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Heme Onc Exam 2 > WBC Path > Flashcards

WBC Path Flashcards

1
Q

Primary cause of death from leukopenia.

A

Infection/sepsis

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2
Q

What is Felty Syndrome?

A

Combination of rheumatoid arthritis and splenomegaly resulting in neutropenia.

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3
Q

Name the antipsychotic that is associated with neutropenia.

A

Clozapine

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4
Q

How is leukocytosis distinguished from acute leukemia?

A

Leukocytosis will have a high number of mature WBCs in the peripheral blood. Leukemia will have a high number of “blast” cells in the peripheral blood.

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5
Q

What is a leukemoid reaction and name 3 things that cause it.

A

A form of non-neoplastic leukocytosis that mimics acute or chronic leukemia. Chronic Infection, Chronic inflammation and steroids can stimulate such a high rate of WBC production that the number of blast cells in the periphery elevates just like leukemias.

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6
Q

What type of biopsy is best to examine a lymph node from possible malignancy?

A

Excisional Biopsy done by a surgeon

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7
Q

What are the 5 classes in the WHO Lymphoma classification?

A
  1. Precursor B cell neoplasm
  2. Peripheral B cell neoplasm
  3. Precursor T cell neoplasm
  4. Peripheral T cell and NK cell neoplasm
  5. Hodgkin Lymphoma (Reed Sternberg Cells)
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8
Q

Cluster of Differentiation (CD) marker found on Reed-Sternberg cells that differentiates Hodgkin Lymphomas from Non-Hodgkin lymphomas.

A

CD30

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9
Q

Main CD marker on NK cells.

A

CD56

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10
Q

CD marker common to all leukocytes.

A

CD45

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11
Q

CD marker on all plasma cells.

A

CD138

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12
Q

What is Terminal deoxynucleotide Transferase (TdT)?

A

A nucleotide that is detectable on the surface of malignant lymphoblastic cells in Acute Lymphoblastic Lymphoma. This nucleotide differentiates this neoplasm from those in the myeloid lineage.

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13
Q

When does the diagnosis of a peripheral B cell lymphoma change to a leukemia?

A

When greater than 4,000 transformed lymphocytes are detected in circulation and/or the bone marrow is involved.

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14
Q

What are the 5 subtypes of Hodgkins Lymphomas?

A
  1. Nodular Sclerosis
  2. Mixed Cellularity
  3. Lymphocyte-Rich
  4. Lymphocyte Depletion
  5. Lymphocyte Predominance (no CD30 Reed Sternberg cells)
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15
Q

What are B symptoms associated with Hodgkins lymphomas?

A

Fevers
Chills
Night Sweats

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16
Q

What two things are required to make a diagnosis of NH lymphoma?

A
  1. Major Cell Type(s)
  2. Pattern of Growth
    (nodular/follicular pattern or diffuse pattern)
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17
Q

Genetics of Follicular Lymphoma

A

Chromosome 14:18 translocation
-14 contains a very active heavy chain immunoglobulin gene that fuses with a very inactive bcl-2 anti-apoptotic gene in 18 leading to expression of the bcl-2 gene and cellular proliferation

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18
Q

Why does Diffuse Large B cell Lymphoma require prompt treatment?

A

This cancer very often invades the CNS causing permanent damage even if the cancer is sent into remission.

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19
Q

Genetics of Burkitt Lymphoma.

A

Chromosome 8:14 translocation

-14 heavy Ig chain fuses with transcription activator c-myc gene on chromosome 8 leading to cellular proliferation

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20
Q

Population likely to develop Burkitt Lymphoma.

A

HIV infected pts in US
Malaria patients in Africa

Both with a co-infection of EBV

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21
Q

How does a biopsy showing Burkitt Lymphoma appear.

A

Many macrophages ingesting apoptotic cells leading to a Starry Sky appearance.

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22
Q

Genetics of Mantle Zone Lymphoma.

A

Chromosome 11:14 translocation

-14 Ig heavy chain gene fuses to Cyclin D1 gene on 11 promoting G to S phase of the cell cycle in B cells

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23
Q

How can Mantle Zone Lymphomas be diagnosed on biopsy?

A

Cyclin D1 can be immune-stained and show up on light microscopy.

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24
Q

What does Tartrate Resistant Acid Phosphatase (TRAP)+ indicate?

A

It indicates a cell or tissue that is normally rapidly dividing like in the skin, liver, or even in pregnant women in the first 8 weeks of pregnancy. In hematology/oncology it is also a marker for hairy cell leukemia.

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25
Q

Why is hairy cell leukemia actually classified as a lymphoma?

A

When HCL was discovered, the “hairy cells” were found in the peripheral blood, so it was termed a leukemia. However, as more cases arose it was discovered that lymph tissue in the spleen was the source of the proliferating B cells and that by the time most cases presented the spleen had become so full that the cells leaked into the periphery.

26
Q

What is Mycosis Fungoides?

A

A T cell lymphoma where the CD4 T cells are directed against the patient’s skin causing a dermatitis reaction. It originally looked like a fungal infection.

27
Q

What syndrome is associated with Mycosis Fungoides?

A

Sezary Syndrome

-patients present with erythroderma (red inflamed skin) along with lymphadenopathy and splenomegaly.

28
Q

What are the two microscopic characteristics associated with Sezary Syndrome?

A
  1. Sezary Cell: cerebriform T cells with nuclei that look like a cerebrum
  2. Pautrier Microabscesses
29
Q

Morphology of CD30+ Reed Sternberg cells found in Hodgkins Lymphoma.

A

Mummified: shrunk pyknotic nuclei

Bi nucleated cells

30
Q

What are the 4 stages of Hodgkins Lymphoma?

A
  1. One lymph node or region affected
    1e. involvement of a single extralymphatic node site
  2. 2 or more lymph nodes or regions affected on the same side of the diaphragm
  3. Lymph nodes involved on both sides of the diaphragm or an organ involved.
  4. Multiple organs involved
31
Q

Describe the pathology of Nodular Scerosis.

A

Lymphoma involving infiltration of T cells, eosinophils, macrophages, and plasma cells into a lymph node. The result is fibrous bancs of connective tissue forming in the node which can be stained on biopsy.

32
Q

What are Bence-Jones proteins?

A

Chunks of aggregated Abs or pieces of Abs that end up in the urine. Occurs as a result of plasma cell dyscrasias.

33
Q

Describe the condition: Monoclonal Gammopathy of Undetermined Significance (MGUS).

A

Plasma cell dyscrasia with non-specific over production of Abs. There is a 1% increase every year after diagnosis that the MGUS will progress to a multiple myeloma.

34
Q

How is MGUS differentiated from Multiple Myeloma?

A

Blood Tests
MGUS:
1. Bone Marrow plasma cells less than 10%
2. M-protein level less than 3g/dL
Multiple Myeloma has levels greater than the ones listed.

(the M protein here refers to immunoglobulin light chains that accumulate in serum in plasma cell dyscrasias. Not to be confused with the Strep pyogenes M protein)

35
Q

Describe Multiple Myeloma

A

Plasma cell dyscrasia with non-specific over production of Abs. Diagnosed with Bone Marrow Plasma cells greater than 10% and M protein level in the serum greater than 3g/dL

36
Q

When do you treat multiple myeloma?

A

When symptoms arise.

37
Q

What are the symptoms of multiple myeloma?

A

CRAB

  1. Calcium Levels rise
  2. Renal Failure: accumulation of Igs in glomeruli
  3. Anemia: crowded bone marrow space
  4. Bone involvement: lytic bone lesions
38
Q

How does multiple myeloma appear on blood smear?

A

Rouleaux Formation

-the RBCs appear stacked on each other like a stack of coins

39
Q

Describe Waldenstrom Macroglobulinemia

A

Infiltration of B cells and Plasmacytoid B lymphocytes only producing IgM Abs.

40
Q

What condition results from Waldenstrom Macroglobulinemia?

A

Hyperviscosity Syndrome

  • high levels of IgM thicken blood
  • patients develop lymphadenopathy, hepatomegaly, and splenomegaly
41
Q

Describe Primary or Immunocyte-Associated Amyloidosis (IAA).

A

Proliferation of plasma cells that only secrete light chains (incomplete Abs). Usually accompanies multiple myeloma. The proteins are deposited as amyloid, commonly in the skin, around the eyes, on the tongue.

42
Q

How can IAA be diagnosed with microscopy.

A

Amyloid stains Congo red and turns green with immunofluorescence (apple green birefringence)

43
Q

Describe what occurs in Acute leukemias and where most of the complications arise.

A

Acute leukemias occur in both the myeloid (AML) lineage and lymphoid or lymphoblastic lineage (ALL). The progenitor blast cells for each lineage only make copies of one another rather than differentiating into specific blood cell types. Depending on which cell type is depleted, different complications can arise:
neutrophils- infection
platelets- bleeding
RBCs- anemia

44
Q

Which acute leukemia more commonly affects the CNS?

A

ALL

45
Q

What 2 factors are associated with a worse prognosis in patients with ALL?

A
  1. Age outside the range of 2-10yrs
  2. Presence of t(9:22) bcr/abl translocation
    - Philadelphia chromosome
46
Q

What is the requirement to diagnose AML?

A

More than 20% of blood cells in the bone marrow must be myeloblasts

47
Q

Describe the genetics of the M3 class of AML (the only one he really wanted us to study).

A

M3: Acute Promyelocytic Leukemia
15:17 translocation (RARA/PML)

48
Q

Main cause of death in patients with M3 AML

A

Development of early DIC, patients clot first and then eventually bleed to death.

49
Q

What are Auer Rods?

A

Clumps of azurophilic granular material that form elongated needles seen in the cytoplasm of leukemic blasts in AML.

50
Q

Describe myelodysplastic syndromes.

A

Hyperproliferation of usually one type of myeloid cell. Occurs usually in older patients that present with a specific complain of bleeding, infection, or anemia symptoms. Curable with a bone marrow transplant

51
Q

Charasteristic of neutrophils on microscopy in patients with myelodysplastic syndromes.

A

Pseudo Pelger - Huet Cell: bi-lobed neutrophil

52
Q

Characteristic of Chronic Lymphoblastic Leukemia (CLL) on peripheral blood smear.

A

Smudge Cells

-lymphocytes are very fragile that they lyse in the slide preparation

53
Q

What is the difference between myelodysplastic syndromes and myeloproliferative disorders?

A

Myleodysplastic Syndromes: one myeloid lineage cell does not form because the myeloblast does not differentiate into that type. Ex. neutrophils, a patient will present with infections because his or her myeloblasts won’t differentiate into neutrophils.

Myeloproliferative disorders are the opposite. One (sometimes multiple) cell type of the myeloid lineage are overproduced.

54
Q

What genetic mutation occurs in a majority of Polycythemia Vera?

A

Jak2 mutation

-results in overproduction of RBCs and increased risk of thrombotic events

55
Q

Unique symptom of polycythemia vera.

A

Aquagenic Pruritis: itching after hot shower or bath

56
Q

Genetic mutation very common with Chronic Myeloid Leukemia (CML).

A

Philadelphia Chromosome
t(9:22) BCR/ABL translocation
-treatable with BCR/ABL tyrosine kinase inhibitors

57
Q

How does a CML blood smear appear?

A

Looks like bone marrow due to a left shift (lots of band cells)

58
Q

Describe Myelofibrosis with Myeloid Metaplasia (MMM).

A

Neoplastic transformation of multipotent myeloid stem cells along with deposition of collagen within the bone marrow space.

59
Q

How do patients with MMM present?

A

The collagen deposition in the marrow space reduces the capacity of bone marrow to produce blood cells. So the liver and spleen start to contribute leading to hepatomegaly and splenomegaly. The splenomegaly pushes against the stomach resulting in early satiety.

60
Q

What is DiGeroge Syndrome?

A 
Congenital thymic hypoplasia or aplasia.
Catch 22
-due to deletion on chromosome 22
-cardiac anomalies
-abnormal facies
-thymic aplasia
-cleft palate
-hypoparathyroidism w/ hypocalcemia

Heme Onc Exam 2 (9 decks)

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