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Y3 CBLs > CBL_7 Haematology > Flashcards

CBL_7 Haematology Flashcards

1
Q

Normal hematopoiesis diagram

A
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2
Q

What’s the most preferred location for bone marrow biopsy?

A

upper pelvic bone (posterior iliac crest) -> no major blood vessels or organs are located nearby

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3
Q

Do malignant cells function normally?

A

No

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4
Q

Why we can see abnormal blood count in leukemia?

A

Leukaemia cells proliferating in the bone marrow will replace normal cells -> reduce other elements of the bone marrow -> abnormal blood counts

*as bone ,arrow will become ‘over-crowded’

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5
Q

What type of leukemia is more common in old age?

A

Acute Myeloid Leukemia (AML)

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6
Q

What type of leukemia is more common in children?

A

Acute Lymphoblastic Leukemia (ALL)

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7
Q

What’s the Philadelphia chromosome?

A

Chromosome 22

*in chronic myeloid leukemia: arms of chromosomes 22 and 9 switches the places (translocation)

This combination causes BCR-ABL genes to combine -> this switches Tyrosine Kinase -> uncontrolled proliferation

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8
Q

(2) characteristics of myelodysplastic syndrome

A
  • defective maturation of myeloid cells
  • build up of blasts (in the bone marrow)
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9
Q

What % of blasts is seen in:

A. Myelodysplastic syndrome

B. ALL

A
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10
Q

Risk factors for Acute Leukemia

A
  • Down Syndrome
  • exposure to radiotherapy (e.g. used in Rx for other malignancy)
  • exposure to alkylating chemotherapy
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11
Q

Symptoms of AML and ALL

A
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12
Q

Why is there hepatosplenomegaly and lymphadenopathy in leukemia?

A

Blasts (T cells) migrate to the organs

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13
Q

What does peripheral blood smear show in AML and what in ALL? (simply)

A
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14
Q

Features of myeloblasts in leukemia on peripheral blood smear

A

myeloblasts in leukemia = AML

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15
Q

Features of lymphoblasts in leukemia on peripheral blood smear

A

Lymphoblasts = ALL

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16
Q

What are (2) markers for lymphoblastic leukemia in immunophenotyping ?

A
  • CD10 -> surface marker for pre B cells
  • TdT -> DNA polymerase only in lymphoblasts
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17
Q

What is the key distinction between Acute and Chronic Leukemias?

A

Acute -> cells do not mature at all

Chronic -> cells mature only partially

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18
Q

What is a simple difference in pathophysiology of CML and CLL?

A
  • CML -> cells divide too quickly
  • CLL -> cells do not die as they should

Result of both: too many premature cells (as chronic leukemia = cells develop only partially)

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19
Q

Symptoms of Chronic Myeloid and Chronic Lymphoid Leukemia

A
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20
Q

The difference on a peripheral blood smear in CML and CLL

A
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21
Q

Clinical features of Acute Leukemias

A

–Tiredness, infection, bruising/bleeding

–High white cell count

–Low haemoglobin (anaemia)

–Low platelet count (thrombocytopenia)

–Low neutrophil count (neutropenia)

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22
Q

What type of cancer is it?

A

Auer Rod = Acute Myeloid Leukemia

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23
Q

What’s therapy for AML? (2)

A

AML

–3 to 4 cycles of combination chemotherapy

–Haemopoietic stem-cell transplant (HSCT) for some patients

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24
Q

What’s myelodysplasia?

A

Myelodysplasia -> an acquired neoplastic disorder of hematopoietic stem cells, they are pre-leukaemia and are most likely to progress to AML

They are more common with age, and they present with bone marrow failure

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25
Q

In what type of cancer gum hypertrophy can be seen?

A

Acute Myeloid Leukemia

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26
Q

DIagnostic features of AML (3)

A
  • WCC is often high, but this can be normal or low
  • Blast cells may be few in the peripheral blood
  • Auer Rods are diagnostic of AML
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27
Q

What’s the supportive management of AML?

A

Supportive:

  • Blood/platelet transfusion
  • IV fluids.
  • Allopurinol and this is to prevent tumour lysis syndrome
  • Insert Hickman line for IV access (central venous catheter used for administration of chemo)
  • Walking can relieve the fatigue
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28
Q

Chemotherapy in AML

  • two main drugs used in chemo
A
  • very intensive, resulting in long periods of marrow suppression with neutropenia and low platelets.

Two main drugs used in chemo:

Daunorubicin

Cytarabine

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29
Q

What’s Myelodysplastic syndrome?

A
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30
Q

What’s the diagnosis of myelodysplastic syndrome?

A
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31
Q

What’s the management of myelodysplastic syndrome?

A
32
Q

Supportive Mx of ALL

A
  • Blood/platelet transfusion
  • IV fluids
  • Allopurinol and this is to prevent tumour lysis syndrome
  • Insert Hickman line for IV access.
33
Q

In what type of hematological cancer CNS involvement is common?

A

ALL

34
Q

Investigations done in ALL

A
  • Characteristic blast cells on blood film and bone marrow
  • WCC are high
  • CXR and CT scan to look for mediastinal and abdominal lymphadenopathy.
  • Lumbar puncture should be done and that is to see if there is any CNS involvement.
35
Q

Management of infections in ALL

A

Infections are dangerous and that is because of neutropenia caused by the disease

  • Immediate IV antibiotics
  • Prophylactic antibiotics, antivirals and antifungals
  • Neutropenic regimen (specific combination of ABx)
36
Q

Steps in chemotherapy in ALL (3)

A
  1. To induce remission (different chemo agents e.g. vinicristine)
  2. Consolidation: medium dose chemo over few weeks
  3. Maintenance: prolonged chemotherapy, mercaotopurine, methotrexate and vincristine and prednisolone for 2 years
37
Q

What’s given in terms of CNS protection in ALL?

A

ALL = often CNS involvement

CNS prophylaxis: intrathecal or high dose IV methotrexate or CNS radiation

38
Q

What condition overproduction of these mature blood cells may result in

Overproduction of:

A. Neutrophils

B. RBCs

C. Platelets

A
39
Q

What’s the most common leukemia seen in adults?

A
  • Chronic lymphocytic leukaemia (CLL) is caused by a monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells (99%)
  • It is the most common form of leukaemia seen in adults
40
Q

Features of CLL

A
  • often none -> found on blood test
  • constitutional: anorexia, weight loss
  • bleeding, infections
  • lymphadenopathy more marked than CML
41
Q

What’s Richter’s transformation?

A

Chronic Lymphocytic Leukemia (CLL) -> possible transformation to high-grade lymphoma (Richter’s transformation)

42
Q

What is typical finding on blood smear in CLL?

A

Smudge cells (aka smear cells)

43
Q

What type of cancer is Philadelphia Chromosome mostly associated with?

A

CML (chronic myeloid leukemia)

44
Q

Presentation of CML

A

Usually in 60-70 years

  • anaemia: lethargy
  • weight loss and sweating are common
  • splenomegaly may be marked →abdo discomfort
  • decreased leukocyte alkaline phosphatase
  • bone pain
45
Q

Management of CML

A
  • imatinib is now considered first-line treatment
  • hydroxyurea
  • interferon-alpha
  • allogenic bone marrow transplant

Imatinib

inhibitor of the tyrosine kinase associated with the BCR-ABL defect (Philadelphia chromosome)

very high response rate in chronic phase CML

46
Q

What’s Imatinib?

A

Imatinib

  • inhibitor of the tyrosine kinase associated with the BCR-ABL defect (Philadelphia chromosome)
  • very high response rate in chronic phase CML
47
Q

What’s ‘blast crisis’?

A

blast crisis’ – i.e. transformation of CML to Acute Leukaemia (can either be ALL of AML)

48
Q

What’s myeloma?

What’s the peak incidence for myeloma?

A

Myeloma is neoplasm of a bone marrow

Peak incidence 60-70 y

49
Q

What are the clinical features of myeloma?

A

Clinical features

  • bone disease: bone pain, osteoporosis + pathological fractures (typically vertebral), osteolytic lesions
  • lethargy
  • infection
  • hypercalcaemia
  • renal failure
  • other features: amyloidosis e.g. Macroglossia, carpal tunnel syndrome; neuropathy; hyperviscosity
50
Q

Investigations for myeloma (3)

A
  • urine and bloods -> characteristics of myeloma: monoclonal proteins (usually IgG or IgA) in the serum and urine (Bence Jones proteins)
  • Whole body MRI -> to look for bone lesions
  • X-rays: ‘rain-drop skull’ (random pattern of dark spots)
51
Q

What are the characteristic findings in serum and urine in myeloma? (2)

A
  • monoclonal proteins (serum) -> usually IgA, IgG
  • Bence Jones proteins in urine
52
Q

What are the diagnostic criteria for myeloma?

A

The diagnostic criteria for multiple myeloma requires one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma.

Major criteria

  • Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
  • 30% plasma cells in a bone marrow sample
  • Elevated levels of M protein in the blood or urine

Minor criteria

  • 10% to 30% plasma cells in a bone marrow sample.
  • Minor elevations in the level of M protein in the blood or urine.
  • Osteolytic lesions (as demonstrated on imaging studies).
  • Low levels of antibodies (not produced by the cancer cells) in the blood.
53
Q

Why is there hypercalcaemia in myeloma?

A

Hypercalcaemia in myeloma

  • primary factor: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
  • much less common contributing factors: impaired renal function, increased renal tubular calcium reabsorption and elevated PTH-rP levels
54
Q

Treatment for myeloma

A

–Induction with combination chemotherapy

–Autologous stem-cell transplant in first remission

55
Q

What is the sign?

What’s the diagnosis?

A

‘Rain drop’ skull

In multiple myeloma

56
Q

What is the kidney failure a result of in multiple myeloma?

A

Deposition of abnormal proteins (e.g. abnormal monoclonal antibodies) produced by malignant cells

57
Q

What’s the mnemonic and meaning for the presentation of multiple myeloma?

A

C constipation, nausea, poor appetite -> due to hypercalcaemia

R - Renal failure (due to deposition of proteins produced by malignant plasma change) - may present with thirst

A- Anaemia - may presence with fatigue and pallor (due to crowded bone marrow, depletion of RBCs)

B - bone lesions/ fractures/ Back pain - as cytokines produced by malignant plasma cells increase bone turnover -> more calcium into the blood -> fragile bones

58
Q

What’s that called?

What condition is it?

A

Rouleaux of RBCs -> RBCs attached in chains

Multiple myeloma

59
Q

What (in general) lymphoma is?

A
  • Lymphomas are disorders caused by malignant proliferation of lymphocytes
  • These accumulate in the lymph nodes caused lymphadenopathy, but may also be found in peripheral blood or infiltrate organs
  • Tumours of lymphatic system: lymph nodes, MALT, splee, bone marrow
60
Q

Classification of lymphomas

A
61
Q

What is (2) peak incidence for Hodgkin lymphoma?

A
  • 15 - 30
  • >65
62
Q

What are the cells characteristic of Hodkin’s lymphomas?

A

The characteristics of Hodgkin’s are cells with mirror-image nuclei, and these are called Reed-Sternberg cells

63
Q
A
64
Q

Which lymphoma (Hodgkins or Non-Hodgkins) have a better survival?

A

Hodgkins have better survival

65
Q

Symptoms for Hodgkins lymphoma

A

enlarged, painless, non-tender ‘rubbery’ superficial lymph nodes, typically the cervical, also the axillary and the inguinal

The lymph nodes may grow bigger or decrease in size

  • Night sweats
  • Fever
  • Weight loss
  • Pruitis
  • Lethargy
66
Q

What cancer may present with alcohol-induced lymph nodes pain?

A

Hodgkins lymphoma

67
Q

What is the Ann-Arbor system used for?

A

Ann-Arbor system -> in Hodgkins lymphoma, for prognosis and treatment

68
Q

Stages on Ann-Arbor system

A
69
Q

What are B symptoms in the Hodgkin lymphoma?

A

B symptoms - indicate worse prognosis:

  • weight loss in the last 6 months
  • unexplained fever >38 C
  • night sweats (needing a change of clothes)
70
Q

What is the difference between Hodgkin and Non-Hodgkin lymphoma?

A

There is an absence of Red Steenberg cell in Non-Hodgkin lymphoma

71
Q

Treatment of Hodgkins lymphoma

A

both chemo and radiotherapy are used

72
Q

What infection is linked with Hodgkin’s lymphoma?

A

Infection with Ebstein Barr virus is linked to the condition (particularly mixed cellularity lymphoma

73
Q
A
74
Q

What has better prognosis: T cell lymphoma or B cell lymphoma?

A

T-cell lymphomas tend to do less well then those with B-cell lymphomas

(B cell lymphomas - better prognosis)

75
Q

Types of stem cell transplants (2)

A
  • autogenous: from patient’s own stem cells, curative/ or extent remisison
  • allogenic: from a donor, curative intent (all types of hemo ca, but most often acute leukemia)
76
Q
A

Y3 CBLs (13 decks)

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