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30 Cards in this Set
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Increased neutrophils (or any kind of leukocyte)
Due to acute inflammation to bacteria Dohle bodies in neutrophils (aggregates of RER) * increased LAP = leukocyte alkaline phosphatase Ddx: CML has decreased LAP |
Leukocytosis
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Increased Monocytes
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think TB or chronic disease (ie. Inflammatory bowel disease)
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Increased lymphocytes
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acute viral infection
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MCC = EBV --> heterophile positive
EBV binds CD21 (CR2) receptors on B cells CD8+ cells respond to atypical lymphocytes (Downey cells - enlarged) . Atypical cells can be found in the paracortex (Tcells) of lymph nodes (DONT confuse with Hodgkins disease) Heterophile Abs – abs used against other species of RBCs --> used for monospot test Downey cells Enlarged – theyre enlarged T cells that have attacked B cells Look like monocytes, but THEY ARE NOT!! (hence the name) |
Infectious Mononucleosis
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Lymphoblasts are positive for: TdT, PAS, acid phosphatase . Neg for MPO
Can be B or T cell lineage (look at surface marker) B cell: sIg, t12:21 (good prognosis), CD10 (CALLA) +, Comes from precursor B cells T9:22 (bad prognosis), 4 year old – highest proliferation of B cells T cell: Mediastinal mass in 12 year old boy – highest proliferation of T cells (Thymus is in mediastinum genius) Pre T cell ALLs -> TAL-1 (+) |
Acute Lymphoblastic Leukemia (ALL)
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What is SLL?
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Proliferation of small B cells with B cell markers and one T cell marker = CD5+, CD23+, CD10-
Lymphocytosis in peripheral blood, smudge cells Mean age – 60 Infiltrative neoplastic cells |
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Major distinction:
If patient presents with blood findings = CLL If patient presents with lymph node findings = SLL |
Distinctions between the 2.
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95% of cases – B cell; 5% of cases – T cell
Lymphocytosis in peripheral blood, smudge cells Mean age – 60 CD23+, CD10-, CD5+ (same as SLL in this) Associated with warm autoimmune hemolytic anemia (+direct coombs, will see spherocytes) Richter syndrome – when CLL transfers to a worse lymphoma – DLCL – p53 mutation |
Chronic Lymphocytic Leukemia
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Hair-like cytoplasmic projections
Dry tap of BM TRAP positive Older males |
Hairy Cell Leukemia
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Derived from B cells
t14:18 14 – Ig heavy chain 18 - Bcl-2 50% of cases progress to diffuse large cell lymphoma (DLCL – a NHL) Variants: can find small cleaved cells – centrocytes or follicular large cells |
Follicular Lymphoma
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Easy – large cells with diffuse growth pattern
CD19+, CD20+, CD 10, surface Ig, BCL 6 2 subtypes: If EBV present -- immunodeficiency associated B cell lymphoma If advanced HIV is present - thru body cavity – large B cell lymphoma ( KSHV/HHV8 present) |
Diffuse Large B cell Lymphoma
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Starry sky due to tingible body macrophages – phagocytosis of apoptotic tumor cells
t8:14 14 - Ig heavy chain 8 - c-myc Two types: African type – look for jaw (young boy), EBV American type – abdomen/AIDS |
Burkitts Lymphoma
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CD19+, CD20+, CD5+, CD23-
t11:14 14 - Ig heavy chain 11 – L-1 = cyclin D – poor prognosis |
Mantle Cell Lymphoma
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May arise extranodally
Begins as reactive polyclonal expansion --> probably autoimmune disorder --> MALToma |
Marginal Zone Lymphoma (MALToma)
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MC primary tumor of bone in adults
M spike in serum electrophoresis --> IgG spike (60%), IgA (20%), Bence-Jones proteins (20%) --> found in urine Rouleaux in peripheral blood Multiple lytic bone lesions --> due to osteoclast activating factor (OAF) = IL-6 --> *hypercalcemia and bone pain (Look for holes in skull in xray) Predisposes to plasmacytoma Aggregates of plasma cells in bone or usually respiratory tract Primary amyloidosis MCC of death = infection |
Multiple Myeloma
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M spike found in 1-3% of asymptomatic people >50 years
20% of these people will develop into plasma cell disorder in 10-15 years (don't choose this in a multiple choice, probably a distraction) |
Monoclonal Gammopathy of Undetermined Significance (MGUS)
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(SLL with plasmacytic differentiation)
Think of it as multiple myeloma and SLL M spike (IgM) --> cold agglutination, patient may present with Raynaud's infiltrative neoplasm Can have: Russell bodies – cytoplasmic immunoglobulin Dutcher bodies – nuclear immunoglobulin Differential with MM – no increase in Ca++, no bone lesions |
Lymphomaplasmacytic lymphoma (Waldenstrom's macroglobulinemia)
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CD4+ T cell disorder caused by HTLV-1
Will see hyperlobulated “4-leaf-clover” lymphocytes |
Adult T cell leukemia/lymphoma
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CD4+ cell disorder --> pathogenesis – (eczema gone wild)
Patient wil lhave erythemstous rash --> develops into nodule(s) Cerebriform nuclei in CD4+ Th |
Mycosis Fungoides
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1) Lymphocyte Predominance
If there isn't a lot of RS cells – good prognosis CD15-/CD30- Has L-H cells (popcorn cells) 2) Mixed cellularity CD15+/CD30+ IL-5 levels increased, therefore you will see eosinophils and plasma cells 3) Lymphocyte depleted Few lymphocytes Many RS (poor prognosis) CD15+/CD30+ 4) Nodular Sclerosis Most common type – lymph node has broad collagen bands. RS variant = lacunar cells --> due to a clear space surrounding the cell |
Hodgkins Diease (4 variants needed to differentiate)
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CD15+/CD30+
“owl eye” nuclei: bilobed mirror image nuclei with prominent nucleoli |
Reed-Sternberg Cells
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RS cells
Stays in lymph nodes(mostly) Involves midline LN: cervical, paraortic, mediastinal Contiguous spread thru lymph nodes Does not involve waldeyers-ring |
Hodgkins
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No RS cells
Extranodal spread Involves peripheral lymph nodes Skips around lymph nodes Usually involves waldeyers ring = tonsils and adenoids |
Non-Hodgkins
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Myeloblasts have inctracytoplasmic rods (M3 type) – Auer rods = abnormal lysosomes
Auer rods stains with MPO = myeloperoxidase or sudan-black Vitamin A – very good differentiator in tumors M3 subtype: Auer rods and cytoplasmic granules, may get DIC, t15:17, hence treat with all trans-retinioic acid M4 subtype: both myeloblasts and monoblasts M5 subtype: monocytic leukemia – you will see monoblasts, MPO-, esterase +, gingival infiltrates (pt presents with bleeding gums) M6 subtype: erythroleukemia --> huge binucleate cells, also has Auer rods M7 subtype: see atypical megakaryocytes, increase PDGF release --> myelofibrosis --> teardrop shaped RBCs |
Acute Myelogenous Leukemia
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Neoplastic proliferations of myeloid stem cells
All four have in common? Increased eosinophils and basophils What are the 4 types? CML Polycythemia vera Essential Thrombocythemia Myelofibrosis |
Myeloproliferative Syndromes
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t9:22 – philadelphia chromosome
Massive splenomegaly (crosses midline) Hypercellularity of all cells in bone marrow Peripherally – increased neutrophils, increase eosinophils, increased basophils Decreased LAP, differential from leukemoid reaction |
Chronic Myelogenous Leukemia
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Increased hematocrit, increased blood viscosity, decreased erythropoietin, increase LAP, increased red cell mass, therefore decreased MCHC
This disease is due to an increase in erythroid precursors, increased activity of granulocytic and megakaryocytic precursors Clinical patients are plethoric (red- excessive release of histamine from basophils) and then later cyanotic (blue – histamine --> gastric ulcer--> increased bleeding--> anemia) |
Polycythemia vera
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Increased megakaryocytes, increased platelets (>1,000,00) and increased leukocytes
Clinical signs – excessive bleeding (purpura), increased bleeding time, therefore something wrong with platelets (qualitative error) |
Essential Thrombocythemia
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Dry tap of bone marrow
Megakaryocytes release excessive PDGF --> proliferation of fibroblasts --> fibrosis Extramedullary hematopoiesis (in spleen) --> massive splenomegaly Teardrop RBC |
Myelofibrosis (idiopathic)
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mycosis fungoids and *systemic blood involvment
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Sezary syndrome
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