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Leukaemia Flashcards

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1
Q

what is acute leukaemia?

A

Uncontrolled proliferation of partially developed white blood cells, also called blast cells, which build up in the blood over a short period of time.

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2
Q

what are the 2 consequences of the causative mutations in leukaemia?

A

causes precursor blood cells to lose ability to differentiate into mature blood cells
blast cells divide uncontrollably

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3
Q

what is the consequence of cells not maturing in leukaemia?

A

stuck as blast cells, don’t function properly

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4
Q

what are the consequence of uncontrollable cell division of blast cells?

A

Take a lot of space and nutrition in bone marrow
Other cells get crowded out
Causes cytopenia’s = Anaemia, Thrombocytopenia, Leukopenia

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5
Q

what happens when blast cell numbers increase?

A

they spill into blood:
Lymphoblasts = settle in liver and spleen
Pre-t cell settle in Thymus and Lymphnodes – enlargement
Acute promyelocytic anaemia -
Promyelocytes activate the clotting process, combined with decreased platelets = DIC

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6
Q

what are the shared clinical features of acute leukaemia?

A
  • Fatgie – anemia
  • Bleeding – thrombocytopenia
  • Increased infections – leukopenia
  • Pain and tenderness in the bones – increased cell production
  • Abdominal fullness – hepatosplenomegaly
  • Pain in lymphnodes (lymphadenopathy)
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7
Q

what are clinical features more indicative of ALL?

A

hepatosplenomegaly and lymphadenopathy more common
o Thymus enlargement in T-ALL – mass in mediastinum
o Also testicular
o Cranial nerve palsies

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8
Q

what are clinical features more indicative of AML?

A

monocytic variety causes swelling of guns

Violaceous skin lesions

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9
Q

what are the common investigations done for Acute leukaemia?

A 
FBC,
Blood film,
Coagulation screen
Bone Marrow Aspirate +/- Biopsy 
CXR and CT scan 
Lumbar puncture
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10
Q

what is the general management of acute leukaemia?

A

Chemo
Biological therapy
stem cell transplants
bone marrow transplants

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11
Q

what will FBC show in acute leukaemia?

A

decreased haemaglobin
increased wcc (tho blasts so not functioning)
decreased platelets

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12
Q

what will the blood film in AML show?

A

large cells, fine chromatin, auer rods (crystalised aggregates of the myeloperoxidase enzyme), myeloid blasts

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13
Q

what will the blood film in ALL show?

A

smaller cells, coarse chromatin, little cytoplasm (glycogen granules) – lymphoblasts

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14
Q

what will the morphology of a bone marrow aspirate show?

A

 ↓erythropoiesis; ↓megakaryocytes, i.e. platelet precursors; > 20% blast cells

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15
Q

what is the immunophenotyping of B lineage acute leukaemia?

A

HLA-DR+, TdT-, CD19+, CD10+, surface IgM+

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16
Q

what is the immunophenotyping of T lineage acute leukaemia?

A

TdT+, cytoplasmic CD3+, CD1a/2/3+, CD5+

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17
Q

what are the additional immunophenotyping findings of acute leukaemia?

A

Anti-MPO, CD13, CD33, CD45, CDxw65, CD117

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18
Q

what is the epidemiology of ALL?

A
  • Most common childhood cancer (Newborn – 14 yeras)

* Most common leukemia overall

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19
Q

what is the difference between acute and chronic leukaemia

A 
Acute = blast (non mature)
Chronic = cytic (slightly more mature)
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20
Q

what can ALL be classified into?

A

o T cell ALL (proliferation of T cell precursors)
o Pre-B cell ALL (proliferation of B cell precursors)
o B-cell ALL

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21
Q

what are the histological features of lymphoblasts?

A

no granules, increased N/C ration, scanty cytoplasm, less prominent nucleolus

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22
Q

what is the spread and consequence of ALL?

A

bone marrow - replaces other cells (pancytopenia)
enter peripheral blood - leukostasis
Metastasize through body - hepatosplenomegaly, lymphadeonpathy, testes enlarge, CNS, bone

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23
Q

what markers are commonly present in ALL?

A

TdT+

Periodic acid shiff (+ve)

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24
Q

what are the common causes of ALL?

A

chromosomal translocations
abnormal chromosome number
genetic conditions
Radiation, smoking, viral infections, folate metabolim polymorphisms, chemotherapy, benzne, multiple myeloma

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25
what are the common chromosomal translocations associated with ALL and what does it cause?
12 and 21 22 and 9 (Philadelphia) Production of abnormal intracellular proteins, affect cell function + division
26
what geentic conditions are associated with ALL?
trisomy 21, Klinefelters, Fanconi anameia, Blooms syndrom
27
what are the features, translocations and markers associated with Pre B-ALL?
o Child o Trisomy o CD10, CD19, CD20 o t(9:22), t(12:21
28
what are the features, translocations and markers associated with B cell ALL?
o t(8:!4), t(8:22), t(2:8) = burkitts lymphoma
29
what are the features, translocations and markers associated with T cell ALL?
o Adult mass in the anterior mediastinum o CD3+, CD7+ o 14q11, 7q34
30
what are the clinical features associated with ALL?
acute, anaemia, infection, fever, malasie, sweats, haemorrhage, lecostasis, bone or joint pain, mediastinal involvement, CNS involvement, widespread lymphadeonpathy, hepatosplenamegaly, rhabdomyosarcoma, Ewings sarcoma
31
what are the signs of haemorrhage seen in ALL?
purpura, menorrhagia, epitaxiss, bleeding gum, retina, rectal
32
what are the signs of leukostasis in ALL?
hypoxia, retinal haemorraghe, confusion or diffuse pulmonary shadowing
33
what does mediastinal involvement in ALL cause?
SVC obstruction
34
what does CNS involvement in ALL cause?
cranial nerve palsy
35
what investigations should be done in ALL?
``` morphologic analysis cytogenic studies cell surface markers molecular markers cytochemical analysis peripheral blood smear ```
36
what will the peripheral blood smear show in ALL?
Normocytic or macrocytic anaemia Platelets <100,000 WBC <10,000 -> 100,000
37
which subsets of ALL can have targeted treatments?
o BCR-ABL+ALL o Burkitts o T-cell ALL o CNH Leukaemia
38
what is the remission induction treatment of ALL?
vincritin, predinisolone, daunorubicin, aspraraginase
39
what is consolidation therapy of ALL treatment?
alternating cycles of induction agents and cytotoxic
40
what CNS prophylaxis is used in ALL?
cranial irradiation plus IT chemotherapy (methotrexate +/- cytarabine, prednisolone)
41
what is the maintenance therapy used in ALL?
daily 6-MP PO and weekly methotrexate PO
42
what are the poor prognostic factors of ALL?
* Age > 60 * WBCs > 100,000 * Mature B or early T cell types * Phildelphia chromosome (ALL bad, CML good)
43
what is the epidemiology of AML?
more common in the elderly (>60s)
44
what is AML?
the clonal expansion of myeloid blasts in the bone marrow, peripheral blood, or extramedullary tissues
45
what is the spread of AML?
* replace most of bone marrow cells crowding out of normal hamatopoeisis * enter the peripheral blood – leukostasis * metasiatisze throughout the body – liver, spleen, CNS, lymphnodes, bone, skin, gum infiltration (m5)
46
what are myeloid cells?
granulocytes
47
what are the causes of AML?
chromosomal translocations myelodysplastic antineoplastic agents, alkylating agents, ionising radiation, benzene aplastic anaemia, myeloproliferative disorders, Fanconi anaemia, PNH
48
what is myelodysplastic syndrome?
Defective maturation of myeloid cells Build of blasts initially <20% blast, but enough to cause decrease in function of red blood cells, granulocytes and platelets as disease progresses the blast percentage may >20% resulting in AML with myelodysplasia
49
what is the classification of AML based on?
the morphology of the myeloblast
50
what are the different classifications of AML?
``` AML without maturation AML with minimal maturation AML with maturation (M2) Acute promyelocytic leukaemia (M3) Acute myelomonocytic leukaemia Acute monocytic leukaemia (M5) Acute erythroid leukaemia Acute megakaryoblastic leukaemia ```
51
what are the features of AML M2?
caused by t8:21 | most common
52
what are the features of acute promyelocytic leukaemia (M3)
Characterised by translocation of chromosome 15:17 which disrupts retinoic acid receptor gene which is required for normal cell division Associated with DIC Treats with Vit A – good prognosis
53
what feature is associated with AML M5
gum infiltration
54
what are the clinical features of AML?
acute, anaemia, infection, fever, malaise, sweats, haemorrhage (M3), gum hypertrophy and skin infiltration (M4/M5), leucostasis
55
what are the diagnostic investigations for
``` morphologic analysis cytogenic studies cell surface markers molecular markers cytochemical analysis peripheral blood ```
56
what will morphological analysis show in posistive AL?
>20% blasts
57
what chemical markers are present in AML?
TdT-, MPO+
58
what will peripheral blood in AML show?
Normocytic or macrocytic anemia Platekets <100,000 WBC <10,000 – 100,000 Auer rods – myeloperoxidase +
59
what is the treatment of AML?
• 2-4 cycles of chemotherapy (5-10 days of chemotherapy followed by 2-4 weeks recovery)
60
what are the poor prognostic factors of AML?
* Age >60 * WBCs >100,000 * Poor performance status * Mutation of FLT3 * 2ry AML
61
what are common complications of treatment in AL?
Bone Marrow Suppression - anaemia, neutropenia, thrombocytopenia Ohers - n+v, hair loss, liver, renal dysfunction, tumour lysis syndrome, infection, hyperviscosity sundrome late effects - loss of fertility, cardiomyopathy
62
AL - presence of auer rods in blood?
ALL - none | AML - always
63
AL- presence of lymphoblast's in blood
ALL - always present | AML - may or may not be present
64
AL - bone and joint pain
ALL - more common | AML - less common
65
AL - hepatosplenomegaly
ALL - more common | AML - less common
66
AL - organ infiltration
ALL - more common | AML - quite unusual
67
AL - Immunophenotyping
ALL - B Cell (CD19, cytoplasmic CD22, cytoplasmic CD79a, CD10), T cell (CD4, CD2, CD7) AML - Anti-MPO, CD13, CD33, CD45, CDxw65, CD117
68
what is the pathophysiology of chronic leukaemia?
Cells only mature partially Too many premature cells = accumulate Leukocytes accumulate in bone marrow and eventually spill out – blood and tissues Accumulated cells causes healthy cells to get crowded out
69
What is the affect of cell dysfunction in each type of CL?
CML - divide too quickly | CLL - don't die as they should
70
most is the epidemiology of CLL?
* Most common type in Western countries | * adults – increased risk with increasing age (>60s)
71
what type of cells does CLL impact?
T and B cells
72
what is the underlying pathophysiology of CLL?
• B cell interfere with pathways of B cell receptors, which should only be activated during infection – to activate specific tyrosine kinase o Brutons tyrosine kinase which stops lymphoids developming developing o Interaction with each other – causes them to die slowly
73
what markers are expressed in CLL?
CD5, CD19, CD23
74
what is the spread of leukocytes in CLL?
• Premature leukocytes build up in bone marrow, spill in blood and move to lymphatic system – primarily lymph nodes – lymphadenopathy then lymphomas o Richter transformation – small lymphomas collect into masses
75
What are the consequences of cell spread in CLL?
Autoimmune haemolytic anaemia Hypogammaglobulinemia Cytopenia
76
what are the clinical features of CLL?
asymptomatic lymphadenopathy lymphocytosis “smudge cells” marrow failure – anaemia, neutropenia and thrombocytopenia recurrent infection weight loss, night sweats, malaise massive hepatosplenamegaly autoimmune haemolytiv anameia – DAT, warm type 10% develop diffuse large cell lymphoma = aggressice (fever, increased LDH and LD size)
77
what investigations can be done in CLL?
``` blood count blood film immunophenotyping immunoglobulins cytogenics ```
78
what will a blood count in CLL show?
lymphocytosis, platelets normal or low
79
what will a blood film in CLL show?
increased lymphhocytes, smear cells
80
what will immunophenotyping in CLL show?
o CD5, CD19 and CD23 + | o CD2 and FMC7 -ve
81
what will immunoglobulins in CLL show?
hypogammaglobulinemia
82
what is the cytogenic of CLL?
13q –, 11q –, 12q +, 17p –, 6q –, +12
83
what staging system is used for CLL?
The RAI system: o Stage 0 lymphocytosis (low) o Stage 1 lymphocytosis and adenopathy (mid) o Stage 2 lymphocystosis and hepatosplenomegaly (mid) o Stage 3 anemia (high) o Stage 4 thrombocytopenia (high)
84
what are the indications for treatment in CLL?
o weight loss of more than 10% over 6 months o extreme fatigue o fever related to leukemia for longer than 2 weeks o night sweats for longer than 1 month o progressive marrow failure (anemia or thrombocytopenia) o autoimmune anemia or thrombocytopenia not responding to glucocorticoids o progressive or symptomatic splenomegaly o massive or symptomatic lymphadenopathy o progressive lymphocytosis, as defined by an increase of greater than 50% in 2 months or a doubling time of less than 6 months
85
What is the 1st line treatment for CLL?
Chlorambucil +/- prednisolone
86
what is the epidemiology of CML?
elderly
87
what are the causes of CML?
Translocation that effects granulocytes = Philadelphia chromosome (t(9;22) = 22 Radiation Chronic myeloproliferative – CML, p.vera, ET, MMM
88
what cell does CML affect?
myeloid cells: granulocytes and their precursors other lineages (platelets)
89
how does the Philadelphia chromosome cause CML?
• Philadelphia chromosome produces BCR gene sites next to ABL = BCR-ABL gene • Produces BCR-ABL protein o Activates tyrosine kinases (causes abnormal phosphorylation = signalling) – on/off switch always on o Switch on cell division – myeloid cells divide more quickly  causes buildup in bone marrow, spill into blood
90
what is natural progression of CML?
o chronic phase – increased WCC <10% of blast cells in blood o aggressive/accelerated phase – more likely to find blast cells in the blood – 10-10%, more systemic symptoms o blast phase/crisis – blood contains >20% blast cells  increased mutatuons as cells divide more quickly
91
what are the clinical features of CML?
* presents in chronic phase * many asymptomatic * fatigue, lethargy, weight loss, sweats * hepatospenomegaly – feeling of abdominal fullness (due to build up of cells) * gout, brusing/bleeding, splenic infarction, priapism * retinal haemorraghe, dyspnoea and cough
92
what are the clinical features of a blast crisis?
rapid increase in blast cells, fever, bone pain, fatigue, increased severity of anemia and thrombocytopnia, splenomegaly, large clusters of blasts in bone amrrow
93
what investigations can be used in CML?
``` FBC blood film NAP score decreased, ESR reduced BM biopsy cytogenic analysis FiSH ```
94
what is the management of CML?
Imatinib Interferon Alpha Stem Cell Transplant SOKAL - prognosis
95
how does Imatinib work in CML management?
o tyrosine kinase inhibitor that prevents the action of the BCR-ABL fusion protein, i.e.this is the abnormal protein produced by the Ph mutation.
96
what is the diagnostic feature of blast cells in CML?
<10%
97
what will the blood film and FBC show in CML?
increased WBC o normal/↓Hb o leucocytosis with neutrophilia and myeloid precursors (myelocytes – of all stages), eosinophilia, basophilia o thrombocytosis o Rapid turnover – raised uric acid and LDH
98
what will cytogenic analysis in CML show?
t9:22
99
what will FiSH anaylsis in CML show?
BCR-ABL

Haematology (13 decks)

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