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WBC Conditions

Lymphoma, myeloma, leukemias, etc.

QuestionAnswer
What organ infiltrations can cause acute leukemia? Marrow expansion as well as spleen, liver, lymph nodes, CNS, gums, and mouth infiltrations can cause acute leukemia.
What is the WHO criteria related to the FAB classification AML-M2? AML with t(8;21).
What is the WHO criteria related to the FAB classification AML-M4? AML with inv(16). Can also include FLT3 mutation and 11q23 abnormalities.
What is the WHO criteria related to the FAB classification AML-M5? Can include FLT3 mutation or 11q23 abnormalities.
characteristic cells in AML-M1? Ton of myeloblasts in PB and BM(90% of nucleated cells). Auer rods possible, loose, open, lacy chromatin, distinct nucleoli, immature cytoplasm, most have no granules, but nothing more mature than blasts
characteristic cells in AML-M2? at least 20% myeloblasts, may have auer rods and are +MPO. Likely to see other stages of neut development. If t(8;21), myelocytes have a clump of specific granules in cytoplasm and extra long auer rods.
characteristic cells in AML-M3? must see >20% promyelocytes, wome with bundles of auer rods (faggot cells) virtually all have t(15;17).
characteristic cells in AML-M4? dual lineage: lots of myeloblasts and lots of monocytic cells all together equalling >20% of nucleated cells. If inv(16), big Eos w/ dark granules present (AML-M4 Eo). increased incidence of extramedullary involvement.
characteristic cells in AML-M5A? lots of monoblasts (acute monoblastic) which are poorly differentiated. Neut component must be <20% and monocytic lineage must be at least 80%. 20% of the cells are monoblasts in this one.
characteristic cells in AML-M5B? lots of promonocytes (acute monocytic) which are well differentiated. Neut component must be <20% and monocytic must be at least 80%. 20% of cells are promonocytes in this one.
characteristic cells in AML-M6? at least 20% myeloblasts and lots of erythroid precursors (usually >50% of all nucleated cells). erythroid may be larger than normal and abnormal in appearance. megaloblastic changes, dyserythropoiesis, and ineffective erythropoiesis.
characteristic cells in AML-M7? at least 20% megakaryoblasts, discovered via flow cytometry since these blasts look the same as others.
Tx of AML? chemotherapy (2/3 go into short lived remission from this). BMT best chance for full remission, but risky.
Prognosis of AML? 80% of pts die w/in 3 years. older have worse prognosis than younger (inversely proportional to age.
WBC inclusions for Chediak-higashi? big gray-green peroxidase pos bodies in granulocytes and cells of tissues. Cannot fight off infections.
WBC inclusions for Pelger Huet Anomaly? hypolobated neutrophils that function normally.
WBC inclusions for Alder Reilly? large purplish granules in leukocytes, accompanies conditions like Hunter's and Hurler's syndromes.
WBC inclusions for May Hegglin? large basophilic and pyroninophilic inclusions similar to Dohle bodies. May have bleeding disorder due to giant hypogranular platelets w/ short lives.
What is the associated name for AML-M1? AML without maturation
What is the associated name for AML-M2? AML with maturation
What is the associated name for AML-M3? Acute Promyelocytic leukemia
What is the associated name for AML-M4? Acute Myelomonocytic Leukemia
What is the associated name for AML-M5A? acute monoblastic leukemia
What is the associated name for AML-M5B? Acute monocytoic leukemia
What is the associated name for AML-M6? Acute Erythroblastic Leukemia
What is the associated name for AML-M7? Acute Megakaryoblastic leukemia
The three types of Acute Lymphoblastic leukemias (ALL) are? B-Lymphoblastic Leukemia, T-Lymphoblastic Leukemia, and Burkitt's Leukemia
T cell ALL clinical features mediastinal mass and very high WBC count. occurs more in teenage years.
Precursor B ALL clinical features Petechiae and infections, rapid course
Burkitt's Leukemia Large lymphoblasts w/ deep blue cytoplasm and sharply punched out vacuoles. associated w/ t(8;14), t(2;8), and t(8;22). Seen in older children w/ fast-growing abdominal mass.
Common genetic abnormality of CML. philadelphia chromosome, t(9;22) creates BCR-ABL gene which produces causative protein.
What is characteristic of CML? marked proliferation of neutrophils, eosinophils, and neutrophilic precursors in blood and granulocytic hyperplasia in BM. often have LOTS of basophils.
Lab picture of CML? 45-55 year old, male, exposed to alkylating agents, benzene, or ionizing radiation with basophilia. Present w/ fevers, night sweats, weight loss, bone pain, anemic symptoms, and maybe leukostasis.
Treatment of CML? Gleevec, inhibits activity of BCR-ABL gene. BMT is only cure.
Presentation of Polycythemia Vera 60 year old male typically with headache, weakness, pruritus, and dizziness. May also show vascular stasis due to increased blood viscosity. Hepatomegaly and "plethora" a redness of head and neck are possible as well.
Cause of Polycythemia vera? intrinsic abnormality of myeloid cells (JAK-2) which is primary, or increased erythropoietin secretion from physiologic mechanisms (living at high altitude) or inappropriate mechanisms (solid tumor).
Treatment of PV? therapeutic phlebotomy (450 mL of whole blood per week or 2x weekly or removal of just RBCs via apheresis to hit target HCT), myelosuppressive drugs if pt cannot tollerate therapeutic phlebotomies or have thrombotic risk factors.
complications of treatment of PV by therapeutic phlebotomy? iron difficiency occurs, meaning transfusions only required every 3-6 months.
Presentation of essential thrombocythemia? usually: 60 year old female who is asymptomatic or may present w/ MI, stroke, DVT, excessive bleeding due to acquired von Wilebrand disease, mild splenomegaly, pallor and tachycardia if anemic, erythromelagia (pain, redness and swelling in the hands/feet)
cause of Essential thrombocythemia? increased platelet count not related to Chronic Myelofibrosis, CML, iron deficiency anemia, or cancer.
Presentation of Idiopathic Myelofibrosis? usually mid-late 60s, presents over a long time, initially as splenomegaly, Sx of anemia, fever, anorexia, weight loss, night sweats, pruritis, bone pain. Few are asymptomatic at Dx.
Causes of Idiopathic Myelofibrosis? May have familial connection, but undefined inheritance mode. May be associated w/ exposure to chemicals or radiation.
What is leukoerythroblastic reaction? blasts and early RBCs are pushed out of marrow into PB and teardrops also present due to the cramped space in BM due to fibrosis there.
What is the order of severity in Myelodysplastic syndromes? Refractive anemia, Refractive Anemia w/ ringed sideroblasts, Refractory Anemia w/ excess blasts, and finally Chronic Myelomonocytic Leukemia. (RA, RARS, RAEB (RAEB-t), CMML
What classifies it as Refractory Anemia? BM contains <5% blasts, <15% ringed sideroblasts, supported when clonal chromosomal abnormality can be found that supports BM and PB findings
What classifies it as Refractory Anemia w/ Ringed Sideroblasts? at least 15% ringed sideroblasts in BM with <5% blasts. usually macrocytic or normocytic w/ dual population of hypo- and normochromic RBCs.
What classifies it as Refractory Anemia w/ Excess Blasts? More dysplastic than RA or RARS with hyposegmented & hypogranulated WBCs, decreased PLT count (large and agranular), RBCs: macrocytic/normochromic and ovalocytes and dacrocytes present. BM shows 5-20% blasts dysmegakaryocytopoiesis and dyserythropoiesis.
What classifies it as Refractory Anemia w/ Excess Blasts in Transformation? 20-30% blast count in BM, >5% blasts in blood possible. Confirmed by Auer rods present. Can mimic AML-M2 when blast count is 25-35%.
How to differentiate between AML-M2 and RAEB-t? More dysplasia in BM with RAEB-t and presence of t(8;21) may be present in AML-M2 but is never present in RAEB-t.
What classifies it as Chronic Myelomonocytic leukemia? CMML1: <5% blasts in PB, <10% blasts in BM. CMML2: 5-19% blasts in PB, 10-19% blasts in BM.
Which Myelodysplastic syndrome is WHO classified w/ cytogenetic abnormality? 5q syndrome, due to deletion of the long arm of chromosome 5. has female predominance and around 66 year old at Dx.
lab findings of 5q syndrome macrocytic anemia, moderate leukopenia, normal to inc. PLTs. BM shows <5% blasts, normal to increased dysplastic megakaryocytes.
general morphological features of myelodysplasia? segs funky looking and dysplastic, hypolobulation/hypogranulation.
How do RBCs look in myelodysplastic syndrome? May look like myegaloblastic red cells and ovalocytes like in megaloblastic anemia.
WHO classifies RAEB-t as? There is no RAEB-t in the WHO classification, these all fall under leukemia now, specifically AML-M2 under WHO.
What are type I blasts? typical myeloblasts and unclassifiable cells. Nuclear chromatin is finely dispersed w/ prominent nucleoli cytoplasm has no granules.
What are type II blasts? resemble type I except cytoplasm contains fewer than 20 granules and nucleus is more central w/ lower N:C ratio than Type I
What are type III blasts? resemble type II except contain more than 20 granules in the cytoplasm.
What stain is specific to Hairy Cell Leukemia? Tartrate-resistant acid phosphatase (TRAP) which changes hairy cell leukemia cells red (the hairy lymphocytes)
What is characteristic of Hairy Cell Leukemia? PB usually pancytpenia and splenomegaly as well as marrow fibrosis. Shaggy lymphocytes (messy, blurry cell border w/ hair like projections). BM hypercellular w/ "moth-eaten" appearance and fibrotic re: in marrow traps cells in BM with reticulin strands
Clinical presentation of hairy cell leukemia? usually 40-60 year old male w/ splenomegaly and no lymphadenopathy.
Which lymphoproliferative disorders are B-cell disorders? Hairy Cell Leukemia, Prolymphocytic leukemia
Which lymphoproliferative disorders are T-cell disorders? Large granulated Lymphocyte Leukemia (both subtypes),
Most common chromosomal abnormality w/ CLL? presence of an extra chromosome 12 (trisomy 12).
What is gives CLL the worse prognosis? trisomy 12 with other chromosomal abnormality (13q14) is the worst prognosis.
What is the characteristic cell in Hodgkin Lymphoma? Reed-Sternberg Cell: 45um diameter
folicular B cell lymphoma characteristic cell? "buttocks" cell.
mycosis fungoides characteristic? mushroom like purplish tumor on skin.
sezarv's syndrom characteristic? limphoma from skin to BM and other tissues. scaly erythematous rash. PB contains cerebriform lymphocytes (look like brains)
How are Multiple Myeloma and Waldenstrom's alike? M-protein has light chain kappa or lambda. serum concentration is greater than 1g/dL.
How are Multiple Myeloma and Waldenstrom's different? Waldinstrom's has enlarged liver, spleen, and lymphnodes. Serum is hyperviscous, and M-protein's heavy chain is always IgM. Myeloma has bone lesions and bone pain and the M-protein's heavy chain is rarely IgM.
basic testing scheme for MM and Waldenstrom's? serum electrophoresis separates and quantifies the different protein fractions of serum. if M-spike is present Immunofixation electrophoresis is done which overlays monoclonal antibodies on electrophoresis gel directed toward their chains.
Gaucher's cells 20-100um diameter, eccentric nucleus (or multiple nuclei), light blue cytoplasm w/ crumpled tissue paper appearance.
features of Plasma cell Leukemia? plasma cell count in PB >20% of WBCs. high calcium increased anemia and thrombocytopenia, significant organ involvement.
Niemann Pick cells 20-90um diameter, inconspicuous nucleus, cytoplasm filled with uniformly sized lipid droplets.
Alder-Reilly Inclusions prominent, dark-staining, coarse cytoplasmic granules in granulocytes, monocytes, and occasionally lymphocytes. looks similar to toxic granulation.
Sea-Blue Histiocytes 20-60um, contain blue-to-green staining granules that vary in size, shape and degree of stain uptake.
Cause of Gaucher's disease deficiency of beta-glucocerebrosidase, leads to unmetabolized glucocerebroside in reticuloendothelial cells.
Cause of Niemann-Pick Disease deficiency in sphingomyelinase, leads to accumulation of unmetabolized lipid sphinomyelin and cholesterol.
Cause of Tay-Sachs disease autosomal recessive disorder leading to deficiency of enzyme hexosaminidase B. results in unmetabolized GM2 ganglioside in tissues, especially CNS and eye.
cause of Mucopolysaccharidoses deficiency in one of the enzymes responsible for the breakdown of mucopolysaccharides. it's autosomal recessive and results in accumulation of unmetabolized mucopolysaccharides in reticuloendothelial cells.
Cause of Alder-Reilly autosomal recessive disorder.
cause of Sea-Blue Histiocyte Syndrome genetic disorder w/ unclear mode of inheritance and unidentified enzyme deficiency.
What does Myeloperoxidase and sudan Black stain for? myeloperoxidase and lipid.
What are the MPO and Sudan Black Stains useful for diagnosis in? AML M1-M4 (+) AML-M5 (-) ALL (-)
What does Specific esterase stain for? esterase in granulocyte precursors
What is Specific esterase stain useful for Dx of? AML M1-M4 (+) AML-M5 (-)
What does Non-Specific esterase stain for? non-specific esterase in monocyte precursors
What is Specific esterase stain useful in DX of? AML M4 (+) AML M5 (++) With fluoride inhibition step, M5 (-)
What does Periodic Acid Schiff stain for? Glycogen
What is Periodic acid shiff stain useful for Dx of?? erythroleukemia (M6) ALL ("Chunky" positive)
What does LAP stain for? Alkaline Phosphatase
What is LAP stain useful for Dx of?? Increased in Leukemoid Reaction Decreased in CML
What does TRAP stain for? Tartrate Resistant Acid Phosphatase
What is TRAP stain useful for Dx of?? Hairy Cell Leukemia
What does Prussion Blue stain for? Iron
What is Prussian Blue stain useful for Dx of?? Sideroblastic Anemia.
Created by: wulfmannwarrior