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Haematology and Immunology > Malignancy > Flashcards

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
Describe stem cell Tx in AML
Allogenic HLA matched donors Aim to conoslidate remission/potentially cure
26
What does myeloid blast cell count <15% mean
Myelodysplastic disorders
27
Describe remission
State where blood counts have returned to near normal state independent of transfusion Blast count <5%
28
New developments in AML treatment
Targeted Ab Targeted small molecules New delivery systems
29
Pathology of chronic myeloid leukaemia
Affects myeloid cells: Ongoing proliferation AND Ongoing differentiation ast a higher rate
30
Features of CML
``` Anaemia Splenomegaly Abdo pain Weight loss Gout ```
31
Features of hyperleukostasis
Fundal haemorrhage Venous congestion Altered consciousness Resp failure
32
What is hyperleukostaiss
Medical emergency Commonly associated with CML Extremely elevated blast cell counts and symptoms of decreased tissue perfusion
33
Symptoms of CML
Mostly chronic and insidious W.t loss Fever Fatigue Sweats
34
Lab features of CMl
Increased WCC Increased platelets Decreased Hb (anaemia)
35
Blood film features of CML
All stages of WCC differentiation are increased
36
Ix for CML
FBC Blood film Bone marrow biopsy Dx
37
Which chromosomal anomaly is associated with CML
Philadelphia chromosome
38
Describe philadelphia chromosome
Small chromosome 22 Result of balance translocation between chromosome 9 and 22 Forming fusion BCR-ABL oncogene
39
Which oncogene is formed in Philadelphia chromosome
BCR-ABL
40
Why are Tyroskine kinase inhibitors used to treat CML
Because BCR-ABL oncogene (from Philadelphia chromosome) has tyrosine kinase activity
41
1st line RX for CML
Tyrosine Kinase Inhibitors: e.g Imatinib Direct inhibitor of BCR-ABL 1st line in all patient’s now
42
2nd line Rx CML
Allogenic Tx Few now Carried sig. morbidity and mortality
43
When would allogenic Rx be used in CML
Failure of tyrosine kinase inhibitors
44
Who is the Philadelphia chromosome found in
Most patients with CML | Some patients with AML
45
Who does CLL mainly affect
Older
46
What is the commonest leukaemia worldwide
CLL
47
Aetiology of CLL
Potentially genetic | But relatively unknown
48
Dx criteria for CLL
Blood > 5 x 10 to 9/L lymphocytes | Bone marrow > 30% lymphocytes
49
Pathology of CLL
Affects lymphoid cells so that Ongoing proliferation AND Ongoing differentiation at a higher rate
50
Clinical features of CLL
Bone marrow failure: Anaemia Thrombocytopenia Lymphadenopathy (enlarged, rubbery, non-tender) Splenomegaly Fever and sweats
51
What is the commonest presentation of CLL
Often asymptomatic | Patients picked up on routine bloods for something else e.g anaemia
52
Ix for CLL
FBC Blood film Bone marrow biopsy
53
Which staging is used for CLL
Binet
54
Describe Binet stage A
<3 groups LN affected | Increased WCC
55
Describe Binet stage B
>3 groups of enlarged LN affected | And increased WCC
56
Describe Binet Stage C
Enlarged LN or spleen Increased WCC Decreased RBC Decreased platelets
57
Rx for CLL
Often nothing 1/2 require chemo 1/2 require observation
58
Potential Rx treatments for CLL
Cytotoxic chemotherapy Monoclonal antibodies Novel agents Radiotherapy
59
Which monocloncal ab can be used to Rx CLL
Rituximab
60
Which novel agents cn be used to Rx CLL
Bruton tyrosine kinase inhibtors | PI3K inhibitor
61
What can radiotherapy be used to Rx in CLL
Splenomegaly | Lymphadenopathy
62
Indications for RX in CLL
``` Progressive bone marrow failure Massive lymphadenopathy Progressive splenomegaly Lymphocyte doubling time <6 months Systemic symptoms Autoimmune cytopenias ```
63
Poor Prognostic factors CLL
``` Advanced disease Atypical lymphocyte morphology Rapid lymphocyte doubling time CD38+ expression Loss/mutation p53 ```

Haematology and Immunology (7 decks)

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