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Hem Yr 2 Sem 2 > Acute leukimia > Flashcards

Acute leukimia Flashcards

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1
Q

What is Acute leukemia

A

Rapid clonal proliferation in BM of LYMPHOID or MYELOID progenitor cells

Lymphs and Myelos

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2
Q

What is the FAB classification of acute leukemia

A

-based on morph and cytochemical staining to diff lymphs from myeloblasts

need to have more than 20% blasts when diagnosing acute leukemias as per WHO

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3
Q

What is tumor lysis syndrome

A

-complication in patients with malignancy - lymphoma and leukemia with or without treatment

-causes breakdown products of dying cells that cause acute uric acid nephropathy and renal failure

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4
Q

What is tumor lysis syndrome characterized by

A

HyperKalemia - high K = fatal
hypokalemia - low K
Hyperuricemia - excess uric acid due to cell turnover
Hyperphosphatemia - increased PHO4 due to cell lysis and bone destruction
Hypocalcemia - low calcium due to bone destruction

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5
Q

Laboratory Findings of Acute Leukemia

What we see in BM :
how does it manifest
-Anemia low RBC
Thrombocytopenia
granulocytopenia
expanding leukimic cells

A

-Fatigue malaise, pallor

bruising , bleeding

fever, infections

bone or joint pain

check slide 7

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6
Q

What are required tests for leukemia as per FAB and WHO

A

FAB
CBC & hem tests
BM
Flow

WHO
Cytogenetics
Molecular Diagnostics

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7
Q

What will a general CBC/PBS show in Acute Leukemia

A

CBC
Anemia - N/N
decreased platelets
WBCS variable

PBS
Blasts
NRBCs
Dysplastic features

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8
Q

The BM aspirate for AL should show

A

% Blasts in all ANC
>20% for acute leukemia
- variable M:E ratio
-look at megakaryocytes

%blasts in non myeloid cells (NEC)
-used for FAB classification

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9
Q

What do you look for in a BM biopsy

A

Cellularity - hyper cellular not too much fibrosis
Overall structure

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10
Q

What are some reflex hematology tests included in a BM panel

A

Retic - RBC destruction . BM production or release is response to the anemia

ESR - increased in inflammation and infection but in leukemia its just slightly increased
exception in multiple myloma as it increases IgG in plasma and increasing ESR due to cell stacking

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11
Q

What are the types of cytochemical cells we can use

A

-help diff between acute myeloid and acute lymphoid

Myeloperoxidase (MPO/MPX) - enzyme stain - granulocytes , primary granules of myeloid cells

Sudan Black B (SBB) - lipid stains (1 and 2 myeloid) and lysosome stain in monocyte

Esterases - Specific(primary granular like myeloblast) stain & Non-specific (positive in monocytes) enyzme stain

Periodic Acid Schiff (PAS)- glycogen stain - abnormal RBC precursors and lymphs

NBE - enzyme stain - alpha napth but esterase monocyte marker

if positive diff between all and aml

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12
Q

What is flow cytometery good for

A
  • produces scatter plot like diff
    -addition of monoclonal AB to detect Cluster of differentiation antigens
    -CD markers associated with lineage and maturity
    34- immature myeloblast and Lymp progenitors
    33 - pan myeloid marker
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13
Q

What does cytogenetics help with

A

-detects chromosomal abnormalities

-Numerical - Trisomy

Structural - deletions, inversions, translocations

Karyotypes and FISH - uses a probe that binds to a chromosome

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14
Q

how does molecular diagnostics help detect residual disease after treatment

A
  • looks at DNA at molecular level - not just chromosome form
    -PCR amplifies DNA to detect DNA sequence
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15
Q

What does real time PCR do

A
  • detects single malignant cell amongst millions with labeled probes
  • to detect how much residual disease is left
    -detects 1(15, 17) to measure minimal residual disease after treatment
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16
Q

What are ALL

A
  • disease of childhood and adolescence
    -25% of childhood cancers
    -peak between 2-5 years

-rare in adults
-risk increases with age , adults who get are older than 50
-subtype of ALL is important indicator for survival
-Adults have poorer outlook

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17
Q

What are the WBC counts in ALL

A

WBC increased
Extreme leuocytosis in <15% ALL
Leukopenia in 25%

counts vary

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18
Q

Clonal proliferation in B cell lymphoid progenitors results in =
what do the patients present with

A

B cell ALL - most common type of ALL

Pts present with
Fatigue due to anemia
Fever - due to neutropenia and infection
Muconutaneous bleeding due to thrombocytopenia

enlarged lymphs
splenomegaly
haptomegaly
bone pain (intramedullary growth of leukemic cells)
-BLASTS WILL BE SEEN IN CSF

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19
Q

What is T cell ALL

symptoms

A
  • when pts have mass in mediastinum

Fatigue from anemia
Fever from neutropenia and infection
Mucocutaneous bleeding and thrombocytopenia
Organomegaly
Bone pain

leukopenia is less severe than B cell ALL

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20
Q

What does the prognosis of ALL depend on

A
  • age at time of diagnosis
    -lymphoblast load
    -immunophenotype (T cell and Mature B cell have a worse outcome than immature B cell)
    -genetic abnormalities
    -genetic translocation associated with poorer prognosis

lymphoblast >20-30 X 10^9/L, hepatosplenomegaly , and lymphadenopathy are associated with worse outcome

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21
Q

What are the two morphologic types of lymphs

Small lymphs
large lymphoblast

A

Small lymph - most common
1-2 times the size of a normal one
-scant blue cytoplasm
indistinct nucleoli

Larger lymphoblast (looks like a MYELOBLAST)
2-3 times the size of lymph (larger ones can be confused with blasts of AML)
PROMINENT nucleoli
nuclear membrane irregularities

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22
Q

What do BM myeloblasts look like

Study These Flashcards
A

3-5x larger then lymph
moderate blue/grey cyto
-uniform chromatin
2-3 PROMINENT nucleoli maybe AUER RODS

23
Q

What are the 4 types of immunologically classifed ALL

how are they sorted by genetic abnormality

Study These Flashcards
A

done through CD markers

Early B ALL - pro B or Pre Pre B
Intermediate B ALL - Common B
Precursor or Pre B ALL
T- ALL

B-ALL 9 types of specific genetic abnormalities t(9, 22)

T ALL no specific genetic abnormalities

24
Q

Where is T cell ALL seen

Study These Flashcards
A
  • seen in teenage males with:
    -mediastinal mass
  • increased peripheral blast counts
    -causes of neurological problems with the meninges of the brain being invovled
    -infiltration of extra marrow sites

t cell markers are CD2, CD3, CD4, CD5, CD7, CD8

25
What type of gene does T ALL have
- gain of function mutation -NOTCH1 gene alternation that is a signalling pathway responsible for normal T cell development
26
What type of ALL has the worst prognosis
B cell LL with t(9,22) translocation , BCR-ALB1 mutation Philadelphia Chromosome - Positive ALL -most common in adults than in children
27
B cell vs T cell
B cell Most childhood ALL -better prognosis -many levels of B cell markers -genetic abnormalities 9 diff classification T cell 1% of childhood ALL -poor prognosis -not specific genetic abnormalities -less correlation with treatment outcome
28
What are the 3 groups that the FAB system separates ALL
L1 l2 l3 but this is no longer valid most places rely on immunophenotypic, cytogenetic and molecular findings
29
What does the L1 classficiation have
-uniform population of blasts -scant cytoplasm homogenous pattern inconspicuous nucleoli -regular nuclear shape and occasional clefting
30
What does the L2 classification have
-cellular hetergeneity - some blasts look like L1 some are larger with abundant cytoplasm loose chromatin pattern prominent nuceoli -nuclear clefting and indentation seen
31
What does the L3 classification seen as
- large blast with deeply vacuolated basophilic cytoplasm -Round - Oval nucleus -known as Burkett type because its similar to what we see in Burkitt's leukemia
32
What is AML symptoms
- most common type of Leukemia -Peak at 40 -less common in children fatigue, pallor, bruising , bleeding, fever Splenomegaly Bone, joint pain
33
What does AML present as clinically
non specific decreased production of BM element CBC with PBA BM aspirate and biopsy WBC count can be normal, increased, or decreased Myeloblasts in PB in 90% of cases -treatment and prognosis depends on exact diagnosis anemia, thrombocytopenia, neutropenia, hypercellular BM >20% blast (depending if aberrations are present) DIC, malignant cells into gums and mucosal sites, splenomegaly, Tumor Lysis Syndrome
34
Abberation T(8, 21)
-mutation in 5% of AML -children and young adults -myeloblasts with dysplastic, granular cytoplasm, Auer rods -similar to Fab M2 -see Pseudo Pelger Huet and hypo granulation -eosinophilia
35
t(16,16)
5-8 of AML chromosomal INVERSION increase in myeloid and monocytic lines -PB- myeloblasts, monoblasts and promyelocytes BM- eosinophilia -central system is site of relapse mostly younger pts
36
What is t (15, 17) or APL
- found in younger patients 5-10 of AML cases -hyper granular promyleocytes - can have AUER rods -when promylos release their primary granule contents DIC is initiated - sometimes in APL granules are so small that cells look like they have no granules
37
What is the microgranular variant present in some APL cases
can be confused with other presentation of AML -presence of Auer rods , butterfly or coin on coin nucleus,
38
t(9, 11)
rare in AML -in children -associated with gingival, skin involvement and DIC -increase in monoblast and immature monocyte iwth pseudopodia -blasts are large with lots of cytoplasm and fine chromatin
39
Acute MYELOID Leukemia -FAB classification grouped on
morph flow cytometery phenotyping limited cytochemical reactions -needs a blast percentage of 20% for peripheral blood -this category has 25 % of all AML
40
As per FAB classification what are we looking for in the BM
% blasts and % mature cells Early myeloblasts - NO auer rods Myeloblasts (AUER RODS) alone or with maturation (pros, myelo, and meta) -promye and blasts -combo of myelo and mono -monos only -RBC mainly -megakaryocyte
41
What is AML - FAB MO
Acute myeloid leukemia with minimal differentiation  Mostly Large Agranular Blasts in PB with thrombocytopenia -Blasts in AML with minimal differentiation - CD13+, CD33+, CD34+, and CD117+ -AUER RODS absent -no evidence of cellular maturation Myeloperoxidase - Negative Sudan black B - Negative report ABCL unless you see Auer rods then you would say AML
42
AML fab m1
Acute myeloid leukemia without maturation  Mostly Blasts and Thrombocytopenia in PB Blasts in AML without maturation are CD13+, CD33+, and CD117+ (CD34 -90% nonerythroid cells in BM - have Auer Rods -less than 10% of leukocytes show maturation to promyelocyte stage Myeloperoxidase - Positive Sudan black B - Positive report this as an ABCL or as an AML if you see Auer rods in the blasts.
43
AML - FAB M2
Acute myeloid leukemia with maturation  Blasts with some maturation and thrombocytopenia in PB Blasts in AML with maturation >20% blasts in BM 10% maturing cells in neutrophil line = promyelo and metamyelo <20% precursors with monocytic lineage -Auer Rods present Myeloperoxidase - Positive Sudan black B - Positive we would report it as either an ABCL or an AML if we see Auer rods.
44
AML - FAB M3
Acute promyelocytic leukemia  Mostly Hypergranular promyelocytes in PB -nuclei is bilobed or kidney shaped - Auer rods in blasts and promyleo can be in bundles -severe thrombocytopenia Diagnostic mutation: t(15;17) Same as WHO Myeloperoxidase - Strongly Positive Sudan black B - Strongly Positive report this as either an acute promyelocytic leukemia (APL) or M3.
45
What do monoblasts look like
- large with ltos of cytoplasm, small granules, pseudopodia -large nuc, immature with many nucleoli
46
AML - FAB M4
Acute myelomonocytic leukemia significantly increased WBC with thrombocytopenia -presence of myeloid and monocytoid cells in PB and BM -left shift with monocytosis in PB Blasts, Pros, Myelocytes, Monoblasts, Promonocytes, Monocytosis (both 20%) positive for the myeloid antigens CD13 and CD33 and the monocytic antigens CD14, CD4, CD11b, CD11c, and CD64. myeloblast can have auer rods MPO/MPX positive NBE positive report it as an acute myelomonocytic leukemia or an M4.
47
AML - FAB M4 Eo
Acute myelomonocytic leukemia with Eosinophilia -Same as AML FAB M4, but with >5% eosinophils -left shift with myeloblasts -monocytoid cells -thrombocytopenia
48
AML - FAB M5 (M5a and M5b)
Acute monocytic leukemias – poorly & well differentiated Divided into monoblastic and monocytic based on how mature the monocytic cells in PB or BM are -more than 80% of cells in Marrow will be monocytic CD14+, CD4+, CD11b+, CD11c+, and CD64+. Nonspecific esterase – Positive MPO/MPX - Positive NBE - Positive
48
AML - FAB M5a
Acute monocytic leukemia – poorly differentiated Mostly Blasts with thrombocytopenia in PB Monoblasts are large abundant basophilic cytoplasm -1 or more prominent nucleoli -fold cleft nuc - if there is maturation the cells are called promonocytes M5a is suspected, report as an ABCL.
49
AML - FAB M5b
Acute monocytic leukemia – well differentiated Mostly monocytes and promonocytes with thrombocytopenia in PB - can look like a monocytosis >20% blasts in BM Promonocytes Large Abundant Basophilic Cytoplasm Irregular Nucleus Granules Vacuoles report this as a M5b.
50
AML - FAB M6 What are the two types
Acute Erythroleukemia (Erythroid/Myeloid) Pure Erythroid Leukemia Dimorphic RBCs and RBC precursors with thrombocytopenia in PB
51
Acute Erythroleukemia (Erythroid/Myeloid)
type of M6 50% normoblasts - all RBC stages >20% myeloblast in BM NRBC and myeloid precursor
52
Pure Erythroid Leukemia
50% Pronormoblasts with >30% basophilic normoblasts 80% of the BM is made up of very immature erythroid cells - precursors will have multinucleation , megaloblastic asynchrony, NRBC in high numbers in PB
53
AML - FAB M7
Acute megakaryoblastic leukemia Micromegakaryocytes, pleomorphic blasts with agranular cytoplasm - giant plts or normal ones -delicate chromatin with prominent nucleoli - immature MK can have light blue cytoplasmic blebs -CD42b positive

Hem Yr 2 Sem 2 (12 decks)

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