WBC Flashcards
(70 cards)
1
Q
Causes of neutropenia
A
Drug toxicity (chemo with alkylating agents) Infection (neutrophils move into cells)
2
Q
Treatment for neutropenia
A
GM-CSF or G-CSF
3
Q
Causes of lymphopenia
A
Immunodeficiency High cortisol (cushing) Autoimmune destruction (SLE) Radiation (lymphocytes are most sensitive)
4
Q
Causes of neutrophilic leukocytosis
A
Bacterial infection, tissue necrosis or high cortisol state
5
Q
What is a left shift?
A
Increased release of neutrophils causing increased % of immature cells
6
Q
How is an immature neutrophil identified?
A
Decreased Fc receptors (CD16)
7
Q
Causes of monocytosis
A
cx inflammation and malignancy
8
Q
Causes of esoinophilia
A
T1HS, parasites, Hodgkin lymphoma
9
Q
Causes of basophilia
A
CML
10
Q
Causes of lymphocytic leukocytosis
A
viral infxn, Bordetella
11
Q
Characteristic findings of EBV
A
Elevated WBC with atypical lymphocytes and CD8 t cells
12
Q
Mechanism of monospot
A
Detects heterophiles abs (IgM that react with horse or sheep blood)
13
Q
Characterization of ALL
A
positive nuclear staining for TdT (not present on myeloid cells or mature cells)
14
Q
Population of pts with ALL
A
Most commonly arises in children; associated with Down syndrome (after age of 5 years)
15
Q
Most common type of ALL?
A
BALL
16
Q
Features of BALL
A
Characterized by lymphoblasts (TdT+) that express CD10, CD19, and CD20.
Excellent response to chemotherapy; requires prophylaxis to scrotum and CSF
17
Q
Features of TALL
A
Lymphoblasts (TdT+) that express markers ranging from CD2 to CD8 (no CD10)
18
Q
Cells characterized by positive cytoplasmic staining for myeloperoxidase (MPO)
A
Myeloblasts (AML)
Crystal aggregates of MPO: Auer rods
19
Q
Subtypes of AML
A
acute monocytic leukemia, acute promyelocytic leukemia, acute megakaroblastic leukemia
20
Q
Features of APL
A
Type of AML
t(15;J7), translocation of retinoic acid receptor (RAR) on c17 to c15; blocks maturation and promyelocytes (blasts) accumulate
Abnormal promyelocytes contain primary granules: increase the risk for DIC
21
Q
Features of Acute monocytic leukemia
A
Type of AML
Proliferation of monoblasts; usually lack MPO
Characteristically infiltrate gums
22
Q
Features of Acute megakaryoblastic leukemia
A
Type of AML
Proliferation ol megakaryoblasts; lack MPO
Associated with Down syndrome (usually arises before the age of 5)
23
Q
Neoplastic proliferation of mature circulating lymphocytes; characterized by a high WBC count
A
Chronic leukemia
24
Q
Chronic Lymphocytic Leukemia (CLL)
A
Naive B cells; co-express CD5 and CD20
Most common leukemia overall
Increased lymphocytes and smudge cells on blood smear
Generalized lymphadenopathy
25
Complications of CLL
Hypogammaglobulinemia: infection is most common cause of death
Autoimmune hemolytic anemia
Transformation to diffuse large B-cell lymphoma (Richter transformation)
26
Hairy Cell Leukemia
Mature B cells w/hairy cytoplasmic processes
+ tartrate-resistant acid phosphatase (TRAP)
Splenomegaly (accumulation of hairy cells in red pulp) and "dry tap" on bone marrow aspiration (due to marrow fibrosis)
NO lymphadenopathy
Excellent response to 2-CDA (cladribine)
27
Adult T-Cell leukemia/Lymphoma (ATLL)
Mature CD4 T cells
Associated with HTLV-1; most commonly in Japan and Caribbean
Rash (skin infiltration), generalized Lymphadenopathy w/ hepatosplenomegaly
Lytic bone lesions with hvpercalcemia
28
Mycosis Fungoides
Mature CD4T cells that infiltrate skin: rash, plaques, and nodules
Aggregates of neoplastic cells in epidermis: Pautrier microabscesses
Cells spread to involve blood -> Sezary syndrome: Characteristic lymphocytes with cerebri form nuclei (Sezary cells) on blood smear
29
Chronic Myeloid Leukemia
Mature myeloid cells, esp granulocytes and
precursors; basophils characteristically increased
t(9;22) (Philadelphia chromosome): generates a BCR-ABL
Treatment is imatinib: blocks tyrosine kinase activity
Splenomegaly
Can transform to AML (2/3 of cases) or ALL (1/3 of cases); mutation in pluripotent stem cell
30
CML is distinguished from a leukemoid reaction (reactive neutrophilic leukocytosis) by
1. Negative leukocyte alkaline phosphatase (LAP) stain (leukemoid reaction are LAP +)
2. Increased basophils (absent with leukemoid reaction)
3. t(9;22) (absent in leukemoid reaction)
31
Polycythemia Vera
Mature myeloid cells, esp RBCs
JAK2 kinase mutation
Sx d/t hyperviscosity of blood:
Blurry vision, HA, DVTs
Flushed face due to congestion (plethora)
Itching, esp after bathing (histamine release from increased mast cells)
Treatment is phlebotomy; second-line is hydroxyurea
32
Distinguish PV from reactive polycythemia
1. In PV, EPO decreased and SaO is normal.
2. In reactive polycythemia due to high altitude or lung disease, SaO is low and EPO is increased.
3. In reactive polycythemia due to ectopic EPO production from renal cell carcinoma, EPO is high,and SaO is normal.
33
Essential Thrombocytopenia
Mature myeloid cells, esp platelets (RBCs and granulocytes also)
JAK2 kinase mutation
Sx related to increased risk of bleeding and/or thrombosis
34
Myelofibrosis
Mature myeloid cells, esp megakaryocytes
JAK2 kinase mutation
Megakaryocytes produce PDGF -> marrow fibrosis
1. Splenomegaly: extra medullary hematopoiesis
2. Leukoerythroblastic smear (tear-drop RBCs, nucleated RBCs, and immature
granulocytes)
3. Increased risk of infection, thrombosis, and bleeding
35
Lymphoma
Neoplastic proliferation of lymphoid cells that forms a mass
36
Non-Hodgkin Lymphoma
60%
malignant lymphoid cells; mass made of lymphoid cells
Painless lymphadenopathy, usually arises in late adulthood
Spread is diffuse
Leukemic phase occurs
37
Hodgkin Lymphoma
40%
Malignant Reed-Sternberg Cells (CD15 and CD 30 +)
Mass made of reactive cells
Painless lymphadenopathy occasionally with 'B' symptoms, usually arises in young adults
Radiation is the mainstay of treatment
No leukemic phase
38
Follicular Lymphoma
Small B cells (CD20+); form follicle-like nodules
Presents in late adulthood with painless lymphadenopathy
Driven by t(14;18): BCL2 on 18 to IgH on 14: inhibition of apoptosis
Treatment is low-dose chemotherapy or rituximab (anti-CD20 antibody)
Progression to diffuse large B-cell lymphoma is a complication (enlarging lymph node)
39
Follicular lymphoma is distinguished from reactive follicular hyperplasia by
1. Disruption of normal lymph node architecture (maintained in follicular hyperplasia)
2. Lack of tingible body macrophages in germinal centers (tingible body macrophages are present in follicular hyperplasia)
3. Bcl2 expression in follicles (not expressed in follicular hyperplasia)
4. Monoclonality (follicular hyperplasia is polyclonal)
40
Mantle Cell Lymphoma
Small B cells (CD20+) that expand the mantle zone
Presents in late adulthood with painless lymphadenopathy
Driven by t(ll;14): cyclin D to IgH: over expression of cyclin D1 promotes G1 to S
41
Marginal Zone Lymphoma
Small B cells (CD20+) that expands the marginal zone
Associated with chronic inflammatory states such as Hashimoto thyroiditis, Sjogren syndrome, and H pylori gastritis
MALToma is marginal zone lymphoma in mucosal sites
42
Burkitt Lymphoma
Intermediate-sized B cells (CD20+); associated with EBV
Driven by translocations of c-myc for IgH-> promotes cell growth
'Starry-sky' appearance on microscopy
43
African form of Burkitt Lymphoma
Involves the jaw
44
Sporadic form of Burkitt lymphoma
Involves the abdomen
45
Diffuse large B-cell Lymphoma
Large B cells (CD20+); grow diffusely in sheets
Most common form of NHL
Clinically aggressive (high-grade)
46
Neoplastic cells of Hodkin Lymphoma and features
Reed-Slernberg (RS) cells: large B cells with multilobed nuclei and prominent nucleoli; CD15 and CD30+, secrete cytokines
1. Occasionally results in 'B' symptoms (fever, chills, and night sweats)
2. Attract reactive lymphocytes, plasma cells, macrophages, and eosinophils
3. May lead to fibrosis
47
HL subtypes
1. Nodular sclerosis
2. Lymphocyte-rich
3. Mixed cellularity
4. Lymphocyte-depleted
48
Most common subtype of HL
Nodular sclerosis; 70%
Presentation is enlarging cervical or mediastinal lymph node in a young adult, usually female
Lymph node is divided by bands of sclerosis; RS cells are present in
lake-like spaces
49
HL with best prognosis
Lymphocyte-rich
50
Most aggressive HL
Lymphocyte-depleted; usually seen in the elderly and HIV-positive individuals
51
Multiple Myeloma
Malignant proliferation of plasma cells in the bone marrow
Most common primary malignancy of bone
High serum IL-6
52
Presentation of MM
Bone pain with hypercalcemia: Neoplastic plasma cells activate RANK receptor on osteoclasts -> bone destruction
Lytic, 'punched-out' skeletal lesions on XR
Elevated serum protein— cells produce (IgG or IgA)
Increased risk of infection— lacks antigenic diversity; Infection is the most common cause of death
Rouleaux formation of RBCs
Primary AL amyloidosis
Proteinuria—Free light chain is excreted in the urine as Bence Jones protein
53
Monoclonalgammopathy of Undetermined Significance (MUGS)
Increased serum protein with M spike
54
Waldenstrom Macroglobulinemia
B-cell lymphoma with monoclonal IgM production
1. Generalized lymphadenopathy, lytic bone lesions are absent.
2. Increased serum protein with M spike (comprised of IgM)
3. Visual and neurologic deficits (e.g., retinal hemorrhage or stroke)—IgM (large
pentamer) causes serum hyperviscosity.
4. Bleeding—Viscous serum results in defective platelet aggregation.
treated with plasmapheresis, which removes IgM from the serum
55
Letterwise disease
A. Malignant proliferation of Langerhans cells
B. Classic presentation: skin rash and cystic skeletal defects in an infant (< 2 years old).
C. Multiple organs involved; rapidly fatal
56
Esosinophilic Granuloma
A. Benign proliferation of Langerhans cells in hone
B. Classic presentation is pathologic fracture in an adolescent; skin is not involved
C. Biopsy shows Langerhans cells with mixed inflammatory cells, including numerous eosinophils
57
Hand - Shuller- Christian Disease
A. Malignant proliferation of Langerhans cells
B. Classic presentation is scalp rash, lytic skull defects, diabetes insipidus, and
exophthalmos in a child
58
What is IM?
Reactive CD8 cells due to EBV infection of B cells
59
What is acute leukemia?
Neoplastic proliferation fo blasts (>20%); can be lymphoblastic or myeloblastic
60
Characterization of acute leukemia
Large, immature cells with punched out nucleoli
61
BALL with t(12;21)
Good prognosis; more common in children
62
BALL with t(9;22)
Poor prognosis; more common in adults (Philadelphia+ ALL)
63
Presentation of TALL
In teenagers as a mediastinal (thymic) mass (called acute lymphoblastic lymphoma because the malignant cells form a mass)
64
Treatment for APL
Treat with all trans retinoic acid
65
What is myelodysplastic syndrome?
AML from pre-existing dysplasia d/t exposure to alkylating agents or radiotherapy
66
What is the Richter transformation?
CLL to diffuse large B cell lymphoma
| Seen as enlarging lymph node or spleen
67
Treatment for Hairy Cell Leukemia
2-CDA (cladribine)
68
Two leukemias with punched out bone lesions and how do you differentiate
ATLL and MM
| ATLL has a rash
69
Sezary cells
Characteristic lymphocytes with cerebri form nuclei seen on blood smear in mycosis fungicides
70
Treatment for CML
Imatinib: blocks tyrosine kinase activity
