WBCs, LN, Spleen, Thymus Flashcards by Vince Baroña

Clinically significant neutropenia (<500/mm3)

Agranulocytosis (most commonly caused by drug toxicity)

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Rare type of leukocytosis indicative of myeloproliferative disorder

Basophilic leukocytosis

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Seen in LN when there is predominant humoral response

Follicular hyperplasia

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Seen in LN when there is predominant cell-mediated response

Paracortical hyperplasia

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Two main parts of a LN

Cortex and medulla

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Seen in LN follicles

B cells (CD 20; secondary follicles are stimulated)

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Seen in LN paracortex

T cells (CD3)

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Three areas of a secondary LN follicle

Germinal center, mantle zone, marginal zone

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

Centroblast (BCD - blasta, centro, dark zone)

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

Sinus histiocytosis (usually seen in malignancies, but nonspecific)

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Most common cancer in children

ALL (acute lymphoblastic leukemia)

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Two types of ALL

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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Notable mutations associated with B-cell ALL

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

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Notable mutations associated with T-cell ALL

NOTCH-1 (70%)

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Unique metastatic site of ALL

CNS (meningeal spread) and testis (sanctuary site)

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Kind of ALL seen more in early childhood

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

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Neoplastic proliferation of myeloid precursors

AML (acute myeloid leukemia)

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AML with best prognosis

Acute promyelocytic leukemia

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AML with very poor prognosis

Therapy-related AML

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Diagnostic cut-off of myeloblasts in bone marrow for AML

> = 20% myeloblasts

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Absence of blasts in peripheral blood

Aleukemic leukemia (seen in AML)

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Genetic mutation of APML

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

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Seen in APML, needle-like azurophilic granules

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

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APML is curable in 80% of cases using this substance

All-trans retinoic acid

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Age of onset of AML

Generally adults, while ALL more common in children

Most common leukemia of adults in the Western world

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

Only difference between CLL and SML

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

Seen in PBS of CLL/SML

Small lymphocytes with smudge cells

Notable sequelae of CLL/SML

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

Genetic mutation seen in CML

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

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

Preferential proliferation of granulocytic and megakaryocytic lines

Parameters for diagnosis of CML

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

Clinical phases of CML

Chronic, accelerated, blast (can "transform" into AML)

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

Tyrosine kinase inhibitor (imatinib / Gleevec)

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

Chloroma

Distinguishes CML from leukemoid reaction

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

LN involvement of Hodgkin's lymphoma

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

LN involvement of Non-Hodgkin's lymphoma

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

Characteristic cell seen in Hodgkin's lymphoma

Reed-Sternberg cells

Two pathologic microscopic features of Hodgkin's lymphoma

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

Five subtypes of Hodgkin's lymphoma

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

Subtypes of Hodgkin's associated with EBV

Mixed cellularity and lymphocyte depleted (more aggressive)

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

CD15 and CD30

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

CD20

Most common subtype of Hodgkin's

Nodular sclerosis

Subtype of Hodgkin's associated with HIV

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

Subtypes of non-Hodgkin's B-cell lymphomas

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

Most common indolent lymphoma of adulthood

Follicular lymphoma

Notable mutation associated with follicular lymphoma

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

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

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

IHC stains used for diffuse large B-cell lymphoma

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

Three types of Burkitt's lymphoma

Endemic, sporadic, HIV-associated

The fastest growing human tumor

Burkitt's lymphoma

Features that would favor a neoplastic follicle

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

Type of Burkitt's associated with EBV

Endemic (100%)

Notable mutation associated with Burkitt's

MYC t(8;14) / Burk-EIGHT

Histologic finding of Burkitt's lymphoma

Starry sky pattern

Cell of origin of marginal zone lymphoma

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

T-cell non-Hodgkin's lymphoma

Mycosis fungoides or cutaneous T-cell lymphoma

Cells found in mycosis fungoides or cutaneous T-cell lymphoma

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

Occurs in mycosis fungoides

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

Most important plasma cell neoplasm

Multiple myeloma

Pathophysiology behind multiple myeloma

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

Two PAS (+) findings in MM

Russell bodies (cytoplasmic) and Dutcher bodies (nuclear)

Renal finding in MM

Bence Jones proteinuria (Ig light chain)

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

MDS

Cellular morphology found in MDS

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

Chronic myeloproliferative disorders asociated with JAK2 mutations

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

Paraneoplastic syndrome associated with thymomas

MG, PRCA, other autoimmune diseases