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Heme and Lymph > Diseases of WBCs, LNs, Spleen, and Thymus > Flashcards

Diseases of WBCs, LNs, Spleen, and Thymus Flashcards

1
Q

What are the three categories of myeloid neoplasms?

A

acute myeloid leukemia’s, chronic myeloproliferative disorders, myelodysplastic syndromes.

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2
Q

What are histiocytoses?

A

uncommon proliferative lesions of macrophages and dendritic cells.

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3
Q

What are some predisposing genetic factors for developing acute leukemias?

A

down syndrome, type 1 NF, Faconi anemia, bloom syndrome, ataxia telangiectasia.

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4
Q

HTLV-1 is associated in what cancer?

A

adult T cell leukemia/ lymphoma.

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5
Q

How can reactive and malignant lymphocytosis be differentiated?

A

Based on clonality: monoclonal is malignant and polyclonal is reacitve.

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6
Q

What is the most common childhood cancer?

A

Acute Lymphoblastic Leukemia/ lymphoma

Children <15

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7
Q

What is the most common type of ALL?

A

B-ALL makes up 85%

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8
Q

Ethnicity of ALL?

A

white-3x more likely.

hispanics have highest risk

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9
Q

Peak age of B-ALL?

A

3

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10
Q

Peak age of T-ALL?

A

15

- predominately adolescent males

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11
Q

70% of T-ALLs have what genetic mutation?

A

NOTCH-1

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12
Q

What translocation is associated with B-ALL?

A

balanced t(12;21)

*other genes include PAX6,E2A,EBF

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13
Q

What is the morphology of the marrow in leukemic presentations?

A

Hyper cellular and packed with lymphoblasts.

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14
Q

What are the morphological features of a peripheral smear in a patient with ALL?

A

Punched out nuclei, blasts appear larger, chromatin is delicate and finely stippled.

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15
Q

What are the differentiating features of myeloblasts compared to lymphoblasts?

A

Lymphoblasts have more condensed chromatin, less conspicuous nucleoli, and smaller amounts of cytoplasm that usually lacks granules.

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16
Q

What stain can be used to identify myeloblasts?

A

myeloperoxidase (MPO)

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17
Q

Lymphoblasts are characterized by positive nuclear staining for what?

A

TdT.

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18
Q

What CDs are expressed in B-ALLs?

A

CD-10, 19, 20

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19
Q

What CDs are expressed in T-ALLs?

A

CD-1,2,5,7

** not CD-10!

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20
Q

What are the common symptoms associated with ALL?

A

Anemia (fatigue), thrombocytopenia (bleeding), neutropenia (infection)

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21
Q

What is the prognosis of ALL in children?

A

aggressive chemotherapy–> 95% success rate

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22
Q

What factors favor a good prognosis in ALL?

A

t(12;21), age 2-10, hyperdiploidly, trisomy of chromosomes 4,7,10.

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23
Q

What translocation in ALL yields a poor prognosis?

A

t(9;22)

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24
Q

What fusion gene is created in the t(9;22) form of ALL?

A

BCR-ABL tyrosine kinase

  • Philadelphia +
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25
Q

What is the most common leukemia of adults in the world?

A

Chronic Lymphocytic Leukemia

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26
Q

What staining can be used on peripheral smear for AML?

A

MPO

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27
Q

What microscopic feature is found in AML?

A

Auer rods-> distinctive needle-like azurophilic granules.

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28
Q

What is the average age of onset for AML?

A

50-60 years of age

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29
Q

What is the translocation that leads to acute promyelocytic leukemia?

A

t(15;17) that creates a fusion gene encoding a chimeric protein consisting of the retinoid acid receptor.

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30
Q

What is the treatment for acute promyelocytic leukemia?

A

all-trans retinoid acid or arsenic trioxide.

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31
Q

What is necessary for a diagnosis of AML?

A

presence of at least 20% myeloid blasts in the bone marrow

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32
Q

What is characteristic of myeloblasts?

A

delicate nuclear chromatin, two to four nucleoli, and more cytoplasm than lymphoblasts.

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33
Q

What are some clinical features of AML?

A
  • fatigue, fever, spontaneous mucosal and cutaneous bleeding.
  • Infections of the oral mucosa, skin, lungs, kidneys, bladder, and colon.
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34
Q

What is the prognosis of AML?

A

60% obtain complete remission with chemotherapy.

t(15;17)->best prognosis
t(8;21)->good prognosis in absence of KIT mutations.

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35
Q

What are Myelodysplastic syndromes (MDS)?

A

group of clonal stem cell disorders characterized by maturation defects that are associated with ineffective hematopoiesis and a have a high risk of transformation to AML.

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36
Q

What are the two causes of MDS?

A

Either primary (idiopathic) or secondary to previous genotoxic drug of radiation therapy.

*Genotoxic drugs have highest rate of transformation to AML

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37
Q

How do patients present with MDS?

A

Cytopenias, hypercellular bone marrow, increased myeloid blasts.

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38
Q

what is a common abnormality seen in MDS within the erythroid series?

A

Ring Sideroblasts. Erythroblasts with iron-laden mitochondria visible as perinuclear granules in Prussian blue-stained aspirates or biopsies.

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39
Q

What morphological features can be seen in MDS?

A
  • megaloblastic maturation
  • nuclear budding abnormalities
  • Pseudo-Pegler-Huet Cells (neutrophils with only two nuclear lobes)
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40
Q

What are the clinical features of MDS?

A
  • primarily affects older people only (>70)

- weakness, infections, hemorrhages

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41
Q

What is the prognosis of MDS?

A

primary-> 9-29 months

secondary-> 4-8 months

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42
Q

What is a common theme of the Myeloproliferative disorders?

A

presence of a mutated, constitutively, activated tyrosine kinase.

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43
Q

What are the common features of myeloproliferative disorders?

A
  • increased proliferative drive in the bone marrow
  • extramedullary hematopoiesis (splenomegaly)
  • marrow fibrosis
  • variable transformation to acute leukemia
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44
Q

What is the translocation and mutation that is found in Chronic Myelogenous Leukemia?

A

t(9;22) BCR-ABL fusion gene that results in a constitutively active tyrosine kinase.

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45
Q

What is the morphology of CML?

A
  • bone marrow is hypercellular (especially basophils)

- scattered macrophages with abundant green-blue cytoplasm (sea-blue histiocytes)

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46
Q

What does the blood count revel in CML?

A

Leukocytosis with consists of predominantly of neutrophils, band forms, metamyelocytes, myelocytes, eosinophils, and basophils.

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47
Q

What is the average age of onset of CML?

A

5-6th decade of life

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48
Q

What are the common presenting symptoms in patients with CML?

A

insidious onset of mild-moderate anemia, hypermetabolism leading to fatigibility, weakness, weight loss, and anorexia.

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49
Q

How is CML best differentiated from other myeloproliferative disorders?

A

detection of the BCR-ABL fusion gene

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50
Q

What activating mutation is seen in polycythemia vera?

A

activating point mutations in the tyrosine kinase JAK2

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51
Q

What cells are increased in polycythemia vera?

A

red cells, granulocytes, and platelets.

*but the increase in red cells is what causes most clinical symptoms.

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52
Q

What are the levels of erythropoietin in primary polycythemia compared to secondary forms of polycythemia?

A

primary-> low

secondary-> high

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53
Q

What is the level of hematocrit in primary polycythemia vera?

A

elevated and leads to increased viscosity and sludging

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54
Q

What are patients with PCV at risk for?

A

prone to both thrombosis and bleeding.

  • DVT, MI, Stroke
  • budd-chiari syndrome
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55
Q

What is the morphology of PCV?

A

increase in red cell progenitors as well as an increase in granulocytic precursors and megakaryocytes.

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56
Q

What is the morphology of late phase PCV?

A

“spent phase” characterized by marrow fibrosis that displaces hematopoietic cells.
-extramedullary hematopoiesis in spleen and liver

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57
Q

What are the clinical symptoms of PCV?

A
  • plethoric and cyanotic
  • HA, dizziness, HTN, and GI symptoms
  • intense pruritus and peptic ulceration
  • hyperuricemia and gout
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58
Q

What mutations are often associated with Essential Thrombocytosis?

A

JAK2 -50%

MPL- 5/10%

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59
Q

How is essential thrombocytosis separated from PCV and primary myelofibrosis?

A

absence of polycythemia and marrow fibrosis

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60
Q

What cell types are increased in Essential Thrombocytosis?

A

Megakaryocytes (large platelets), RBCs and granulocytes are also increased.

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61
Q

What is a characteristic finding of Essential Thrombocytosis?

A

Erythromelalgia –> burning and throbbing of hands and feet caused by occlusion of small arterioles by platelet aggregation.

  • can also be seen in PCV
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62
Q

What is the hallmark finding in Primary Myelofibrosis?

A

Development of obliterative marrow fibrosis

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63
Q

What does primary myelofibrosis lead to?

A

extensive extramedullary hematopoiesis and cytopenias

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64
Q

What is the chief pathologic feature of primary myelofibrosis?

A

Extensive deposition of collagen in the marrow by non-neoplastic fibroblasts

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65
Q

What two growth factors are associated with primary myelofibrosis?

A

PDGF and TGF-beta

66
Q

With progression of primary myelofibrosis, what morphological features are seen?

A

marrow becomes hypocellular and diffusely fibrotic

67
Q

Marrow distortion in primary myelofibrosis leads to what?

A

-premature release of of nucleated erythroid and early granulocytic cells progenitor cells (leukoerythroblastosis)

68
Q

What is the name of the damaged cells that are released into circulation from the fibrotic marrow in primary myelofibrosis?

A

Tear-drop cells

69
Q

What are some clinical features of primary myelofibrosis?

A

left upper quadrant fullness, fatigue, weight loss, night sweats, hyperuricemia and gout

70
Q

What type of anemia is seen in primary myelofibrosis?

A

moderate to severe normochromic mocmocytic anemia accompanied by leukoerythroblastosis.

71
Q

What is a characteristic finding in Langerhans Cells Histiocytosis?

A

Birbeck granules in the cytoplasm.

Tennis racket like in appearance

72
Q

What do the tumor cells express in Langerhans Cells Histiocytosis?

A

HLA-DR, S-100+, CD1a+

73
Q

What is Letterer-Siwe Disease?

A
  • Malignant proliferation of langerhans cell
  • Classic presentation is skin rash and cystic skeletal defects
  • <2 YOA
74
Q

What is Eosinophilic Granuloma?

A
  • Benign proliferation of langerhans cells in bone
  • Presents as pathological fractures or multiple erosive bone masses
  • affects young children
75
Q

What is Hand-Schuler-Christian Disease?

A

-triad of calvarial bone defects, diabetes insidious, and exopthalamus in a child.

76
Q

What are the most common chromosomal deletions in CLL and SLL?

A

deltions in 13q14.3, 11q, 17p, and trisomy 12q

77
Q

What is seen on a blood smear in patients with CLL?

A

increased lymphocytes and smudge cells

78
Q

What morphological feature is pathognomonic for CLL/SLL?

A
  • proliferation centers

- small lymphocytes with condensed chromatin and can’t cytoplasm

79
Q

What cell markers can be found in CLL/SLL?

A

CD 5,19,20, 23

80
Q

What are some complications of CLL/SLL?

A
  • Hypogammaglonulinemia–> infections

- Autoimmune hemolytic anemia

81
Q

What is Richter syndrome?

A
  • Transformation of CLL/SLL to a more aggressive diffuse large B-cell lymphoma.
  • Heralded by development of a rapidly enlarging mass within a lymph node or spleen
82
Q

What is the most common form of indolent NHL in the US?

A

Follicular Lymphoma

83
Q

What is the demographics of follicular lymphoma?

A
  • affects middle aged individuals

- men=women

84
Q

What is the translocation that is associated with follicular lymphoma?

A

t (14;18) involving the BCL2 gene that inhibits apoptosis

85
Q

In addition to BCL2, what else is mutated in 90% of cases of follicular lymphoma?

A

MLL2–> encodes histone methyltransferase that regulates gene expression

86
Q

What is the morphology of follicular lymphoma?

A

nodular or nodular to diffuse growth pattern is observed in involved lymph nodes

87
Q

What two cells can be found in follicular lymphoma?

A
  • Centrocytes: small cleaved cells

- Centroblasts: several nucleoli with modest amounts of cytoplasm

88
Q

What cell markers are expressed in follicular lymphoma?

A

CD 10,19,20

89
Q

How does follicular lymphoma present?

A

painless generalized lymphadenopathy

90
Q

What is the most common form of NHL?

A

Diffuse large B-cell lymphoma (median age 60)

91
Q

What is a frequent pathological event in DLBCL?

A

dysregulation of BCL6

92
Q

What is the morphology of DLBCL?

A

Large cell size and a diffuse pattern of growth

93
Q

What cell markers are seen in DLBCL?

A

CD 19 ,20 with variable expression of CD10 and BCL6

94
Q

How does DLBCL present?

A

Rapidly enlarging mass at a nodal or extra nodal site.

95
Q

What is the prognosis of DLBCLs?

A

With intensive combination chemotherapy, 60-80% gain complete remission

96
Q

What translocation is associated with all types of Burkitt Lymphomas?

A

MYC gene on chromosome 8

  • most commomy the t(8;14)
97
Q

All endemic Burkitt lymphomas as latently infected with what?

A

EBV

98
Q

What is the morphology of Burkitt lymphoma?

A
  • high mitotic index and contains numerous apoptotic cells
  • “starry sky” pattern due to phagocytes with abundant clear cytoplasm
  • royal blue cytoplasm containing clear cytoplasmic vacuoles
99
Q

What are the cell markers that are present in Burkitt lymphoma?

A
  • CD 10, 19, 20
  • surface IgM
  • BCL6
100
Q

What are the common sites affected in the sporadic form and endemic form of Burkitt Lymphoma?

A

Sporadic-> abdomen

Endemic-> jaw

101
Q

What is the prognosis of Burkitt Lymphoma?

A

Responds very well to aggressive chemotherapy

102
Q

What is multiple myeloma?

A

Plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia, renal failure, ad acquired immune abnormalities.

103
Q

The proliferation and survival of myeloma cells is most dependent on what cytosine?

A

IL-6

  • high levels are associated with a poor prognosis
104
Q

What activates osteoclasts activity in multiple myeloma?

A

MIP1 alpha upregualtes expression of NF-kappaB ligand (RANKL) resulting in increased osteoclast activity

105
Q

What are the most commonly involved bones in multiple myeloma and how do they appear?

A

vertebral column, ribs, skull, pelvis, femur

punched-out defects

106
Q

What is the Rouleaux formation?

A

RBCs stick together in a linear pattern

107
Q

What is excreted in the urine in multiple myeloma?

A
  • free light chains are excreted in the urine as Bence Jones proteins.
  • Deposition in the kidney tubules leads to risk for renal failure
108
Q

What cell marker is present in multiple myeloma?

A

CD 138

109
Q

What are the clinical features of multiple myeloma?

A

pathological fractures, hypercalcemia, bone pain

110
Q

What is the elevated serum protein in multiple myeloma show up as?

A

“M spike” that is present on serum protein electrophoresis (SPEP).
Most commonly due to monoclonal IgG for IgA

111
Q

What is the most common plasma cell dycrasias?

A

monoclonal gammopathy of uncertain significance (MGUS)

1% will develop multiple myeloma

112
Q

What age population does MGUS affect?

A

3% >50

5%>70

113
Q

What is the common translocation that is associated with mantel cell lymphoma?

A

t(11;14) involving the IgH locus on chr 14 and cyclin D1 on chr 11

114
Q

What does cyclin D1 promote in mantel cell lymphoma?

A

G1-S transition in mitosis

115
Q

What do a majority of patients present with at diagnosis of mantel cell lymphoma?

A

generalized painless lymphadenopathy

116
Q

What cell markers can be found in mantel cell lymphoma?

A

CD 5,19, 20

*CD23- which helps distinguish it from CLL/SLL

117
Q

What is the prognosis of mantel cell lymphoma?

A

poor; 3-4 year survival

118
Q

What are marginal cell lymphomas associated with?

A
  1. chronic inflammation: sjogrens, Hashimoto thyroiditis, helicobacter gastritis
  2. remain localized until late in course
  3. regress if inciting agent is removed (H. pylori removed MALToma risk back to 0)
119
Q

What mutations are seen in over 90% of Hairy Cell Leukemias?

A

BRAF mutations- a serine/threonine kinase

120
Q

What is the morphology of Hairy Cell Leukemia?

A

Fine hairlike projections with round, oblong, or reniform nuclei with moderate amounts of pale blue cytoplasm,

121
Q

What are the cell markers that are seen in Hairy Cell Leukemia?

A

CD 19,20

CD11c, 25, 103, annexin A1

122
Q

What is the most common clinical feature of Hairy Cell Leukemia?

A
  • Splenomegaly

- some patients will have pancytopenia

123
Q

What is the prognosis of Hairy Cell Leukemia?

A
  • very sensitive to chemotherapy although the tumors tend to return.
  • respond well to same drug on second chemo course
124
Q

What is characteristic of Peripheral T-cell Lymphoma, Unspecified?

A

Tumors are composed of a pleomorphic mixture of variably sized T cells.

125
Q

How do patients present with Peripheral T-cell Lymphoma, Unspecified?

A

Generalized lymphadenopathy, sometimes accompanied by eosinophilia, pruritus, fever, and weight loss.

126
Q

What is Anapestic Large-Cell lymphoma defined by?

A

uncommon entity defined by presence of rearrangement of the ALK gene on chromosome 2p23

127
Q

What cells are found in Anapestic Large-Cell lymphoma?

A

“hallmark cells” with horseshoe shaped nuclei

128
Q

What neoplasm is associated with HTLV-1?

A

Adult T-cell leukemia/lymphoma- neoplasm of CD4+ cells

129
Q

Where is Adult T-cell leukemia/ lymphoma most commonly occur?

A

southern japan, west africa, and the caribbean

130
Q

What are the common findings in Adult T-cell leukemia/ lymphoma?

A

Skin lesions, generalized lymphadenopathy, HSM, hypercalcemia

131
Q

What is Mycosis Fungoides?

A

manifestations of a tumor of CD4+ helper T cells that home to the skin

132
Q

Histologically, where do the CD4 T cells localized in Mycosis Fungoides?

A

Epidermis and upper dermis and have a cerebriform appearance

133
Q

What is Sezary syndrome?

A

variant in which skin involvement is manifested as a generalized exfoliative erythroderma.

134
Q

What is a difference seen morphologically between B cell and T cells?

A

T cells tend to have more cytoplasm than B cells and larger nuclei

135
Q

What translocation has a favorable prognosis in CML but a unfavorable prognosis in ALL?

A

t(9;22)

136
Q

What is the most common form of indolent NHL in the US?

A

Follicular Lymphoma

137
Q

Where do HL arise and how does it spread?

A

Arises in a single node or chain of nodes and spreads first to anatomically contiguous lymphoid tissue.

138
Q

Waldeyer ring and mesenteric node involvement is characteristic of HL or NHL?

A

NHL

139
Q

What is the neoplastic cell found in HL?

A

Reed-Sternburg Cells

140
Q

Average age of diagnosis of HL?

A

32

141
Q

What CD marker are Reed-Sternburg Cells positive for?

A

CD 15, CD 30, PAX 5

142
Q

Activation of what transcription factor is a common event in classical HL?

A

NF-kappaB

*EBV can active this via LMP-1

143
Q

What is the morphology of a Reed-Sternburg Cell?

A
  • multiolobed nuclei with prominent nucleoli.

- can appear “owl eyed”

144
Q

What type of cells are seen in the nodular sclerosing type of HL?

A

Lacunar cells- delicate, folded, or multilobate nuclei and abundant pale cytoplasm.

145
Q

What type of cells are seen in the lymphocyte predominance subtype of HL?

A

Lymphohistiocytic variant- polyploid nuclei, inconscpicious nucleoli, and moderately abundant cytoplasm.

146
Q

What is the most common form of HL?

A

Nodular Sclerosing type

  • deposition of collagen in bands that divide the LN into circumscribed nodules
  • uncommonly associated with EBV
147
Q

What types of HL have a strong association with EBV?

A

Mixed-Cellularity type -70%

Lymphocytic Depletion type -90%

148
Q

Who is affected most commonly by the mixed-cellularity type of HL?

A

men, older age, and systemic symptoms (night sweats)

149
Q

What is the morphology of the Lymphocyte-Rich type of HL?

A

Reactive lymphocytes make up the vast majority of cellular infiltrate.

150
Q

Who is affected by lymphocyte depletion HL?

A

Older adults, HIV+ individuals, nonindustralized countries.

151
Q

What is the “nonclassical” type of HL?

A

Lymphocyte Predominance Type

152
Q

What is the morphology of Lymphocyte Predominace type of HL?

A

-Reed-Sternburg cells are difficult to find.

  • Nodes are effaced by nodular infiltrate of small lymphocytes admixed with variable numbers of macrophages.
  • Eosiniphils and plasma cells are absent
153
Q

Who is most commonly affected by the L&H variant of HL?

A

35 y/o male with cervical or axillary lymphadenopathy.

154
Q

How does HL most commonly present?

A

painless lymphadenopathy

155
Q

What is the predicted pattern of HL spread?

A

nodal disease–> splenic diseae–> hepatic disease–> marrow involvemt.

156
Q

What cell markers are expressed by the lymphocyte predominate type of HL?

A

CD 20+

*CD15, CD30-, EBV -

157
Q

What is a common presenting symptom in HL?

A

Fever related to release of cytokines

158
Q

What type of lymphoma is associated with KSHV/HHV-8?

A

Primary Effusion Lymphoma

159
Q

What is associated with Immunodeficiency-assoacited large B-cell lymphoma?

A

EBV

160
Q

Waldeyer ring is frequently involved in what cancer?

A

DLBCL

161
Q

What is characteristic of Lymphoplasmacytic lymphoma?

A
  • No bone destruction, or secretion of Ig light chains.
  • Most commonly a monoclonal IgM is secreted
  • 6th-7th decade of life
  • Hyperviscosity

Heme and Lymph (4 decks)

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