cure

Palliative

Hydroxyurea helps with splenomegaly, leukocytosis and thrombocytosis

Biologic drugs against JAK (mutation)

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15
Q

What is the difference between allogenic and autologous bone marrow transplants?

A

Autologous: patient’s own cells, taken from patient and frozen before transplant conditioning

Allogenic: donor stem cells which match patient’s HLA

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16
Q

What is meant by transplant conditioning?

A

Preparing a patient for bone marrow transplant

It’s the giving of high dose chemo or radiation to eradicate the malignancy

(This causes irreparable damage to stem cells, hence the transplant)

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17
Q

Which leukaemia can myelofibrosis transform to?

A

Acute myeloid leukaemia

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18
Q

What does poikilocytosis mean?

A

Variable shaped RBCs

They can be pencil shaped: iron deficiency

They can be tear-drop shaped in myelofibrosis

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19
Q

What’s the difference between lymphoma and leukaemia?

A

They’re both cancers of haemopoietic stem cells

In leukaemia cancer cells are in bone marrow

In lymphoma the cancer cells are in the lymph nodes or other tissues

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20
Q

Types of lymphoma? How are they differentiated?

Which is more common? Which is worse?

A

Hodgkin’s: Reed-Sternberg cells present

Non-Hodgkin’s: no Reed Sternberg cells, more common, more likely to disseminate

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21
Q

What are Reed-Sternberg cells?

A

Mutli-nucleated giant cells

Seen in Hodgkin’s lymphoma but not in Non-Hodgkin’s

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22
Q

What subtypes of Non-Hodgkin’s lymphoma are there?

A

B cell (90%) and T cell types

  • Burkitt’s lymphoma
  • MALT lymphoma

These are B cell lymphomas

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23
Q

Who gets Hodgkin lymphoma? What are some risk factors?

A

15-30 years

EBV
HIV
Smoking

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24
Q

What are the symptoms of both types of lymphoma?

A

Painless lymphoid swelling

  • often supraclavicular in HL
  • peripheral in NHL
Cough, SOB
Fatigue
Fever
Night sweats
Pruritus
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25
Q

Investigations of lymphoma?

A

FBC

  • anaemia
  • WCC

ESR: the higher the worse prognosis

HIV test

Lymph node biopsy: look for Reed Sternberg cells

CXR, CT to look for other affected lymph nodes and staging

Bone marrow biopsy for staging

26
Q

How are H and NH lymphoma staged?

A

Ann Arbor

Stage I to IV

Subscript letters represent extralymphatic involvement

27
Q

Management of HL?

A

Chemoradiotherapy

They need pneumococcal and influenza vaccines

28
Q

Complications of Hodgkin’s lymphoma?

A

Leukaemia (from the chemo)

Solid tumours (from the chemo and radiotherapy)

Melanoma
Pancreatic Ca
Hypothyroidism
Cardiovascular disease

29
Q

Who gets Non-Hodgkin lymphoma? What are some risk factors?

A

Middle aged people

EBV
Hep C
Toxins
Autoimmunity
H pylori
30
Q

What is Burkitt’s lymphoma?
Pathophysiology?
Who gets it?
Clinical features?

A

B cell, from a mutation

Children
Immunosuppressed: HIV, immunosuppressing drugs

Affects ileocaecal region

Abdominal mass and obstruction
Jaw and thyroid swellings
CNS involvement

31
Q

What is MALT lymphoma?
Pathophysiology?
Who gets it?
Clinical features?

A

Cancer of mucosa associated lymphoid tissue (commonly in stomach)

But any mucosal site can be affected

Women over 60

Dyspepsia, nausea gastric bleeding

32
Q

Investigations of Burkitt’s lymphoma?

What about MALT lymphoma?

A

Burkitt’s: BMA, LP

MALT: endoscopy + gastric biopsy, CT

33
Q

Management of NHL?

A

Multi-chemotherapy (r-CHOP)

34
Q

What does r-CHOP stand for?

A

A combintation of chemotherapy drugs

Rituximab
Cyclophosphamide
Hydroxydaunorubicin
Oncovin (Vincristine)
Prednisolone
35
Q

Management of Burkitt’s and MALT lymphoma?

A

Burkitt’s: Multi-chemotherapy

MALT: H pylori eradication, chemotherapy if advanced

36
Q

What is leukaemia?

A

Malignancy of haempoietic stem cells

Resulting in overproduction of abnormal white cells

Diffuse replacement of bone marrow with these abnormal cells

Supression of production of normal blood cells

37
Q

What 4 types of leukaemias are there?

A

Acute myeloid
Acute lymphoblastic:
Chronic myeloid
Chronic lymphocytic

38
Q

Clinical presentation of leukaemias?

A

Acute: within weeks
Chronic: months - years

Bone marrow failure:

  • neutropenia: infections
  • anaemia: fatigue, pallor, palpitations, SOB
  • thrombocytopenia: bleeding, epistaxis, menorrhagia, bruising

Also

  • lymphadenopathy
  • hepatosplenomegaly
  • bone and joint pain
  • persistent fever
  • weight loss
39
Q

Who is affected by each type of leukaemia?

A

AML: older people

ALL: children, esp under 6

CML: older people

CLL: older people

40
Q

Which type of leukaemia is associated with the philadelphia chromosome?

A

CML

41
Q

What investigations would you do for leukaemia?

A

FBC:
anaemia, leukopenia, thrombocytopenia

Lactate dehydrogenase and uric acid raised (due to high cell turnover)

Blood film: blast cells visible

CXR: may show pneumonia, heart disease, mediastinal mass, lytic bone lesions

Bone marrow biopsy

Immunophenotyping
Cytogenic studies

42
Q

What are the differences in chronic and acute leukaemias?

A

Onset:

  • acute = weeks
  • chronic = months-years

Cells:

  • acute = immature cells
  • chronic = more mature cells
43
Q

What are risk factors for leukaemia?

A

Age (in all but ALL)

Cytogenic abnormalities

Trisomy 21 (ALL, AML)

Aplastic anaemia, myelodysplastic disorder (AML)

Exposure to radiation and toxins, chemotherapy

44
Q

High cell turnover causes raised levels of what in the blood?

A

Lactate dehydrogenase

Uric acid

45
Q

What is needed in blood or bone marrow for a diagnosis of leukaemia?

A

Over 20% blasts in peripheral blood or bone marrow

46
Q

Management of leukaemia?

A

Multi-chemotherapy

+ methotrexate (ALL)

In CML give imatinib

Bone marrow transplant (allogenic or autologous)

47
Q

Which leukaemia is treated with imatinib?

What type of drug is it?

A

CML

A biologic: a tyrosine kinase inhibitor

48
Q

What is multiple myeloma?

A

Malignant proliferation of plasma cells

Resulting in overproduction of a monoclonal antibody

And diffuse bone marrow infiltration causing bone marrow failure

49
Q

How are myelomas classified?

What’s the most common?

A

By the type of antibody produced

IgG is most common

50
Q

Clinical features of multiple myeloma?

A

Bones:
Pain
Pathological fractures
Spinal cord/nerve root compression

Anaemia
Leukopenia
Thrombocytopenia

Cardiac failure
Impaired renal function

Hypercalcaemia

Fatigue, nausea, constipation, dehydration

Hyperviscosity syndrome

51
Q

What are the symptoms of hypercalcaemia?

A

Bones (pain)
Stones (renal)
Abdominal groans (constipation)
Psychic moans (confusion)

52
Q

Why does multiple myeloma cause bone problems?

A

Imbalanced bone remodelling

Osteoclast actvity increased, osteoblast activity reduced

So lytic bone lesions
Fractures

53
Q

Why does multiple myeloma cause hypercalcaemia?

A

Because of bone breakdown

Osteoclast activity increased, osteoblast activity reduced

54
Q

Why does multiple myeloma cause renal problems?

A

Accumulation of the immunoglobulins in the kidneys

55
Q

What is hyperviscosity syndrome?

A

Symptoms caused by an increase in viscosity of blood

Headache
Visual disturbance
Seizures
Cerebrovascular events

56
Q

Investigations of multiple myeloma?

A

FBC, ESR, U+E
Plasma viscosity

Electrophoresis: serum (shows which immunoglobulin) and urine (look for Bence Jones’ protein)

XR: lytic bone lesions

Bone marrow aspirate and biopsy

57
Q

What is Bence Jones’ protein?

A

A monoclonal globulin protein or immunological light chain

Found in urine in multiple myeloma

58
Q

Management of multiple myeloma?

A

Incurable

Chemotherapy

High dose steroids

Allogenic stem cell transplant

Bisphosphonates and pain killers

59
Q

A patient with CLL suddenly become acutely unwell, what could have happened?

A

Richter’s transformation: transformation to a high grade B cell lymphoma

Warm autoimmune haemolytic anaemia: haemolysis occuring at high temperatures

60
Q

A patient with CML becomes suddenly acutely unwell, what could have happened?

A

Transformation to AML or ALL (less common)

Dermatology & Haematology (8 decks)

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