Heme - Lymphocytes And Lymph Nodes

Front 1

Lymph node disease clinical manifestations

Back 1

Local enlargement - tender or nontender

Compression of adjacent structures (e.g. GI or pulm)

Release of cytokines producing systemic sx (fever, weight loss, night sweats).

Front 2

Are primary neoplasms of the lymph nodes always malignant?

Back 2

yes

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Primary immune organs

Back 3

Sites of initial maturation - to become immunocompetent

Bone marrow (B)
Thymus (T)

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Secondary immune organs

Back 4

Sites of antigen drive replication and differentiation into committed effector cells.

Lymph nodes
Spleen
Mucosal associated lympoid system (lines GI and resp tracts)
"Everywhere else"

Lymph nodes are the largest secondary organ and the major site of lymphoid pathology.

Front 5

Lymph node anatomy (inside to outside)

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Medullary sinus - macrophages
Medullary cords - macrophages and plasma cells.
Paracortex - Mostly T cells
Lymphoid follicle - Mostly Bs
Cortex - Site of b cell amplification and maturation in response to stimuli.

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What presents to B cells in lymph node?

Back 6

Dendritic reticulum cells.

Front 7

Lymphocyte homing b cells

Back 7

B CELLS
Primary lymphoid organ to blood, then homing to follicles and medullary cords in the lymph node and other secondary organs.

In follicles - Respond to antigens.
In medullary cords - Aggregation of plasma cells and release of Igs into efferent lymph.

Front 8

Lymphocyte homing t cells

Back 8

Goes to paracortex

Front 9

Small lymphocyte features

Back 9

Dark blue dots. Round nucleus. Clumped chromatin (not proliferating). Small/absent nucleolus. (can't tell if they are B or T - location can help)

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B cell - where in node are they found?

Back 10

Primary follicles, mantle zone of secondary follicles, medullary cords.

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T cells - where in node are they found?

Back 11

Paracortex and minor pop in germinal center.

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Noncleaved cells/centroblasts

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In the follicular center

Replicating with larger round nuclei and open chromatin (nucleoli seen)

"Large" or "small" is based on nucleus comparison to a macrophage nucleus.

Found in dark zone of a follicle.

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Small cleaved cells/centrocytes

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Non-replicating.

Post-mitotic memory or plasma cell precursors.
Clumped chromatin, irreg folded/cleaved nuclear profiles.

Found in light zone of a follicle

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Immunoblasts

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Replicating large cells found outside germinal centers - Bs or Ts

Nuclear characteristics similar to replicating lymphocytes (open chromatin and nucleoli seen)

Front 15

Accessory cells (2 types)

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Antigen presenting cells and macrophages (histiocytes)

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APCs

Back 16

Type of accessory cell
Either interdigitating reticulin cells (T cell paracortex) or dendritic reticulin cells (B cell germinal centers)

Invisible in normal lymph node.

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Macrophages/histiocytes

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Phagocytic cells of lymph node.
In germinal center - tingible body macrophages
There are also medullary and subcapsular sinus macrophages
Abundant pale cytoplasm
Oval nucleus that is single and small.

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Reasons there would be pathology of lymph nodes

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Infections - bacterial will have acute inf and abscess formation. There can also be granulomatous, caseous and noncaseous.

Reactive hyperplasia

Sarcoidosis

Metastatic tumor

Malignant lymphoma
NHL or Hodgkin's

Front 19

Types of reactive hyperplasia

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These can cause lymph node pathology

Exaggeration of normal histology

Follicular hyperplasia - germinal centers take up huge part of the node.

Interfollicular hyperplasia

Sinus histiocytosis

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Causes of Follicular hyperplasia

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Germinal centers spread into paracortex and medullary areas.


collagen vascular disease

systemic toxoplasmosis

Syphillis

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Causes of interfollicular hyperplasia

Back 21

Seen in the paracortex - so mainly a t cell response

Skin disease
viral inf
drug rxn

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Aggressive lymphomas due to...

Back 22

lymphocyte frozen at a stage associated with high replication.

Front 23

Indolent lymphoma due to...

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Lymphoma frozen at stage associated with recirculation or final function.

Front 24

Where are malignant lymphomas?

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Mainly outside the bone marrow at sites of normal lymphoid homing.

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How to dx malignant lymphomas?

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Microscopic ID of dominant cell type supplemented with immunologic and molecular techniques.

Tx and px based on dominant cell type, extent of spread, underlying health.

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2 types of classifications of lymphomas

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Clinical (indolent, aggressive, highly aggressive)
and
biological (very hazy)

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Can you cure a "low" aggression lymphoma?

Back 27

No

And you can cure a highly aggressive one.

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3 main subclassifications of REAL/WHO system

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B cell neoplasms (Precursor [e.g. ALL] or peripheral

T cell/NK cell neoplasms (precursor Ts or periph T/NKs)

Hodgkin's lymphoma


WHO classification tries to define lymphoma based on cell of origin.

Ancillary studies needed to define characteristics seen at each stage of development.

Front 29

Two major activities for normal lymphoid maturation

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Production of unique receptor on surface

Expression of several surface proteins needed for antigen recog, cell-cell comm and cell activation.

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Receptor on B cells

Back 30

Two heavy and two light chains.
(pick one heavy chain antigen and only one of two kappa or lambda light chains)

D and J brought together, then V added, then C brought in for heavy. If not succ, try other chrom. If that doesn't work, cell dies.

Then light - DJ together. If that doesn't work, try second kappa, then try lambda. (this explains 2:1 ratio of kappa to lambda)

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Receptor o nT cells

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Select one of two heterodimeric receptors.
(alpha/beta is more common than gamma/delta)

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B cell markers

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19, 20, 22, 23

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T cell markers

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3, 4, 5, 8

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Reason to use flow cytometry

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Analyze population of cells to get frequencies.
(e.g. light chains establish clonality in B cells)

(uses antibodies)

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Reason to use immunohistochemistry

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Correlating morphology with immunology.

(uses antibodies)