WBC pathology Flashcards

(45 cards)

1
Q

What is the normal range for total WBC?

A

4000-10000/fl

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2
Q

Decreased count of which cell type is the most common reason for leukopenia? What is second?

A

most common: neutrophils (neutropenia)

also possible: lymphocytes (lymphopenia)

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3
Q

Generally, what are potential reasons for leukopenia?

A
  • congenital d/o’s
  • post glucocorticoid or cytotoxic drug therapy
  • autoimmune d/o’s
  • malnutrition
  • certain acute viral infections
  • advanced HIV infection
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4
Q

Marked reduction in PMN count and increased susceptibility to infx are hallmarks of ______?

A

agranulocytosis

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5
Q

What are the four sub-types of leukopenia due to decreased production? What are the underlying conditions associated with each?

A

(1) suppression of myeloid stem cells:
• aplastic anemia
• infiltrative marrow d/o’s – tumors, granulomatous dz.
(2) Drug suppression of granulocytic precursors:
• alkylating agents – bone marrow suppression
• antimetabolites used in cancer tx- bone marrow suppression
• Aminopyrine – Aby mediated
• Sulfonamides – Aby mediated
(3) Defective precursors in marrow:
• megaloblastic anemia
• myelodysplastic syns
(4) Genetic defects:
• rare inherited conditions (Kostmann syn).

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6
Q

What are the three sub-types of leukopenia due to increased PMN removal? What are the underlying conditions associated with each?

A

(1) Immune mediated injury:
•SLE
•drugs
(2) Splenic sequestration:
•inc. destruction d/t enlargement of spleen.
(3) Increased peripheral utilization:
•overwhelming infxs from bacteria, fungal or rickettsial pathogens (lyme dz).

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7
Q

What would be the expected bone marrow morphology if there is excessive white cell destruction in the body?

A

hypercellular, filled with granulocyte precursors

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8
Q

What are some areas of increased infx in patients with leukopenia? What will be the state of he lymph nodes?

A

ulceration and necrotization in the oropharynx region. also life-threatening infxs in the lung and urinary tract.

regional lymph nodes will be enlarged and inflamed

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9
Q

What are the general reasons for leukocytosis and their underlying causes?

A
  • INC. release from marrow stores:
    • Endotoxemia = bacteria
    • acute infxn
    • hypoxia
  • DEC. margination:= MORE IN CIRCULATION
    • exercise
    • epinephrine
  • DEC. extravasation into tissues:
    • glucocorticoid therapy
  • INC. numbers of marrow precursors:
    • chr.infxnor inflammation
    • tumors
    • myeloproliferative d/o’s
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10
Q

To what does toxic granulation refer? What is likely to be going on in a patient that has it? What is causing it?

A

toxic granulation: dark, coarse granules in peripheral granulocytes…usu neutrophils. it is a dilated ER. they suggest an inflammatory process.

patient presumed to have sepsis until proven otherwise.

it occurs b/c the cytoplasm is not given time to mature due to the high demand for cells.

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11
Q

What are the non-neoplastic bases for elevations of the following:

  • neutrophils
  • toxic granulation
  • eosinophils
  • monocytes
  • lymphocytes
  • band cells
A
  • neutrophils: bacterial infx; acute inflamx; MI
  • toxic granulation: sever infx; bacterial sepsis
  • eosinophils: allergy; parasitic infx
  • monocytes: chronic inflamx; mono; recovery post-infx
  • lymphocytes: acute viral infx; chronic inflamx
  • band cells: infx
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12
Q

What are the three types of chronic lymphadenitis and which portion of the LN does each affect? What is the stimulus for each?

A
  • follicular hyperplasia: two types within the cortex.
    1. affects the germinal centers secondary to an infx triggering humoral immunity - B-cell and M0 stimulation
    2. lymphoid cell hyperplasia through the mantle zone surrounding the germinal centers.
  • paracortical lymphoid hyperplasia: in the paracortical region, drugs/viral infxs stimulate T-cell production.
  • sinus histiocytosis (aka reticular hyperplasia): within the sinus; distention secondary to some type of cell (often breast cancer) getting stuck when draining through.
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13
Q

What genetic abnormalities are present in the majority of WBC neoplasms?

A

chromosomal translocations (t#:#) and oncogenes

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14
Q

Which d/o would be associated with the following causes?

  • H. pylori
  • gluten-sensitive enteropathy
  • HIV infx
  • radiotherapy/chemo tx
A
  • H. pylori: gastric B-cell lymphoma
  • gluten-sensitive enteropathy: intestinal T-cell lymphoma
  • HIV infx: B-cell lymphoma
  • radiotherapy/chemo tx: myeloid & lymphoid neoplasm due to mutation of progenitor cells.
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15
Q

Which type of lymphoma can exist outside the LN itself?

A

non-hodgkin’s. about 1/3 are extranodal (skin, stomach, brain)

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16
Q

How is it possible to differentiate between early lymphoma and reactive leukocytosis?

A

In lymphoma, the WBCs will be monoclonal

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17
Q

What impact does lymphocytic leukemia have on hematopoiesis?

A

Suppression. Tumor steals nutrients and also takes up space, forcing immature cells into circulation. Bleeding d/o and anemia result.

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18
Q

What kind of cell comprises a plasms-cell neoplasm? From where does it arise?

A
  • terminally differentiated (mature) B-cells.

- arise in the bone marrow.

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19
Q

With what do most patients with multiple myeloma present? What causes it?

A

pain from multiple fractures. bence jones proteins take up a lot space within the bone and ruin the structural integrity.

20
Q

What type of cells are Reed-Sternberg cells and what gives them their ‘owl eye’ appearance?

A

They are B lymphocytes from a crippled germinal center. They do not express their antibody.

Multi-nucleated or bi-lobed nucleus gives them the owl eye appearance.

21
Q

Reed-Sternberg must not only be present but do what in order to be diagnostic for ________ lymphoma?

A

Hodgkin’s lymphoma.

Must be able to chemo-attract normal lymphocytes.

22
Q
Are Reed-Sternberg cells +/- for the following markers?
CD15
CD20
CD30
CD45
A

CD15 +
CD20 -
CD30 +
CD45 -

23
Q

Which dz comes from a tumor of B and T cell precursors?

Who is most often affected by pre-B and pre-T?

A

Acute Lymphoblastic Leukemia (ALL)

Pre-B ALL: white children ~4 yrs when pre-B lymphoblasts peak.

Pre-T ALL: adolescence when thymus reaches max size.

24
Q

How do the cells appear in ALL?

A

Cells are huge lymphocytes with condensed chromatin and scant cytoplasm.

25
What is the common presentation for patients with ALL?
present pale, fatigued, bruised, sick (due to pancytopenia) pain from periosteum general LAD hepatosplenomegaly may also see: testicular enlargement CNS involvement (HA, meningitis) sudden onset (thus ALL and not CLL)
26
What is the pathogenesis of ALL? What conditions make for a good/poor prognosis?
Chromosomal changes impact expression of transcription factors for normal hematopoietic cell development. Philadelphia chromosome t(9:22) is worse than t(12:21). Age 2-10 is better than either side. Worse if peripheral blast count exceeds 100000
27
Peripheral B-cell neoplasms are made of what type of cell?
mature B cells
28
Which leukemia is the most common among Western adults?
chronic lymphocytic leukemia (CLL)
29
Which is the only leukemia not associated with radiation or drug exposure?
chronic lymphocytic leukemia (CLL)
30
Which other d/o is morphologically, phenotypically, and genotypically indistinguishable from CLL? How can you tell the difference?
small lymphocytic lymphoma (SLL) the difference is the degree of lymphocytosis
31
How does CLL appear on a PBS?
small lymphocytes with condensed chromatin and scant cytoplasm. tumor cells can present as 'smudge cells'. their fast growth leads to poor membrane integrity.
32
What tissue is involved in all cases of CLL/SLL? Where does SLL like to go?
all cases involved the bone marrow. SLL infiltrates red and white pulp of the spleen as well as hepatic portal tracts.
33
What other cell types does CLL impact? How?
RBCs/platelets: AIHA and thrombocytopenia d/t dev. of Ab against them. agranulocytosis: inversely proportional to lymphocytes d/t taking up LN space.
34
How does CLL present clinically?
Age 50+ Asymptomatic LA or: wt loss, anorexia, DOE, organomegaly, abdominal fullness
35
What is the cardinal diagnostic criteria for CLL? SLL?
CLL: lymphocyte count greater than 45000 SLL: no blood lymphocytosis
36
What can SLL and CLL transform into? How frequently? How does this change prognosis?
Can become aggressive lymphoid neoplasms (prolymphocytic leukemia or diffuse large B-cell lymphoma) 10-30% of the time. Normal prognosis is 4-6 yr survival. With transformation, less than a year.
37
What is the most common form of NHL in the US?
follicular lymphoma....45% of adult cases
38
In follicular lymphoma, how often is lymphocytosis present? How often is the bone marrow involved? What other tissues are also frequently involved?
Lymphocytosis: 10% Bone marrow involvement: 85% Other tissue: white pulp of spleen and hepatic triads.
39
What abnormal cells will be found on histological examination of follicular lymphoma?
centrocytes: small lymphoid cells with condensed chromatin and irregular/cleaved nuclear outlines centroblasts: larger cells with nucleoli (look like Reed-Sternberg cells)
40
In follicular lymphoma, genetic translocation causes overexpression of which gene? How can this help differentiate a reactive from a neoplastic follicle histologically?
BCL2, an atagonist of apoptosis. Can use an immunohistochemical stain. Ractive follicle: will have a stained ring of BCL2 on the outside of the mantle zone. Neoplastic follicle: strong stain in the center.
41
Much like CLL, follicular lymphoma can undergo transformation into what? How does this impact prognosis?
A diffuse large B-cell lymphoma in 30-50% of cases. Follicular lymphoma has 7-9 yr survival normally. With transformation it less than 1 yr.
42
What is the most common presentation of follicular lymphoma?
painless, generalized LA
43
How does a diffuse large B-cell lymphoma appear morphologically?
large: 4-5X bigger than normal lymphocyte multiple nucleoli: 2-3 cytoplasm: abundant, pale or basophilic
44
What kind of transcription is involved in the pathogenesis of diffuse large B-cell lymphomas? Which gene is affected?
zinc finger transcription | BCL6 gene
45
Diffuse large B-cell lymphomas grow (fast or slow?). As a result they are often (symptomatic or asymptomatic?).
fast growing. symptomatic as a result.