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Heme Week 2 > Pathoma Chapter 6: Part 1 > Flashcards

Pathoma Chapter 6: Part 1 Flashcards

1
Q

Myeloid stem cells give rise to what?

A
  • Erythroblasts (RBCs)
  • Myeloblasts (neutrophils, basophils, eosinophils)
  • Monoblasts (monocytes)
  • Megakaryoblasts (Megakaryocytes)
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2
Q

What is a normal white cell count?

A

4.4-11.3 K/ul

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3
Q

What are some causes of neutropenia?

A
  • drug toxicity (chemo with alkylating agents)

- severe infection (gram- species)

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4
Q

How do chemo alkylating agents cause neutropenia?

A

they damage stem cells resulting in decreased production

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5
Q

How do severe infections cause neutropenia?

A

increased movement of neutrophils into tissue results in decreased circulating neutrophils

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6
Q

What are some causes of lymphopenia?

A
  • immunodeficiency (DiGeorge or HIV)
  • High cortisol state (Cushing’s of exogenous corticosteroids)
  • Autoimmune destruction (SLE)
  • Whole body radiation
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7
Q

How does a high cortisol state cause lymphopenia?

A

it induces apoptosis of lymphocytes

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8
Q

What are some causes of eosinophilia?

A
  • type I hypersensitivity
  • parasitic infections
  • Hodgkin lymphoma
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9
Q

What are some causes of basophilia?

A
  • acute myeloid leukemia
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10
Q

What are some causes of lymphocytosis?

A
  • viral infections
  • Bordetella pertussis infection (via lymphocytosis promoting factor secreted by the bacteria which prevents them from leaving blood to enter lymph)
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11
Q

What is acute leukemia?

A

neoplastic proliferation of blasts; defined as an accumulation of 20+% of blasts in the bone marrow or peripheral blood

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12
Q

Why is it called “acute” leukemia?

A

increased blasts crowd-out normal hematopoiesis, resulting in an acute presentation

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13
Q

Clinical presentation of acute leukemia?

A
  • anemia (fatigue)
  • thrombocytopenia (bleeding)
  • possible neutropenia (infection)
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14
Q

T or F. WBC is usually elevated in acute leukemia

A

T. due to blasts entering the blood stream

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15
Q

What is acute lymphoblastic leukemia defined as?

A

accumulation of 20+ % of lymphocytes in the bone marrow

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16
Q

How are lymphoblasts identified?

A

via positive nuclear staining for TdT, a DNA polymerase

TdT is absent in myeloid blasts and mature lymphocytes

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17
Q

ALL is common in what patient population?

A 
usually kids (associated with down syndrome)
presents after 5 y/o typically
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18
Q

Subclasses of ALL?

A

B-ALL (most common) and T-ALL based on surface markers

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19
Q

How is B-ALL identified?

A

usually characterized by lymphoblasts (TdT) that express CD10, CD19, and CD20.

20
Q

Clinical course for B-ALL?

A

requires prophylaxis to scrotum and CSF- great response

21
Q

Prognosis of B-ALL?

A

based on cytogenetic abnormalities

i. t(12,21)-kids- has a good prognosis
ii. t(9,22)-adults- has a poor prognosis (philadelphia)

22
Q

What is T-ALL characterized by?

A

lymphoblasts (TdT+) that express markers ranging from CD2 to CD8 (e.g. CD3/4/7).

don’t express CD10

23
Q

What patient population is common for T-ALL?

A

usually presents in teenagers as a mediastinal (thymic) mass (called acute lymphoblastic lymphoma because the malignant cells form a mass)

24
Q

What is acute myeloid leukemia defined as?

A

20+% of immature myeloid precursors (myeloblasts) in the bone marrow

25
Q

How are myeloblasts identified?

A

positive cytoplasmic staining for MPO (crystals of MPO commonly seen as Auer rods)

26
Q

Patient population for AMLs?

A

older adults (avg 50-60 y/o)

27
Q

High-yield subtypes of AML (based on cytogenetics, lineage of immature myeloid cells, and surface markers):

A
  • Acute promyelocytic leukemia (APL)
  • Acute monocytic leukemia
  • Acute megakaryoblastic leukemia
28
Q

What causes APL?

A

t(15,17) PML-RARa. The fusion protein causes enhancement of RARa function, which is to disrupt myeloid differentiation, but proliferation is unaffected so promyeloblasts accumulate

29
Q

What is a common risk associated with APL?

A

DIC

30
Q

What is the treatment for APL?

A

ATRA (vitamin A derivative) which binds the receptor and causes the blasts to mature (and eventually die)

31
Q

What causes acute monocytic leukemia?

A
  • proliferation of mono blasts that usually lack MPO

- these blasts characteristically infiltrate gums

32
Q

What causes acute megakaryocytic leukemia?

A

-proliferation of megakaryoblasts that usually lack MPO

33
Q

What is acute megakaryocytic leukemia associated with? When does it present?

A

Down syndrome (usually arise BEFORE age 5)

34
Q

What else can AML arise from?

A

-pre-existing dysplasia (myelodysplastic syndromes)

35
Q

How does myelodysplastic syndromes usually present?

A
  • cytopenias
  • hyper cellular bone marrow
  • increased blasts (but less than 20%)
36
Q

Outcome of myelodysplastic syndrome patients?

A

most die from infection or bleeding, though some progress to acute leukemia

37
Q

What causes chronic leukemia?

A

neoplastic proliferation of mature circulating lymphocytes (high WBC count)

38
Q

Patient population for chronic leukemia?

A

insidious onset in older adults

39
Q

What causes chronic lymphocytic leukemia (CLL)?

A

neoplastic proliferation of naive B cells that co-express CD5 and CD20 (most common leukemia overall)

40
Q

What are some complications with CLL?

A
  • hypogammaglobinemia
  • autoimmune hemolytic anemia
  • Transformation to diffuse large B-cell lymphoma (Richter transformation)
41
Q

Hairy cell leukemia (HCL) patients are positive for what?

A

TRAP (tartrate-resistant acid phosphatase)

42
Q

Clinical features of HCL?

A
  • splenomegaly due to accumulation of hairy cells in red pulp
  • dry tap on bone marrow aspiration (due to marrow fibrosis)
  • no lymphadenopathy
43
Q

How is HCL treated?

A

excellent response to 2-CDA (Cladribine), an adenosine deaminase inhibitor

44
Q

What is adult T-cell leukemia/lymphoma (ATLL) caused by?

A

neoplastic proliferation of mature CD4+ T cells

associated with HTLV-1

45
Q

Clinical presentation of ATLL?

A
  • rash (skin infiltration)
  • generalized lymphadenopathy with hepatosplenomegaly
  • lytic (punched out) bone lesions with hypercalcemia
46
Q

Normal counterpart in mycosis fungicides (chronic leukemia type)?

A

mature CD4 T cells

47
Q

When MF spreads to include peripheral blood it is called _____.

A

Sezary syndrome

Heme Week 2 (18 decks)

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