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2.2 Haematology > Haematological Malignancies 2 > Flashcards

Haematological Malignancies 2 Flashcards

(55 cards)

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1
Q

What is Hodgkin lymphoma
(5)

A

Clonal B-cell malignant that develops within the lymphatic system

The malignant Reed-Sternberg Cell typically has a bilobed nucleus that gives an “owls eyes” appearance

Diagnosis, excisional lymph node biopsy

Spreads in an orderly fashion to adjacent nodes

Painless lymphadenopathy, constitutional “B” symptoms (fever, night sweat, weight loss), pruritus, hepatosplenomegaly

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2
Q

Write about Reed-Sternberg

A

Cell may contain more than one nucleus

Presence in peripheral blood indicate advanced stage of disease

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3
Q

What are the three main types of lymphoma

A

NK cell
B cell
T cell

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4
Q

What cells are involved in leukaemia

A

Neutrophil
Monocyte
RBC
Megakaryocyte

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5
Q

Write about acute lymphoblastic leukaemia

A

Usually occurs before 14 years of age

Peak incidence between 2 and 9 years

Less common in adults -> peak at about 50

Low RCC, Hb, Hct, platelet count, low normal or high WBC count

Accumulation of malignant, poorly differentiated lymphoid cells within the Bone marrow, peripheral blood and 20% of the time at extramedullary sites

Chromosomal aberrations are the hallmark of ALL, but are not sufficient to generate leukaemia.

Characteristic translocations

More recently, a variant with a similar gene expression profile to Ph positive ALL but without the BCR-ABL1 rearrangement has been identified (poor prognosis)

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6
Q

Comment on the prevalence of ALL

A

Usually occurs before 14 years of age

Peak incidence between 2 and 9 years

Less common in adults -> peak at about 50

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7
Q

What are the clinical findings of ALL?
(5)

A

Low RCC
low Hb
low Hct
low platelet count
low normal or high WBC count
Increased lymphoblast

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8
Q

What exactly happens in ALL

A

Accumulation of malignant, poorly differentiated lymphoid cells within the Bone marrow, peripheral blood and 20% of the time at extramedullary sites

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9
Q

What causes ALL

A

Chromosomal aberrations are the hallmark of ALL, but are not sufficient to generate leukaemia.

Characteristic translocations

More recently, a variant with a similar gene expression profile to Ph positive ALL but without the BCR-ABL1 rearrangement has been identified (poor prognosis)

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10
Q

Write about the clinical findings of bone marrow aspirate in ALL

A

Hypercellularity
High lymphoblasts greater than 20%

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11
Q

Write about acute myeloid leukaemia

A

Most common type of acute leukaemia in adults

Accounts for 30% of all leukaemia

300-400 cases of AML in Ireland/year

Outcome in patients with AML ranges from death within a few days of beginning treatment to likely cure

The major reason patients are not cured is resistance to treatment, often manifested as relapse from remission, rather than, even in older patients, treatment related mortality, whose incidence is decreasing

Knowledge of the pre-treatment mutation statis of various genes has improved our ability to assign initial treatment and, of particular importance, knowledge of whether patients apparently in remission have measurable residual disease should influence subsequent management

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12
Q

What is the most common type of leukaemia in adults

A

Acute myeloid leukaemia in adults

Accounts for 30% of all leukaemia in adults

300-400 cases per year

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13
Q

Comment on the severity of AML

A

One of the harder leukaemias to beat

Outcome in patients with AML ranges from death within a few days of beginning treatment to likely cure

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14
Q

Why is AML so hard to cure

A

The major reason patients are not cured is resistance to treatment, often manifested as relapse from remission, rather than, even in older patients, treatment related mortality, whose incidence is decreasing

Knowledge of the pre-treatment mutation statis of various genes has improved our ability to assign initial treatment and, of particular importance, knowledge of whether patients apparently in remission have measurable residual disease should influence subsequent management

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15
Q

How is AML classified

A

M0 -> M7

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16
Q

What is M0 AML

A

Undifferentiated acute myeloblastic leukaemia
5%

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17
Q

What is M1 AML

A

Greater number of myeloblasts with less than 10% granulocytic differentiation

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18
Q

What is M2 AML

A

Myeloblasts in great number with granulocytic differentiation >10%

NSE < 20%

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19
Q

What is M3 AML

A

Promyelocytes that are hyper granular with many Auer rods on CAE or Wright-stain and variant form cells with reniform nuclei, multilobed or bibbed, primeval cells with multiple Auer rods or relative scarcity of Hypergranular promyelocytes

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20
Q

What is M4 AML

A

> 20% but <80% NSE-butyrate positivity in Monocytic cells

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21
Q

What is M5 AML

A

Monocytic cells with >80% NSE positivity

a. Monocytic differentiated
b. Monocytic, differentiated

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22
Q

What is M6 AML

A

> 30% myeloblasts with more than 50% erythroblasts eliminating the erythrois cells

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23
Q

What is M7 AML

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A

Acute megakaryoblastic leukaemia <5%

24
Q

Write about CLL
(7)

Study These Flashcards
A

Most common leukaemia, usually B lineage

Normally B cells produce antibody in CLL they don’t

Often diagnosed on routine check up

BM aspirate not useful in early stages

Rai Binet staging system

Flow cytometry needed for diagnosis

Richters transformation: very rare, very severe, CLL> Prolymphocytic leukaemia

25
What are the clinical symptoms of CLL
Lymphocytosis B Smudge/smear cells up Reticulocyte up Haemoglobin down
26
Write about the use of flow cytometry in CLL
Needed for diagnosis Neoplastic B-cells with co-expression of CD19, CD5, CD23, with weak CD20 and monoclonal surface immunoglobulin expression
27
What is a telltale feature of CLL
Hairy Cell
28
What are some laboratory findings of peripheral blood? (4)
Hairy cells Pancytopenia Neutropenia Flow cytometry
29
Explain how flow cytometry is used for CLL (2)
The cells are strongly positive for CD20 In contrast to other B cell disorders they also express CD25, CD103 and CD123 They are CD5 negative
30
Write about hairy cell trapping
Hairy cells are trapped in the bone marrow and that's why you get a dry tap They are also trapped everywhere else, therefore, they don't show up in the lymph nodes and that's why the clinical finding of lymphadenopathy is absent
31
Write about the clinical findings of plasma cell myeloma (7)
Rouleaux formation RBCC down Neoplastic plasma cells Neoplastic plasma cells in BM aspirate Bence-Jones in urine electrophoresis Paraprotein in serum electrophoresis IG up in serum electrophoresis
32
Write about the use of flow cytometry in plasma cell myeloma (3)
Usually lack surface light chain with monotypic cytoplasmic Ig Express bright CD38, CD138, often CD56+ or CD117+ May have partial CD45, usually negative for CD20, CD19 and CD10
33
What are MPNs
Myeloproliferative neoplasms
34
What does Ph negative MPN mean
Philadelphia chromosome negative myeloproliferative neoplasms
35
What are the four types of philadelphia chromosome negative MPNs
Myelofibrosis Polycythemia vera Essential thrombocythemia Other
36
What are some clinical findings of CML (6)
RBCC down Little to no platelets WBCC up Neutrophils myelocytes PHL Chromosome in BM Hypercellularity in bone marrow > 90% Blasts
37
Write about myelodysplastic Neoplasms
Cytopenias Dysplasia in one or more of the major myeloid cell lines Ineffective haematopoiesis Increased risk of development of acute myeloid leukaemia (AML)
38
What are the thresholds for crytopenias ? (4)
The thresholds for crytopenias as recommended in the International Prognostic Scoring System (IPSS) for risk stratification in the MDS are: - Haemoglobin < 10 g/dL - Absolute neutrophil count (ANC) < 1.8 x10^9/L - Platelets < 100 x 10^9/L
39
What happens in MDS
Bone marrow does not produce enough healthy blood cells Average age of diagnosis is between 60 and 75 years Risk factors include smoking and exposure to automobile exhaust
40
What are the symptoms of MDS
Fever Fatigue Weakness Easy bruising
41
How is MDS diagnosed
Blood tests Bone marrow examination Karyotyping
42
Comment on the severity of MDS
Death is mostly caused by bleeding and infections Average survival after diagnosis is 6-12 months
43
How is MDS treated
Chemotherapy Stem cell transplantations
44
What morphological signs are there for MDS
Dysgranulopoiesis Dyserythropoiesis Dysmegakaryopoiesis
45
What is meant by dysgranulopoiesis?
Formation of asynchr
46
What is meant by dyserythropoiesis
Formation of macrocytic, megaloblastic cells
47
What is meant by dysmegakaryopoiesis
Formation of Rund, non-lobules megakaryocytes
48
How does MDS become AML
Normal stem cells undergo aberrant epigenetic programs to become MDS stem cells MDS stem cells undergo aberrant growth signals and reduced apoptosis to become AML This results in inhibited differentiation and uncontrolled blast cell proliferation Thought to be due to epigenetics
49
How do we diagnose and monitor haematological neoplasms (5)
FBC and morphology Flow cytometry Cytogenetics, FISH, Karyotyping, Array CGH Molecular sequencing Molecular methods e.g. RQ-PCR, dPCR, RT-PCR
50
How do we use PCR to quantify disease burden (3)
Real time PCR used to quantify amount of disease that is there e.g. cycle numbers in covid If you have to use cycle numbers then there is a very low disease dose Real time PCR allows us to find out exactly how much of a disease they have -> used to monitor disease and the effectiveness of drugs The higher the disease burden, the more fusion transcripts present so the more template cDNA present and the earlier products appear during PCR cycles e.g PML-RAR, BCR-AbI
51
Write about next generation sequencing
Making its way to all of the labs A sequencing method Allows us to discover mutations Allows us to see what DNA base pairs are present
52
What are the four types
Extraction Library Prep Sequencing Analysis
53
How are malignancies treated (6)
Chemotherapy - usually combination of drugs is used, 7+3 regimen Epigenetic therapies - demethylating agents and HDACs Stem cell transplant (younger patients, allogeneic versus autologous) Radiotherapy Immunotherapy - stimulate the patients own immune system to mount a response against the malignant cells - Monoclonal antibodies - examples include Rituximab - CAR-T cell therapy Small molecule inhibtiors e.g. Tyrosine Kinase inhibitors - Imatinib (Gleevec), JAK2 inhibitors, BTK inhibitors
54
What is chimeric antigen receptor (CAR) T-cell therapy ? (6)
Used in lymphoid leukaemias and lymphoma patients Can cure patients Patients own T cells are taken and genetically engineered to fight their own leukaemia Patients remain cancer free afterwards Works well in lymphoid => targets CD19 -> expressed on malignant cells Phase 1 trials for AML (there isn't one antigen i.e. CD molecule for myeloid)
55
What is meant be hide and seek
Leukaemia cells can move to lymph nodes (lymphoma) or hide in the bone marrow

2.2 Haematology (38 decks)

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