Leukemia Flashcards

1
Q

What is cytogenetics

A

Cytogenetic testing is the examination of chromosomes to determine chromosome abnormalities such as aneuploidy and structural abnormalities.

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2
Q

What is Immunophenotype

A

Immunophenotyping is a technique that couples specific antibodies to fluorescent compounds to measure specific protein expression within a cell population.

The protein expression is used to identify and categorize the tagged cells.

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3
Q

What are the two types of leukemia

A

Acute

  • Sudden onset
  • Bone marrow blasts ≥ 20%
  • Progress quickly with devastating clinical course if untreated

Chronic

  • Insidious onset
  • Bone marrow blasts <20%
  • May persist for years even without treatment
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4
Q

What is the age differnce for Acute Myeloid vs Acute Lymophoblastic Leukemia

A

AML: OLD

ALL: KIDs
All kids get leukemia

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5
Q

If you see Auer Rods…

Think

A

AML

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6
Q

Auer Rods + Anemia+ Thrombocytopenia

Think

A

AML

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7
Q

What the age for AML

A

OLD

Think “Old Mamma Aymel”

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8
Q

What is the WHO classification for AML

A
  1. AML with recurrent genetic abnormalities
  2. AML with myelodysplasia-related changes
  3. Therapy-related AML
  4. AML, not otherwise specified (NOS)
  5. Myeloid sarcoma
  6. Myeloid proliferations related to Down syndrome
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9
Q

What are the 4 most common variants for AML

A

Four most common
-T(8;21)
—Good prognosis
—Most frequent genetic abnormality in kids with AML

-APL with the PML-RARA fusion gene
—Acute promyelocytic leukemia (APL)!!
—Good prognosis; responsive to treatment

-Inv(16)
—Good prognosis

-T(9;11)
—poorer prognosis

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10
Q

What is APL

Acute Promyelocytic Leukemia

A

Variant of AML
-Infiltration of the marrow by promyelocytes

Has a vary good prognosis

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11
Q

A pt presents with fatigue, pallor, weakness, palpitations, and dyspnea on exertion

+bruising, petechiae, epistaxis, and gingival bleeding

+GINGIVIAL HYPERTROPHY!!

Think

A

Acute Myelogenous Leukemia

Look for (Auer Rods) 
(Acute is > 20% Blasts) 

Treatment: relative emergency

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12
Q

Lymphoblastic that are accumulating in the meninges!!, gonads, thymus, liver, spleen or lymph nodes

Think

A

ALL

Acute Lymophoblastic Leukemia

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13
Q

Etiology of ALL

A

Originates in a single B- or T-lymphocyte progenitor

Proliferation and accumulation of clonal blast cells in the marrow result in suppression of hematopoiesis

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14
Q

How do you determine the subtype of ALL

A

Immunophenotyping

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15
Q

Classifications of ALL

A

B-ALL

  • With recurrent genetic abnormalities
  • Not otherwise specified

T-ALL

Early T Cell Precursor ALL

NK Cell ALL

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16
Q

Clinical presentation for ALL

A

Typically abrupt onset of symptoms

Variable presentation however, may also present insidiously

Fever
-Either from infection or from the leukemia itself

Pallor, fatigue, lethargy, weakness
Bone pain!!!!, arthralgia
-Leukemic expansion of the marrow or infiltration of the periosteum

Hepatomegaly, splenomegaly
Lymphadenopathy

Signs of bleeding
-Petechiae, purpura, epistaxis, gingival bleeding

17
Q

What is an essential Dx procedure for a kid with ALL

A

Examination of the cerebrospinal fluid (CSF) is an essential diagnostic procedure

Requires lumbar puncture to evaluate for potential leukemic involvement of the CNS

Presence of leukemic blasts in CNS requires intrathecal chemotherapy

18
Q

A WBC above 100,000 is indicative of…

A

Acute Leukemia

Emergency treatment is required witching 48hours

19
Q

CLL is considered identical to…

A

Non-Hodgkin Lymphoma

20
Q

Clinical presentation for CLL

A

Most common CA in western countries

As/s

Lymphadenopathy
(Cervical, Supraclavicular, and axillary)

Splenomegaly/Hepatomegaly

Immune Hemolytic Anemia

21
Q

What is the hallmark of CLL

A

Hallmark of CLL is isolated
Lymphocytosis

Cytopenias may be present but not severe
-Neutropenia, anemia, thrombocytopenia

22
Q

Peripheral smear for CLL

A

Small mature-appearing lymphocytes

+ smudge cells

23
Q

What is Richters Transformation

A

An isolated lymph node transforms into a diffuse large B cell lymphoma (very aggressive)

Sudden clinical deterioration characterized by:

  • Rapid development of B symptoms
  • Rapidly progressive lymphadenopathy
  • Increased splenomegaly
  • Increased lactate dehydrogenase (LDH)
  • Anemia and thrombocytopenia

5-8 months of survival

24
Q

Most cases of Therapy related AML are 2/2 s

A

Most cases associated with two classes of chemotherapeutic agents
-Alkylating agents (e.g., cyclophosphamide, cisplatin)
Treat solid tumors, CML, leukemia, lymphoma
Latency period 5-7 years

-Topoisomerase II inhibitors (e.g., etoposide, doxorubicin)
Treat solid tumors
Breast cancer, testicular cancer, small cell lung tumors