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SBL 1 > Pathology of WBC, LN, Spleen, and Thymus > Flashcards

Pathology of WBC, LN, Spleen, and Thymus Flashcards

1
Q

When does an ANC become serious?

A

below 500

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2
Q

What can cause severe neutropenia

A
  • Drug toxicity
  • Aplastic anemia
  • Megaloblastic anemia
  • Immune destruction
  • Hypersplenism
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3
Q

What happens as a result of severe neutropenia?

A
  • Overwhelming bacterial and fungal infections
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4
Q

What causes leukocytosis?

A
  • Increased marrow priduction
  • Increased release from marrow
  • Decreased margination
  • Decreased extravasation into tissues
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5
Q

What is acute suppurative lymphadenitis?

A

painful “fluctuant” LAD

suppurative material due to infections with pyogenic organisms

Neutrophils are in the upper half of the image

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6
Q

List the 7 types of B cell non hodgkin leukemia/lymphoma

A
  • Chronic lymphocytic leukemia/Small lymphocytic lymphoma
  • Follicular lymphoma
  • Diffuse large B cell lymphoma
  • Burkitt lymphoma
  • Mantle cell lymphoma
  • Marginal zone lymphoma
  • Hairy cell leukemia
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7
Q

What falls under category of lymphoid neoplasia?

A
  • B cell and T cell
  • Plasma cell
  • Hodgkin
  • NK cell
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8
Q

what falls under myeloid neoplasia?

A
  • AML
  • Myelodysplasia
  • Myeloproliferative neoplasia
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9
Q

Differentiate leukemia vs lymphoma?

A

Leukemia is in the blood or bone marrow and lymphoma is in lymph nodes

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10
Q

Most common cancer of kids? How does it present?

A
  • Acute Lymphoblastic Leukemia/Lymphoma
  • Sudden onset of:
    • Fatigue
    • Fever
    • Bleeding bruising
    • Pain
    • Headache
    • N/V
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11
Q

What is ALL?

A
  • Occurs when there are mutations to lymphoid stem cells resutling in a “leukemic stem cell”
    • this means it can self renew and it also causes arrest of maturation resulting in blasts
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12
Q

How could a bone marrow aspirate of a patient with ALL look?

A
  • It may not aspirate at all if the bone marrow is densely packed with the leukemic cells, it is too “sludge-y”
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13
Q

what cancer is this and how do you know?

A
  • ALL
  • Cells are large with dark nuclear chromatin and scant agranular cytoplasm
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14
Q

In patients with ALL what will flow cytometry markers be?

A
  • TdT (seen in prolymphocytess)
  • B cell markers:
    • CD19, CD20, CD10, and Pax-5
  • T cell markers:
    • CD1-CD5, CD7, CD8
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15
Q

With ALL what factors play into a good prognosis vs bad?

A

Good:

  • 2-10 yo
  • Low peripheral WBC count
  • Hyperdiploidy
  • t(12:21)

Bad:

  • Age <2 or adolescent/adult
  • High WBC count greater than 100K
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16
Q

What is this?

A

CLL/SLL

  • Peripheral smear demonstrates lymphocytosis with small matrue lymphocytes and smudge cells
  • Non Hodgkins B cell
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17
Q

When staining for CLL/SLL what can indicate that it is CLL?

A

Using a CD5 stain

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18
Q

What is richter transformation?

A
  • Transformation from CLL/SLL to an aggressive tumor
  • Mutations usually involve P53 or MYC
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19
Q

Describe the translocation seen in follicular lymphoma?

A
  • t(14:18)
  • This moves the IgH gene next to BCL-2 and anti-apoptotic factor
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20
Q
A

Left: follicular hyperpasia

Righ: Follicular lymphoma

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21
Q

Diffuse large B cell lymphoma?

A
  • Large tumors in the LN or the spleen, this is an aggressive fast growing cancer
  • Two special types:
    • Immunodeficiency relatetd LCL linked to EBV activation
    • Primary effusion lymphoma linked to HHV-8
22
Q

In DLBCL, what is the frequent somatic mutation seen?

A

BCL-6

23
Q
A

Burkitt lymphoma a B cell non Hodgkin lymphoma

“starry sky”

24
Q

In burkitt lymphoma, what are the “stars”?

A

Tingible body macrophages

25
Q

Describe the translocation in Burkitts lymphoma?

A
  • Extremely fast growing tumors
  • t(8:14), moves IgH next to MYC
26
Q

3 major types of Burkitt lymphoma?

A
  1. Endemimc african burkitt lymphoma, EBV universal and mandibular growth occurs
  2. Sporadic
  3. HIV related

They respond well to treatment especially younger patients

27
Q

What is this

A

Mantle cell lymphoma

  • Small mature appearing cells, very aggressive tumor
28
Q

Describe mantle cell lymphoma

A
  • B cell malignancy resembling the mantle cell layer
  • Small mature looking cells, but very aggressive
  • t(11:14) moves IgH next to cyclinD1
29
Q

Describe Marginal Zone Lymphoma

A
  • Can occur in LN or at extranodal sites
  • Picture was of a MALT-oma, this is an extranodal example
    • They are assoc. with chronic inflammation caused by H pylori
  • Hashimoto thyroiditiws can result in MZL of thyroid
  • Chronic sialadenitis can be assoc with MZL of salivary glands
30
Q

Describe Hairy Cell lymphoma

A
  • Non Hodgkins B cell
  • Neoplastic B cells have hair like projections on them to keep distance betwen cells
  • Bone marrow is packed with cells
  • Induction of reticulin fibrosis leads to dry tap
  • MASSIVE splenomegaly
  • CD25 and CD11c
31
Q

How does Myeloma presesnt?

A
  • Lytic bone lesions, spontaneous fractures
  • Hypercalcemia
  • Renal failure
  • Immune abnormalities
32
Q

Describe what is seen.

A
  • Plasma cells left
  • Plasmablasts below left
  • Mott cells below
  • Dutcher nbodies bottom right
33
Q

What are the CRAB criteria for multiple myeloma?

A
  • C: hypercalcemia due to osteolysis, may present as altered mental status, Short QT, siezures, N/V, constipation
  • R: renal insufficiency due to immunoglobins that are being filtered and combining with renal glycoproteins forming casts called Bence Jones proteins, proteinuria, systemic amyloidosis AL
  • A: anemia as result of marrow infiltration of myeloma, IL-6 and other suppressive cytokinds, renal disease, MOST COMMON OF ALL CRAB
  • B: bone lesions
34
Q

What is seen?

A

multiple myeloma

35
Q

Lymphoplasmacytic lymphoma?

A
  • B cell clonal neoplasm of small mature B cells with plasmacytic differentiation
  • Waldenstrom’s macroglobulinemia
    • Monoclonal gammopathy
    • Hyperviscosity
36
Q

What is seen

A

Classic HL wit hreed sternberg cells, which are positive for CD15, CD30 and Pax-5

37
Q

Describe Nodular LP hodgkin lymphoma

A
  • Lymphohistiocytic variants (LH) cells aka popcorn cells are present
  • Positive for CD20 and negative for CD15 and CD30
  • Can transform into DLBCL
38
Q

What is used to diagnose ALL, B cell NHL, Myeloma, and HL?

A
  • ALL: morphology, staining, flow cytometry
  • B cell NHL: Morphology staining flow cytometry
  • Myeloma: Morphology staining, SPEP/Immuno fix
  • HL: Morphology and staining
39
Q

anaplastic large cell lymphoma (ALCL)

A
  • May be ALK +, seen in younger patients and has better prognosis
  • ALK -, seen in older with worse prognosis
40
Q

Adult T cell leukemia/lymphoma?

A
  • Assoc. with HTLV-1 infection
  • Leukemia has poor prognosis and you can see a cloverleaf cell
  • Skin involvement is common and you can see exfoliation to necrotizing nodules
41
Q

Describe Myucosis fungoides and Sezary syndrome.

A
  • MF: t cell lymphoma that presents with cutanoeous lesions, starting as a plaque and progressing to tumors
  • SS: T cell lymphoma presenting with erythroderma and leukemia
    • “Red Man”
  • NOT assoc. with HTLV-1
42
Q

What is seen

A

AMLm you can see the blasts and there are granules so that tells you they are of myeloid descent

43
Q

How does AML present?

A
  • Fever fatigue bleeding bruising
  • May have blasts in the peripheral smear and >20% blasts in the marrow
  • May also be an Aleukemic Leukemia, nothing in peripheral blood
44
Q

Describe AML with t(8:21)

A
  • AML with neutrophilic maturation, seen in younger patients and has a good prognosis and response to tx
  • RUNX-1 and RUNX1T1 fusion disrupts the core binding factor mediated hematopoetic differentiation and maturation
45
Q

Describe AML with t(15:17), what are these patients at risk for, how is it treated?

A
  • Referred to Acute Promyelocytic Leukemia (APL)
  • Auer rods are seen in the smear
  • RARa/PML translocation, this blocks RA from binding RAR and this stalls differentiation resultig in leukemic blasts
  • RISK FOR DIC
    • ​these cells express tissue factor which activates facctor X triggering clotting
  • Can treat with all transRA
46
Q

What is myelodysplastic syndrome?

A
  • Clonal DO with morphologic manifestations that go through many cell lineages
  • This is a precursos to AML
    • transformation to AML is more likely if MDS is due to priro cytotoxic therapy/radiation
47
Q

How does myelodysplastic syndrome manifest?

A
  • Cytopenias present, tap BM to see
  • Classification is based on:
    • Dysmorphic features of 1+ lineages
    • Chromosomal analysis
    • If the blast count is increased but not yet criteria for AML
48
Q

what is this

A

CML

Proliferation of mature myeloid cells

49
Q

Describe CML.

A
  • Philadelphia chromosome, the BCR-ABL tyrosine kinase, this can be treated with a tyrosine kinase inhibitor
  • You see marked leukocytosis with WBC > than 100K, splenomegaly and extramedullary hematopoiesis
50
Q

What is Langerhans cell histiocytosis?

A
  • Clonal proliferations of immature dendritic cells
  • Grooved nuclei of langherhans cells are seen as well as tennis racket shaped Birbek granules in electron microspy
51
Q

What causes congestive splenomegaly?

A

Liver dysfunction

52
Q

Differentiate hyperslenism and splenomegaly.

A

Hyeprsplenism has cytopenias with it and splenomegaly does not

SBL 1 (8 decks)

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