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White Blood cell disorders Flashcards

1
Q

What is the marker for hematopoietic stem cells? (CD(__))?

A

CD34

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2
Q

What are the two divisions of the lymphoid route of stem cell maturation?

A 
B cells (to plasma cells)
T cells to CD4 or CD8 cells
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3
Q

What are the four myeloid cells that stem cells can differentiate into?

A

Erythroblasts
Myeloblasts
Monoblasts
Megakaryblasts

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4
Q

What are the three cells that myeloblasts give rise to?

A

Neutrophils
Basophils
Eosinophils

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5
Q

What are the two major causes of neutropenia?

A

Drug toxicity

Severe infection

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6
Q

What is the treatment for neutropenia? (2)

A

G-CSF

GM-CSF

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7
Q

What are the four major causes of lymphopenia? (3)

A
  • Immunodeficiency
  • High cortisol state
  • Autoimmune disease (e.g. SLE)
  • Whole body radiation
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8
Q

What are the most sensitive cells to radiation?

A

Lymphocytes

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9
Q

When does neutrophil leukocytosis occur? (3)

A
  • Bacterial infection
  • Tissue necrosis
  • High cortisol state
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10
Q

What is a left shift?

A

Increased band cells

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11
Q

What does premature neutrophils lack as compared to normal neutrophils? What is the marker that identifies this?

A

Fc receptors

CD16

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12
Q

Decreased CD16 indicates what?

A

Proliferation of immature neutrophils and a lack of Fc receptors

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13
Q

What is the MOA of neutrophilic leukocytosis with high cortisol states?

A

Causes PMN detachment from endothelial cells of the blood vessels (loss of marginated pool)

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14
Q

What are the two causes of monocytosis?

A
  • Malignancy

- Chronic inflammatory states

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15
Q

What are the three causes of eosinophilia?

A
  • Allergic reaction
  • Parasitic infection
  • Hodgkin lymphoma
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16
Q

In what malignancy is there a high amount of eosinophils present? What causes this?

A
  • Hodgkin’s lymphoma

- Increased IL-5 production

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17
Q

Basophilia is seen in what malignancy?

A

CML

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18
Q

What general type of infectious diseases cause a lymphocytic leukocytosis? Which bacteria can cause this, and why?

A
  • Virus infection

- Bordetella pertussis, which produces a lymphocyte promoting factor, preventing leukocytes from leaving the blood

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19
Q

What are the two viral causes of mononucleosis?

A
  • EBV infection predominate

- CMV less common cause

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20
Q

What is the T cell type that predominates in infectious mononucleosis? What does this result in (3)?

A

CD8 + T cells

  • Generalized LAD
  • Splenomegaly
  • High white count
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21
Q

Which are of the lymph node will be enlarged in a viral infection?

A

Paracortex

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22
Q

Where are B cells found in a lymph node?

A

Cortex

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23
Q

What is in the white pulp part of the spleen? Red pulp?

A

Red pulp = blood

White pulp = cells

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24
Q

What part of the white pulp of the spleen is enlarged in viral infections?

A

Periarterial lymphatic sheath (PALS)

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25
Q

Where are the T cells present in the spleen?

A

Around the blood vessels

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26
Q

What does the monospot test assess for?

A

-IgM to heterophile antibodies

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27
Q

A negative monospot usually indicates that what virus is usually causing the mono-like symptoms?

A

CMV

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28
Q

What is the definitive test for mono?

A

EBV viral capsid antigen

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29
Q

A rash can develop if a patient with Mono is given what abx?

A

PCN

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30
Q

How long do patients with mono have to avoid contact sports d/t the chance of splenic rupture?

A

1 year

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31
Q

What is the basis for acute leukemia?

A

Accumulation of blast cells d/t cell inability to mature properly

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32
Q

Acute leukemia is defined as when there is more than what percent of blasts in the bone marrow?

A

When there is >20% of blasts in the bone marrow

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33
Q

What is the cause of the ssx of acute leukemia? Why?

A

Loss of a type or many types of cell lines, d/t blast cells crowding out normal cells/not producing normal cells (so anemia, neutropenia, leukopenia etc)

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34
Q

Why is there a high WBC count if there are not any mature cells being produced in leukemia?

A

Tons of blasts

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35
Q

What are the histological findings of acute leukemia?

A

Large, immature cells with punched out nucleoli

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36
Q

What is the marker for ALL? AML?

A 
ALL = tdt
AML= myeloperoxidase
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37
Q

tdt in the nucleus of an immature WBC = what disease? What is tdt?

A

ALL

DNA pol for lymphoid cells

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38
Q

Auer rod = what disease? What is an auer rod?

A
  • AML

- myeloperoxidase

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39
Q

Down syndrome is associated with what hematological malignancy? What age does this appear after?

A

ALL

After age of 5 yo

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40
Q

What age group usually gets ALL?

A

Children

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41
Q

What are the two divisions of ALL?

A
  • B-ALL

- T-ALL

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42
Q

B-ALL surface markers = which three?

A

CD10
CD19
CD20

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43
Q

What is the prognosis for B-ALL?

A

Good with chemo

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44
Q

What parts of the body need to be given prophylaxis of chemo for B-ALL?

A

scrotum and CSF

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45
Q

What are the two translocations associated with B-ALL? Which is associated with children and has a good prognosis, and which with adults and has a bad prognosis?

A
  • t(12;21) = kids

- t(9;22) = adults (philadelphia chromosome)

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46
Q

What are the cell markers for T-ALL? Which CD marker is not expressed on T cells, but is on B cells for ALL?

A

CD2 through CD8

CD10

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47
Q

What is the usual presentation of T-ALL that distinguishes it from B-ALL?

A

Thymic mass in a teenager

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48
Q

What are auer rods?

A

Crystallized myeloperoxidase–an enzyme only found in myeloblasts, hence why these are pathognomonic for AML

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49
Q

Punched out nucleolus = what type of cell?

A

Lymphoblasts

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50
Q

What is the age range that usually gets AML?

A

Old people (50-60)

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51
Q

What are the three types of classification in AML?

A
  • Cytogenetic abnormalities
  • Lineage of myeloblasts
  • Surface markers
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52
Q

What is the chromosomal translocation found in acute promyelocytic leukemia?

A

t(15;17)

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53
Q

What disease is caused by a t(15;17)? how? What is the treatment and prognosis?

A
  • Acute promyelocytic leukemia
  • Retinoic acid receptor disrupted, inhibiting promyelocyte maturation
  • Treat with ATRA (great prognosis)
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54
Q

Promyelocytes that contain numerous Auer rods, as seen in acute promyelocytic leukemia, poses a risk for what emergent complication?

A

DIC

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55
Q

What is the treatment for acute promyelocytic leukemia?

A

ATRA (all trans-retinoic acid)–very good prognosis

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56
Q

What is the cause of acute monocytic leukemia? What is the telltale sign of this?

A
  • Proliferation of monoblasts that lack MPO

- Infiltration of the gums = gingival hypertrophy

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57
Q

What is the cause of acute megakaryoblastic leukemia? What disease is associated with this?

A

Proliferation of megakaryocytes that lack MPO

Down syndrome BEFORE age 5)

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58
Q

What is the CA that appears before the age of 5 for down syndrome pts? After?

A
  • Before = acute megakaryoblastic leukemia

- After = ALL

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59
Q

What chemotherapeutic agent can lead to AML?

A

Alkylating agents

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60
Q

What is myelodysplastic syndrome? What can this progress to?

A

Cytopenia with hypercellular bone marrow from blasts, but less than 20% blasts

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61
Q

Most patients who have myelodysplastic syndrome die from what complication?

A

Infection or bleeding

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62
Q

What, generally, are chronic leukemias?

A

Neoplastic proliferation of mature circulating lymphocytes

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63
Q

Is the WBC high or low in chronic leukemia?

A

high

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64
Q

Who usually gets chronic leukemia? What is the course?

A
  • Older adults

- Slow onset and slow progression

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65
Q

CLL is caused by what? What are the cell markers that distinguish this from other proliferations?

A

Neoplastic proliferation of naive B cells

CD5 and CD20

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66
Q

Increased lymphocytes and smudge cells = ?

A

CLL

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67
Q

How does CLL progress to small lymphocytic lymphoma?

A

When bad B cells go to lymph nodes, will cause “lymphoma”

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68
Q

What are the classical hematological findings with CLL? (2)

A
  • Hypogammaglobulinemia

- Autoimmune hemolytic anemia

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69
Q

What is the cause of the autoimmune hemolytic anemia seen in CLL?

A

Bad B cells producing crappy Igs that attack RBCs

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70
Q

CLL can progress to what? What is the classic presentation of this?

A

Large B cell lymphoma (enlarging spleen/lymph node)

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71
Q

What, generally, is hairy cell leukemia?

A

Neoplastic proliferation of mature B cells that have hairy cytoplasmic processes

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72
Q

What are the two findings for hairy cell leukemia? (histological, and protein)

A

Hairy cytoplasmic processes

Cells are TRAP +

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73
Q

What are the three clinical features of hair cell leukemia (bone tap, LAD, splenomegaly)?

A
  1. Splenomegaly (red pulp)
  2. Dry bone marrow aspiration
  3. Lymphadenopathy is absent
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74
Q

What is odd about the splenomegaly in hairy cell leukemia, as opposed to other leukemias?

A

Enlargement is found in the red pulp

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75
Q

What is the best way to remember the clinical features of hairy cell leukemia?

A

“TRAPt”

  • Tartrate-resistant acid phosphatase (TRAP) +
  • B cells Trapped in the red pulp
  • B cells trapped in the bone marrow
  • B cells trapped so no lymphadenopathy
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76
Q

What is the drug that is used to treat hair cell leukemia? MOA? Prognosis?

A
  • 2-CDA (cladribine)
  • Adenosine deaminase, which is used in the purine degradation pathway, and results in the death of neoplastic cells
  • Excellent
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77
Q

What is ATLL caused by? What infection is this associated with? Where in the world is this usually seen?

A

Neoplastic proliferation of CD4+ T cells

HTLV-1 (Japan and the caribbean)

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78
Q

What are the clinical features of ATLL? (3)

A
  • Rash
  • Generalized LAD with HSM
  • Lytic bone lesions w/ hypercalcemia
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79
Q

Lytic bone lesions = what two diseases in your ddx? What can help differentiate these?

A

Multiple myeloma OR
ATLL

ATLL will have a rash

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80
Q

What is mycosis fungoides?

A

Neoplastic proliferation of mature CD4+ T cells

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81
Q

What are the clinical features of mycosis fungoides?

A

Rash/plaques/nodules

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82
Q

Pautrier microabscesses = ?

A

skin abscesses of Mycosis fungoides (CD4+)

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83
Q

What is Sezary syndrome? What are the histological characteristics of the cells that are found in this?

A
  • Neoplastic CD4+ T cells proliferating in the skin (advanced mycosis fungoides)
  • lymphocytes with cerebriform nuclei
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84
Q

lymphocytes with cerebriform nuclei = ?

A

Sezary syndrome

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85
Q

Chronic myelogenous leukemia is what?

A

Overproduction of mature myeloblasts (PMNs, basophils, eosinophils)

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86
Q

Chronic overproduction of RBCs is what? Is this the only cell line that is overproduced in this?

A

Polycythemia vera, not the only cell line

87
Q

Chronic overproduction of megakaryocytes is what?

A

essential thrombocythemia

88
Q

Who usually gets myelodysplastic syndromes?

A

Older adults

89
Q

What are the WBC and bone marrow findings in myelodysplastic syndrome?

A
  • High WBCs

- Hypercellular bone marrow

90
Q

True or false: in any myelodysplastic syndrome, all cells of myeloid lineage are increased

91
Q

Why is there an increased risk for hyperuricemia and gout in myelodysplastic syndrome?

A

Increased production/turnover of all myeloid cells

92
Q

What causes the “burnt out” phase of myelodysplastic syndromes?

A

Bone marrow fibrosis

93
Q

What can myelodysplastic syndromes lead to?

A

Acute leukemias

94
Q

What is chronic myeloid leukemia?

A

Neoplastic proliferation of mature myeloid cells, especially granulocytes

95
Q

What cell type is classically increased in CML?

96
Q

CA with Basophilia =?

97
Q

What is the genetic translocation and mutation in CML? Medication for this? MOA?

A
  • t(9;22) causing an increase in tyrosine kinase

- Imatinib–blocks Y-kinase activity

98
Q

True or false: splenomegaly is uncommon in CML

A

False–common, and may indicate the transition from chronic to accelerated phase

99
Q

How can you tell if CML is progressing or not?

A

Increasing spleen size

100
Q

CML can lead to which neoplastic diseases? Why?

A

Acute leukemia (AML or ALL)

Genetic cause is in the HSC, and is predisposed to forming other neoplastic processes

101
Q

What are the three ways to differentiate leukocytosis due to CML vs infection?

A

CML has:

  1. Granulocytes that are Leukaline phosphatase (LAP) -
  2. Increased basophils
  3. t(9;22)
102
Q

What is polycythemia vera? What is the mutation that leads to this?

A

Proliferation of mature myeloid cells, especially RBCs

JAK2 kinase mutation

103
Q

What are the clinical symptoms of polycythemia vera? (4)

A
  • Blurry headache
  • Budd-chiari syndrome
  • Flushed face
  • Itching after bathing
104
Q

What is Budd-Chiari syndrome, and how does it relate to polycythemia vera?

A

a condition caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement.

Increased thrombosis

105
Q

Why does polycythemia vera present with itching following bathing?

A

Increased production of mast cells that can be activated by heat

106
Q

What is the treatment for polycythemia vera? (2)

A
  • Phlebotomy

- Hydroxyurea

107
Q

What is reactive polycythemia?

A

some disease causing increased RBC (hypoxemia, EPO producing tumor etc)

108
Q

How do you distinguish polycythemia vera from reactive polycythemia?

A

Decreased EPO in polycythemia vera, whereas there is an increased production of EPO if reactive

109
Q

What is the cause of essential thrombocythemia? Genetic mutation?

A

Neoplastic proliferation of mature myeloid cells, especially platelets

JAK2 kinase

110
Q

What must essential thrombocythemia be differentiated from? Why?

A
  • Fe deficiency anemia

- Looks very similar

111
Q

What other cells are overproduced in essential thrombocythemia?

A

RBC and granulocytes

112
Q

What are the symptoms of essential thrombocythemia? Why?

A

Increase bleeding/thrombosis

Crappy platelets = increased bleeding, or lots of okay platelets and thrombosis

113
Q

Is there a risk for hyperuricemia or gout with essential thrombocythemia? Why or why not?

A

No, because platelets do not have nuclei or DNA

114
Q

How often does essential thrombocythemia progress to acute leukemia?

115
Q

What is primary myelofibrosis? Which cell in particular is overproduced? Mutation that causes it?

A

Increased proliferation of mature myeloid cells, especially megakaryocytes

JAK2 Kinase mutation

116
Q

What is the pathophysiology of the marrow fibrosis in primary myelofibrosis?

A

Neoplastic megakaryocytes cause increased PDGF, causing fibroblasts proliferation in the bone marrow

117
Q

What is the cause of Splenomegaly in primary myelofibrosis?

A

Extramedullary hematopoiesis occurs due to a loss of marrow

118
Q

What is the leukoerythroblastic smear in primary myelofibrosis, and what causes it?

A

Normally, Reticulin in the bone inhibits reticulocytes from leaving early, but this is not found in the spleen. Thus, when there is extramedullary hematopoiesis, immature cells have nothing stopping them from escaping, allowing large, immature cells from leaving the spleen prematurely

119
Q

What is the cause of the increase in thrombosis, infx, and bleeding in primary myelofibrosis?

A

not enough cell produced from the spleen, relative to the entirety of the bone marrow

120
Q

Tear drop cells = ?

A

Primary myelofibrosis due to a lack of reticulin in the spleen, where RBC production shifts

121
Q

What is the ddx of painless LAD? (3)

A
  • Chronic inflammation
  • Metastatic carcinoma
  • Lymphoma
122
Q

Expansion of the follicles of lymph nodes is usually found in what two diseases?

A
  • RA

- Early HIV

123
Q

Expansion of the paracortex in lymph nodes is usually due to what type of infections? Why?

A

viral infection

T cell proliferation

124
Q

Where do T cells live in lymph nodes? B cells?

A

T cells = paracortex

B cells = cortex

125
Q

Where do histiocytes live in lymph nodes?

A

Sinuses of the medulla

126
Q

What are the three major types of lymphomas that arise from lymph nodes?

A
  • Follicular
  • Mantle
  • Marginal
127
Q

Where do lymphoma generally arise?

A

LN or extranodal tissues

128
Q

What are the two general categories of lymphoma? Which is more common?

A

NHL (60%)

HL (40%)

129
Q

What is the dark area that immediately surrounds the follicle of a lymph node?

130
Q

What is the area immediately around the mantle of a LN?

131
Q

What is follicular lymphoma? When and how does it usually present?

A

t(14;18) causing Neoplastic proliferation of small B cells in the follicles of lymph nodes

Presents in late adulthood with generalized, painless LAD

132
Q

What is the cell marker for follicular lymphoma?

133
Q

What are the histological findings of follicular lymphoma?

A

Proliferation of follicles of lymph nodes

134
Q

What is the chromosomal translocation for follicular lymphoma? What is the protein that is coded for in these chromosomal regions? What does this result in?

A

t(14;18)

BCL-2 on chr 18 translocates to a heavy chain Ig locus on 14

Results in overexpression of Bcl-2, which inhibits apoptosis of B cells

135
Q

What is the treatment for follicular lymphoma? What are the criteria for treatment?

A

Low dose CTX or rituximab, i.f.f. symptomatic

136
Q

What may follicular lymphoma progress to? How will this present?

A

Progression to diffuse large B cell lymphoma, which presents as an enlarging lymph node

137
Q

What is the monoclonal antibody that is used to treat follicular lymphoma, and how does it work?

A

Rituximab–Anti CD20 antibody

138
Q

How do you distinguish follicular lymphoma from follicular hyperplasia? (4)

A

Follicular lymphoma has:

  • disrupted LN architecture
  • Lack of tingible macrophages in the LN
  • Expression of BCL-2 in follicles
  • Monoclonal
139
Q

What is the importance of tingible body macrophages in LNs?

A

Macrophages in LNs eat up apoptotic cells or bacteria, and are normally found in lymph nodes.

This can help distinguish between follicular lymphoma, and follicular hyperplasia secondary to infection

140
Q

BCL-2 within LNs is diagnostic of what?

A

Follicular lymphoma

141
Q

How can you tell if the cells in follicular lymphoma is a normal reaction to infection, or the result of monoclonal expansion?

A

Expressing only one ab is characteristic of tumors, whereas polyclonal is suggestive of infection

142
Q

What is mantle cell lymphoma?

A

Neoplastic proliferation of small B-cells that expand the mantle zone of a lymph node follicle

143
Q

What is the marker for B cells?

144
Q

What are the ssx of mantle cell lymphoma?

A

Painless LAD in late adulthood

145
Q

Neoplastic proliferation of cells that expands the region immediately adjacent to the LN follicle = ?

A

Mantle cell lymphoma

146
Q

What is the translocation involved in mantle cell lymphoma? What is the protein that is overexpressed here?

A
  • t(11:14)

- Cyclin D1 on chr 11 translocates to Ig heavy chain on chr 14

147
Q

Overexpression of what protein is the cause of mantle cell lymphoma? What does this protein do?

A

Cyclin D1–promotes G1/S transition in cell cycle

148
Q

What is marginal zone lymphoma?

A

Neoplastic Proliferation of B cells in the marginal zone of a LN.

149
Q

What chronic inflammatory states is marginal zone lymphoma associated with? (three, 2 autoimmune, and 1 infx)

A
  • Hashimoto’s thyroiditis
  • Sjogren’s syndrome
  • H.pylori infx
150
Q

When are marginal zones present within lymph nodes normally? How does this relate to marginal zone lymphoma?

A

During infection to expand the B cell population.

Thus certain infectious/inflammatory conditions can lead to marginal zone expansion

151
Q

What is a MALToma?

A

Marginal zone lymphoma in mucosal sites

152
Q

What is the usual cause of MALToma? What is the treatment?

A
  • H.pylori infection

- Treat the H.pylori infection

153
Q

What is Burkitt’s lymphoma?

A

Neoplastic proliferation of intermediate sized B cells, that is associated with EBV infections

154
Q

What is the infectious agent that is associated with Burkitt’s lymphoma?

155
Q

What is the usual presentation of Burkitt’s lymphoma?

A

Extranodal mass in children or young adults, usually in african children’s jaw

156
Q

The sporadic form of Burkitt’s lymphoma usually presents how?

A

Abdominal mass

157
Q

What is the translocation that drives Burkitt’s lymphoma? What are the oncogenes involved?

A
  • t(8;14) resulting in

- overexpression of c-myc

158
Q

Starry-sky appearance on histology = ?

A

Burkitt’s lymphoma

159
Q

What is responsible for the starry sky appearance of Burkitt’s lymphoma on histology?

A

“Blue sky” = over proliferating B cells

“Stars” = tingible body macrophages eating up bad B cells

160
Q

What is diffuse large B cell lymphoma? How does it grow?

A

Neoplastic proliferation of large B cells that grow diffusely in sheets

161
Q

Proliferation of large B cells in diffuse sheets = ?

A

Diffuse large B cell lymphoma (DLBCL)

162
Q

What is the most common form of NHL?

163
Q

Is DLBCL aggressive or indolent? What CA lead to progress from?

A

Aggressive

-May be a transformation of follicular lymphoma

164
Q

What is a typical presentation of DLBCL (age, s/sx)?

A

Late adulthood as an enlarging LN or extranodal mass

165
Q

What is the key difference between Hodgkin’s lymphoma and NHL?

A

Hodgkin’s lymphoma is caused by a single type of cell that proliferates amongst other, normal cells to form a mass, and draws in other inflammatory cells

166
Q

What is the key cell responsible for HL? What are this cell’s histological characteristics?

A

Reed-sternberg cells

Large B cell with multilobed nuclei (“owl eyes”)

167
Q

What are the two CD markers on Reed-Sternberg cells?

A

CD15 and CD30

168
Q

What is the cause of B symptoms in HL?

A

Reed-sternberg cells secreting cytokines

169
Q

Why can HL lead to fibrosis?

A

Reed-sternberg cells secreting cytokines

170
Q

Unlike NHL, HL tumor are made up mostly of what?

A

Non-cancerous cells (e.g. lymphocytes)

171
Q

What are the four common subtypes of HL?

A
  1. Nodular sclerosis
  2. Lymphocyte rich
  3. Mixed cellularity
  4. Lymphocyte depleted
172
Q

What is the usual presentation of nodular sclerosis? Who usually gets this? Is this HL or NHL?

A

Enlarging cervical or mediastinal LN in young, female adult

HL

173
Q

What is the classic histology of nodular sclerosis?

A

Broad bands of fibrosis cut into lymph into nodules, with lacunar areas of RS cells

174
Q

What subtype of HL has the best prognosis (nodular sclerosing, lymphocyte rich, mixed cellularity, or lymphocyte poor)? Which has the worst?

A 
Best = Lymphocyte rich
Worst = lymphocyte depleted
175
Q

Mixed cellularity HL is associated with which granulocyte cell? What is the cytokine produced here?

A

Eosinophils

IL-5

176
Q

What subtype of HL has the worst prognosis? Who usually gets this?

A

**Lymphocyte depleted

Elderly and HIV+**

177
Q

What is multiple myeloma?

A

Malignant proliferation of plasma cells in the bone marrow

178
Q

What is the most common primary malignancy of bone?

A

Multiple myeloma

179
Q

What is the cytokine that can be elevated in multiple myeloma? Why?

A
  • IL-6

- Growth factor for plasma cells

180
Q

Neoplastic plasma cells activate what receptor on osteoclasts? What is the consequence of this?

A

RANK

causes “punched out” lytic bone lesions

181
Q

What bones usually have lytic bone lesions with multiple myeloma?

A

Vertebrae and skull

182
Q

What is the major issue with the lytic bone lesions seen with multiple myeloma?

A

Increased risk of fracture

183
Q

What is the cause of the ostalgia and hypercalcemia seen with multiple myeloma?

A

Activation of osteoclasts by neoplastic plasma cells

184
Q

What is the “M-spike” seen in multiple myeloma?

A

Increased monoclonal antibody seen in S-PEP (serum protein electrophoresis) of some type of Ig

185
Q

What is the M protein seen in multiple myeloma?

A

Monoclonal Ig class of some type (IgA, IgG, IgE etc), but usually IgG or IgA

186
Q

What are the two subclasses of abs that are usually elevated in multiple myeloma?

187
Q

What is the major complication of producing only one type of ab, as is found in multiple myeloma?

A

Loss of antigenic diversity, thus increases the chance of infection

188
Q

Why are patients with multiple myeloma susceptible to infection?

A

Only one class of Ig produced, thus lower antigenic diversity

189
Q

What is the most common cause of death in pts with multiple myeloma?

190
Q

Rouleaux formation on blood smear = ?

A

Multiple myeloma

191
Q

What is the cause of the rouleaux formation seen in multiple myeloma?

A

Increased serum protein decreases charge between RBCs

192
Q

What is the cause of amyloidosis in multiple myeloma?

A

Increased production of free light chain in serum deposits in

193
Q

What are bence jones proteins?

A

Free light chain ab excreted in urine of pts with multiple myeloma

194
Q

What is the cause of renal failure in multiple myeloma?

A

Deposition of light chain antibodies in the tubules

195
Q

What is MGUS? Why is this concerning?

A

Increased serum protein with M spike on SPEP, but without any symptoms of multiple myeloma

May progress to multiple myeloma

196
Q

What is Waldenstrom’s macroglobulinemia?

A

B cell lymphoma with monoclonal IgM production

197
Q

What are the clinical features of Waldenstrom’s macroglobulinemia? (3)

A
  • Generalized LAD, withOUT lytic bone lesions
  • Visual and neurological defects
  • Bleeding
198
Q

What is the cause of bleeding and visual/neurological defects in Waldenstrom’s macroglobulinemia?

A

Hyperviscosity secondary to increased pentamer of IgM

199
Q

What is the treatment for Waldenstrom’s?

A

Plasmapheresis

200
Q

What is Langerhans cell histiocytosis?

A

Neoplastic proliferation of Langerhans cells

201
Q

What are Langerhans cells?

A

APCs in the epidermis, derived from bone marrow monocytes

202
Q

Tennis racket (birbeck) granules on EM = ?

A

Langerhans cell histiocytosis

203
Q

What are the cell markers for Langerhans cells? (2)

A

CD1a and S100

204
Q

There are three subtypes of Langerhans cell histiocytosis. If the disease is named after someone, what does this indicate?

A

It is malignant and involves the skin

205
Q

There are three subtypes of Langerhans cell histiocytosis. If there are two names in the disease, what does this indicate?

A

Occurs in children

206
Q

There are three subtypes of Langerhans cell histiocytosis. If there are three names in the disease, what does this indicate?

A

Occurs in children >3 yo

207
Q

What is Letterer-Siwe disease?

A

Malignant subtype of Langerhans cell histiocytosis with skin rash, and multiple organ failure. Occurs in children

208
Q

What is eosinophilic granuloma? S/sx?

A

Benign proliferation of Langerhans cells in bone

Pathological fractures in adolescent, without skin involvement

209
Q

Biopsy of Eosinophilic granuloma will show what?

A

Langerhans cells with mixed inflammatory cells, including eosinophils

210
Q

What is Hand-Schuller-christian disease? Presentation? Age?

A
  • -Malignant proliferation of Langerhans cells.
  • Scalp rash, lytic skull defects, DI, exophthalmos
  • Usually >3 yo
211
Q

What is the effect of cortisol on lymphocytes?

A

Induces apoptosis

212
Q

What are the histological characteristics of mononucleosis?

A

Atypical lymphocytes with a large, odd shaped nucleus

213
Q

Where does the EBV virus remain dormant?

214
Q

What is the cancer that classically causes excess EPO production, and secondary polycythemia?

All the things (36 decks)

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