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Pathoma > White blood cell disorders > Flashcards

White blood cell disorders Flashcards

1
Q

CLL “chronic lymphocytic leukaemia “

A

Neoplastic proliferation of naive B cells

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2
Q

CLL it’s cells coexpress

A

CD5 , CD20

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3
Q

CLL blood smear

A

Increased lymphocytes and smudge cells

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4
Q

CLL complications

A

Hypogammaglobulinemia
Autoimmune haemolytic anemia
Transformation to diffuse large B cell lymphoma

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5
Q

Hairy Cell leukaemia

A

Neoplastic proliferation of mature B cells

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6
Q

Hairy cell leukaemia characterized by

A

Hairy cytoplasmic processes

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7
Q

Hairy cell leukaemia are positive for

A

TRAP “tartrate resistance acid phosphatase “

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8
Q

Hairy cell leukaemia clinical features

A

Splenomegaly “ expansion of red pulp”
Dry tab with bone marrow aspiration
Lymphadenopathy is usually absent

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9
Q

Hairy cell leukaemia has excellent response to

A

2-CDA “ adenosine deaminase inhibitor “

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10
Q

ATLL “adult T cell leukaemia lymphoma “

A

Neoplastic proliferation of mature CD4 T cell

Associated with HTLV1 “ Japan and Caribbean “

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11
Q

ATLL clinical features

A

Rash
Generalised LAD and hepatosplenomegaly
Lytic bone lesions with hypercalcemia

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12
Q

Mycosis fungoides

A

Neoplastic proliferation of mature CD4 T cells

In which the cells infiltrate skin producing rash , plaque , nodules

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13
Q

Aggregates of neoplastic T cells in epidermis are called

A

Pautreir microabscesses

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14
Q

If the cells of mycosis fungoides involve the blood it cause

A

Sezary syndrome

Has characteristic lymphocytes with cerebriform nuclei on blood smear

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15
Q

Myeloproliferative disorders definition

A

Neoplastic proliferation of mature cells of myeloid lineage

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16
Q

Myeloproliferative disorders complications

A

Increase risk for hyperuricemia and gout
Progression to marrow fibrosis
Transformation into acute leukaemia

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17
Q

Chronic myeloid leukaemia highly associated with

A

Basophilia

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18
Q

CML driven by ,,,,,,,,,,,

A

t (9,22)BCR-ABL fusion increase tyrosine kinase activity

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19
Q

CML treated by

A

Imatinib “block tyrosine kinase activity “

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20
Q

CML can be transformed into either

A

AML (2/3) or ALL (1/3)

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21
Q

CML must be distinguished from leukemoid reation by

A

CML associated with :
LAP negative “leukocyte alkaline phosphatase”
Increased basophils
t(9,22)

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22
Q

Polycythemia vera is associated with

A

JAK2 kinase mutation

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23
Q

Polycythemia vera clinical symptoms

A

Blurred vision and headache
Venous thrombosis
Flushed face
Itching after bathing

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24
Q

Polycythemia vera must be distinguished from reactive polycythemia

A

PV : SaO2 normal , EPO low
In reactive polycythemia: SaO2 low , EPO increased “lung disease “
In reactive polycythemia : EPO high due to ectopic production and SaO2 normal

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25
Q

Essential thrombocythemia

A

Also associated with JAK2 kinase mutation

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26
Q

No significant risk for hyperuricemia or gout with ,,,,,,,,,,,,,

A

Essential thrombocythemia

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27
Q

Myelofibrosis

A

Neoplastic proliferation of mature myeloid cells especially megakaryocytes

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28
Q

Painful LAD”lymphadenopathy” is seen with

A

Acute infection

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29
Q

Painless LAD is seen with

A

Chronic inflammation , metastatic carcinoma , lymphoma

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30
Q

Expansion of follicles is seen with

A

Rheumatoid arthritis ,early HIV

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31
Q

Expansion of paracortex is seen with

A

Viral infection

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32
Q

Expansion of region where the sinus histiocytes live is seen with

A

Cancer

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33
Q

Lymphoma may arise in ………… or …………..

A

Lymph node or extranodal tissue

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34
Q

Lymphoma classified into

A

Non Hodgkin lymphoma and Hodgkin lymphoma

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35
Q

Follicular lymphoma

A

Neoplastic small B cells (CD20+) that make follicle-like nodules

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36
Q

Follicular lymphoma driven by

A

t(14-18)BCL2 translocates from 18 to 14 result in overexpression of BCL2 which inhibit apoptosis

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37
Q

Follicular lymphoma treatment

A

Rituximab

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38
Q

Follicular lymphoma complication

A

Progression to diffuse large B cell lymphoma

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39
Q

Follicular lymphoma distinguished from follicular hyperplasia by

A
  1. disruption of normal LN architecture
  2. lack of tingible body macrophages in germinal centre
  3. expression of BCL2 in follicles
  4. monoclonality
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40
Q

Mantle cell lymphoma

A

Neoplastic small B cells CD20+that expand the mantle zone “region immediately adjacent to the follicle”

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41
Q

Mantle cell lymphoma driven by

A

t(11:14) cyclin D1 translocation leads to overexpression and promotion of G1/S transition in cell cycle

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42
Q

Marginal zone lymphoma

A

Neoplastic small B cells CD20+ that expand marginal zone

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43
Q

Marginal zone lymphoma associated with chronic inflammatory states like:

A

Hashimoto’s thyroiditis , sjogren syndrome , H pylori gastritis

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44
Q

Burkitt lymphoma

A

Neoplastic intermediate sized B cells CD20+

Associated with EBV

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45
Q

Burkitt lymphoma has two forms :

A

African form usually involve jaw

Sporadic form usually involve abdomen

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46
Q

Burkitt lymphoma driven by

A

t(8;14) c-myc translocation

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47
Q

Burkitt lymphoma has a characteristic

A

Starry sky appearance

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48
Q

DLBCL “diffuse large B cell lymphoma”

A

Neoplastic large B cells that grow diffusely in sheets

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49
Q

Most common form of non Hodgkin lymphoma is

A

DLBCL

50
Q

Hodgkin lymphoma definition

A

Neoplastic proliferation of Reed-Sternberg cells “large B cell with multilobed nuclei “
CD15+ and CD30+

51
Q

Hodgkin lymphoma subtypes

A
  1. Nodular sclerosis(70% of cases)
  2. lymphocyte rich
  3. mixed cellularity
  4. lymphocyte depleted
52
Q

Classic presentation for nodular sclerosis HL

A

Enlarging cervical or mediastinal LN in young adult usually female

53
Q

Nodular sclerosis HL histology

A

Reed-Sternberg cells are present in lake like spaces(lacunar cells)
LN separated by bands of fibrosis

54
Q

HL subtype has the best prognosis

A

Lymphocyte rich HL

55
Q

HL subtype has the worst prognosis

A

Lymphocyte depleted HL

56
Q

Lymphocyte depleted HL seen in

A

Elderly and HIV+ indivuals

57
Q

Mixed cellularity HL is associated with

A

Abundant eosinophils (due to IL5 secretion)

58
Q

Multiple myeloma

A

Malignant proliferation of plasma cells in bone marrow

59
Q

Most common primary malignancy of bone is

A

Multiple myeloma

60
Q

High serum …….. is sometimes present in multiple myeloma

A

IL6

61
Q

Neoplastic plasma cells activate

A

RANK receptor on osteoclasts

62
Q

Multiple myeloma symptoms

A
  1. Bone pain with hypercalcemia
  2. Lytic (punched out) lesion seen on X-ray
  3. Elevated serum protein
63
Q

M spike is present on ‘serum protein electrophoresis’ SPEP in multiple myeloma due to

A

Monoclonal IgG or IgA

64
Q

Monoclonal antibody lacks

A

Antigenic diversity ” lead to increase risk of infection “

65
Q

Increase serum protein in multiple myeloma decrease charge between RBCs lead to

A

Rouleaux formation on blood smear

66
Q

Proteinuria with multiple myeloma lead to

A
  1. bence Jones proteins in urine “free light chains”

2. deposition in kidney tubules “risk for renal failure”

67
Q

MGUS (monoclonal gammopathy of undetermined significance)

A

.Increased serum protein with M spike on SPEP

.Other features of Multiple myeloma are absent

68
Q

MGUS common in

A

Elderly

69
Q

Waldenstrom macroglobulinemia

A

B cell lymphoma with monoclonal IgM production

70
Q

Waldenstrom macroglobulinemia clinical features

A

.Generalized LAD
.Increased serum protein with M spike (IgM)
.Visual and neuronal deficits
.Bleeding

71
Q

Waldenstrom macroglobulinemia treatment

A

Plasmapheresis”remove IgM”

72
Q

Langerhans cells histiocytosis

A

Neoplastic proliferation of langerhans cells

73
Q

Langerhans cells histiocytosis characterized by

A

Birbeck(tennis racket) granules seen on EM

CD1a+ and S100+

74
Q

Letterer-siwe disease

A

Malignant proliferation of langerhans cells
Skin rash and cystic skeletal defects in infant <2yrs
Multiple organ may be involved
Rapidly fatal

75
Q

Eosinophilic granuloma

A

.Benign proliferation of langerhans cells in bone
.present with pathological fracture in adolescent
.biopsy show langerhans cells with inflammatory cells including eosinophils

76
Q

Hand-schuller-Christian disease

A

.Malignant proliferation of langerhans cells

.present with scalp rash, lytic skull defect , diabetes insipidus and exophthalmos in a child

77
Q

Normal WBC count

A

5-10 K

78
Q

Neutropenia seen in

A

Drug toxicity

Severe infection

79
Q

Lymphopenia seen in

A

Immunodeficiency
High cortisol state
Autoimmune destruction
Whole body radiation

80
Q

In neutrophilic leukocytosis there is an increase in number of

A

Immature neutrophils “ with decreased Fc receptor”

81
Q

A marker of decreased Fc receptors is

A

CD16

82
Q

Neutrophilic leukocytosis seen in

A

.Bacterial infection
.Tissue necrosis
.High cortisol state”by disrupting adhesion of marginated neutrophils”

83
Q

Monocytosis seen in

A

Chronic inflammatory state

Malignancy

84
Q

Eosinophilia seen in

A

.Allergic reaction
.Parasitic infection
.Hodgkin lymphoma “due to high IL5”

85
Q

Basophilia seen in

A

CML

86
Q

Lymphocytic leukocytosis seen in

A

.Viral infection

.Bordetella pertussis

87
Q

Infectious mononucleosis seen with

A

.EBV infection

.CMV (less common)

88
Q

EBV primarily infect

A

Oropharynx
Liver
B cells

89
Q

EBV infection results in CD8+ T cell response with

A

.Generalised LAD “ paracortex hyperplasia “
.Splenomegaly “ periarterial lymphatic sheath”
.high white count with atypical lymphocytes

90
Q

Monospot test is used for screening of

A

Infectious mononucleosis

91
Q

Monospot test detect

A

IgM heterophile antibodies

92
Q

Negative monospot test suggests

A

CMV infection

93
Q

Definitive diagnosis for infectious mononucleosis by EBV is made by
(زيادة تأكيد)

A

Testing for EBV viral capsid antigen

94
Q

Complications of Infectious mononucleosis :

A

Increased risk of splenic rupture
Rash if exposed to penicillin
Dormancy of virus in B cells

95
Q

Acute leukaemia

A

Accumulation of >20% blasts in the bone marrow

96
Q

In AL the blasts crowd out normal hematopoiesis , results in

A

Acute presentation with anemia , thrombocytopenia or neutropenia

97
Q

Blasts enter blood result in

A

High WBCs count

98
Q

Blasts definition

A

Large immature cells , often with punched out nucleoli on blood smear

99
Q

Acute leukaemia subdivided into

A

AML and ALL

100
Q

ALL

A

Neoplastic proliferation of lymphoblasts

101
Q

Positive nuclear staining for TdT(DNA polymerase) with

A

ALL

102
Q

ALL most commonly arise in

A

Children associated with Down syndrome (after the age of 5)

103
Q

The most common type of ALL

A

B-ALL

104
Q

B-ALL classically express

A

CD10 , CD19 and CD20

105
Q

B-ALL has excellent response to

A

Chemotherapy

106
Q

B-ALL prognosis based on cryogenic abnormalities :

A

t(12;21) good prognosis >kids

t(9;22) poor prognosis > adults

107
Q

T-ALL express

A

Ranging from CD2 to CD8

108
Q

T-ALL present as

A

Mediastinal “thymic” mass in a teenager

Known as Acute lymphoblastic lymphoma

109
Q

AML characterized by staining for

A

MPO (myeloperoxidase )

110
Q

Crystal aggregate of MPO may be seen as

A

Auer rods

111
Q

AML most commonly arise in

A

Older adults (50-60yrs)

112
Q

Acute promyeloctyic leukaemia characterized by

A

t(15;17) , RAR “retinoacidic receptor” distrupted ; promyelocytes accumulate

113
Q

Promyeloctyes contain

A

Numerous Auer rods , risk for DIC

114
Q

Acute promyelocytic leukaemia treatment

A

ATRA (all-trans-retinoic acid)

Cause blasts to mature

115
Q

Acute monocytic leukemia

A

Proliferation of monoblasts , lack MPO

116
Q

Blasts in acute monocytic leukemia characteristically infiltrate

A

The gums

117
Q

Acute magakaryblastic leukemia

A

Proliferation of megakaryblasts ; lack MPO

118
Q

Acute megakaryoblastic leukemia associated with

A

Down syndrome ( before the age of 5)

119
Q

AML may arise from exposure to…………….. or ……………….

A

Alkylating agents or radiotherapy

120
Q

Notes about Myelodysplastic syndrome

A

.cytopenia with hypercellular bone marrow
.abnormal maturation with increased blasts (<20%)
.may progress to acute leukemia (>20%)
Most patients die from infection or bleeding

Pathoma (4 decks)

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