6: WBCs, LNs, Spleen, Thymus Flashcards

1
Q

NK Cell two markers

A

CD16, CD56

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2
Q

Early myeloblast marker vs early lymphoblast marker

A

Myeloblast: CD34

Lympho last: TdT

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3
Q

Leukocyte common antigen marker

A

CD45

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4
Q

Three B cell markers

A

CD19, CD20, Pax-5

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5
Q

Neutropenia vs agranulocytosis

A

Neutropenia: reduced neutrophils in blood
Agranulocytosis: marked neutropenia

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6
Q

Normal WBC range for blood

A

4.5-11

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7
Q

Typical differential for WBCs on blood sample

A
  1. 67% neutrophils
  2. 27% lymphocytes
  3. 4% monocytes
  4. 2% eosinophils
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8
Q

Absolute Neutrophil Count (ANC) equation***

A

% neutrophils + % bands x WBCs

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9
Q

What ANC is seriously low

A

<500

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10
Q

Examples of things that can cause severe neutropenia

A
  1. Not enough made: drugs, aplastic anemia, megaloblastic anemia
  2. Too much destroyed: immune destruction, hypersplenism
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11
Q

What happens as a result of severe neutropenia

A

Overwhelming infections (bacterial, fungal)

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12
Q

How to treat febrile neutropenic pts

A

Abx + G-CSF

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13
Q

4 Causes of Leukocytosis and examples of them

A
  1. Increased marrow production: chronic inflammation, paraneoplasm, myeloproliferative neoplasms
  2. Increased release from marrow store: acute/chronic inflammation
  3. Decreased margination: exercise, catecholamines
  4. Decreased extravasation into tissues: glucocorticoids
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14
Q

Major causes of the five types of leukocytosis (based on WBC)

A
  1. Neutrophilic: acute bacterial infection
  2. Eosinophilic: asthma, parasites, drug reactions
  3. Basophilic: rare, neoplasm
  4. Monocytosis: random infection/inflammation
  5. Lymphocytosis: viral infections
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15
Q

Acute suppurative lymphadenitis

A

Painful, fluctuant lymphadenitis with pus due to pyogenic organisms + prominent neutrophilic infiltrates

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16
Q

Sinus histiocytosis

A

Increased macrophages in LN sinuses seen in many conditions (malignancy, draining foreign material)

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17
Q

Three major contributors to white cell neoplasia

A
  1. Genetic mutations (proto-oncogenes)
  2. Viral infection (HTLV-1, EBC, HHV-8)
  3. Chronic infection (H pylori)
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18
Q

Leukemia vs lymphoma

A

Leukemia: blood/bone marrow neoplasia
Lymphoma: LN neoplasia

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19
Q

What causes fever, fatigue, cruising, pain, and HA in ALL?

A
  1. Fever: opportunistic infection
  2. Fatigue: anemia
  3. Bleeding/bruising: no platelets
  4. Pain: expansion of cells
  5. HA: goes to the meninges
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20
Q

What is BCL-2?

A

Apoptosis suppressor

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21
Q

How to demonstrate clonality and light chain restriction in B cell clonal neoplasms?

A

Flow cytometry

22
Q

What does MGUS stand for?

A

Monoclonal gammopathy of undetermined significance

23
Q

What does protein electrophoresis do

A

Separate proteins according to charge

24
Q

Two light chains in Abs

A

Kappa, lambda

25
What does the CRAB criteria help diagnose?**
Myeloma
26
Explain renal insufficiency in myeloma
Igs are filtered through -> clog tubes and damage tubular ep + create Bence-Jones proteins + systemic AL amyloidosis (light chain amyloids)
27
What does urine look like in renal insufficiency in myeloma
Proteinuria due to light chains spilled into urine
28
Three causes of anemia in CRAB criteria in myeloma
1. Marrow infiltration of myeloma 2. IL-6 and other cytokines 3. Renal disease / decreased EPO
29
LNs involves in Hodgkin vs Non-Hodgkin lymphoma
Hodgkin: more localized, orderly spread, extranodal presentation is rare Non-Hodgkin: multiple peripheral nodes, noncontiguous spread, extranodal presentation common
30
How do we Dx ALL, B cell NHL, and myelomas vs Hodgkin Lymphoma
ALL, BCNHL, Myeloma: morphology, staining, flow cytometry | HL: morphology and staining**
31
Why is Hodgkin lymphoma not great with flow cytometry
Cells that are neoplastic clones are too diluted by other cells
32
Aleukemic leukemia
Nothing in peripheral blood
33
Mechanism of AML with t(8;21) genetic feature
RUNX1-RUNX1T1 fusion -> disrupts core binding factors in hematopoeitic differentiation
34
Translocation and mechanism in Acute Promyelocytic Leukemia
PML/RARa translocation -> RAR does not want RA anymore -> differentiation stalls -> accumulation of leukemic blasts
35
How to treat Acute Promylelocytic Leukemia
All-trans RA that the RAR will actually accept
36
Some unusual presentations of AML
ST mass formation, granulocytic sarcoma/myeloid sarcoma/Chloroma (greenish tumors)
37
RAEB II
Refractory anemia with excess blasts II, found in myelodysplastic syndrome
38
Four types of myeloproliferative neoplasms
1. Chronic myeloid leukemia 2. Polycythemia Vera 3. Essential thrombocythemia 4. Primary myelofibrosis
39
Eosinophilic granuloma
Eosinophils predominating in a unisystem LCH
40
Functions of the spleen
1. Phagocytosis 2. Ab production 3. Hematopoeisis 4. Sequestration of blood cells
41
Two causes of splenomegaly
1. Reactive splenitis due to viral infection | 2. Congestive splenomegaly: due to hepatic dysfunction
42
What does hypersplenism cause
Cytopenias
43
ITP: idiopathic thrombocytopenic purpura
Platelets are opsonized, spleen clears them
44
Two big causes of splenic rupture
Trauma, mononucleosis
45
Type of malignancy that most commonly causes splenic neoplasia
Hematologic malignancies
46
Two major causes of splenic infarct
1. Outgrows its vascular supply | 2. Clog, like in sickle cell (cause it has no collaterals, just one A and V)
47
Three major pathologies of the thymus to know
1. Thymic hyperplasia 2. Thymoma 3. Myasthenia gravis
48
Myasthenia gravis
Auto-Abs produced in either thymic hyperplasia or thymoma
49
What organism is it important to look out for in neutropenic fever
Pseudomonas aeruginosa
50
How does DIC start from APL
APL leukemic cells display tissue factor on surface -> starts coagulation cascade -> lots of clots