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Hemotology > Leukemias and WBC disorders > Flashcards

Leukemias and WBC disorders Flashcards

1
Q

What is considered a leukemoid reaction?

A

Absolute Leukocyte Count – 50,000+
Any type can become elevated.
Exaggerated response to infection.

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2
Q

What are the most common causes of leukemoid reaction?

A

Perforating Appendicitis
Whooping Cough - Bordella Pertussis
Cutaneous Larva Migrans

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3
Q

What is a leukoerythroblastic reaction and why?

A

When immature bone marrow cells are found in the peripheral blood. Infiltrative Disease or Marrow Stress.

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4
Q

What are the common causes of neutrophilia?

A

Increased neutrophil count

  • Infection
  • Sterile inflammation due to necrosis
  • Drugs (Prednisone, etc.)
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5
Q

If you see Basophillia, what should be at the top of the differential list?

A

Chronic Myelogenous Leukemia (CML)

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6
Q

What are the classifications of a myeloproliferative disorder?

A

Excessive proliferation of one or more of the myeloid lineages. Usually all of them will be elevated, but one more than the others that subclassifies it.

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7
Q

What are the features of the myeloproliferative neoplasms and population?

A

Older individuals – 50-70 years

– HYPERCELLULAR Marrow WITH effective hematopoiesis — thus increased lineages.

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8
Q

How is myeloproliferative different from dysplastic syndrome?

A

MPN – Hypercellular BM WITH hematopoiesis
++ leukocytosis
MDS – Hypercellular BM WITHOUT hematopoiesis
++ leukocytopenias

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9
Q

What is the characteristic genetics of Chronic Myelogenous Leukemia?

A

(9; 22) Translocation – BCR-ABL fusion gene

– tyrosine kinase activity

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10
Q

What would laboratory blood counts find in CML?

A

Diffuse Leukocytosis with hypercellular BM and numerous immature myeloids in plasma.
– most lineages are elevated, so if you see basophilia most likely CML can have others elevated too.

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11
Q

What is the treatment for CML and other pathologies with overactive tyrosine kinase?

A

Gleevec – Imatinib (Tyrosine Kinase Inhibitors)

– life long, or sometimes can cure –

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12
Q

What is it called when myeloproliferative disorder increases RBCs?

A

Polycythemia Vera

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13
Q

What is the most common mutation present in Polycythemia Vera?

A

JAK2 mutation, causes Jak-Stat pathway to be continuously activated.

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14
Q

What are characteristic clinical findings of polycythemia vera?

A
    • Hepatic Vein Thrombosis
    • Gout
    • Pruritus post-bathing, peptic ulcer disease (Histamine)
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15
Q

How is EPO affected during polycythemia vera compared to other pathologies with elevated RBCs?

A

Polycythemia Vera - Decreased EPO (negative feedback)
However in chronic hypoxia EPO will be elevated since trying to produce more RBCs on purpose.
Renal tumors commonly express too much EPO causing increased RBC.

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16
Q

What are the common bone marrow findings of primary myelofibrosis?

A

Rapid development of bone marrow fibrosis and hematopoiesis occurring in other parts of the body like the spleen, liver, nodes. Cytopenais
Clusters of atypical megakaryocytes

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17
Q

When you find a tear drop cell in the peripheral blood, what should you be suspicious of?

A

Primary Myelofibrosis (or another fibrosis of BM)

18
Q

What kind of disorder would present with thrombocythemia with atypical platelet morphology and numerous thrombosis?

A

Essential Thrombocythemia

19
Q

What is the common mutation responsible for essential thrombocythemia and what’s the treatment?

A 
JAK2 Mutation (50%)
Treated with Alkylating Agents to lower platelet count
20
Q

What is the common characteristic of myelodysplastic syndrome?

A

Ineffective hematopoiesis into a single lineage or multiple, due to cells being dysfunctional there is increased apoptosis and cytopenias.
(Less than 20% blast cells)

21
Q

What are unique histological findings of myelodysplastic syndrome?

A

Hypogranular or Hypolobular Neutrophils
Disfigured platelets and granulocytes
Ring Sideroblasts (granules around nuclei clustered)

22
Q

What are common chromosomal abnormalities of myelodysplastic syndrome?

A

Hypoploidy – Missing Chromosome 5 or 7

23
Q

What does myelodysplastic syndrome have a specific risk of?

A

Progression into acute myeloblastic leukemia

MDS is usually present in the very old

24
Q

What is a common treatment for myelodysplastic syndrome?

A

Hypomethylating Agents – Increases gene expression to hopefully allow proper differentiation.

25
Q

What defines acute leukemia?

A

Greater than 20% blast cells (either myeloid or lymphoid)

26
Q

Who common gets each kind of acute leukemias?

A

AML — Adults avg 60

ALL — Children, under age 18

27
Q

What are the key differences between AML and ALL histologically?

A

AML — Larger Cells with cytoplasm, More Nucleoli, Granules Present, Auer Rods Present
ALL — Smaller Cells, less nucleoli (1-2), No auer rods

28
Q

If you stain a sample taken from a patient with numerous undifferentiated cells with Non-specific esterase and it is illuminated, what kind of leukemia do you most likely have?

A

Monoblastic Leukemia

29
Q

If a sample from a patient suspected of having leukemia is successfully stained with Myeloperoxidase, what is the most likely type?

A

Myeloblastic Leukemia

30
Q

What are specific T-cell lineage antigenic markers?

A

CD1 – CD8

31
Q

What are specific B-cell lineage markers?

A

CD19, CD20, and CD22

32
Q

If a CD117 if found on a cell type, what is the most likely cell type?

A

CD117 – immature myeloblast c-KIT

33
Q

What is a common marker of immaturity of ALL?

A

TdT — DNA Polymerase

CD1a – T-cell immaturity ONLY

34
Q

What common antigenic marker would you find for monoblastic leukemia?

A

CD14

35
Q

What correlates with prognosis of AML?

A

–Recurrent Cytogenic Anormalities – Good Prognosis

–If related to myelodysplastic changes and nonspecific dysplasias of cells, Poor Prognosis

36
Q

What are favorable cytogenetic abnormalities of AML?

A

t(8, 21) – AML1/ETO
inv(16) – CBFbeta/MYH11
t(15;17) – PML/RARalpha

37
Q

If histologic examination of a patient’s cells with AML uncovers cells with multiple auer rods, what is likely the translocation?

A

t (15;17) PML/RARalpha– Acute Promyelocytic Leukemia

–EMERGENCY–

38
Q

What are the clinical outcomes of the translocation (15;17) with AML?

A

DIC – disseminated coagulability = highly fetal

Mutated Retinoic acid receptor, preventing the maturation of leukocytes.

39
Q

What is the pharmacologic treatment of translocation (15,17) in AML?

A

ATRA – allows binding of mutated receptor and progression of the maturation, immediately. Need to take the rest of their life.

40
Q

What is a characteristic findings of Langerhans cell histiocytosis on EM?

A

“Tennis Racket” appearance on EM with CD1a surface markers.

Hemotology (9 decks)

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