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Pathology > WBCs, LN, Spleen, Thymus > Flashcards

WBCs, LN, Spleen, Thymus Flashcards

1
Q

Clinically significant neutropenia (<500/mm3)

A

Agranulocytosis (most commonly caused by drug toxicity)

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2
Q

Rare type of leukocytosis indicative of myeloproliferative disorder

A

Basophilic leukocytosis

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3
Q

Seen in LN when there is predominant humoral response

A

Follicular hyperplasia

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4
Q

Seen in LN when there is predominant cell-mediated response

A

Paracortical hyperplasia

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5
Q

Two main parts of a LN

A

Cortex and medulla

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6
Q

Seen in LN follicles

A

B cells (CD 20; secondary follicles are stimulated)

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7
Q

Seen in LN paracortex

A

T cells (CD3)

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8
Q

Three areas of a secondary LN follicle

A

Germinal center, mantle zone, marginal zone

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9
Q

Cells seen in the dark zone of a secondary follicular LN germinal center

A

Centroblast (BCD - blasta, centro, dark zone)

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10
Q

Morphology of LN wherein there is increase in size and number of cells lining lymphatic sinusoids

A

Sinus histiocytosis (usually seen in malignancies, but nonspecific)

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11
Q

Most common cancer in children

A

ALL (acute lymphoblastic leukemia)

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12
Q

Two types of ALL

A

Pre B-cell ALL (more common, 85%) and pre T-cell ALL (not good! generally T cell involvement is more difficult to treat)

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13
Q

Notable mutations associated with B-cell ALL

A

t(12;21) and t(9;22)

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14
Q

Notable mutations associated with T-cell ALL

A

NOTCH-1 (70%)

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15
Q

Unique metastatic site of ALL

A

CNS (meningeal spread) and testis (sanctuary site)

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16
Q

Kind of ALL seen more in early childhood

A

B-cell ALL (vs T-cell ALL which is in adolescence)

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17
Q

Neoplastic proliferation of myeloid precursors

A

AML (acute myeloid leukemia)

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18
Q

AML with best prognosis

A

Acute promyelocytic leukemia

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19
Q

AML with very poor prognosis

A

Therapy-related AML

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20
Q

Diagnostic cut-off of myeloblasts in bone marrow for AML

A

> = 20% myeloblasts

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21
Q

Absence of blasts in peripheral blood

A

Aleukemic leukemia (seen in AML)

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22
Q

Genetic mutation of APML

A

t(15;17) vs B-cell ALL (t12:21 and t9:22) and T-cell ALL (NOTCH-1)

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23
Q

Seen in APML, needle-like azurophilic granules

A

Auer rods inside faggot cells (faggots love rods and DICs, kasi APML is associated with DIC)

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24
Q

APML is curable in 80% of cases using this substance

A

All-trans retinoic acid

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25
Q

Age of onset of AML

A

Generally adults, while ALL more common in children

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26
Q

Most common leukemia of adults in the Western world

A

CLL (chronic myelogenous leukemia) or SML (small lymphocytic lymphoma)

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27
Q

Only difference between CLL and SML

A

Peripheral blood lymphocytosis (>5000 in CLL, < 5000 in SML)

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28
Q

Seen in PBS of CLL/SML

A

Small lymphocytes with smudge cells

29
Q

Notable sequelae of CLL/SML

A

Richter syndrome (progression to diffuse large B-cell lymphoma)

30
Q

Genetic mutation seen in CML

A

BCR-ABL t(9;22), the Philadelphia chromosome

31
Q

Result of BCR-ABL t(9;22) Philadelphia chromosome mutation

A

Preferential proliferation of granulocytic and megakaryocytic lines

32
Q

Parameters for diagnosis of CML

A

WBC >100000 and thrombocytosis, blasts <10% in peripheral blood

33
Q

Clinical phases of CML

A

Chronic, accelerated, blast (can “transform” into AML)

34
Q

Common treatment modality between ALL and CML due to BCR-ABL t(9;22)

A

Tyrosine kinase inhibitor (imatinib / Gleevec)

35
Q

Solid focus of leukemia outside bone marrow seen in blast crisis of CML

A

Chloroma

36
Q

Distinguishes CML from leukemoid reaction

A

Leukocyte alkaline phosphatase (LAP); high LAP means reactive process, low LAP is malignant

37
Q

LN involvement of Hodgkin’s lymphoma

A

Single, axial group of nodes (cervical, mediastinal, paraaortic) (with contiguous spread, less aggressive)

38
Q

LN involvement of Non-Hodgkin’s lymphoma

A

Multiple, peripheral nodes (with non contiguous spread, more aggressive)

39
Q

Characteristic cell seen in Hodgkin’s lymphoma

A

Reed-Sternberg cells

40
Q

Two pathologic microscopic features of Hodgkin’s lymphoma

A

Reed-Sternberg cells and mixed inflammatory cell infiltrate (T-cells, eosinophils, histiocytes + inflammatory background)

41
Q

Five subtypes of Hodgkin’s lymphoma

A

Nodular sclerosis (most common), mixed cellularity, lymphocyte rich, lymphocyte depleted, lymphocyte predominant (mostly reactive B cells, compared to others with T cells)

42
Q

Subtypes of Hodgkin’s associated with EBV

A

Mixed cellularity and lymphocyte depleted (more aggressive)

43
Q

Markers used in Hodgkin’s lymphoma (can stain Reed-Sternberg cells)

A

CD15 and CD30

44
Q

Marker used for lymphocyte predominant Hodgkin’s that can stain B-cells

A

CD20

45
Q

Most common subtype of Hodgkin’s

A

Nodular sclerosis

46
Q

Subtype of Hodgkin’s associated with HIV

A

Lymphocyte depleted (+ B cell lymphoma + Kaposi’s sarcoma)

47
Q

Subtypes of non-Hodgkin’s B-cell lymphomas

A

Follicular, diffuse large B-cell, Burkitt’s, marginal zone

48
Q

Most common indolent lymphoma of adulthood

A

Follicular lymphoma

49
Q

Notable mutation associated with follicular lymphoma

A

BCL2 (anti-apoptotic)/t(14;18) Follicular FOURTEEN

50
Q

Most common form of non-Hodgkin’s and most common lymphoma of adults

A

Diffuse large B-cell lymphoma (anaplastic, aggressive, rapidly fatal without treatment)

51
Q

IHC stains used for diffuse large B-cell lymphoma

A

CD45 (lymphoid), CK (epithelial), and vimentin (mesenchymal)

52
Q

Three types of Burkitt’s lymphoma

A

Endemic, sporadic, HIV-associated

53
Q

The fastest growing human tumor

A

Burkitt’s lymphoma

54
Q

Features that would favor a neoplastic follicle

A

Increase in desnity of follicles, size, and number; more uniform appearance; attenuation of mantle zones; follicles in perinodal fat

55
Q

Type of Burkitt’s associated with EBV

A

Endemic (100%)

56
Q

Notable mutation associated with Burkitt’s

A

MYC t(8;14) / Burk-EIGHT

57
Q

Histologic finding of Burkitt’s lymphoma

A

Starry sky pattern

58
Q

Cell of origin of marginal zone lymphoma

A

Memory B-cell (arises from tissues in chronic inflammation like salivary glands in Sjogren, thyroid in Hashimoto’s, stomach in gastritis) / sore memories that become cancer

59
Q

T-cell non-Hodgkin’s lymphoma

A

Mycosis fungoides or cutaneous T-cell lymphoma

60
Q

Cells found in mycosis fungoides or cutaneous T-cell lymphoma

A

Sezary cells (T cells with cerebriform nuclei, causing Pautrier microabscesses)

61
Q

Occurs in mycosis fungoides

A

Sezary syndrome (generalized exfoliative erythroderma with leukemia of Sezary cells)

62
Q

Most important plasma cell neoplasm

A

Multiple myeloma

63
Q

Pathophysiology behind multiple myeloma

A

Production of monoclonal immunoglobulin (M protein) vs polyclonal Ig production if reactive

64
Q

Two PAS (+) findings in MM

A

Russell bodies (cytoplasmic) and Dutcher bodies (nuclear)

65
Q

Renal finding in MM

A

Bence Jones proteinuria (Ig light chain)

66
Q

Disorder of defective hematopoietic maturation with increased risk of transformation to AML

A

MDS

67
Q

Cellular morphology found in MDS

A

Ringed sideroblasts (erythroid), granulocytic (pseudo-pelget Huet cells), Pawn ball megakaryocytes

68
Q

Chronic myeloproliferative disorders asociated with JAK2 mutations

A

Polycythemia vera, essential thrombocytosis, primary myelofibrosis (BCR-ABL for CML; all responsive to tyrosine-kinase)

69
Q

Paraneoplastic syndrome associated with thymomas

A

MG, PRCA, other autoimmune diseases

Pathology (13 decks)

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