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103 Theme 2 - Blood > Symposium 2 - Leukaemia > Flashcards

Symposium 2 - Leukaemia Flashcards

1
Q

Complete the diagram on haematopoiesis

A
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2
Q

What is G-CSF?

A

G-CSF promotes neutrophil proliferation
G-CSF = granulocyte colony stimulating factor

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3
Q

What is cancer?

Transformed cell phenotype?

Genetic?

Epigenetic?

A

Transformed cell phenotype

–Uncontrolled proliferation

–Failure to undergo apoptosis

Genetic

–Oncogenes

–Tumour suppressor genes

Epigenetic

–Dysregulated gene expression

–Aberrant DNA methylation

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4
Q

Complete the diagram on types of DNA mutation

A
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5
Q

What are the clinical features of leukaemia?

A

Myelofibrosis (causes massive splenomegaly)

Polycythemia rubra vera (too many red cells)

Essential thrombocythemia (too many platelets)

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6
Q

What does this blood smear show?

A
  1. Polycythemia rubra vera
  2. Myelofibrosis
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7
Q

What does this blood smear show?

A

Leucoerthyroblastic blood picture

Nucleated RBC and immature leucocytes

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8
Q

What is JAK-STAT signalling?

A

Signal transduction pathway for EPO and G-CSF

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9
Q

What signalling pathway is mutated in the majority of acute myeloid leukaemia cases?

A

JAK-STAT signalling
Signal transduction pathway for EPO and G-CSF

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10
Q

Complete the diagram

A
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11
Q

Why does myelofibrosis cause splenomegaly?

A

When bone marrow becomes fibrotic, spleen takes over

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12
Q

What is myelofibrosis?

A

Fibrotic bone marrow

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13
Q

What is a myeloproliferative state?

A

Overproduction of a type of blood cell

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14
Q

Whats the diagnosis?

A

Too many white cells - chronic myeloid leukaemia

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15
Q

What chromosome is associated with chronic myeloid leukaemia?

A

“Philadelphia chromosome”

Chromosome 22->9

t(9;22) translocation

BCR gene from chromosome 22 and ABL gene from chromosome 9 come together.

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16
Q

What test is this?

A

“FISHing” for CML
FISH = fluorescent in situ hybridisation

17
Q

What does imatanib target?

A

The BCR-ABL oncogene

18
Q

What effect does imatinib have on chronic myeloid leukaemia patients?

A

Normalises blood counts

Improves survival in CML

19
Q

Which leukaemia can occasionally turn into AML?

A

CML

20
Q

What is acute myeloid leukaemia?

A

Uncontrolled proliferation of primitive cells in the bone marrow

21
Q

Name 3 causes of bone marrow failure in acute myeloid leukaemia

A

–Anaemia

–Infections

–Bleeding

22
Q

What does this show?

A

AML

Leukaemic blasts - very high nucleus:cytoplasm ratio

23
Q

What are the clinical features of AML?

A
  1. Anaemia
  2. Infections
  3. DIC
  4. Ulcers
  5. Infiltration
  6. Bruising
24
Q

What are the 5 ways of diagnosing AML?

A
  1. Morphology - blood film
  2. Immunophenotyping
  3. Genetic
  4. Cytogenetic
  5. Molecular
25
Q

What are the 3 treatments for AML?

A

Chemotherapy – kills rapidly dividing cells:

Supportive therapy:

–Antibiotics, antifungals

–Transfusions of blood and platelets

Allogeneic stem cell transplantation:

26
Q

What are the steps for the donor and recipient in a allogeneic stem cell transplant?

A
27
Q

What are the 2 options for an allogenic stem cell transplant donor?

A

Sibling (1-in-4 chance of being a match)

Matched unrelated donor (Anthony Nolan

28
Q

What chemotherpy is used for AML?

A

–Combination regimes

–Myelo-ablative cycles of treatment

29
Q

What 3 supporting measures are needed for AML patients?

A
30
Q

How would you manage a patient with neutropenic sepsis?

A

MEDICAL EMERGENCY – High risk of death

  • Blood cultures and blind antibiotic therapy if fever > 38°C

1st line – Tazocin (Piperacillin/Tazobactam) +/- Gentamicin

2nd line – Switch to Meropenem +/- Teicoplanin (for Gram +ve)

3rd line – Add anti-fungal e.g. Ambisome (Amphotericin)

Resuscitate patient with i.v. fluids if hypotensive

May require inotropic support on ITU

31
Q

In neutropenic sepsis are gram positive or gram negative bacteria more dangerous?

A

Gram negative

32
Q

What type of pneumonia can AML patients develop?

A

Pneumocystis pneumonia

33
Q

What is graft vs host disease? (acute/chronic)

A
  • Caused by donor/host mismatches in major and minor HLA loci
  • Results in acute GVH (<100 days) and chronic GVH (>100 days) post-transplant
34
Q

How is graft vs host disease prevented?

A

–T-cell depletion of infused donor cells (graft)

–Immunosuppression of recipient (ciclosporin)

35
Q

What are the clinical manifestations of graft vs host disease?

A

–Skin rash, sometimes severe

–Diarrhoea, can be bloody

–Deranged liver function, can lead to liver failure

36
Q

What is graft vs leukaemia?

A

•Graft-vs-leukaemia effect is how the stem cell transplant cures leukaemia

37
Q

_____________ post-Tx can treat relapse by augmenting GVL effect

A

Donor lymphocyte infusions (DLI)

38
Q

What mutation occurs as a young baby but takes years to cause AML?

A

DNMT3A methyltransferase

103 Theme 2 - Blood (10 decks)

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