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MD3 Pathology > Heme Pathology 3 > Flashcards

Heme Pathology 3 Flashcards

1
Q
A

Myeloblast

Earliest precursor with large, rounder oval nucleus. Fine chromatin, evenly dispersed, few primary granules

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2
Q
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Promyelocyte

Nucleus about the same, but the cytoplasm starts to accumulate basophilic granules. Pale regions in nucleus = nucleoli

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3
Q
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Neutrophilic Myelocyte

Nucleus round, but chromatin more coarse. More cytoplasm

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4
Q
A

Metamyelocyte

Kidney bean shaped nucleus

If indentation >1/2 = band

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5
Q
A

Band

Not segmented into separate lobes yet

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6
Q
A

Maure Neutrophil

3-5 Lobes

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7
Q
A

Lymphocyte

Mononuclear cell

Nucleus is the same size as an RBC. Very little cytoplasm

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8
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A

Lymphocyte

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9
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Acute Myeloid Leukemia

Malignancy of Myeloblasts. Hypercellular

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10
Q
A

Acute Myeloid Leukemia

Monoclonal population of -blasts

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11
Q
A

Acute Myeloid Leukemia

-Blasts

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12
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A

Acute Myeloid Leukemia

R-rod = linear configuration of granules

Only seen in neoplastic myeloblasts

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13
Q
A

Acute Myeloid Leukemia

R-rods within myeloblasts

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14
Q
A

Acute Myeloid Leukemia

Acute Promyelocytic leukemia (M3) - cytoplasm filled with granules and some R-rods

>20% blasts to diagnose leukemia

More procoag and fibrinolytic factors in cytoplasm - lead to problems with DIC

Translocation between ch. 15 & 17 T(15,17): PML gene (ch. 15) and Retinoic acid receptor alpha gene (ch. 17) switch –> fusion gene –> fusion protein –> prevents cell from maturing beyond promyelocyte stage. Can target with all-trans retinoic acid to aid maturation.

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15
Q
A

Acute Myeloid Leukemia

Acute Promyelocytic leukemia (M3) - cytoplasm filled with granules and some R-rods

>20% blasts to diagnose leukemia

More procoag and fibrinolytic factors in cytoplasm - lead to problems with DIC

Translocation between ch. 15 & 17 T(15,17): PML gene (ch. 15) and Retinoic acid receptor alpha gene (ch. 17) switch –> fusion gene –> fusion protein –> prevents cell from maturing beyond promyelocyte stage. Can target with all-trans retinoic acid to aid maturation.

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16
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A

AML

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17
Q
A

AML (M4/5) Gingival infiltration by leukemia

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18
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A

AML M4/M5

Leukemia Cutis

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19
Q
A

Normal bone marrow

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20
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A

Chronic Myelogneous Leukemia

Chronic leukemia of myeloid cells. Neoplasm of pluripotent stem cell -> leukocytosis, elevated platelets,

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21
Q
A

Chronic Myelogneous Leukemia

Full spectrum of hematopoietic precursors

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22
Q
A

Chronic Myelogneous Leukemia

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23
Q
A

Chronic Myelogneous Leukemia

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24
Q
A

Chronic Myelogneous Leukemia

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25
Q
A

Chronic Myelogneous Leukemia

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26
Q
A

Chronic Myelogneous Leukemia Philadelphia Chromosome

Characteristic T(9,22) translocation (90-95%). Others have a cryptic (microscopic) translocation

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27
Q
A

Chronic Myelogenous Leukemia

ABL gene breaks off and translocates to BCR gene –> ABL-BCR -> tyrosine kinase gene product -> always turned “On” -> 2nd msnger pathways -> cell proliferation/survival

Can diagnose CML based on this translocation

Can be used with a tyrosine kinase inhibitor

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28
Q
A

Acute Lymphoblastic Leukemia

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29
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A

Acute Lymphoblastic Leukemia

Don’t see R-rods.

TDT - terminal deoxynucleotidal transferase (enzyme that is only found in lymphoblasts) so can stain just for that

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30
Q
A

Acute Lymphoblastic Leukemia

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31
Q
A

Acute Lymphoblastic Leukemia

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32
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A

Acute Lymphoblastic Leukemia

Better prognosis than AML (60-80% remission)

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33
Q
A

Chronic Lymphocytic leukemia

Middle aged-elderly, M>F, usually asymptomatic w/ leukocytosis and inverted differential (50% lymphocytes, 30% neutrophils)

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34
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A

CLL

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35
Q
A

CLL

“Snickerdoodle”

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36
Q
A

Chronic Lymphocytic Leukemia

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37
Q
A

Hairy cell

Malignancy of B-cells. Cytoplasm has projections that look like hair.

Rare, indolent, curable

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38
Q
A

Hairy Cell Leukemia

Usually also present with pancytopenia & massive splenomegaly

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39
Q
A

Bone marrow of Hairy Cell Leukemia

Fried egg appearance

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40
Q
A

Hairy cell leukemia

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41
Q
A

TRAP stain - titrate resistant acid phosphatase for Hairy Cell Leukemia

2CDA cure - few side effects, very effective.

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42
Q
A

Hairy Cell Leukemia

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43
Q
A

Hodgkin Lymphoma

Painless lymphadenopathy

Often localized to single axial group of nodes, orderly spread by contiguity, Mesenteric nodes and Waldeyer’s ring rarely involved, Extranodal involvement uncommon

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44
Q
A

Hodgkin Lymphoma

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45
Q
A

Hodgkin Lymphoma

Reed-Sternberg cells are characteristic, but are the minority of cells.

46
Q
A

Hodgkin Lymphoma

Reed-Sternberg cells are characteristic, but are the minority of cells.

47
Q
A

Hodgkin Lymphoma

Reed-Sternberg Cells

48
Q
A

Hodgkin Lymphoma

Reed Sternberg Cells

49
Q
A

Hodgkin’s Lymphoma Nodular Sclerosis subtype

Separated by Collagen bands

50
Q
A

Hodgkin Lymphoma

Nodular Sclerosis Subtype

51
Q
A

Hodgkin Lymphoma

Nodular Sclerosis Subtype

52
Q
A

Hodgkin Nodular Sclerosis subtype

Lacunar cell

53
Q
A

Normal Lymph node

54
Q
A

Benign Lymphoid follicles

55
Q
A

Follicular Lymphoma

Follicles are all different sizes and scattered throughout lymph node

Characteristic translocation T(14,18)

14 (immunoglobulin heavy chain); 18 (BCL2 - anti-apoptosis)

56
Q
A

follicular lymphoma (Non-H)

57
Q
A

Normal follicles

BCL2 immunostain (Normal follicles don’t stain)

58
Q
A

Follicular lymphoma Non-Hodgkin

BCL2 stain

59
Q
A

Follicular lymphoma (non-H)

Sometimes can end up in peripheral blood (Butt cells)

60
Q
A

Diffuse large B-cell lymphoma

Larger than normal lymphocytes

Can develop from follicular lymphoma

Aggressive high grade lymphoma, but can be treated

61
Q
A

Burkitt Lymphoma

“Starry sky”

  1. Endemic form (from Africa) usually involves jaw/abdominal organs of children. Strongly associated with EBV.
  2. Non-endemic (US) usually involves terminal ileum/ abdominal lymph nodes.
  3. Immunodeficient patients.
62
Q
A

Burkitt Lymphoma

“Starry sky”

63
Q
A

Burkitt Lymphoma

Translocation T(8,14)

c-myc (ch. 8) and Ig heavy chain (ch. 14)

64
Q
A

Multiple Myeloma

Malignancy of plasma cells. Usually affects middle-aged to older adults. Proliferate in bone marrow - so break down bone.

CRAB - Hypercalcemia, Renal failure, Anemia, Bone (decreased density)

65
Q
A

Multiple myeloma

66
Q
A

Multiple myeloma

Prominent pale-staining golgi (normal plasma cells)

67
Q
A

Multiople myeloma

Plasma cells

68
Q
A

Multiple myeloma

Lytic lesions (areas of decreased bone density)

69
Q
A

Multiple myeloma

Lytic lesions

70
Q
A

Multiple myeloma

Breakdown of bone in vertebrae

71
Q
A

Rouleaux formation (RBCs) in multiple myeloma

RBC normally have net-negative charge (zeta potential), but with all the protein, loss of negative charge that normally repel, so aggregate into stacks

72
Q
A

1st group has good prognosis

2nd group has unfavorable prognosis

3rd group (variable)

73
Q
A

Monoclonal protein immunoelectrophoresis

74
Q

What are leukemias?

A

Malignant neoplasms of hematopoietic stem cells. Pathogenesis in most cases is unknown.

Spill into blood, & may also infiltrate liver, spleen, lymph nodes & other tissues

75
Q

What are the differences between acute and chronic leukemia?

A

Acute

  • Symptoms that result from suppression of normal marrow function: anemia (fatigue), fever (infection) and/or bleeding (thrombocytopenia)
  • Fatal w/in wks if untreated
  • Characterized by presence of immature blasts

Chronic

  • Non-specific symptoms: fatigue, weight loss, anemia, or abonromal sensation in abdomen caused by splenomegaly
  • Longer survival
  • Associated with mature cells (but may have acute phase blast crisis)
76
Q

Besides acute vs. chronic, how else can you classify leukemia?

A

Lymphoblastic (originate from precursor of B/T cells) vs. myeloid (precursor of granulocytes, monocytes, erythrocytes, or megakaryocytes)

77
Q

What are the 4 types of leukemias?

A

Acute myeloid leukemia (AML)

Chronic myelogenous leukemia (CML)

Acute lymphoblastic leukemia (ALL)

Chronic lymphocytic leukemia (CLL)

78
Q

AML accounts for ___% of acute leukemias and is more commonly seen in ________

A

AML

90% of acute leukemias

More commonly seen in adults

79
Q

How to AML patients present?

A

Anemia, thrombocytopenia, leukocytosis/leukopenia

80
Q

How do we diagnose AML? (amount of blasts?)

A

>20% myeloblasts in bone marrow OR peripheral blood

81
Q

On what factors was the French-American-British (FAB) classification based?

A

Based on type of myeloid precursor (neutrophilic, monocytic, erythroid, or megakaryocytic) and degree of differentiation/maturation (FAB M0-M7)

82
Q

What is the acute myeloid leukemia in which neoplastic promyelocytes predominate?

A

AML - FAB M3 Acute Promyelocytic Leukemia

t(15,17) translocation found affecting APL gene and retinoic acid receptor gene (functions in cell maturation)

Also mutations FLT3 gene (tyrosine kinase promoting cell proliferation and survival)

83
Q

What is a common complication of AML?

A

DIC - as cells release progcoagulants and fibrinolytic factors contained in abnormal granules

84
Q

What is the treatment for AML?

A

Retinoic acid induces cell maturation, reducing risk for DIC

85
Q

Describe the myelobasts in AML

A
  1. Uniform in appearance
  2. 25-30 um
  3. Fine chromatin and 1-3 prominent nucleoli
  4. Scanty blue cytoplasm may or may not have azurophilic granules
  5. Auer rods (abnormal linear arrangement of azurophilic granules) may be present
  6. Usu. myeloperoxidase +, Tdt negative
86
Q

Describe the pathophysiology of AML

A

Blasts accumulate in marrow, displacing normal progenitors with immature, neoplastic nonfunctional cells

Untreated, AML is lethal within weeks to months

87
Q

WHO Classification

A

I: AML with genetic abberations

II: AML with MDS-like features

III: AML Therapy Related

IV: Other

88
Q

What is CML?

A

Chronic myeloproliferative disorder

Characterized by effective hematopoiesis & massively large spleen (extramedullary hematopoiesis)

Thought to be due to proliferation of pluripotent myeloid stem cell without maturation arrest

Presentation: leukocytosis, anemia, thrombocytopenia/cytosis

89
Q

What do you see in the peripheral blood in CML? Bone marrow?

A

Peripheral blood:

  1. Increased # leukocytes with left shift
  2. Increased # basophils/eosinophils

Bone marrow

  1. Hypercellular with increased # morphologically normal precursors
  2. Varying degrees of marrow fibrosis
90
Q

How do you diagnose CML?

A

Based on combo of clinical, morphologic, and cytogenetic findings

Characteristic translocation t(9,22) ABL-BCR - fusion results in protein with tyrosine kinase activity (Philadelphia Chromosome)

91
Q

What are some other chronic myeloproliferative disorders?

A
  1. Polycythemia vera (increased RBC count; JAK2 mutation in 95%)
  2. Primary myelofibrosis (marrow fibrosis with extramedullary hematopoiesis & massive splenomegaly; JAK2 mutation in 50%)
  3. Essential thrombocythemia (Marked thrombocytosis; JAK2 mutation in 40-50%)
92
Q

What is ALL?

S/Sx

Diagnosis

A

Acute Lymphoblastic Leukemia/Lymphoma

Arises from neoplastic stem cell committed to lymphoid lineage. Blasts accumulate in marrow, crowd out normal progenitors, and spill into peripheral blood.

S/Sx: anemia/thrombocytopenia with high WBC and circulating blasts

Dx: Lymphoblasts must comprise at least 20% of nucleated marrow cells or blood leukocytes

93
Q

What is the morphology of lymphoblasts in ALL?

A
  1. Typically 20-30um
  2. Bland, finely reticulated chromatin
  3. Nucleoli indistinct
  4. Cytoplasm sparse and lacks granules
  5. Usually express TdT (terminal deoxynucleotidyl transferase), CD10, but negative for myeloperoxidase
94
Q

What is CLL?

Who does it affect?

S/sx

A

Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma

Chronic, usually indolent neoplasm of mature lymphocytes

Affects middle age to older adults; M:F = 2:1

S/Sx: Elevated lymphocyte count (10K-150K/ul);anemia; thrombocytopenia; usu asymptomatic

95
Q

What is the morphology of CLL?

A
  1. Lymphoid cells in CLL are slightly larger than the normal lymphocyte
  2. Tend to have “blocky” chromatin and sparse cytoplasm
96
Q

What causes CLL?

A

Most cases due to monoclonal B cell population

Expression of pan-B-cell markers CD19/20 with co-expression of CD5 and CD23

Surface immunoglobulin weakly expressed and light chain restriction is present

97
Q

What is the natural course of CLL?

A

Indolent (survival from 5-10 Years) and most don’t need treatment at time of Dx

Eventually, cytopenias occur, leading to infection or bleeding complications

Autoimmune disorders common (esp. autoimmune hemolytic anemia, thrombocytopenia, neutropenia)

98
Q

What is Hairy Cell Leukemia?

Who does it affect?

A

Rare (2% of all leukemias), Low grade neoplasm of mature B cells

Older adult males (median age=55; M:F = 5:1)

Usu present with enlarged spleen and pancytopneia with absolute neutropenia and monocytopenia

Usu only a few “hairy cells” found in peripheral blood smear

99
Q

What is the morphology of Hairy Cell Leukemia?

A
  1. Medium sized with round or oval nucleus
  2. Moderate amount of cytoplasm with fuzzy border
  3. Tartrate-resistant acid phosphatase (TRAP stain)
100
Q

Course, prognosis, and treatment of hairy cell leukemia?

A

Indolent course

Good prognosis

Treat with 2CDA (2 chlorodeoxyadenosine)

101
Q

What is Hodgkin Lymphoma?

Who gets it?

A

~40% of all adult lymphomas

Adults, slightly more common in men (except nodular sclerosis type)

102
Q

How do you diagnose Hodgkin lymphoma?

A
  1. Presence of Reed-Sternberg cells (binucleated with prominent nucleoli)
  2. Mononuclear Hodgkin cells in background of reactive eosinophils, plasma cells, and histiocytes
103
Q

What are the 5 types of Hodgkin Lymphoma?

A
  1. Nodular Sclerosis
  2. Mixed cellularity
  3. Lymphocyte-rich
  4. Lymphocyte depletion
  5. Lymphocyte predominance
104
Q

How do you stage Hodgkin Lymphoma?

A

Ann Arbor System

  1. Involves single lymph node or extranodal site
  2. Involves 1+ lymph nodes on same side of diaphragm
  3. Involves lymph node regions on both sides of diaphragm
  4. Multiple disseminated foci of 1+ extralymphatic organs
105
Q

What are the differences between Hodgkin and Non-Hodgkin lymphoma?

A
106
Q

What is follicular lymphoma?

What mutation is it associated with?

How does it present?

A

A non-Hodgkin lymphoma (indolent but incurable)

40% of adults with non-Hodgkin lymphoma

Derives from germinal center

t(14,18) causes overexpression of bcl-2, interfering with apoptosis

Presents with painless generalized lymphadenoptahy and frequent marrow involvement

30-50% tranform to higher grade lymphoma over time

107
Q

What is diffuse large B-cell lymphoma?

What is it derived from?

How does it present?

A

50% of adults with non-Hodgkin lymphoma

Wide age range (children to elderly)

Derives from germinal center or post-germinal center B cell

Rapidly enlarging lymphadenopathy, extranodal disease (30%), GI tract, CNS

Fatal if untreated, but potentially curable (40-50%)

108
Q

What is Burkitt’s lymphoma?

What are the differences between the 2 types?

What is it associated with?

What is its morphology?

A

30% of non-Hodgkin lymphoma

American type: GI tract, para-aortic lymph nodes

African (endemic) type: Jaw involvement (100% latently infected with EBV)

Bone marrow and peripheral blood involvement is common

Association with EBV and t(8,14) translocation involving c-myc

Morphology = “starry sky” with many lymphoma cells and tingible-body macrophages

109
Q

What is a multiple myeloma?

Who does it affect?

What is the clinical presentation?

A

Monoclonal proliferation of neoplastic plasma cells with involvement of the bone marrow @ multiple sites

Affects middle aged to elderly

Clinical presentation:

  1. Heme: Normocytic anemia, occasional thrombocytopenia/leukopenia, Rouleaux formation due to increased serum Ig
  2. Bone: pain/pathologic fractures (lytic lesions in skull, vertebrae, ribs, pelvis)
  3. Hypercalcemia
  4. Renal failure
  5. Infection
110
Q

What are some complications of multiple myeloma?

A

M (monoclonal) protein: serum protein electrophoresis detects monoclonal immunoglobulin or light chains produced by neoplastic plasma cells

Bence-Jones protein: free light chains in urine, which contribute to renal failure

Amyloidosis: Ig or light chains may form amyloid (beta-pleated sheet conformation) and may result in organ dysfunction

Plasmacytoma: solitary focus of neoplastic plasma cells

111
Q

Translocations:

  • CML
  • Burkitt lymphoma
  • Follicular lymphoma
  • M3 type of AML
A
  • CML: t(9;22) (bcr-abl hybrid)
  • Burkitt lymphoma t(8,14) (c-myc activation)
  • Follicular lymphoma t(14;18) (bcl-2 activation)
  • M3 type of AML: t(15;17) (responsive to all-trans retinoic acid)

MD3 Pathology (4 decks)

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