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MedEd Path > Haematology 1 > Flashcards

Haematology 1 Flashcards

Acute Leukaemias Chronic Myeloid Leukaemia and Myeloproliferative disorders Chronic Lymphocytic Leukaemia Lymphomas Myeloma Myelodysplastic syndromes & Bone Marrow Failure Bone Marrow Transplantation

1
Q

Leukaemia literal meaning

A

white blood

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2
Q

Pathophysiology of Leukaemia

What types exist

A

Caused by mutations in white blood cells or their precursors
Mutations cause proliferation through a variety of mechanisms
Can be rapidly progressive or indolent – (Acute vs Chronic)

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3
Q

List myeloid cell types

A

Branching off from multipotential haematopoietic stem cell
Common Myeloid Progenitor
Megakaryocyte, Mast Cell, Erythroblast, Myeloblasts: Basophil, Eosinophil, Neutrophil, Monocytes –> Macrophage

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4
Q

List Lymphoid cell types

A

Branching off from multipotential haematopoietic stem cell
Common Lymphoid Progenitor
Natural Killer Cell, Small Lymphocytes: T Lymphocytes, B Lymphocytes –> Plasma Cells

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5
Q

Which cells does acute leukaemia affect?

A

The more acute the leukaemia, the higher up it affects the chain of blood cell production

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6
Q

What cell does AML and CML affect?

A

Common Myeloid Progenitor

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7
Q

What causes CML?

A

BCR-ABL mutation in the myeloid progenitor or prior stem cell line

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8
Q

What is myeloma?

A

Myeloma – Plasma cell dyscrasia – proliferation of PLASMA cells in bone marrow

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9
Q

What cells does CLL affect?

A

Small Lymphocytes: T Lymphocytes and B Lymphocytes

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10
Q

What cell does ALL affect?

A

Common Lymphoid Progenitor

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11
Q

Clinical Presentation of Leukaemia

A

anaemia, thrombocytopenia, leukopenia/neutropenia

Splenomegaly less common than chronic leukaemias

Bone pain common

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12
Q

Pathophysiology of Leukaemia:

A

Rapid proliferation of cells, causing packed bone marrow

Results in bone marrow failure

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13
Q

3 overheading signs of Leukaemia

A

Anaemia, Thrombocytopenia, Leukopenia

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14
Q

3 overheading signs of Acute Leukaemia and associated symptoms

A

Anaemia: shortness of breath, chest pain on exertion, fatigue
Thrombocytopenia: easy bruising, petechial rashes, spontaneous bleeding e.g. epistaxis
Leukopenia: frequent or severe infections including opportunistic infections e.g. fungal infections
Additionally, bone pain

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15
Q

How does chronic leukaemia differ from acute leukaemia?

A

Slower proliferation of malignant cells
Less burden of disease in bone marrow
Clonal cells can pool in lymph nodes or in the spleen
Clinical manifestations – lymphadenopathy, splenomegaly

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16
Q

Key features of ALL in the history

A

Child – typically 2-5 yrs old
Hepatosplenomegaly (usually in chronic L, but children have small organs so occurs in ALL too)
Bone pain / limp (can be this alone - KEY FACT!)
Fevers
CNS symptoms
Testicular swelling (rare but specific - pooling of cells) (bALLs)

Adults – similar to AML, lymphadenopathy

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17
Q

Key features of ALL on blood tests

A

LOW PLATELETS (THROMBOCYTOPENIA)
LOW HB (ANAEMIA)
HIGH WCC
CIRCULATING BLASTS

Usually present with thrombocytopenia and anaemia
High white cell count (if severe, will be normal or suppressed)
Some analysers will indicate presence of blasts but sometimes these will be flagged as lymphocytes.
Circulating blasts are abnormal (should be in bone marrow)

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18
Q

https://imgur.com/2ZABq6m

interpret this blood film

A

High nucleus – cytoplasm ratio

It is not possible to tell ALL from AML on blood film most of the time!

This is Precursor B-cell ALL

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19
Q

What are key Ix for ALL?

A

Flow Cytometry and Bone Marrow Biopsy

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20
Q

What is Flow Cytometry?

A

a technique used to detect and measure physical and chemical characteristics of a population of cells or particles. A sample containing cells or particles is suspended in a fluid and injected into the flow cytometer instrument.

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21
Q

What causes ALL?

what is a method of remembering this?

A

BCR-ABL1 t(9;22) associated with 20-30% of ALL in adults

ALL can affect testicles - Balls - B-ALL spells out BALL.
B standing for BCR-ABL1 t(9:22) mutation

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22
Q

How is ALL treated?

A

Chemotherapy - Imatinib or other TKI for BCR-ABL1

Induction –> Consolidation –> Maintenance –> Remission
Possible transplant

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23
Q

Key features of AML in the history

A

Incidence increases with age
Might have had pre-existing MDS (myelodysplastic syndromes can transform into ALL)
Symptoms of cytopenias

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24
Q

Key features of AML on blood tests

A

anaemia (low haemoglobin) (bone marrow suppression)
high WCC
low platelets (bone marrow suppression)
neutropenia (lack of mature white cells due to xs blasts)
high blasts
normal INR - normal for AML
Abnormal INR - possible DIC due to acute promyelocytic leukaemia

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25
Q

https://imgur.com/ERMjP3z

what is the feature and dx

A

Auer Rods

AML (one is enough to diagnose AML or MDS)

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26
Q

https://imgur.com/0YTUM0h

what is the feature and dx

A

Auer Rods

AML (one is enough to diagnose AML or MDS)

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27
Q

https://imgur.com/Oe1u3pi

what is the feature and dx

A

Auer Rods

AML (one is enough to diagnose AML or MDS)

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28
Q

https://imgur.com/HUniyD6

what is the feature and dx

A

Auer Rods

AML (one is enough to diagnose AML or MDS)

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29
Q

https://imgur.com/oerYgPF

what is the feature and dx

A

Faggot Cells (stacks of Auer Rods)

AML

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30
Q

Next steps if suspecting AML but no Auer Rods?

Positive Result?

A

Flow Cytometry

MPO

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31
Q

Important subtype of AML?
Significance?
Treatment?

A

T(15;17) Acute Promyelocytic Leukaemia
Presents with DIC. Good prognosis
Treat with: All-Trans Retinoic Acid (ATRA) aka Vitamin A: Forces cells to differentiate, stops proliferation

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32
Q

AML treatment?

Prognosis?

A

Similar to ALL - Imatinib or similar TKI
Possibility of targeted agents in future
Poor prognosis particularly in elderly who won’t tolerate stem cell transplant

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33
Q

What are myeloproliferative Neoplasms?

A

These are increased production of the myeloid lineage i.e. anything following the Common Myeloid Progenitor in the chain

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34
Q

What is the myeloproliferative neoplasm affecting megakaryocytes?
Diagnosis? Associated Mutation?

Treatment?

A

Essential Thrombocytopenia

Platelet count consistently >450
JAK2 Mutation in 55%

Aspirin to reduce stroke risk
Hydroxycarbamide to lower count

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35
Q

What is the myeloproliferative neoplasm affecting Erythrocytes?
Diagnosis? Other features? Risks? Associated Mutation?

Treatment?

A

Polycythaemia Vera

Haematocrit >0.52 / 0.48 (M/F)
Often thrombocytothaemia as well
High Risk of thrombotic events e.g. stroke, MI, Budd-Chiari Syndrome (very dense, thick blood)

JAK2 Mutation 95%

Aspirin to reduce stroke risk
Venesection (taking blood to lower haematocrit)
Hydroxycarbamide to lower count

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36
Q

What is Haematocrit?

A

the ratio of the volume of red blood cells to the total volume of blood.

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37
Q

Meaning of ‘Polycythaemia’?

A

Excess production of Red Blood Cells

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38
Q

What is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement.

A

Budd–Chiari syndrome

affects 1 in 1 million

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39
Q

What causes proliferation of stem cells in the bone marrow & subsequent fibrosis? Pathophysiology?

Associated mutation? Ix results?

Blood film finding?
Pathagnomonic Ix and Result?

Treatment?

A

Myelofibrosis
clonal proliferation of stem cells (first cell in the chain)
results in cytokine release and fibrosis of bone marrow
The fibrosis causes reduced production of all cell lineages

JAK2 Mutation in 50%
Pancytopenia
Splenomegaly (can be massive splenomegaly)

Tear Drop Cells
Bone Marrow aspiration - Dry Tap (no aspirate)

Stem cell transplant likely only cure
Ruloxitnib - JAK inhibitor

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40
Q

What is a key type of MPN?

A

A key type of myeloproliferative neoplasm is CML

Increased production of the Myeloid Lineage

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41
Q

What are key features of CML in the history?

A

Typically onset age 35-55 in EMQs
LUQ pain - Splenomegaly
Mostly ASYMPTOMATIC if diagnosed in chronic phase
May present with symptoms of acute leukaemia if in accelerated / blast phase (~10%)

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42
Q

Typical age of onset of CML?

A

35-55

Ahmed - Saeid

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43
Q

Key features of CML on blood tests

A

Haemoglobin - normal (unlikely v anaemic)
WCC - 30 (v. v. high - Leukocytosis)
Platelets 450 (high - if chronic may have dropped, 50% have elevated platelet count)
Neutrophils 15 (neutrophilia)
Basophils (might be elevated blood count)
Monocytes (

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44
Q

Clinical Presentation of Chronic Leukaemia (4 points)

A

Slower proliferation of malignant cells
Less burden of disease in bone marrow
Clonal cells can pool in lymph nodes or in the spleen
Clinical manifestations – lymphadenopathy, splenomegaly

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45
Q

CELLS WITH HIGH NUCLEUS - CYTOPLASM RATIO ON BLOOD FILM

A

ALL (maybe AML - can’t tell apart)

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46
Q

Ix for ALL

A

Bone Marry Biopsy & Flow Cytometry

47
Q

BCR-ABL1 t(9;22) associated with?

A

20-30% of ALL in adults

may indicate CML too

48
Q

Mx for ALL?

A

Imatinib

or other tyrosine kinase inhibitor for bCR-ABL1

possibly transplant

49
Q

Key features of AML on blood tests

A 
low hb
high WCC
low platelets
low neutrophils
raised blasts
INR normal (AML)
INR high (DIC due to acute proteomyelocytic leukaemia)
50
Q

Auer Rods?

A

AML

possibly MDS

51
Q

what are faggot cells?

A

stacks of auer rods - indicate AML

52
Q

Ix for AML if no auer rods seen?

A

Flow Cytometry - (MPO)

53
Q

What is acute promyelocytic leukaemia?

A

type of AML with good prognosis and different mx (w/ ATRA) that presents with DIC (clotting and procoagulant depletion - clots & difficulty forming more clots - low PLT and fibrinogen)

54
Q

AML treatment

A

Imatinib

similar to ALL - (chemotherapy)
poor prognosis, particularly in elderly who can’t tolderate stem cell transplant

bone marrow transplant if treatment not working

55
Q

What are myeloproliferative neoplasms?

A

Excess production of red cells, white cells or megakaryocytes or any other myeloid cell.

56
Q

What are myeloproliferative neoplasms?

A

INCREASED PRODUCTION OF MYELOID LINEAGE CELLS

57
Q

PLATELET COUNT >450 CONSISTENTLY (no hx of recent infection where it can be raised)

KEY COMPLICATION

MX

A

ESSENTIAL THROMBOCYTHAEMIA

STROKE

HYDROXYCARBAMIDE
& ASPIRIN (to reduce stroke risk)

58
Q

What are the 4 main myeloproliferative disorders?

A

Polycythaemia Vera (RBCs)

Essential Thrombocythaemia (PLTs)

CML (granulocytes)

Myelofibrosis (stem cells fibrose bone marrow - all cell lineages REDUCED)

59
Q

What medication lowers myeloid cell count?

A

Hydroxycarbamide

60
Q

Haemocrit >0.5 ±0.2
High PLT

dx
mutation %
important complication
mx

A

POLYCYTHAEMIA VERA

JAK2 MUTATION 95%

MX
ASPIRIN to reduce stroke risk
VENESECTION to lower haematocrit
HYDROXYCARBAMIDE to lower count

61
Q

Low RBC
Low WCC
Low PLT

Dx & Ix
Mutation & %
features
Mx

ASSOCIATION ON BLOOD FILM

A

Myelofibrosis - clonal proliferation of stem cells in bone marrow –> cytokine release and fibrosis of bone marrow –> reduced prod. all myeloid cell lineages

Ix: BONE MARROW BIOPSY - DRY TAP!!

JAK2 MUTATION in 50%

Pancytopenia
SPLENOMEGALY - can be MASSIVE SPLENOMEGALY

Mx:
STEM CELL TRANSPLANT likely only cure
RULOXITINIB - JAK inhibitor!

TEARDROP CELLS

62
Q

age range of CML?

common presenting complaints?

A

35-55

LUQ pain & splenomegaly

63
Q 
mildly low Hb
v high WCC
high PLT
high NEUT
possibly high basophils
low monocytes
A

CML

64
Q

Left Shift on blood film

A

CML

65
Q

CML blood film features

A 
Features:
“Left shift” 
Leukocytosis
Eosinophilia
Basophilia

Hypolobated megakaryocytes in bone marrow

66
Q

The bigger the cells the more _____ they are

A

immatrure

67
Q

mutation in CML

which Ix used?

A

PHILADELPHIA CHROMOSOME

aka BCR-ABL1 fusion gene

translocation t(9;22)

FISH (fluo in situ hybridisation)

68
Q

What are the phases of CML?

A

3 phases

Chronic (85-90%)
Accelerated (gradually more blasts in bone marrow)
Blast Phase (20% blasts in bone marrow - behaves like AML)

69
Q

Management of CML

Prognosis

worst case scenario?

A

Tyrosine Kinase Inhibitors:
1st gen: Imatinib
2nd gen: Dasatinib, Niltinib, Bosutinib
3rd gen: Pontaninib

> 90% 10 yr survival

Small percentage of patients will fail treatment and need transplants

70
Q

Signs and Symptoms of CLL

A 
ASYMPTOMATIC
dx on bloods
AGE >50 - incidence increases w age
Men:Women 2:1
can present with lymphadenopathy/splenomegaly, ITP/haemolytic anaemias
71
Q 
Normal Hb (occasionally low)
EXTREMELY high WCC (100)
PLT normal
NEUT normal
Lymphocytes 95 (WCC made up of mature lymphocytes)
A

CLL

72
Q

Smear cells (blood film)

A

CLL

73
Q

Smudge Cells (blood film)

A

CLL

74
Q

Ix with CLL?

A

Flow cytometry

Usually B-cell but can get T-cell CLL
Same pathology as small lymphocytic lymphoma but different distribution: blood/marrow vs lymph nodes - i.e.more lymph nodes than blood

75
Q

Mx w CLL

A

STAGE DEPENDENT:

A - no cytopenia, <3 areas of lymphoid involvement
B – no cytopenia, 3+ areas of lymphoid involvement
C – cytopenias

A – watch and wait
B – consider treatment
C – treat

Richters syndrome: transformation of CLL to aggressive disease (ALL / high grade lymphoma)

Treat with either:
IBRUTINIB (Brutons TK Inhibtor)
FCR (fludarabine, cyclophosphamide, rituximab)
Stem Cell Transplant

76
Q

2 other ways of describing the philadelphia chromosome?

how is it detected?

A

BCR-ABL1 fusion gene
t(9;22)

by FISH (fluorescene in situ hybridisation)

77
Q

CML Treatment? if fails?

A

Imatinib

Transplants

78
Q

how does CML present?

A

RUQ pain and splenomegaly

79
Q

how does CLL present?

A

asymptomatic - picked up on routine blood tests

80
Q

What is pathagnomonic for CLL?

A

Smear Cells / Smudge Cells

81
Q

Blood film of CLL

A

Lymphocytosis

SMEAR/SMUDGE CELLS

82
Q

Treatment of CLL?

A

(if stage C) Ibrutinib or FCR (fludarabine, cyclophosphamide, rituximab)

if failing, Stem cell transplant

83
Q

Which leukaemia is associated with very high lymphocytes?

A

CLL

lymphoid lineage

84
Q

Which leukaemias are indicated by:
Auer Rods

Smear Cells

Left Shift

A

Auer rods - AML

Smear/Smudge Cells - CLL

Left Shift (more immature cells, less mature cells) -CML

85
Q

Way of remembering what smear/smudge cells indicate?

A

They are chronic
and they are LL
lymphoblastic leukaemia because they are S/S
i.e. double letter

86
Q

Which leukaemia is associated with high basophils?

A

CML

myeloid lineage

87
Q

Which leukaemias are associated with higher levels of blasts in the marrow?

A

Acute Leukaemias have over 20% blasts in the bone marrow

88
Q

Which leukaemia can have a high platelet count?

A

CML (myeloid lineage)

89
Q

Which leukaemia is associated with high eosinophils?

A

CML

myeloid lineage

90
Q

Which leukaemias have blast cells in the blood?

A

I think all of them can have them, however blasts are more characterisitc of acute leukaemias

91
Q

What can go on to form AML?

A

Myelodysplastic Syndromes?

92
Q

What are Myelodysplastic Syndromes?

A

Dysplastic changes - abnormal cells
1 or more myeloid cell lines (erythroids, megakaryocyte,
granulocyte)

Usually asymptomatic - however there is risk of progression to AML
Present with incidental cytopenia

93
Q

Pelger Huet Cells =

A

Hyposegmented Neutrophils

Pseudo-Pelger Anomally

causes:
Congenital (lamin B Receptor mutation) Acquired (myelogenous leukaemia and myelodysplastic syndromes (granulocytic lineage))

94
Q

How does MDS present?

A

Clinical Features
• BM failure and cytopenias – infection, bleeding, fatigue
• Hypercellular BM
• Defective cells:
o RBCs e.g. ring sideroblasts (abn nucleated blast surrounded by iron granule ring)
o WBCs – hypogranulation, Pseudo-Pelger-huet anomaly (hyposegmented neutro)
o Platelets – micromegakaryocytes, hypolobated nuclei
N.B. In the exam – use an ‘investigative approach’ to pick out clues that lead to classification

95
Q

Key difference between MDS and Leukaemia?

A

<20% blasts in MDS, >20% blasts acute leukaemia

96
Q

What are Myelodysplastic Syndromes?

A

Heterogeneous group of progressive disorders featuring ineffective proliferation and differentiation of abnormally maturing myeloid stem cells.
• Characterised by: peripheral cytopenia; qualitative abnormalities of cell maturation; risk of AML transformation.
• Typically seen in the elderly; symptoms usually develop over weeks/months (incidental)
• By definition all patients have <20% blasts (>20% blasts = acute leukaemia)

97
Q

Treatment of MDS?

A

Treatment
• Supportive – transfusions, EPO, G-CSF, ABx
• Biological modifiers – immunosuppressive drugs, lenalidomide, azacytidine
• Chemotherapy – similar to AML
• Allogeneic SCT

98
Q

Where are the different types of MDS found and what are the types?

A 
BLOOD
RBCs: Refractory Anaemia (RA) +/
ring sideroblasts ( RARS )
PLATELETS: MDS w/ 5q deletion
MDS unclassified
WBCs: Refractory Cytopenia with Multilineage Dysplasia (RCMD) +/ ring sideroblasts ( RCMD RS )

BONE MARROW
Refractory anaemia with excess blasts
(RAEB I) <5% Blasts
(RAEB II) 5-19% Blasts

99
Q

Explain staging of both Hodgkin’s and Non-Hodgkin’s Lymphoma

A

Ann-Arbor Staging
Stage I - IV

Stage I - One Group of Lymph Nodes (e.g. axillary, cervical, mediastinal)
Stage II - More Than One Group of Lymph Nodes That Are Above The Diaphgragm
Stage III - More Than One Group of Lymph Nodes That Are Above and Below the Diaphragm
Stage IV - Bone Marrow / Spleen Involement

100
Q

How are Lymphomas classified?

A

Hodgkin’s vs Non-Hodgkin’s
Hodgkin’s has 4 types
Non-Hodgkin’s is B-cell vs T-Cell (ATLL)
Very High vs High vs Low Grade

101
Q

What is pathagnomonic for Hodgkin’s Lymphoma?

A

Reed-Sternburg Cells

owl eye cells

102
Q

Hodgkin’s Lymphoma - profile and typical presentation

prognosis

A

affects young
pc: lymphadenopathy (often mediastinal) or B symptoms
Reed-Sternburg Cells are diagnostic

usually good prognosis, stem cell transplant used if fails

103
Q

What disease is associated with Hodgkin’s Lymphoma?

A

EBV

Ebstein Barr Virus infection

104
Q

What is the most common subtype of Hodgkin’s Lymphoma?

A

Nodular Sclerosing

105
Q

What is the most common slow growing (indolent) lymphoma?

A

Follicular

106
Q

Lymph node biopsy shows large numbers of centroblasts

A

Follicular Lymphoma

107
Q

t(14;18) ?

A

causes fusion of BCL2 gene

follicular lymphoma

108
Q

What does centroblast look like on biopsy?

A

perfect circle of many cells

109
Q

What are the 4 types of Hodgkin’s Lymphoma?

A

nodular sclerosis classical Hodgkin lymphoma

mixed cellularity classical Hodgkin lymphoma

lymphocyte-rich classical Hodgkin lymphoma

lymphocyte-depleted classical Hodgkin lymphoma

110
Q

Features of Follicular Lymphoma

How does it present?

Risk?

A

Small lymphocytic lymphoma similar to CLL but disease with disease in NODES

Presents with lymphadenopathy, usually few very large nodes

Risk of transformation to high grade lymphoma

111
Q

Treating Follicular Lymphoma

A

Is Non-Hodgkin’s Lymphoma subtype

Expectant management unless high burden of disease

112
Q

Key features of Non-Hodgkin’s Lymphoma

A

Many sub-types – mostly B-cell origin, can be T-cell (ATLL)

Present with B-symptoms or lymphadenopathy

Incidence increases with age

113
Q

Treatment of Hodgkin’s Lymphoma

A

Treatment is with ABVD chemotherapy usually + radiotherapy
Most patients have a good chance of cure
Stem cell transplants for rare cases who fail treatment

MedEd Path (5 decks)

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