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WBC Disorders (Non-Neoplastic), Non-Neoplastic White Cell Disorders Acute Nonspecific Lymphadenitis -direct microbiologic drainage mostly Teeth->cervical area Extremities->axilla, inguinal Appendiitis & others->mesenteric Nodes become swollen, gray-red, engorged Prominence of lymphoid follicles, large GCs -histiocytes w/ debris or bacteria -follicle may necrotize, suppurate->scarring -if less severe, neutrophilic infiltrate around follics Overlying skin red, can become site of infx., Leukocytosis-common for inflammation varieties -can look like neoplasm Periph Leukocyte Count influenced by: -size of myeloid (grans, monos), lymphoid pools -enlargement via IL-1, TNF in chronic infx -rate of release from pool into circ.(IL-1, TNF) -marginating pool -rate of extravasation If septic or severe inflam dz (Kawasaki) ->morpho. changes in neutrophils-Dohle bodies; toxic granulations (coarse purple)-ABNL primary grans; cytoplasmic vacuoles Types Neutrophilic Leukocytosis Eosinophilic Leukocytosis-IL-5, allergies Basophilic Leukocytosis Monocytosis Lymphocytosis-c-kit, IL-7, Non-Neoplastic White Cell Disorders LEUKOPENIA Neutropenia ('Agranulocytosis' if real bad) -reduced # of granulocytes->predisposes to infx cells/mm^3, is real bad Tx-broad spectrum Antibx, G-CSF after chemo MOST SIGNIFICANTLY PRODUCED BY DRUGS Occurs if: 1. Reduced/ineffective production -Suppresses myeloid stems-aplastic anemia, marrow dzs --> pancytopenia -Suppressed committed gran'cyte blasts (drugs) -Ineffective production b/c megaloblastic anemia, MDS --defective precursors->intramedullary death -Impaired gran'cyte differentiation (Kostmann Syn) 2. Accelerated removal from periphery -immune-mediated PMN injury via eg.SLE, drugs -Splenic sequestration-destruction 2ndary to enlarging -increased peripheral use, due to infx DRUGS- alkylating agents, antimetabolites for CA Tx -predictable and dose-related -generalized bone marrow suppression ->pancytopenia idiosyncratic drugs-chloramphenicol, sulfas, chlorpromazine-toxic to marrow precursors aminopyrine, thiouracil, some sulfas-immune mediated -sim. to drug-induced hemolytic anemias Suspect autoimmunity if:ABs against neutrophil Ags Could be ass'd w/ Large Granular Lymphocytes (LGLs) Morphology-depends on cause -if due to destruction:marrow full of precursors -MDS, megaloblastic anemias:also hypercellular marrow -ineffective granulopoiesis -if due to suppression of growth, precursors:hypocellular FEATURES-infx can lead to death -ulcerating oral cavity leasions (gingiva, mucosa, etc.) -can also be in GI, vagina, anus, lungs, GU -lymph nodes enlarged/inflamed -malaise, chills, fever, fatigue, Hodgkin Lymphoma (resembles inflam dz) -B Sx = fever, night sweats, weight loss -Single node/chain->contiguous spreading(node->spleen->liver) -Morph-REED-STERNBERG CELLS -neoplastic giant cells -bi-/multinucleated, owl-eyed nuclei (lympho-size) -induce accum of reactive lymphos, histiocytes, grans (via IL-4, IL-5, TNF-a, GM-CSF, TGF-b) -only make up 1-5% of total tumor mass -ESSENTIAL ID FOR DX- in proper bkgrd of NL inflam cells -B cell origin most likely -One of most common malignancies in young adults avg-32yo -second peak after 50 yo -Slightly higher risk after infectious mono ,EBV in 50% RS cells CLINICAL: -painless lymph node enlargement, usually (-)Sx, pruritus -pain in LNs upon drinking EtOH -reduced immunologic capacity (cutaneous anergy) -Stage III, IV (MC, LD) present w/ B Sx -Cure~100% of I, IIA; 50% of IV w/ XRT, CTX 5% develop the 2nd CA ->MDS, AML (CTX); lung CA NHL, BR CA(XRT) ->pulm. fibrosis, atherosclerosis Resemble solid tissue tumors infectious mononucleosis NHL, Non-Neoplastic White Cell Disorders INFLAMMATORY PROLIFERATIONS Leukocytosis-common for inflammation varieties -can look like neoplasm Periph Leukocyte Count influenced by: -size of myeloid (grans, monos), lymphoid pools -enlargement via IL-1, TNF in chronic infx -rate of release from pool into circ.(IL-1, TNF) -marginating pool -rate of extravasation If septic or severe inflam dz (Kawasaki) ->morpho. changes in neutrophils-Dohle bodies; toxic granulations (coarse purple)-ABNL primary grans; cytoplasmic vacuoles, Non-Neoplastic White Cell Disorders Chronic Nonspecific Lymphadenitis -not tender -frequently in inguinal, axillary 3 Causes: Folllicular Hyperplasia-inf. process activates B cells -large, round/oblong GCs bulges against mantle Bs -dark zone, light zone, tingible body macs, FDCs -Causes: RA, toxoplasmosis, HIV Can be confused w/ follic lymphomas: If hyperplasia: architecture preserved, variation of lymphoid nodules, presence of dark, light, macs -can also have marginal zone B cell hyperplasia Paracortical Lymphoid Hyperplasia-T cell region changes -encroach on/efface B cell follicles -hypertrophy of sinusoidal and vasc. endoth cells -macs/eosinophils infilitrate Drgu Rxns (phenytoin (DYLANTIN)) Acute Viral infx-infectious mononucleosis Certain vaccinations Sinus Histiocytosis (reticular hyperplasia) -distention/prominence of lymphatic sinusoids -lining endoth cells hypertrophied -histiocytes engorge sinuses In LNs draining CAs (breast) -immune response against tumor, Hodgkin Lymphoma (resembles inflam dz) -B Sx = fever, night sweats, weight loss -Single node/chain->contiguous spreading(node->spleen->liver) -Morph-REED-STERNBERG CELLS -neoplastic giant cells -bi-/multinucleated, owl-eyed nuclei (lympho-size) -induce accum of reactive lymphos, histiocytes, grans (via IL-4, IL-5, TNF-a, GM-CSF, TGF-b) -only make up 1-5% of total tumor mass -ESSENTIAL ID FOR DX- in proper bkgrd of NL inflam cells -B cell origin most likely -One of most common malignancies in young adults avg-32yo -second peak after 50 yo -Slightly higher risk after infectious mono ,EBV in 50% RS cells CLINICAL: -painless lymph node enlargement, usually (-)Sx, pruritus -pain in LNs upon drinking EtOH -reduced immunologic capacity (cutaneous anergy) -Stage III, IV (MC, LD) present w/ B Sx -Cure~100% of I, IIA; 50% of IV w/ XRT, CTX 5% develop the 2nd CA ->MDS, AML (CTX); lung CA NHL, BR CA(XRT) ->pulm. fibrosis, atherosclerosis Types Lymphocyte Depleted -(+)CD15, CD30 -frequent RS cells, variants -OLDER MEN w/ disseminated dz -Type IV -in HIV in developing countries -worst prognosis of HD, but still no bad -lots of necrosis, fibrosis, Hodgkin Lymphoma (resembles inflam dz) -B Sx = fever, night sweats, weight loss -Single node/chain->contiguous spreading(node->spleen->liver) -Morph-REED-STERNBERG CELLS -neoplastic giant cells -bi-/multinucleated, owl-eyed nuclei (lympho-size) -induce accum of reactive lymphos, histiocytes, grans (via IL-4, IL-5, TNF-a, GM-CSF, TGF-b) -only make up 1-5% of total tumor mass -ESSENTIAL ID FOR DX- in proper bkgrd of NL inflam cells -B cell origin most likely -One of most common malignancies in young adults avg-32yo -second peak after 50 yo -Slightly higher risk after infectious mono ,EBV in 50% RS cells CLINICAL: -painless lymph node enlargement, usually (-)Sx, pruritus -pain in LNs upon drinking EtOH -reduced immunologic capacity (cutaneous anergy) -Stage III, IV (MC, LD) present w/ B Sx -Cure~100% of I, IIA; 50% of IV w/ XRT, CTX 5% develop the 2nd CA ->MDS, AML (CTX); lung CA NHL, BR CA(XRT) ->pulm. fibrosis, atherosclerosis Types Nodular Sclerosis 65-75% of HD.Has Lacunar cells, Collagen Bands -Scant or abundant fibrosis makes nodules -Lacunar cells on bkgrd of small T cells, eos, plasmas, macs -Tumor cells- (+) CD15, CD30 (-)CD45, B, Tcell markers -Mainly in paracortical T zones, can make nodules in spleen, liver, BM -More common in WOMEN, affects adolescents/young adults -Supraclavic, lower cervical, mediastinal nodes -Excellent Prognosis TGF-b by Eos for collagen production, Nodular Sclerosis 65-75% of HD.Has Lacunar cells, Collagen Bands -Scant or abundant fibrosis makes nodules -Lacunar cells on bkgrd of small T cells, eos, plasmas, macs -Tumor cells- (+) CD15, CD30 (-)CD45, B, Tcell markers -Mainly in paracortical T zones, can make nodules in spleen, liver, BM -More common in WOMEN, affects adolescents/young adults -Supraclavic, lower cervical, mediastinal nodes -Excellent Prognosis TGF-b by Eos for collagen production Same Immunohistochemistry -MHC-II, B7 (APCs) -B cell, T cell-specific Ags -some Ig rearrangements Mixed Cellularity 25% of cases -DIFFUSE EFFACEMENT OF NODES by infiltrate -small lymphos(T), eos, plasma, macs -CLASSIC RS AND MONONUCLEAR RS VARIANTS -Tumor cells- (+) CD15, CD30 (-)CD45, B, Tcell markers -SAME AS NOD SCLEROSIS -Early dz to paracortical T cell zones (sometimes most T cells) ->need to rule out Lymphocyte Predominant, NHL -More common in MEN, older age, B Sx, advanced tumor stage ᡪ% present at Stage III, IV -Good overall prognosis, Hodgkin Lymphoma (resembles inflam dz) -B Sx = fever, night sweats, weight loss -Single node/chain->contiguous spreading(node->spleen->liver) -Morph-REED-STERNBERG CELLS -neoplastic giant cells -bi-/multinucleated, owl-eyed nuclei (lympho-size) -induce accum of reactive lymphos, histiocytes, grans (via IL-4, IL-5, TNF-a, GM-CSF, TGF-b) -only make up 1-5% of total tumor mass -ESSENTIAL ID FOR DX- in proper bkgrd of NL inflam cells -B cell origin most likely -One of most common malignancies in young adults avg-32yo -second peak after 50 yo -Slightly higher risk after infectious mono ,EBV in 50% RS cells CLINICAL: -painless lymph node enlargement, usually (-)Sx, pruritus -pain in LNs upon drinking EtOH -reduced immunologic capacity (cutaneous anergy) -Stage III, IV (MC, LD) present w/ B Sx -Cure~100% of I, IIA; 50% of IV w/ XRT, CTX 5% develop the 2nd CA ->MDS, AML (CTX); lung CA NHL, BR CA(XRT) ->pulm. fibrosis, atherosclerosis Types Lymphocyte-Rich -40% associated w/ EBV -more common in MEN -moderately aggressive course