Malignancy Flashcards

1
Q

What is acute Lymphoblastic leukaemia

A

Acute malignancy of lymphoid cells

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2
Q

Pathology of ALL

A

Affecting lymphoid lineages
Increase proliferation
But failure to differentiate

Uncontrolled proliferation of immature blast cells

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3
Q

Who is ALL common in

A

Children

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4
Q

Clinical features of ALL

A

V. short Hx/V. Acute:

Marrow failure:
Anaemia (Hb)
Infection (WCC)
Bleeding (platelets)
Pallor (due to anaemia)
Petechia (due to platelet dysfunction)

Infiltration:
Hepatosplenomegaly
Lymphadenopathy

CNS involvement:
CN palsies
Meningism

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5
Q

Common infections in ALL

A
Bacterial septicaemia 
Zoster 
CMV 
Measles 
Candiadisis
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6
Q

Blood film in ALL

A

Characteristic blast cells

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7
Q

Bone marrow in ALL

A

Characteristic blast cells

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8
Q

Dx blast cell criteria for ALL

A

> 20% lymphoblasts present in bone marrow

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9
Q

Ix for ALL

A
Blood film 
Bone marrow biopsy 
FBC
Coagulation screen 
U&E's
LFTs
CXR 
CT 
LP
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10
Q

Prognosis in ALL in children compared to adults

A

Cure rates in children 70-90%

Adults = poorer prognosis

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11
Q

Describe CAR therapy

A

Patient/healthy 3rd party T cells harvested
Transfected to express a specific T-cell receptor
Expanded in vitro
Re-infused into the patient

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12
Q

Complications of T cell immunotherapy

A

Cytokine release syndrome

Neurotoxicity

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13
Q

Chemotherapy regimen for ALL

A

Induction therapy
Consolidation therapy
Maintenance chemotherapy

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14
Q

Newer therapies used to treat ALL

A

Bispecific T cell engagers

CAR therapy

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15
Q

CNS directed/prophylaxis Rx in ALL

A

Intrathecal (or high dose) methotrexate +/- CNS irradiation

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16
Q

What is the commonest acute leukaemia in adults

A

AML

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17
Q

Pathology of AML

A

Affects Myeloid cells so that:

Increased proliferation but failure to differentiate or mature

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18
Q

Bone Marrow Failure clinical features in AML

A

Anaemia
Thrombocytopenia (purpura and mucosal membrane bleeding)
Infection (due to neutropenia -> predominantly bacterial and fungal)

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19
Q

Infiltration clinical features of AML

A
Hepatomegaly 
Splenomegaly 
Gum hypertrophy 
Infiltration brain 
Bone pain (bone infiltration)
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20
Q

Blood count features AML

A

Neutropenia
Thrombocytopenia
Decreased Hb

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21
Q

Ix for AML

A

FBC
Blood fim
Bone marrow biopsy

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22
Q

What blast count confirms AML

A

> 20%

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23
Q

When would CSF be Ix in AML

A

If CNS symptoms present

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24
Q

Rx for AML

A

Supportive care
Anti-leukaemic chemotherapy
Stem cell Tx
Targeted treatment

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25
Q

Describe stem cell Tx in AML

A

Allogenic
HLA matched donors
Aim to conoslidate remission/potentially cure

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26
Q

What does myeloid blast cell count <15% mean

A

Myelodysplastic disorders

27
Q

Describe remission

A

State where blood counts have returned to near normal state independent of transfusion
Blast count <5%

28
Q

New developments in AML treatment

A

Targeted Ab
Targeted small molecules
New delivery systems

29
Q

Pathology of chronic myeloid leukaemia

A

Affects myeloid cells:
Ongoing proliferation
AND
Ongoing differentiation ast a higher rate

30
Q

Features of CML

A
Anaemia 
Splenomegaly 
Abdo pain 
Weight loss 
Gout
31
Q

Features of hyperleukostasis

A

Fundal haemorrhage
Venous congestion
Altered consciousness
Resp failure

32
Q

What is hyperleukostaiss

A

Medical emergency
Commonly associated with CML
Extremely elevated blast cell counts and symptoms of decreased tissue perfusion

33
Q

Symptoms of CML

A

Mostly chronic and insidious
W.t loss Fever
Fatigue
Sweats

34
Q

Lab features of CMl

A

Increased WCC
Increased platelets
Decreased Hb (anaemia)

35
Q

Blood film features of CML

A

All stages of WCC differentiation are increased

36
Q

Ix for CML

A

FBC
Blood film
Bone marrow biopsy Dx

37
Q

Which chromosomal anomaly is associated with CML

A

Philadelphia chromosome

38
Q

Describe philadelphia chromosome

A

Small chromosome 22
Result of balance translocation between chromosome 9 and 22
Forming fusion BCR-ABL oncogene

39
Q

Which oncogene is formed in Philadelphia chromosome

A

BCR-ABL

40
Q

Why are Tyroskine kinase inhibitors used to treat CML

A

Because BCR-ABL oncogene (from Philadelphia chromosome) has tyrosine kinase activity

41
Q

1st line RX for CML

A

Tyrosine Kinase Inhibitors: e.g Imatinib
Direct inhibitor of BCR-ABL

1st line in all patient’s now

42
Q

2nd line Rx CML

A

Allogenic Tx
Few now
Carried sig. morbidity and mortality

43
Q

When would allogenic Rx be used in CML

A

Failure of tyrosine kinase inhibitors

44
Q

Who is the Philadelphia chromosome found in

A

Most patients with CML

Some patients with AML

45
Q

Who does CLL mainly affect

A

Older

46
Q

What is the commonest leukaemia worldwide

A

CLL

47
Q

Aetiology of CLL

A

Potentially genetic

But relatively unknown

48
Q

Dx criteria for CLL

A

Blood > 5 x 10 to 9/L lymphocytes

Bone marrow > 30% lymphocytes

49
Q

Pathology of CLL

A

Affects lymphoid cells so that
Ongoing proliferation
AND
Ongoing differentiation at a higher rate

50
Q

Clinical features of CLL

A

Bone marrow failure:
Anaemia
Thrombocytopenia

Lymphadenopathy (enlarged, rubbery, non-tender)
Splenomegaly
Fever and sweats

51
Q

What is the commonest presentation of CLL

A

Often asymptomatic

Patients picked up on routine bloods for something else e.g anaemia

52
Q

Ix for CLL

A

FBC
Blood film
Bone marrow biopsy

53
Q

Which staging is used for CLL

A

Binet

54
Q

Describe Binet stage A

A

<3 groups LN affected

Increased WCC

55
Q

Describe Binet stage B

A

> 3 groups of enlarged LN affected

And increased WCC

56
Q

Describe Binet Stage C

A

Enlarged LN or spleen
Increased WCC
Decreased RBC
Decreased platelets

57
Q

Rx for CLL

A

Often nothing
1/2 require chemo
1/2 require observation

58
Q

Potential Rx treatments for CLL

A

Cytotoxic chemotherapy
Monoclonal antibodies
Novel agents
Radiotherapy

59
Q

Which monocloncal ab can be used to Rx CLL

A

Rituximab

60
Q

Which novel agents cn be used to Rx CLL

A

Bruton tyrosine kinase inhibtors

PI3K inhibitor

61
Q

What can radiotherapy be used to Rx in CLL

A

Splenomegaly

Lymphadenopathy

62
Q

Indications for RX in CLL

A
Progressive bone marrow failure 
Massive lymphadenopathy 
Progressive splenomegaly 
Lymphocyte doubling time <6 months 
Systemic symptoms 
Autoimmune cytopenias
63
Q

Poor Prognostic factors CLL

A
Advanced disease
Atypical lymphocyte morphology 
Rapid lymphocyte doubling time 
CD38+ expression 
Loss/mutation p53