Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

wbc path 1


WBC count Normal: 5-10 K/µL Leukopenia: <5 K/µL Leukocytosis: >10 K/µL
Causes of neutropenia Drug toxicity (e.g. chemotherapy)//Severe infection (e.g. gram
Causes of lymphopenia Immunodeficiency (e.g. DiGeorge syndrome [no thymus] or HIV)// High cortisol state (e.g. exogenous corticosteroids or Cushing syndrome)// Autoimmune destruction (e.g. SLE)// Whole body radiation
Causes of neutrophilic leukocytosis Bacterial infection or tissue necrosis (release of marginated pool and recruitment of bone marrow neutrophils/ High cortisol state (release of marginated pool)
Marginated pool leukocytes "hang" in lung vasculature//cortisol disrupts adhesion, releases marginated pool// causes leukocytosis
Fc receptors Fc receptors help neutrophils recognize immunoglobulin (opsonin for phagocytosis)//lack of CD16 indicates lack of Fc receptors
Causes of monocytosis chronic inflammatory states (autoimmune or infectious)// malignancy
Causes of eosinophilia due to increased IL 5 production//allergic reactions//parasitic infections//Hodgkin lymphoma
Causes of basophilia classically seen in chronic myeloid leukemia
Causes of lymphocytic leukocytosis viral infections//B. pertussis infection
Acute leukemia accumulation of neoplastic blasts (>20% in the bone marrow)//blasts crowd out normal hematopoiesis// blasts enter blood, result in high WBC count with large appearance and "punched out" nucleoli
TdT DNA polymerase in lymphoblasts, but not myeloblasts or mature lymphocytes// can stain for TdT to diagnose ALL
ALL accumulation of >20% lymphoblasts in bone marrow// positive stain for TdT// most commonly arises in children// association with Down syndrome (usually >5yo)// subclassified into B
B- ALL accumulation of TdT+ lymphoblasts expressing CD10, CD19, and CD20//excellent response to chemo// requires prophylaxis to scrotum and CSF// t(12,21) has good prognosis (usually in kids), t(9,22) has poor prognosis (usually in adults)
T-ALL usually presents in teenagers as a thymic mass (called "lymphoma")// remember T's: T cells, teenagers, thymic mass
AML accumulation of >20% myeloblasts in bone marrow// positive stain for myeloperoxidase// crystal aggregates of MPO: Auer rods// may arise from myelodysplastic syndromes
Acute promyelocytic leukemia subtype of AML// has t(15;17): translation of retinoic acid receptor// RAR blocks maturation of promyelocytes// treatment = atra
Acute monocytic leukemia subtype of AML//blasts usually lack MPO //characteristically infiltrate gums//
Acute megakaryoblastic subtype of AML// blasts usually lack MPO //associated with Down syndrome (usually <5yo)
Chronic leukemia accumulation of mature LYMPHOcytes, characterized by a high WBC count with blasts <20%// often insidious onset// usually seen in older adults
CLL accumulation of naive B cells that co// most common type of leukemia// see increased lymphocytes and smudge cells// can involve lymph nodes
Complications of CLL hypogammaglobulinemia (infection most common cause of death)// autoimmune hemolytic anemia//transformation to large B cell lymphoma (will see enlarging lymph nodes or spleen)
Hairy cell leukemia accumulation of mature B cells with "hairy" cytoplasmic processes// TRAP+ // features: splenomegaly (hairy cells in red pulp), "dry" bone marrow tap (due to marrow fibrosis)// excellent response to cxtrpy
Adult T cell leukemia/lymphoma (ATLL) accumulation of mature CD4+ T cells//associated with HTLV// presents with rash, generalized lymphadenopathy, hepatosplenomegaly, punched out bone lesions with hypercalcemia
Mycosis fungoides accumulation of mature CD4+ T cells that infiltrate skin// presents with localized skin rash, plaques, nodules: called Pautrier microabscesses// cells can spread to the blood// characteristic lymphocytes with cerebriform nuclei (Sezary cells)
Myeloproliferative disorders accumulation of mature myeloid cells// usually in late adulthood(50//high WBC count with hypercellular bone marrow// all myeloid cells are increased, but classified based on dominant myeloid cell producedall myeloid cells are increased, but classified bas
Complications of MPD - increased risk for hyperuricemia and gout (high cell turnover) - progression to marrow fibrosis - transformation to acute leukem
CML - type of MPD, granulocytes are predominant cell type - basophils characteristically increased - t(9;22): Philadelphia chromosome --> BCR-ABL fusion protein with increased tyrosine kinase activity
Treatment for CML Imatinib// blocks tyrosine kinase activity of BCR
Outcomes of CML can transform to AML (2/3) or ALL (1/3) because mutation is in the pluripotent stem cell
How to distinguish CML from leukemoid reaction CML will have: negative LAP stain//increased basophils//t(9;22)
Polycythemia vera - type of MPD, RBCs are predominant cell type - assoc with JAK2 kinase mutation - blood becomes hyperviscous, requires phlebotomy (without, death usually within a year)
S/sx of polycythemia vera - splenomegaly (extramedullary hematopoiesis) - leukoerythroblastic smear (teardrop RBCs, nucleated RBCs, immature granulocytes) - increased risk of infection, thrombosis, bleeding
How to distinguish polycythemia vera from reactive polycythemia In polycythemia vera: EPO levels are decreased// oxygen saturation is normal
Essential thrombocythemia type of MPD, platelets are particularly increased// assoc with JAK2 kinase mutation //symptoms related to increased risk of bleeding AND/OR thrombosis (platelets either working really well or not at all)//rarely progresses to marrow fibrosis or acute leuk
Myelofibrosis - type of MPD, megakaryocytes are particularly increased - assoc w/ JAK2 kinase mutation (50% of cases) - megakaryocytes produce excess PDGF --> marrow fibrosis
Causes of painful vs. painless lymphadenopathy lymphadenopathy Painful: usually draining region of acute infection// Painless: seen w/ chronic inflammation, metastatic carcinoma, or lymphoma
Follicular lymphoma - NHL of small CD20+ B cells that form follicle-like nodules - typically late adulthood - can progress to diffuse large B-cell lymphoma
Pathophys of follicular lymphoma - Bcl2 normally inhibits apoptosis in peripheral cells - follicular cells generally lack Bcl2 so they can undergo testing - t(14;19) --> overexpression of Bcl2 --> cells that fail testing no longer die --> neoplasm
Treatment of follicular lymphoma reserved for symptomatic pts//involves low
How to distinguish follicular lymphoma from reactive follicular hyperplasia Follicular lymphoma shows: disruption of LN architecture// lack of tingible body macrophages (white spaces in follicle indicate macrophages are gobbling up apoptotic B cells)// Bcl2 expression //monoclonality
Mantle cell lymphoma NHL of small CD20+ B cells that expand mantle zone around follicle //typically late adulthood
Pathophys of mantle cell lymphoma t(11;14) --> overexpression of cyclin D1 --> promotes G1/S transition in cell cycle --> neoplasm
Marginal zone lymphoma - NHL of small CD20+ B cells that expand the marginal zone around the mantle/follicle - assoc with chronic inflammatory states (e.g. Hashimoto thyroiditis, Sjogren syndrome, H. pylori gastritis)... marginal zone typically only present with chronic inflam
Burkitt lymphoma - NHL of intermediate-sized CD20+ B cells - associated with EBV - translocations of c-myc (nuclear regulator) --> cell growth - high mitotic index and "starry sky" appearance under microscope
Classic presentation of Burkitt lymphoma extranodal mass in a child or young adult extranodal mass in a child or young adult - African form: jaw - Sporadic form: abdomen
Diffuse large B - most common form of NHL - large CD20+ B cells grow diffusely in sheets - clinically aggressive - arises sporadically or from transformation of lower-grade lymphoma - presents in late adulthood
Hodgkin lymphoma overview - proliferation of Reed-Sternberg cells - cytokine release attracts other inflammatory cells, may lead to fibrosis and "B" symptoms (night sweats, fever, chills) - reactive cells are the bulk of the tumor - nodular sclerosis is most common subtype
Reed Sternberg cells - large B cells with multilobed nuclei & prominent nucleoli ("owl eye" appearance) - neoplastic in Hodgkin lymphoma - classically CD15 and CD30+ with NO CD20 expression - secrete cytokines that attract lymphos, plasma cells, macrophages and eosinophils
Nodular sclerosis - most common subtype of Hodgkin lymphoma - classically presents with enlarging cervical or mediastinal lymph node in young adult, usually female - lymph node divided by bands of sclerosis - Reed Sternberg cells present in lake-like spaces (aka lacunar
Best/worst prognosis for Hodgkin lymphoma - lymphocyte-rich subtype has best prognosis - lymphocyte-deprived has worst prognosis (usually in elderly and HIV+)
Multiple myeloma malignant proliferation of plasma cells in marrow// high serum IL //plasma cells overproduce osteoclast activating factor, Igs, light chain
S/sx of multiple myeloma osteoclast activating factor// IgA & IgG// = bence jones protiens
Monoclonal gammopathy of undetermined significance (MGUS) increased serum protein with M spike// other features of multiple myeloma are ABSENT// common in elderly, some will develop multiple myeloma
Waldenstrom macroglobulinemia B cell lymphoma with monoclonal IgM production// similar to multiple myeloma but: no lytic bone lesions// visual and neurologic deficits (due to serum hyperviscosity)// bleeding (defective platelet aggregation)// treat with plasmapheresis
Langerhans cell histiocytosis neoplastic proliferation of Langerhans cells// characteristic Birbeck (tennis racket) granules seen on EM// cells are CD1a+ and S100+//
data source clarebp on quizlet(dot)com
Created by: ljacob2010