WBC disorders Pathoma Flashcards
Leukopenia
low WBC count (less than 5K)
Leutocytosis
high WBC count (above 10K)
Myeloid Stem cells can become
Erythroblast (RBC), Myeloblast (granulocytes = neutrophils, basophils), monoblast (monocytes), & megakaryocytes
Lymphoid stem cells can become
B Cells (plasma cells) & T cells (CD8 & CD4)
Neutropenia
Low neutrophils
Caused by drug toxicity (chemotherapy) & severe infection (out of blood & in tissue)
Treated with granulocyte stimulating factor
Lymphopenia
Low number of circulating lymphocytes
Caused by immunodeficiency , high cortisol state (induce apoptosis), autoimmune destruction, whole body radiation (most sensitive cell in body to radiation)
Neutrophilic leukocytosis
Increase in neutrophils
Caused by bacterial infection, tissue necrosis, & high cortisol states
Bone marrow releases immature neutrophils (left shift) - decreased Fc receptors
CD 16 is marker for FC receptor (also decreased)
Monocytosis
Increases WBC count
Seen in chronic inflammatory states & malignancy
Eosinophilia
Increased number in circulating eosinophils
Caused by allergic reactions, parasitic infection, & Hodgkin lymphoma (by increased IL-5 production)
Basophilia
High basophil count
Seen in CML
Lymphocytic leukocytosis
High lymphocyte count
Seen in viral infections (fought by CD8 T cells) & Bordetella pertussis (even though it is a bacteria - one exception; blocks lymphocytes from entering lymph nodes - stuck in blood)
Infectious Mononucleosis
EBV infection that results in a lymphocytic leukocytosis comprised of reactive CD8 T cells
CMV is less common case
Risk splenomegaly & rupture - avoid contact sports for 1 year
Acute leukemia is a neoplastic proliferation of
blasts
over 20% blasts in bone marrow; 1-2% is normal number
As blasts pile up, they cause
acute presentation of anemia, thrombocytopenia, or neutropenia (as they crowd out normal hematopoiesis)
Blasts enter blood, resulting in
high WBC count.
Look like large, immature cells with punched out nucleoli
Accumulation of myeloid blast is
AML
Accumulation of lymphoblast is
ALL
Hallmark marker for lymphoblast is
TdT in nucleus - DNA polymerase only present in lymphoblasts
Marker for myeloid blast is
MPO
(myeloperoxidase)
Can crystalize into structure called Auer Rod
ALL most commonly arises in
Children
especially associated with Down syndrome (after age 5)
Most common type of ALL
B-ALL
Classical surface markers CD10, CD19, CD20
B-ALL prognosis
t(12;21) good prognosis - in children
t(9;22) poor prognosis - more common in adults (Ph+ ALL)
T-ALL markers
CD2-CD8
Do not express CD10
T-ALL commonly presents in
thymic (mediastinal) mass in teenager
Auer Rod
seen in AML
Acute promylocytic leukemia
Characterized by t(15;17)
Disruption of RAR (retinoic acid receptor) - promyelocytes accumulate
Risk for DIC (activation of coagulation casscade by auer rods)
Treated by ATRA
Acute monocytic leukemia
proliferation of monoblasts; lack MPO
Infiltrate gums
Acute megakaryoblastic leukemia
Proliferation of megakaryoblasts; lack MPO
Association with Down Syndrome (before age of 5)
Myelodysplastic syndrome
Cytopenias (low count of cells in blood) with hypercellular bone marrow
(abnormal maturation with increased blasts,
Chronic leukemia
neoplastic proliferation of mature circulating lymphocytes.
High WBC, usually insidious onset & in older adults
CLL
Neoplastic proliferation of naive B-cells
Co-express CD5 & CD20
CLL blood smear shows
Increased lymphocytes & smudge cells
Small lymphocytic lymphoma
CLL that involves the lymph nodes causing generalized lymphadenopathy
CLL complications
hypogammaglobulinemia (low immunoglobulin - die of infection)
Autoimmune hemolytic anemia (antibodies against own RBC)
Transformation to diffuse large B-cell lymphoma (enlarging lymph node or spleen)
Hairy Cell Leukemia
Neoplastic proliferation of mature B cells
Hairy cytoplasmic processes
Positive for TRAP
Hairy Cell Leukemia clinical features
Splenomegaly (red pulp expansion)
Dry tap with bone marrow aspiration
Lymphadenopathy usually absent
Hairy Cell Leukemia treated with
2-CDA (adenosine deaminase inhibitor)
Adenosine accumulates to toxic levels in neoplastic B cells