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2: SBL Exam 1 > 6: WBCs, LNs, Spleen, Thymus > Flashcards

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
Q

What does the CRAB criteria help diagnose?**

A

Myeloma

26
Q

Explain renal insufficiency in myeloma

A

Igs are filtered through -> clog tubes and damage tubular ep + create Bence-Jones proteins + systemic AL amyloidosis (light chain amyloids)

27
Q

What does urine look like in renal insufficiency in myeloma

A

Proteinuria due to light chains spilled into urine

28
Q

Three causes of anemia in CRAB criteria in myeloma

A
  1. Marrow infiltration of myeloma
  2. IL-6 and other cytokines
  3. Renal disease / decreased EPO
29
Q

LNs involves in Hodgkin vs Non-Hodgkin lymphoma

A

Hodgkin: more localized, orderly spread, extranodal presentation is rare
Non-Hodgkin: multiple peripheral nodes, noncontiguous spread, extranodal presentation common

30
Q

How do we Dx ALL, B cell NHL, and myelomas vs Hodgkin Lymphoma

A

ALL, BCNHL, Myeloma: morphology, staining, flow cytometry

HL: morphology and staining**

31
Q

Why is Hodgkin lymphoma not great with flow cytometry

A

Cells that are neoplastic clones are too diluted by other cells

32
Q

Aleukemic leukemia

A

Nothing in peripheral blood

33
Q

Mechanism of AML with t(8;21) genetic feature

A

RUNX1-RUNX1T1 fusion -> disrupts core binding factors in hematopoeitic differentiation

34
Q

Translocation and mechanism in Acute Promyelocytic Leukemia

A

PML/RARa translocation -> RAR does not want RA anymore -> differentiation stalls -> accumulation of leukemic blasts

35
Q

How to treat Acute Promylelocytic Leukemia

A

All-trans RA that the RAR will actually accept

36
Q

Some unusual presentations of AML

A

ST mass formation, granulocytic sarcoma/myeloid sarcoma/Chloroma (greenish tumors)

37
Q

RAEB II

A

Refractory anemia with excess blasts II, found in myelodysplastic syndrome

38
Q

Four types of myeloproliferative neoplasms

A
  1. Chronic myeloid leukemia
  2. Polycythemia Vera
  3. Essential thrombocythemia
  4. Primary myelofibrosis
39
Q

Eosinophilic granuloma

A

Eosinophils predominating in a unisystem LCH

40
Q

Functions of the spleen

A
  1. Phagocytosis
  2. Ab production
  3. Hematopoeisis
  4. Sequestration of blood cells
41
Q

Two causes of splenomegaly

A
  1. Reactive splenitis due to viral infection

2. Congestive splenomegaly: due to hepatic dysfunction

42
Q

What does hypersplenism cause

A

Cytopenias

43
Q

ITP: idiopathic thrombocytopenic purpura

A

Platelets are opsonized, spleen clears them

44
Q

Two big causes of splenic rupture

A

Trauma, mononucleosis

45
Q

Type of malignancy that most commonly causes splenic neoplasia

A

Hematologic malignancies

46
Q

Two major causes of splenic infarct

A
  1. Outgrows its vascular supply

2. Clog, like in sickle cell (cause it has no collaterals, just one A and V)

47
Q

Three major pathologies of the thymus to know

A
  1. Thymic hyperplasia
  2. Thymoma
  3. Myasthenia gravis
48
Q

Myasthenia gravis

A

Auto-Abs produced in either thymic hyperplasia or thymoma

49
Q

What organism is it important to look out for in neutropenic fever

A

Pseudomonas aeruginosa

50
Q

How does DIC start from APL

A

APL leukemic cells display tissue factor on surface -> starts coagulation cascade -> lots of clots

2: SBL Exam 1 (10 decks)

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