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Rapid Review Pathology > Chapter 13 - White Blood Cell Disorders > Flashcards

Chapter 13 - White Blood Cell Disorders Flashcards

0
Q

Give an example of a disease with a WBC structure defect.

A

Structure defect: Chédiak-Higashi syndrome

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1
Q

What do qualitative WBC defects refer to?

A

Qualitative WBC defects: structure and/or function

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2
Q

Give two examples of WBC function defects.

A

Function defect: selectin deficiency, CD11a/CD18 deficiency

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3
Q

Give an example of a WBC phagocytosis defect.

A

Phagocytosis defect: Bruton agammaglobulinemia

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4
Q

Give two examples of WBC microcidal defect.

A

Microbicidal defect: MPO/NADPH oxidase deficiencies

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5
Q

What are the clinical findings in qualitative WBC defects?

A

Qualitative WBC defects: unusual pathogens, “cold” abscesses, frequent infections

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6
Q

What is Job syndrome?

A

Job syndrome: defect in chemotaxis; ↑IgE

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7
Q

What is the equation to determine the absolute count of WBC?

A

Absolute count = % leukocytes × total WBC count

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8
Q

What is a leukemoid reaction?

A

Leukemoid reaction: benign, exaggerated WBC response

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9
Q

What is leukoerythroblastosis?

A

Leukoerythroblastosis: immature WBCs/nucleated RBCs in peripheral blood

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10
Q

What are the causes of leukoerythroblastosis?

A

Causes: infiltrative disease; metastasis; granulomatous disease; leukemia
Other causes: trauma with multiple fractures; EMH

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11
Q

What is the probable diagnosis if a woman >50 years presents with leukoerythroblastosis?

A

Leukoerythroblastosis in woman >50 yrs: probable breast cancer metastatic to bone

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12
Q

How is neutrophilic leukocytosis defined?

A

Neutrophilic leukocytosis: >7500 cells/mm3

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13
Q

What are the causes of neutrophilic leukocytosis?

A

Causes: bacterial infection, sterile inflammation with necrosis, corticosteroids

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14
Q

Describe the pathogenesis of neutrophilic leukocytosis.

A

Pathogenesis: ↑production, ↓activation neutrophil adhesion molecules

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15
Q

How is neutropenia defined?

A

Neutropenia: <1500 cells/mm3

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16
Q

What are the causes of neutropenia?

A

Causes: aplastic anemia, immune destruction (SLE), septic shock
Causes: drugs (penicillin), tick-borne diseases, viral infections
Causes: bacterial infection (TB, typhoid, brucellosis); systemic fungi; ionizing radiation

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17
Q

Describe the pathogenesis of neutropenia.

A

Pathogenesis: ↓production, ↑destruction, ↑activation neutrophil adhesion molecules

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18
Q

How is eosinophilia defined?

A

Eosinophilia: >400 cells/mm3

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19
Q

What are the causes of eosinophilia?

A

Causes: type I HSR, invasive helminths, D. fragilis, hypocortisolism

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20
Q

What is a cause of eosinopenia?

A

Eosinopenia: hypercortisolism

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21
Q

Which disease should be considered if basophilia is present?

A

Basophilia: consider myeloproliferative disease

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22
Q

How is lymphocytosis defined?

A

Lymphocytosis: >5000 cells/mm3 (adult); >8000 cells/mm3 (child)

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23
Q

What are the causes of lymphocytosis?

A

Causes: viruses (mononucleosis, CMV), bacteria (whooping cough, TB)
Causes: drugs (phenytoin, tetracycline); Graves disease, CLL

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24
Q

What are the causes of atypical lymphocytosis?

A

Atypical: infection (mononucleosis, CMV, toxoplasmosis, viral hepatitis); drugs (phenytoin)

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25
Q

Describe the pathogenesis of atypical lymphocytosis.

A

Atypical lymphocytes: antigenically stimulated

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26
Q

What causes mononucleosis?

A

Mononucleosis: EBV

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27
Q

Describe the pathogenesis of mononucleosis.

A

B cells have CD21 receptor sites for EBV; atypical B cells
Mono: cytotoxic T cells control infected B cells; atypical lymphocytes
Mono: EBV dormant in B cells; relapses may occur

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28
Q

What are the clinical findings of mononucleosis?

A

Mono: fatigue; exudative tonsillitis/petechiae in posterior palate; tender hepatosplenomegaly
Mono: painful lymphadenopathy; pruritic rash with ampicillin/amoxicillin

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29
Q

What are the lab findings in mononucleosis?

A

Mono: atypical lymphocytes >20%
Mono heterophile antibodies: IgM antibodies directed against horse, sheep, bovine RBCs
Anti-VCA lgG/IgM: excellent test if mono screening test is negative

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30
Q

How is lymphopenia defined?

A

Lymphopenia: <3000 cells/mm3 (child)

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31
Q

Describe the characteristics of lymphopenia in HIV.

A

Lymphopenia in HIV: lysis CD4 helper T cells by virus

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32
Q

What benign quantitative WBC disorders are caused by corticosteroids?

A

Corticosteroids produce neutrophilic leukocytosis, eosinopenia, and lymphopenia

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33
Q

How is monocytosis defined?

A

Monocytosis: >800 cells/mm3

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34
Q

What are the causes of monocytosis?

A

Monocytosis: chronic infection, autoimmune disease, malignancy

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35
Q

What is leukemia?

A

Leukemia: malignant transformation marrow stem cells

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36
Q

What are the risk factors for leukemia?

A

Risk factors: Down syndrome; ionizing radiation; benzene; alkylating agents
Risk factors: chronic myeloproliferative disorders, PNH, smoking, immunodeficiency disease

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37
Q

What is the most common leukemia and overall cancer in children?

A

ALL: MC leukemia/cancer in children

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38
Q

Who is affected by AML and CML?

A

AML/CML: 40–60 years old

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39
Q

Who is affected by CLL?

A

CLL: MC >60 years

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40
Q

What is the most common overall type of leukemia?

A

CLL MC overall type of leukemia

41
Q

Describe the pathogenesis of leukemia.

A

Leukemia: arises in marrow → disseminates; never benign

42
Q

Describe the onset of symptoms in acute leukemia.

A

Acute leukemia: abrupt onset

43
Q

Which type of leukemias involve the skin?

A

Skin involvement: T-cell leukemias

44
Q

Where does ALL metastasize to?

A

ALL: CNS, testicle involvement

45
Q

What is the most important test for diagnosing leukemia?

A

Most important test for diagnosing leukemia: bone marrow examination

46
Q

What are the lab findings in leukemia?

A

Leukemia: ↑peripheral count, thrombocytopenia, normocytic/macrocytic anemia
Acute leukemia: blast cells >20% in bone marrow

47
Q

Describe the onset chronic leukemia.

A

Chronic leukemia: insidious onset

48
Q

What are the clinical findings in chronic leukemia?

A

Hepatosplenomegaly, generalized painless lymphadenopathy

49
Q

What are the lab findings in chronic leukemia?

A

Chronic leukemia: blasts <10% in bone marrow

50
Q

What are all myeloid disorders?

A

Myeloid disorders: neoplastic stem cell disorders

51
Q

What is the most common chronic myeloproliferative disorder?

A

Polycythemia vera: MC chronic myeloproliferative disorder

52
Q

What are the general characteristics of the chronic myeloproliferative disorders?

A

Splenomegaly, marrow fibrosis, some transformation to acute leukemia

53
Q

How is polycythemia defined?

A

Polycythemia: ↑Hb, Hct, RBC count

54
Q

How do the RBC count and RBC mass differ?

A

RBC count: # RBCs per microliter (µL)

RBC mass: total # RBCs peripheral blood in mL/kg

55
Q

What are the findings in relative polycythemia?

A

Relative polycythemia: ↑RBC count; ↓PV; normal RBC mass, SaO2, EPO

56
Q

What are the findings in appropriate absolute polycythemia?

A

Appropriate absolute: ↑RBC mass, EPO; normal PV; ↓SaO2

57
Q

What are the findings in inappropriate absolute polycythemia?

A

Inappropriate absolute (ectopic secretion EPO): ↑RBC mass, EPO; normal PV, normal SaO2

58
Q

How is polycythemia vera defined?

A

Polycythemia vera: inappropriate absolute polycythemia

59
Q

What is the mutation in polycythemia vera?

A

Polycythemia vera: mutation in JAK2 gene

60
Q

What are the clinical findings in polycythemia vera?

A

Polycythemia vera: thrombotic events (hepatic vein, dural sinus, retinal vein)
Polycythemia vera: pruritus after bathing, mast cells release histamine
Polycythemia vera: peptic ulcer disease, gout

61
Q

What is the best initial test for polycythemia vera?

A

Polycythemia vera: serum EPO best initial test

62
Q

What are the lab findings in polycythemia vera?

A

Polycythemia vera: ↑RBC mass, ↓EPO; ↑PV, normal SaO2

63
Q

What is the only polycythemia with increased PV and decreased EPO?

A

Polycythemia vera: only polycythemia with ↑PV and ↓EPO

64
Q

What is the treatment for polycythemia vera?

A

Polycythemia vera: phlebotomy reduces viscosity-induced thrombosis

65
Q

Describe the pathogenesis of CML.

A

CML: t(9;22) translocation of ABL proto-oncogene; fusion with BCR

66
Q

What is the Philadelphia chromosome?

A

Philadelphia chromosome = chromosome 22 with translocation

67
Q

What is the most consistent finding in CML?

A

CML: splenomegaly most consistent finding

68
Q

What is the only leukemia with thrombocytosis?

A

CML: only leukemia with thrombocytosis

69
Q

What is the most sensitive/specific test for CML?

A

BCR-ABL fusion gene: most sensitive/specific test for CML

70
Q

How is the LAP score affected in CML?

A

CML: ↓LAP score; little to no alkaline phosphatase in leukemic cells

71
Q

What are the lab findings in CML blast crisis?

A

CML blast crisis: myeloblasts/lymphoblasts; no Auer rods

72
Q

Most cause of myelofibrosis with myeloid metaplasia are due to what mutation?

A

MMM: mutation JAK2 gene

73
Q

What are the findings in MMM?

A

MMM: EMH; marrow fibrosis; massive splenomegaly
MMM: teardrop RBCs; leukoerythroblastosis

74
Q

What is essential thrombocythemia?

A

ET: dysplastic/nonfunctional platelets; ↑platelets

75
Q

Most cases of ET are due to what mutation?

A

ET: mutation in JAK2 gene

76
Q

Describe the clinical findings in ET.

A

ET: bleeding because platelets dysfunctional

77
Q

What are the lab findings of ET?

A

ET: megakaryocytes dysplastic/numerous

78
Q

What is MDS characterized by?

A

MDS: cytopenias; hypercellular marrow

79
Q

What percentage of MDS cases progress to AML?

A

MDS: >30% progress to AML

80
Q

What are the lab findings in MDS?

A

MDS: dimorphic RBC population; leukoerythroblastosis
MDS: ringed sideroblasts in some types (bone marrow)

81
Q

What are the risk factors for AML?

A

AML risks: ionizing radiation, benzene, MDS, Down/Turner/Klinefelter

82
Q

Which chromosome has mutations in AML?

A

AML: mutations chromosome 8

83
Q

What is a clinical finding in acute monocytic leukemia?

A

Acute monocytic leukemia: gum infiltration

84
Q

What is a lab finding of CML?

A

AML: Auer rods in cytoplasm of myeloblasts

85
Q

What lab finding is in AML but not CML?

A

Auer rods: only AML; not CML

86
Q

What is the most common type of acute lymphoblastic leukemia?

A

ALL: pre–B-cell MC type

87
Q

What is the most common type of ALL?

A

ALL: CD10 and TdT positive; MC type (early pre-B cell)

88
Q

What translocation in early pre-B cell ALL offers a favorable prognosis?

A

ALL: t(12;21) offers favorable prognosis

89
Q

What percentage of early pre-B cell ALL cases are considered cured?

A

ALL: ~3/4 cured

90
Q

Where does ALL metastasize to?

A

ALL: B-cell types metastasize to testicles/CNS
ALL: T-cell types metastasize to skin

91
Q

Adult T-cell leukemia is associated with what virus?

A

Adult T-cell leukemia: association with HTLV-1

92
Q

What does the TAX gene do in adult T-cell leukemia?

A

TAX gene: inhibits p53 suppressor gene

93
Q

What are the clinical findings in adult T-cell leukemia?

A

Adult T-cell leukemia: skin lesions; lytic bone lesions with hypercalcemia

94
Q

What is the most common overall leukemia in Western countries?

A

CLL: MC overall leukemia

95
Q

What is the most common cause of generalized lymphadenopathy in individuals >60 years old?

A

CLL: MCC generalized lymphadenopathy >60 years old

96
Q

What are the lab findings in CLL?

A

CLL: hypogammaglobulinemia; smudge cells
CLL: hypogammaglobulinemia common

97
Q

What type of leukemia is hairy cell leukemia? What is the primary site for neoplastic cells?

A

HCL: B-cell leukemia; spleen primary site for neoplastic cells

98
Q

What is uncommon in HCL?

A

HCL: lymphadenopathy uncommon

99
Q

What are the lab findings in HCL?

A

HCL: hair-like projections; positive TRAP stain

100
Q

HCL has a dramatic response to what treatment?

A

HCL: dramatic response to purine nucleosides

Rapid Review Pathology (14 decks)

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