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pathology > WBC pathology > Flashcards

WBC pathology Flashcards

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
Q

What is the common presentation for patients with ALL?

A

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
Q

What is the pathogenesis of ALL? What conditions make for a good/poor prognosis?

A

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
Q

Peripheral B-cell neoplasms are made of what type of cell?

A

mature B cells

28
Q

Which leukemia is the most common among Western adults?

A

chronic lymphocytic leukemia (CLL)

29
Q

Which is the only leukemia not associated with radiation or drug exposure?

A

chronic lymphocytic leukemia (CLL)

30
Q

Which other d/o is morphologically, phenotypically, and genotypically indistinguishable from CLL?

How can you tell the difference?

A

small lymphocytic lymphoma (SLL)

the difference is the degree of lymphocytosis

31
Q

How does CLL appear on a PBS?

A

small lymphocytes with condensed chromatin and scant cytoplasm.

tumor cells can present as ‘smudge cells’. their fast growth leads to poor membrane integrity.

32
Q

What tissue is involved in all cases of CLL/SLL? Where does SLL like to go?

A

all cases involved the bone marrow.

SLL infiltrates red and white pulp of the spleen as well as hepatic portal tracts.

33
Q

What other cell types does CLL impact? How?

A

RBCs/platelets: AIHA and thrombocytopenia d/t dev. of Ab against them.

agranulocytosis: inversely proportional to lymphocytes d/t taking up LN space.

34
Q

How does CLL present clinically?

A

Age 50+
Asymptomatic LA or:
wt loss, anorexia, DOE, organomegaly, abdominal fullness

35
Q

What is the cardinal diagnostic criteria for CLL? SLL?

A

CLL: lymphocyte count greater than 45000
SLL: no blood lymphocytosis

36
Q

What can SLL and CLL transform into? How frequently? How does this change prognosis?

A

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
Q

What is the most common form of NHL in the US?

A

follicular lymphoma….45% of adult cases

38
Q

In follicular lymphoma, how often is lymphocytosis present? How often is the bone marrow involved? What other tissues are also frequently involved?

A

Lymphocytosis: 10%
Bone marrow involvement: 85%

Other tissue: white pulp of spleen and hepatic triads.

39
Q

What abnormal cells will be found on histological examination of follicular lymphoma?

A

centrocytes: small lymphoid cells with condensed chromatin and irregular/cleaved nuclear outlines
centroblasts: larger cells with nucleoli (look like Reed-Sternberg cells)

40
Q

In follicular lymphoma, genetic translocation causes overexpression of which gene?

How can this help differentiate a reactive from a neoplastic follicle histologically?

A

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
Q

Much like CLL, follicular lymphoma can undergo transformation into what?

How does this impact prognosis?

A

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
Q

What is the most common presentation of follicular lymphoma?

A

painless, generalized LA

43
Q

How does a diffuse large B-cell lymphoma appear morphologically?

A

large: 4-5X bigger than normal lymphocyte
multiple nucleoli: 2-3
cytoplasm: abundant, pale or basophilic

44
Q

What kind of transcription is involved in the pathogenesis of diffuse large B-cell lymphomas? Which gene is affected?

A

zinc finger transcription

BCL6 gene

45
Q

Diffuse large B-cell lymphomas grow (fast or slow?). As a result they are often (symptomatic or asymptomatic?).

A

fast growing. symptomatic as a result.

pathology (5 decks)

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