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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
Increased Monocytes
think TB or chronic disease (ie. Inflammatory bowel disease)
Increased lymphocytes
acute viral infection
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
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)
What is SLL?
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
Major distinction:
If patient presents with blood findings = CLL
If patient presents with lymph node findings = SLL
Distinctions between the 2.
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
Hair-like cytoplasmic projections
Dry tap of BM
TRAP positive
Older males
Hairy Cell Leukemia
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
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
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
CD19+, CD20+, CD5+, CD23-
t11:14
14 - Ig heavy chain
11 – L-1 = cyclin D – poor prognosis
Mantle Cell Lymphoma
May arise extranodally
Begins as reactive polyclonal expansion --> probably autoimmune disorder --> MALToma
Marginal Zone Lymphoma (MALToma)
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
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)
(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)
CD4+ T cell disorder caused by HTLV-1
Will see hyperlobulated “4-leaf-clover” lymphocytes
Adult T cell leukemia/lymphoma
CD4+ cell disorder --> pathogenesis – (eczema gone wild)
Patient wil lhave erythemstous rash --> develops into nodule(s)
Cerebriform nuclei in CD4+ Th
Mycosis Fungoides
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)
CD15+/CD30+
“owl eye” nuclei: bilobed mirror image nuclei with prominent nucleoli
Reed-Sternberg Cells
RS cells
Stays in lymph nodes(mostly)
Involves midline LN: cervical, paraortic, mediastinal
Contiguous spread thru lymph nodes
Does not involve waldeyers-ring
Hodgkins
No RS cells
Extranodal spread
Involves peripheral lymph nodes
Skips around lymph nodes
Usually involves waldeyers ring = tonsils and adenoids
Non-Hodgkins
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
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
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
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
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
Dry tap of bone marrow
Megakaryocytes release excessive PDGF --> proliferation of fibroblasts --> fibrosis
Extramedullary hematopoiesis (in spleen) --> massive splenomegaly
Teardrop RBC
Myelofibrosis (idiopathic)
mycosis fungoids and *systemic blood involvment
Sezary syndrome