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Heme/Onc > Pathoma 6 > Flashcards

Pathoma 6 Flashcards

1
Q

Causes of neutropenia

A

drug toxicity or severe infection (gram-negative sepsis)

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2
Q

Treatment of neutropenia

A

GM-CSF or C-CSF

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3
Q

Causes of lymphopenia (name 4)

A
  1. Immunodeficiency (DiGeorge or HIV)
  2. High cortisol state
  3. Autoimmune destruction
  4. Whole body radiation
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4
Q

Why does severe infection (gram-negative sepsis) cause neutropenia?

A

Increased movement of neutrophils into tissues results in decreased circulating neutrophils.

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5
Q

Why does high cortisol state cause lymphopenia?

A

Induces apoptosis of lymphocytes

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6
Q

Causes of neutrophilic leukocytosis (name 2)

A
  1. Bacterial infection or tissue necrosis

2. High cortisol state

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7
Q

How would bacterial infection cause neutrophilic leukocytosis?

A

Induces release of marginated pool and BM neutrophils, including immature forms (left shift).

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8
Q

What characterizes immature neutrophils?

A

decreased Fc receptors (CD16)

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9
Q

Why does high cortisol state cause neutrophilic leukocytosis?

A

Impairs leukocyte adhesion, leading to release of marginated pool of neutrophils

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10
Q

Causes of monocytosis

A

Chronic inflammatory state and malignancy

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11
Q

Causes of eosinophilia

A

allergic reaction (type I HS), parasitic infxn, and Hodgkin lymphoma

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12
Q

What drives eosinophilia?

A

IL5! (–> eosinophilic chemotactic factor)

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13
Q

Cause of basophilia

A

CML

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14
Q

Causes of lymphocytic leukocytosis

A
  1. Viral infection

2. Bordetella pertussis

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15
Q

How does Bordetella pertussis cause lymphocytic leukocytosis?

A

Produces lymphocytosis-promoting factor, which blocks circulating lymphocytes from leaving the blood to enter the lymph node

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16
Q

EBV primarily infects:

A
  1. oropharynx
  2. liver
  3. b cells
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17
Q

clinical symptoms of infectious mononucleosis

A
  1. Generalized LAD (T cell hyp. in LN paracortex)
  2. Splenomegaly (T cell hyperplasia in PALS)
  3. Leukocytosis with atypical lymphocytes (reactive CD8+ T cells)
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18
Q

How does the monospot test work?

A

Screen by detecting IgM antibodies that cross react with horse or sheep RBCs (heterophile antibodies); usually turns positive within 1 week of infection; remember that neg could mean CMV

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19
Q

Definitive diagnosis of infectious mononucleosis after a positive monospot

A

serologic testing for the EBV viral capsid antigen

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20
Q

Complications of infectious mononucleosis

A
  1. Splenic rupture
  2. Rash with ampicillin
  3. Increased risk for B-cell lymphoma
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21
Q

Definition of acute leukemia

A

> 20% blasts in BM –> crowd out normal hematopoiesis

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22
Q

Describe blasts on blood smear

A

large, immature cells with punched out nucleoli

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23
Q

+TdT and CD10+, CD19+, CD20+

A

B-ALL

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24
Q

+TdT and positive for Cd2-8 (no CD10)

A

T-ALL

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25
Q

Neoplastic accumulation of lymph blasts (>20%) in the marrow is called:

A

ALL (acute lymphoblastic leukemia)

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26
Q

In ALL, the nucleus stains positive for:

A

TdT (in lymphoblasts, not myeloplasts)

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27
Q

In what populations does ALL most commonly present?

A

Under 5 and in pts with Down syndrome (>5)

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28
Q

How do you treat B-ALL?

A

chemotherapy with prophylaxis to scrotum and CSF

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29
Q

With what cytogenic abnormalities do you associated B-ALL?

A

t(12;21) - kids, excellent prognosis (12 flipped is 21);

t(9;22) - adults, poor prognosis, Ph+

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30
Q

Thymic mass in a teenager (may present with difficulty swallowing), TdT+, CD2-8+

A

T-ALL

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31
Q

Auer rod

A

AML (acute myeloid leukemia), specifically APL (others may be MPO negative)

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32
Q

t(15;17)

A

APL (acute promyelocytic leukemia; subtype of ALL) - AT disruption blocks maturation and promyelocytes (blasts ) accumulate

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33
Q

Affinity for vitamin A derivative

A

APL

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34
Q

Abnormal promeylocytes in APL contain primary granules that increase the risk for?

A

DIC

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35
Q

Treatment of APL

A

All-trans-retinoic acid

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36
Q

How does ATRA work?

A

binds the altered receptor and causes the blasts to mature (and eventually die)

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37
Q

For what do myeloblasts stain positive?

A

MPO+ (sounds like only APL of all the ALL subtypes)

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38
Q

What do you call a proliferation of monoblasts (usually lack MPO) that characteristically infiltrate the gums?

A

Acute monocytic leukemia (subtype of ALL)

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39
Q

With what condition do you associated a proliferation of megakaryocytes?

A

Down syndrome; onset before 5

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40
Q

AML may arise from pre-existing dysplasia, called what? What patients are most at risk?

A

Myelodysplastic syndromes; prior exposure to alkylating agents or radiotherapy

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41
Q

Cytopenias + hypercellular bond marrow + abnormal maturation of cells + increased blasts (<20%)

A

Myelodysplastic syndromes

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42
Q

Neoplastic proliferation of mature circulating lymphocytes (high WBC count)

A

Chronic leukemia

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43
Q

What is the most common leukemia overall?

A

CLL

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44
Q

Neoplastic proliferation of naive B cells that co-express CD5 & CD20; smudge cells on smear

A

CLL

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45
Q

complications of CLL

A
  1. hypogammaglobulinemia
  2. autoimmune hemolytic anemia
  3. transformation to diffuse large B cell lymphoma (Richter transformation);
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46
Q

How might you tell clinically whether CLL was progressing to large B-cell lymphoma?

A

Enlarging lymph node or spleen

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47
Q

tartrate-resistant acid phophatase (TRAP) positive

A

hairy cell leukemia

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48
Q

Hairy cell leukemia is a proliferation of?

A

mature B cells characterized by hairy cytoplasmic processes; TRAP+

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49
Q

Clinical features of hairy cell leukemia

A

Splenomegaly (hairy cells in red pulp) + dry tap (marrow fibrosis); no LAD

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50
Q

How do you treat hairy cell leukemia?

A

2-CDA (cladribine), an adenosine deaminase inhibitor

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51
Q

How does 2-CDA (cladribine) work?

A

Adenosine accumulates to toxic levels in neoplastic B cells

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52
Q

Neoplastic proliferation of mature CD4+ T cells associated with HTLV-1; most commonly seen in Japan and Caribbean

A

Acute T-cell leukemia/lymphoma (ATLL)

53
Q

rash (skin infiltration);
generalized LAD with HSM;
lytic bone lesions w/ hypercalcemia

A

ATLL

54
Q

neoplastic proliferation of mature CD4+ T cells that infiltrate the skin –> Pautrier microabscesses

A

mycosis fungoides

55
Q

Cells with cerebriform nuclei on blood smear

A

Sezary cells (mycosis fungoides)

56
Q

Types of acute leukemia

A
  1. ALL

2. AML

57
Q

Types of chronic leukemia

A
  1. CLL
  2. Hairy cell
  3. ATLL
  4. Mycosis fungoides
  5. CML (also myeloproliferative disorder)
58
Q

Types of myeloproliferative disorders

A
  1. CML
  2. PV
  3. ET
  4. myelofibrosis
59
Q

Complications of all MPD

A
  1. hyperuricemia and gout (high turnover)

2. progression to marrow fibrosis or transformation to acute leukemia

60
Q

Neoplastic proliferation of mature myeloid cells, esp granulocytes and their precursors; basophilia

A

CML

61
Q

Translocation in CML

A

t(9;22) –> BCR-ABL (non-receptor tyrosine kinase)

62
Q

Treatment for CML

A

imatinib

63
Q

neoplastic proliferation of mature myeloid cells, esp RBCs

A

Polycythemia vera

64
Q

What diseases are associated with a JAK2 kinase mutation?

A
  1. Polycythemia vera
  2. Essential thrombocythemia
  3. myelofibrosis
65
Q

4 clinical symptoms/risks of PV

A
  1. blurry vision + headache
  2. venous thrombosis
  3. flushed/ruddy face (plethora)
  4. Itching, esp after bathing (inc. mast cells)
66
Q

treatment for PV

A

Phlebotomy (second line: hydroxyurea)

67
Q

Prognosis of PV

A

death within a year without treatment

68
Q

EPO and SaO2 in PV

A

low epo; normal SaO2

69
Q

EPO and SaO2 in reactive polycythemia due to high altitude or lung disease

A

high epo; low SaO2

70
Q

EPO and SaO2 in reactive polycythemia due to ectopic EPO from RCC

A

high epo; normal SaO2

71
Q

neoplastic proliferation of mature myeloid cells, esp platelets (also RBCs + granulocytes)

A

Essential thrombocythemia (increased risk of bleeding and/or thrombosis, but rarely other things)

72
Q

neoplastic proliferation of mature myeloid cells, esp megakaryocytes

A

myelofibrosis

73
Q

pathophys of myelofibrosis

A

megakaryocytes produce excess PDGF –> marrow fibrosis

74
Q

tear-drop RBCs + nucleated RBCs + immature granulocytes on blood smear

A

“leukoerythroblastic smear” - myelofibrosis

75
Q

clinical features of myelofibrosis

A
  1. splenomegaly
  2. leukoerythroblastic smear
  3. inc. risk of infxn, thrombosis, bleeding
76
Q

Region of lymph node associated with B cells

A

follicle

77
Q

follicular hyperplasia is seen in:

A

RA + early HIV

78
Q

region of lymph node associated w/ T cells

A

paracortex

79
Q

paracortex hyperplasia is seen in:

A

viral infections (like mono)

80
Q

hyperplasia of sinus histiocytes is seen in:

A

cancer (in LBN draining that area)

81
Q

types of non-Hodgkin lymphomas

A
  1. follicular
  2. mantle cell
  3. marginal celll
  4. burkitt
  5. diffuse large B cell
82
Q

t(14;18)

A

Follicular lymphoma

83
Q

What is the etiology of follicular lymphoma?

A

BCL2 on 18 translocates to the Ig heavy chain locus on 14 –> Bcl2 over expression –> no apoptosis –> cancer

84
Q

Treatment of follicular lymphoma

A

Reserved for symptomatic pts; low-dose chemotherapy or rituximab (anti-CD20 antibody)

85
Q

Presentation & progression of follicular lymphoma

A

presents in late adulthood with painless lymphadenopathy; can progress to diffuse large B-cell lymphoma

86
Q

neoplastic proliferation of small B cells (CD20+) that expands the mantle zone

A

Mantle cell lymphoma

87
Q

Translocation in mantle cell lymphoma

A

t(11,14)

88
Q

Etiology of mantle cell lymphoma

A

Cyclin D1 gene on chromosome 11 translocates to Ig heavy chain on 14 –> over expression of D1 – promotion of G1/S transition in cell cycle –> cancer

89
Q

What cancer is associated with chronic inflammatory states, such as Hashimoto’s thyroiditis, Sjogren syndrome, and H pylori gastritis?

A

Marginal zone

90
Q

What forms the marginal zone?

A

post-germinal center B cells

91
Q

What do you call marginal zone lymphoma in mucosal sites?

A

MALToma (NB: may regress with treatment of H pylori!)

92
Q

High mitotic index plus starry sky on microscopy

A

Burkitt lymphoma

93
Q

neoplastic proliferation of intermediate-sexed B cells associated with EBV

A

Burkitt lymphoma

94
Q

extranodal mass involving jaw in child or young adult

A

African form of Burkitt lymphoma

95
Q

extranodal mass involving the abdomen in child or young adult

A

Sporadic form of Burkitt lymphoma

96
Q

most common translocation in Burkitt lymphoma

A

t(8;14)

97
Q

oncogene in Burkitt lymphoma

A

c-myc

98
Q

etiology of Burkitt lymphoma

A

Translocation of c-myc to the Ig heavy chain locus on 14 –> overexpression of c-myc –> promotes cell growth

99
Q

Most common non-Hodgkin lymphoma

A

diffuse large B-cell lymphoma (neoplastic prolif. of large B cells that grow profusely in sheets)

100
Q

presentation of diffuse large B cell lymphoma

A

in alate adulthood as an enlarging lymph node or an extra nodal mass; clinically aggressive (high grade); sporadic or transformation of a low-grade lymphoma (follicular lymphoma)

101
Q

Enlarging cervical or mediastinal lymph node in a young female

A

Nodular sclerosis subtype (most common) of Hodgkin lymphoma

102
Q

Reed-Sternberg cells

A

Hodgkin lymphoma

103
Q

What are Reed-Sternberg cells?

A

Large B cells with multi lobed nuclei and prominent nucleoli; CD15+ & CD30+

104
Q

fever, chills, weight loss, night sweats

A

B symptoms of Hodgkin lymphoma (sounds like TB)

105
Q

RS cells secrete cytokines –> attraction of

A

reactive lymphocytes, plasma cells, macrophages, eos

106
Q
  1. Nodular sclerosis
  2. Lymphocyte rich
  3. Mixed cellularity
  4. Lymphocyte-depleted
A

Subtypes of HL

107
Q

Lymph node histology in nodular sclerosis subtype of HL

A

lymph node divided by bands of sclerosis; RS cells present in lake-like spaces (lacunar cells <– does he mean spaces?)

108
Q

Which subtype of Hodgkin Lymphoma has the best prognosis?

A

Lymphocyte-rich (and lymphocyte-depleted (elderly & HIV+) is the worst)

109
Q

Why is the mixed cellularity subtype of Hodgkin lymphoma often associated with abundant eos?

A

Because RS cells produce IL-5

110
Q

malignant production of plasma cells in the bone marrow; may have high IL6

A

multiple myeloma

111
Q

Why do people with multiple myeloma (MM) have bone pain with hypercalcemia?

A

Neoplastic plasma cells activate the RANK receptor on osteoclasts –> lytic lesions on x ray, esp vertebrae and skull –> increased risk for fracture

112
Q

Why do ppl w/ MM have elevated serum protein?

A

Neoplastic plasma cells produce Ig –> M spike on SPEP (usually IgG or IgA)

113
Q

Why do ppl w/ MM have an increased risk of infection?

A

lack of antigenic diversity

114
Q

What is a Rouleaux formation of RBCs on x-ray?

A

In multiple myeloma, increased serum protein decreases the charge btwn RBCs –> clump on top of each other like poker chips

115
Q

In MM, free light chains circulate in serum and deposit on tissues. What is this phenomenon called?

A

Primary AL amyloidosis

116
Q

Why are people with MM at increased risk for renal failure?

A

Proteinuria. Free light chain is excreted in urine as Bence Jones protein (deposition in tubules –> myeloma kidney / renal failure).

117
Q

Six clinical features of multiple myleoma

A
  1. Bone pain with hypercalcemia
  2. Elevated serum protein (M spike on SPEP)
  3. Inc risk of infxn
    4 .Rouleaux formation of RBCs
  4. Primary AL amyloidosis
  5. Proteinuria –> Bence Jones protein –> renal failure
118
Q

What proteins cause the M spike on SPEP in multiple myeloma

A

Monoclonal IgG or IgA

119
Q

M spike on SPEP without other features of multiple myeloma

A

think MGUS (common in elderly; 1%/yr –> multiple myeloma)

120
Q

B cell lymphoma with monoclonal IgM production

A

Waldenstrom macroglobulinemia

121
Q
  1. Generalized LAD with no lytic bone lesions
  2. M spike on SPEP
  3. Visual & neurologic deficits
  4. Bleeding
A

Waldenstrom macroglobulinemia

122
Q

What causes the M spike on SPEP in Waldenstrom macroglobulinemia?

A

IgM

123
Q

How do you treat acute complications of Waldenstrom macroglobulinemia?

A

Plasmapheresis

124
Q

What are Langerhans cells?

A

Specialized dendritic cells found predominantly in the skin that present antigen to naive T cells. They are derived from bone marrow monocytes

125
Q

Birbeck (tennis racket) granules on EM; CD1a+ and S100+

A

Langerhans cell histiocytosis

126
Q

Skin rash and cystic skeletal defects in an infant; multiple organs may be involved; rapidly fatal

A

Letterer-Siwe disease

127
Q

Pathologic fracture in an adolescent with no skin findings; biopsy shows Langerhans cells with mixed inflammatory cells, including numerous eos)

A

Eosinophilic granuloma

128
Q

Scalp rash, lytic skull defects, diabetes insipidus, and exophthalmos in a child

A

Hand-Schuller-Christian disease

Heme/Onc (6 decks)

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