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Heme and Lymph Final > DSA: Leukemias and Lymphomas and White cell disorders (from the end of week 2) > Flashcards

DSA: Leukemias and Lymphomas and White cell disorders (from the end of week 2) Flashcards

1
Q

Acute Leukemia EOD

A
  • short duration of symptoms, including fatigue, fever, and bleeding
  • cytopenias or pancytopenia
  • more than 20% blasts in the bone marrow
  • blasts in peripheral blood in 90% of patients
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2
Q

What cell is malignant in Acute leukemia?

A

hematopoietic progenitor cell

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3
Q

What are the clinical findings in acute leukemia due to?

A

replacement of normal bone marrow elements by the malignant cells

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4
Q

What is AML in relation to acute leukemia?

A

a myeloblastic subtype of it

-60 years

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5
Q

What is Acute Promyelocytic anemia characterized by?

A

t(15;17)

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6
Q

What does the t(15;17) make?

A

PML-RAR-alpha

  • blocks retinoic acid…. blocks differntiation
  • can be overcome with retinoic acid
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7
Q

What is the lymphoblastic subtype of acute leukemia?

A

ALL

  • acute lymphoblastic leukemia
  • mostly childhood
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8
Q

AML

A
  • t(8;21) is the a good diagnosis
  • inv(16) is good too
  • monosomy 5 or 7 is bad
  • FLT3 is bad too
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9
Q

APL

A
  • t(15;17)
  • PML-RAR-alpha
  • response to non-chemotherapy treatments
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10
Q

ALL

A
  • hyperdiploidy and t(12;21) is good

- hypodiploidy and t(9;22) and t(4;11) is bad

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11
Q

Mixed Phenotype Acute leukemias

A
  • has blasts that lack differentiation along the lymphoid or myeloid lineage or blasts that express both myeloid and lymphoid lineage-specific antigens
  • high risk and poor prognosis
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12
Q

How do these acute leukemia patients present?

A
  • bleeding
  • infections… we need to treat them or they’ll die
  • gum hypertrophy and bone and joint pain
  • hyperleukocytosis, elevated blast count, impaired circulation, present as headache, confusion, and dyspnea
  • Patients will be pale and have purpura and petechiae
  • rectal fissures`
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13
Q

Lab findings of acute leukemia

A

-pancytopenia and circulating blasts
-bone marrow hypertrophy and dominated by blasts
-pts with ALL with have a mediastinal mass visible on chest radiograph
-Auer rods!!!!! secure the diagnosis
-MPO +
-

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14
Q

What is CD10 known as?

A

the common ALL antigen

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15
Q

differential diagnosis with AML?

A

-myeloproliferative disorders, CML, and myelodysplastic syndromes
-left shifted bone marrow recovering from a previous toxic insult
-

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16
Q

Tx of AML?

A

-anthracycline (rubicin)
-cytarabine
-stem cell transplantation maybe later down the road
-if over 60, bad prognosis
-

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17
Q

Tx of ALL?

A

chemotherapy

-if Ph chromsome is there, kinase inhibitor like dasatinib

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18
Q

prognosis of AML

A

-good if under 60

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19
Q

prognosis for ALL

A

-good if younger than 39 years

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20
Q

Chronic Lymphocytic Leukemia

A
  • B-cell lymphocytosis greater than 5000

- Coexpression of CD19, CD5 on lymphocytes

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21
Q

What is CLL a malignancy of?

A

B- cells

-it’s usually indolent, slowly progressive accumulation of them

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22
Q

How is CCL manifested clinically?

A

by immunosuppression, bone marrow failure, and organ infiltration
-the B cells don’t make normal antibody

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23
Q

Symptoms of CLL

A
  • older ppl
  • lymphocytosis
  • LAD
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24
Q

What is the Rai classification of CLL?

A
  • 0: lymphocytosis only
  • 1: +LAD
  • 2: +organomegaly
  • 3: +anemia
  • 4: +thrombocytopenia
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25
Q

In about 5% of cases of CLL, while the systemic disease remains stable, an isolated lymph node transforms into and aggressive large cell lymphoma… what’s that called?

A

-Richter Syndrome

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26
Q

Lab findings for CLL

A

-hallmark is lymphocytosis
-WBC >20,000
-distinguished from mantle cell lymphoma by presence of CD23 and absence of Cyclin D1 mutation
-if cells have mutated Ig, that’s good!
-if they have ZAP-70, we need to worry
-del 17p (TP53) is the worst prognosis
-

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27
Q

Tx pf CLL

A
  • most cases no specific therapy, observation
  • if bad, cyclophosphamide and fludarabine
  • in older ppl, chlorambucil with obinutuzumab
  • if relapsed or refractory disease, ibrutinib and idelalisib
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28
Q

When should Fludarabine be avoided?

A

in patients with autoimmune hemolytic anemia

-it could exacerbate it

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29
Q

prognosis of CLL?

A

pretty good if it isn’t stage 3 or 4

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30
Q

EOD for CML

A
  • elevated white blood count
  • markedly left-shifted myeloid series but with a low percentage of promyelocytes and blasts
  • Presence of bcr/abl gene (Philadelphia chromosome)
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31
Q

What is CML?

A

it’s just an overproduction of myeloid cells

-remember (9;22)

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32
Q

What happens if CML is untreated?

A

it progresses to an accelerated and then acute blast phase… indistinguishable from acute leukemia

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33
Q

Symptoms of CML

A
  • middle age
  • fatigue, night sweats, fevers
  • enlarged spleen
  • sternal tenderness from marrow overproduction
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34
Q

CML lab findings

A
  • myeloid left shift!!! immature cells
  • hypercellular bone marrow
  • bcr-abl gene
  • the blast phase of CML is diagnosed when blasts are more than 20%
35
Q

tx of CML

A
  • not emergent
  • tyr kinase inhibitor
  • imantinib
36
Q

NHL EOD

A
  • often present with painless LAD

- Pathologic diagnosis of lymphoma is made by pathologic examination of tissue

37
Q

What translocation does Burkitt lymphoma have?

A

t(8;14)

-c myc!

38
Q

Follicular lymphomas translocation

A

t(14;18)

-BCL2

39
Q

Once pathologic diagnosis is established, what do we do next?

A

STAGE IT using whole body PET/CT scan, a bone marrow biopsy, and lumbar puncture if they are really bad

40
Q

Lab findings with NHL

A

-paratrabecular monoclonal lymphoid aggregates in bone marrow

41
Q

What lab finding has an influence on the prognosis of NHL?

A

serum LD

42
Q

Tx of indolent NHL

A
  • follicular, marginal zone, and small lymphocytic lymphoma (CLL)
  • depends on stage
  • localized radiation
  • if disseminated, treat only if symptoms come up
43
Q

Tx of aggressive NHL

A
  • DLBCL
  • short course immunotherapy if localized RCHOP + radiation or 6 cycles of immunochemotherapy without radiation
  • peripheral T-cell lymphomas don’t respond as well to radiation
44
Q

What are factors that mean bad prognosis in NHL?

A
  • > 60
  • elevated serum LD
  • Stage 3 or 4 disease
  • more than one extranodal site of disease
  • poor performance state
45
Q

In treatment of AML, what do we use for induction, consolidation, and maintenance?

A
  • induction: 5+7 (anthracycline and Ara-C)
  • Consolidation: High dose Ara-C (HDAC)
  • Maintenance: All trans retinoic acid (ATRA)… remember that this is for APL ONLY
46
Q

What is APL again?

A
  • Acute promyelocytic leukemia
  • accumulation of granulocytes called promyelocytes
  • M3 subtype of AML
  • responds well to ATRA
47
Q

In treatment of ALL, what do we use for induction, consolidation, and maintenance?

A
  • induction: vincristine+prednisone
  • consolidation: multiple agents+ CNS prophylaxis (MTX or Ara-C)
  • Maintenance: 6MP and MTX
48
Q

Hairy Cell Leukemia

A
  • indolent B-cell lymphoma
  • middle aged males
  • CD103 is the “unique” hairy cell antigen
  • BRAF mutation
  • high levels of IL-2 in serum
  • severe monocytopenias, so infections happen
  • pancytopenia and splenomegaly
  • TRAP resistant
  • treat with 2-Chlorodeoxyadenosine (cladribine)
49
Q

Go through the Rai staging system again.

A

0: Lymphocytosis only
1: +LAD
2: +HSM
3: +anemia
4: +thrombocytopenia
- remember, this is for CLL

50
Q

EOD of Gastric Lymphoma

A
  • symptoms of dyspepsia, weight loss, or anemia
  • variable abnormalities on upper GI series or endoscopy including thickened folds, ulcer, mass, or infiltrating lesions; diagnosis established by endoscopic biopsy
  • abdominal CT and EUS require for staging
51
Q

What kinds of lymphomas are Gastric lymphomas usually?

A
  • Non hodgkin B cell lymphoma

- believed to arise from MALT

52
Q

What is an important risk factor the development of primary gastric lymphoma?

A

-infections with H. pylori

53
Q

clinical findings for Gastric lymphoma

A
  • ab pain, weight loss, or bleeding

- looks like ulcer

54
Q

What should probably be performed if we have Gastric lymphoma?

A

EUS

  • endoscopic ultrasound
  • gives us the stage
55
Q

Tx of Gastric lymphoma

A
  • eradicate H. pylori
  • Endoscopic surveilence every 6 months
  • if we see mutations, radiation maybe required
  • don’t do surgical resection, radiation and chemotherapy will do just fine
56
Q

EOD for Hodgkin Lymphoma

A
  • often painless LAD
  • constitutional symptoms may or may not be present
  • Pathologic diagnosis by lymp node biopsy
57
Q

Clinical findings with HL

A
  • RS cells
  • bimodal age distribution
  • painless mass, commonly in neck
  • constitutional symptoms are fever, weight loss, drenching night sweats and stuff like that
  • pain in lymph node following alcohol ingestion
  • spreads in orderly fashion
  • don’t confuse it with reactive lymphocytosis
58
Q

What is the Ann Arbor staging thing for HL?

A
  • 1: 1 lymph node region involved
  • 2: involvement of 2 or more lymph node regions on one side of the diaphragm
  • 3: lymph node regions involved on both sides of diaphragm
  • 4: disseminated disease with extranodal involvement
  • it’s “A” if there are no constitutional symptoms
  • “B” if there is 10% weight loss over 6 months, fever, or drenching night sweats
59
Q

Tx of HL

A
  • Chemotherapy: ABVD
  • doxorubicin, bleomycin, vinblastine, dacarbazine
  • remember that fibrosis happens with bleomycin
60
Q

What are the 7 things that influence the prognosis of HL?

A
  • Age
  • Stage
  • gender
  • Hgb
  • albumin
  • WBC count
  • lymphocyte count
61
Q

What does the prognosis work for HL?

A
  • 75% if 0-2 risk factors

- 55% when 3 or more

62
Q

When do we see a bad prognosis for HL?

A
  • older
  • bulky disease
  • lymphocyte depletion or mixed cellularity on histologic exam
63
Q

What is a normal peripheral WBC count?

A

7500

64
Q

What is a Leukamoid reaction

A

WBC >50,000

-can be from infections

65
Q

What are some secondary causes of Leukocytosis?

A
  • Chronic Inflammation
  • Ciggarette smoking
  • Stress (catecholamines release marginated pool)
  • Drug induced
  • nonhematologic malignancy
  • marrow stimulation from destructin of RBCs and platelets
66
Q

What is it called when non hematopoietic entities invade the bone marrow?

A

-myelophthisis

67
Q

What are some primary causes of Neutrophilia?

A
  • Hereditary neutrophilia (constant G-CSF on auto dominant)
  • Pelger Huet: looks like a left shift but not
  • Down syndrome: GATA1 mutation
  • Leukocyte Adhesion Deficiency (LAD): delayed separation of umbilical cord
  • Familial Cold Urticaria: rash and hurts when cold
  • post splenectomy
68
Q

How do we tell CML apart from a leukamoid reaction

A

CML has abnormalities in more than one cell line
-t(9;22)
-low LAP (leukocyte alkaline phosphatase) score in CML
-

69
Q

What is Monocytosis defined as?

A

> 500

70
Q

What is eosinophilia defined as?

A

> 400

71
Q

What is neutopenia defined as?

A

<1500

72
Q

Does benign or ethnic familial neutropenia show any increased risk for infection?

A

no

73
Q

What is Cyclic neutropenia?

A
  • periodic neutropenia that lasts about 3-5 days and occurs at 21 day intervals
  • neturophil elastase gene probs
74
Q

Schwachman Diamond syndrome

A
  • isolated neutropenia at first
  • skeletal and pancreas problems
  • SBDS gene: regulation of ribosomal RNA
  • increased risk for leukemic transformation
75
Q

Fanconi Anemia

A
  • mutations involved in DNA repair
  • takes more time for marrow failure to develop
  • short, upper limb anomalies, hyperpigmented cafe au lait spots
76
Q

Dyskeratosis congenita (DKC)

A
  • nail dystrophy, leukoplakia, and skin pgmentation

- neutropenia

77
Q

Chediak-Higashi syndrom

A
  • albinism and neutropenia
  • defects in vesicular trafficking
  • LYST gene
78
Q

what is the most common cause of neutropenia?

A

drug induced neutropenia

-neutrophil recovery is speeded by G-CSF

79
Q

What complement molecule renders neutrophils more adherent and thereby prone to aggregation within the pulmonary vasculature?

A

C5a

  • this happens with pts suffering burns and transfusion rxns
  • PNH
80
Q

What is the characteristic finding in the setting of megaloblastic anemia?

A

hypersegmentation of the neutrophil

81
Q

What is standard treatment for CML?

A

Imatinib mesylate

82
Q

Splenomegaly, cytopenia, and nonaspirable bone marrow in a middle aged man… what do we think of?

A

HCL

83
Q

What is CLL characterized by?

A

lymphocyte counts that range from 5,000-600,000
*if they have autoimmune hemolytic anemia superimposed onto it, the erythroid hyperplasia can be masked by the lymphocyte infiltration of the bone marrow

Heme and Lymph Final (14 decks)

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