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WBC disorders Pathoma Flashcards

1
Q

Leukopenia

A

low WBC count (less than 5K)

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2
Q

Leutocytosis

A

high WBC count (above 10K)

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3
Q

Myeloid Stem cells can become

A

Erythroblast (RBC), Myeloblast (granulocytes = neutrophils, basophils), monoblast (monocytes), & megakaryocytes

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4
Q

Lymphoid stem cells can become

A

B Cells (plasma cells) & T cells (CD8 & CD4)

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5
Q

Neutropenia

A

Low neutrophils
Caused by drug toxicity (chemotherapy) & severe infection (out of blood & in tissue)
Treated with granulocyte stimulating factor

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6
Q

Lymphopenia

A

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)

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7
Q

Neutrophilic leukocytosis

A

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)

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8
Q

Monocytosis

A

Increases WBC count

Seen in chronic inflammatory states & malignancy

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9
Q

Eosinophilia

A

Increased number in circulating eosinophils

Caused by allergic reactions, parasitic infection, & Hodgkin lymphoma (by increased IL-5 production)

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10
Q

Basophilia

A

High basophil count

Seen in CML

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11
Q

Lymphocytic leukocytosis

A

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)

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12
Q

Infectious Mononucleosis

A

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

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13
Q

Acute leukemia is a neoplastic proliferation of

A

blasts

over 20% blasts in bone marrow; 1-2% is normal number

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14
Q

As blasts pile up, they cause

A

acute presentation of anemia, thrombocytopenia, or neutropenia (as they crowd out normal hematopoiesis)

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15
Q

Blasts enter blood, resulting in

A

high WBC count.

Look like large, immature cells with punched out nucleoli

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16
Q

Accumulation of myeloid blast is

A

AML

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17
Q

Accumulation of lymphoblast is

A

ALL

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18
Q

Hallmark marker for lymphoblast is

A

TdT in nucleus - DNA polymerase only present in lymphoblasts

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19
Q

Marker for myeloid blast is

A

MPO
(myeloperoxidase)
Can crystalize into structure called Auer Rod

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20
Q

ALL most commonly arises in

A

Children

especially associated with Down syndrome (after age 5)

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21
Q

Most common type of ALL

A

B-ALL

Classical surface markers CD10, CD19, CD20

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22
Q

B-ALL prognosis

A

t(12;21) good prognosis - in children

t(9;22) poor prognosis - more common in adults (Ph+ ALL)

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23
Q

T-ALL markers

A

CD2-CD8

Do not express CD10

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24
Q

T-ALL commonly presents in

A

thymic (mediastinal) mass in teenager

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25
Auer Rod
seen in AML
26
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
27
Acute monocytic leukemia
proliferation of monoblasts; lack MPO | Infiltrate gums
28
Acute megakaryoblastic leukemia
Proliferation of megakaryoblasts; lack MPO | Association with Down Syndrome (before age of 5)
29
Myelodysplastic syndrome
Cytopenias (low count of cells in blood) with hypercellular bone marrow (abnormal maturation with increased blasts,
30
Chronic leukemia
neoplastic proliferation of mature circulating lymphocytes. | High WBC, usually insidious onset & in older adults
31
CLL
Neoplastic proliferation of naive B-cells | Co-express CD5 & CD20
32
CLL blood smear shows
Increased lymphocytes & smudge cells
33
Small lymphocytic lymphoma
CLL that involves the lymph nodes causing generalized lymphadenopathy
34
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)
35
Hairy Cell Leukemia
Neoplastic proliferation of mature B cells Hairy cytoplasmic processes Positive for TRAP
36
Hairy Cell Leukemia clinical features
Splenomegaly (red pulp expansion) Dry tap with bone marrow aspiration Lymphadenopathy usually absent
37
Hairy Cell Leukemia treated with
2-CDA (adenosine deaminase inhibitor) | Adenosine accumulates to toxic levels in neoplastic B cells
38
ATLL
Neoplastic proliferation of mature CD4 T cells | Associated with HTLV-1 (Japan & Caribbean)
39
ATLL clinical features
Rash Generalized lymphadenopathy with hepatosplenomegaly Lytic bone lesions with hypercalcemia
40
Mycosis fungoides
neoplastic proliferation of mature CD4 T cells | Infiltrate skin - rash, plaques, or nodules
41
Pautrier microabscesses
aggregates of neoplastic T cells in epidermis
42
Sezary syndrome
CD4 T cells (in mycosis fungoides) spread to blood | Cerebriform nuclei on blood smear
43
Myeloproliferative Disorder
Overproduction of mature myeloid cells Get overproduction of all myeloid cells (RBC, granuclocytes, etc.) but named based on predominant cell Late adulthood disease High WBC count with hypercellular bone marrow
44
Myeloproliferative disorder complications
Increased risk for hyperuricemia & gout Progression to marrow fibrosis Transformation to acute leukemia
45
Chronic Myeloid Leukemia (CML)
Neoplastic proliferation of mature myeloid cells, especially granulocytes Basophils characteristically increased
46
CML translocation
t(9;22) - Philadelphia chromosome | BCR-ABL fusion with increased tyrosine kinase activity
47
CML treatment
Imatinib - blocks tyrosine kinase activity
48
CML chronic phase
Enlarged spleen
49
Enlarging spleen (getting bigger) is marker of (what CML phase)
Accelerated phase; transformation to acute leukemia follows shortly (either AML or ALL)
50
CML granulocytes are
LAP negative (leukemoid reaction are LAP positive)
51
Polycythemia Vera
Neoplastic proliferation of mature myeloid cells, especially RBC EPO decreased due to negative feedback Granulocytes & platelets also increased JAK2 kinase mutation
52
Polycythemia Vera symptoms
``` hyperviscosity Blurry vision & headache Increased risk of venous thrombosis Flushed face due to congestion Itching after bathing (high number of mast cells) ```
53
Polycythemia Vera treatment
Phlebotomy | 2nd line treatment hydroxyurea
54
Reactive polycythemia
Polycythemia due to lung disease (has SaO2 low & EPO increased) Due to ectopic EPO production, EPO is high & SaO2 is normal
55
Essential Thrombocythemia
Neoplastic proliferation of mature myloid cells - platelets! RBC & granulocytes also increased JAK2 mutation
56
Essential Thrombocythemia symptoms
Increased risk of bleeding and/or thrombosis Rarely develops into marrow fibrosis or acute leukemia No risk for hyperuricemia or gout
57
Myelofibrosis
Neoplastic proliferation of mature myeloid cells, esp megakaryocytes JAK2 mutation
58
Myelofibrosis
Splenomegaly due to extramedullary hematopoiesis Leukoerythroblastic smear Increased risk of infection, thrombosis, & bleeding Teardrop cells
59
Lymphadenopathy
enlarged lymph nodes Painful with acute infection Painless with chronic inflammation, metastatic carcinoma, or lymphoma
60
Lymphoma
neoplastic proliferation of lymphoid cells that forms a mass | Can be in lymph node or extranodal tissue
61
Most common lymphomas
Non-Hodgkin lymphomas
62
Follicular lymphoma
Neoplastic small B cells (CD20) that make the follicle-like nodules - disrupts normal lymph node architecture Late adulthood with painless LAD Driven by t(14;18), over-expression of BCL2
63
BCL2
Stabilizes mitochondrial membrane & prevents cytochrome c from leaking into the cytoplasm Blocks apoptosis
64
Follicular lymphoma treatment
low dose CTX or rituximab | for symptomatic patients
65
Follicular lymphoma complications
Progression to diffuse large B-cell lymphoma - presents as enlarging lymph node
66
Mantle Cell Lymphoma
Neoplastic small B cells (CD20) that expand mantle zone (immediately adjacent to follicle) Late adulthood with painless LAD Driven by t(11;14) - Cyclin D1 overexpression
67
Cyclin D1
promotes G1/S transition in cell cycle through protein phosphorylation
68
Marginal Zone Lymphoma
Neoplastic small B cells (CD20) that expand marginal zone (outside of the mantle) Associated with chronic inflammatory states (like Hashimoto thyroiditis, Sjogren syndrome, H pylori gastritis)
69
MALToma
marginal zone lymphoma in mucosal sites (stomach example) | Gastric MALToma may regress with treatment of H pylori
70
Burkitt Lymphoma
Neoplastic intermediate-sized B cells | Associated with EBV
71
Burkitt Lymphoma presents as
extranodal mass in child or young adult African form - jaw Sporadic form - abdomen
72
Burkitt lymphoma is driven by
translocations of c-myc (chromosome 8) t(8;14) most common Overexpression of c-myc oncogene promotes cell growth
73
Burkitt lymphoma looks like _____ on histology
starry-sky appearance | Due to rapid growth & turnover
74
DLBCL (Diffuse large b cell lymphoma)
``` Neoplastic large B cells that grow diffusely in sheets Clinically aggressive (poorly differentiated) ```
75
Most common type of nonHodgkin lymphoma is
DLBCL
76
DLBCL presents
late in adulthood as enlarging lymph node or extranodal mass | Arise sporadically or transformation of follicular lymphoma
77
Hodgkin Lymphoma
Reed-Sternberg cells - Large B cell with multilobed nuclei & prominent nucleoli CD15 & CD30
78
RS cells secrete cytokines that
Can cause B symptoms (fevers, chills, night sweats) Attract reactive lymphocytes, plasma cells, macrophages, & eosinophils May lead to fibrosis
79
Most common type of HL is
Nodular sclerosis: Enlarging cervical neck or mediastinal LN & usually a young female LN divided by broad bands of fibrosis RS cells sit in big empty spaces
80
Multiple Myeloma
malignant proliferation of plasma cells in bone marrow Most common primary malignancy of bone High serum IL-6
81
Osteoclast activating factor
Can be produced by plasma cells Activate osteoclasts that eat away at bone - punched out lesions on x-ray seen in vertebrae & skull Leads to bone pain, hypercalcemia, & increase risk of fracture
82
M spike
indicates monoclonal immunoglobulin | Tight & high band on SPEP
83
Most common cause of death from multiple myeloma is
infection | Monoclonal antibody lacks antigenic diversity
84
Immunoglobulin with MM
overproduced by plasma cells | Gives high serum protein with M spike (IgG or IgA) & decreased antigenic diversity
85
Light chain production with MM
Overproduced by plasma cells Deposits in tissue as amyloid (amylodosis) & comes out in urine as Bence-Jones proteins Can deposit in kidney tubules & cause renal failure
86
MGUS
Increased serum protein with M spike on SEP | Other features of multiple myeloma are absent
87
MGUS common in
elderly | can develop into MM
88
Waldenstrom Macroglobulinemia
B cell lymphoma with monoclonal IgM production Presents with generalized LAD; absent lytic bone lesions Increased serum protein with M spike (IgM) Visual & neurological deficits Bleeding
89
Acute complications of Waldenstroms are treated with
plasmapheresis - removes IgM from serum
90
Langerhans cells
specialized dendritic cell found mostly in skin | From bone marrow monocytes
91
Langerhans cell histiocytosis
``` Neoplastic proliferation Characteristic Birbeck (tennis racket) cell ```
92
Letterer-Siwe disease
Malignant proliferation of Langerhans cells | Classic presentation is skin rash and cystic skeletal defects in an infant (
93
Eosinophilic granuloma
Benign proliferation of Langerhans cells in bone | Pathologic fracture in adolescent; skin not involved
94
Hand-Schuller-Christian disease
Malignant proliferation of Langerhans cells Scalp rash, lytic skull defects, diabetes insipidus, exopthalmos In child

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