Acute vs. Chronic Leukemia

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Questions and Answers

In acute leukemia, why does suppressed normal hematopoiesis lead to anemia, infection, and bleeding?

  • Abnormal precursor clones directly attack and destroy normal blood cells.
  • The bone marrow vasculature becomes damaged, causing leakage of blood and immune cells.
  • The accelerated maturation of all blood cell lines exhausts the bone marrow's regenerative capacity.
  • There is decreased production of red blood cells, insufficient mature neutrophils, and reduced platelet formation due to marrow overcrowding. (correct)

Which of the following best describes the difference in cell maturation between acute and chronic leukemia?

  • In acute leukemia, cells proliferate slowly and mature properly; in chronic leukemia, cells proliferate rapidly with maturation arrest.
  • In acute leukemia, cells proliferate rapidly and mature properly; in chronic leukemia, cells proliferate slowly with maturation arrest.
  • In acute leukemia, cells proliferate rapidly with maturation arrest; in chronic leukemia, cells mature properly but proliferate rapidly. (correct)
  • In acute leukemia, cells mature properly but at an increased rate; in chronic leukemia, cell maturation is entirely suppressed.

What is the MOST immediate consequence of the rapid proliferation of leukocyte precursors in acute leukemia?

  • Increased apoptosis of healthy bone marrow cells due to competition for resources.
  • Hyperactivity of mature leukocytes, leading to systemic inflammation.
  • Reduced production of growth factors necessary for immune cell development.
  • An overwhelming environment in the bone marrow, leading to suppressed normal hematopoiesis. (correct)

Why do external factors like alkylating agents, carcinogens, and radiation increase the risk of developing leukemia?

<p>They induce mutations in hematopoietic stem cells, leading to a proliferation advantage and differentiation arrest. (A)</p> Signup and view all the answers

A patient presents with fatigue, fever, and bleeding tendencies. Blood tests reveal a high number of immature cells and a low number of mature blood cells. This clinical presentation is MOST indicative of which condition?

<p>Acute Leukemia (A)</p> Signup and view all the answers

A patient diagnosed with Acute Myeloid Leukemia (AML) is undergoing chemotherapy. Which mechanism explains why hyperuricemia is a common complication during treatment?

<p>The rapid breakdown of leukemic cells releases intracellular contents, including purines that are metabolized to uric acid. (D)</p> Signup and view all the answers

A patient with Acute Myeloid Leukemia (AML) is at risk of developing tumor lysis syndrome (TLS) after starting chemotherapy. Beyond hyperuricemia, which electrolyte abnormalities are associated with TLS?

<p>Hyperkalemia, hyperphosphatemia, and hypocalcemia. (A)</p> Signup and view all the answers

Which of the following genetic abnormalities is associated with Acute Promyelocytic Leukemia (APL)?

<p>t(15;17)(q22;q11-12) (B)</p> Signup and view all the answers

All-trans retinoic acid (ATRA) is a common treatment used for a specific subtype of acute myeloid leukemia due to its ability to induce differentiation. Which AML subtype benefits from ATRA treatment?

<p>Acute Promyelocytic Leukemia (A)</p> Signup and view all the answers

What cytogenetic abnormality defines Core Binding Factor (CBF) leukemias?

<p>Inversion or Translocation involving chromosome 16 or translocation involving chromosomes 8 and 21. (B)</p> Signup and view all the answers

Which genetic abnormality is associated with a subtype of AML that often presents with gingival and skin involvement?

<p>t(9;11)(p21.3;q23.3) (A)</p> Signup and view all the answers

What morphological feature is characteristic of Acute Myeloid Leukemia with t(8;21)(q22;q22.1)?

<p>Cells with Auer rods in myelocytes and mature segmenters and abnormal granules. (B)</p> Signup and view all the answers

A patient with suspected acute leukemia has abnormal granules in their eosinophils within the bone marrow. Which genetic abnormality is MOST likely to be present?

<p>inv(16)(p13.1q22) (B)</p> Signup and view all the answers

Why is Disseminated Intravascular Coagulation (DIC) a common complication in Acute Promyelocytic Leukemia (APL)?

<p>The procoagulant activity of primary granules released from promyelocytes. (D)</p> Signup and view all the answers

What is the main difference between therapy-related myeloid neoplasms (t-MN) and de novo acute myeloid leukemia?

<p>t-MN is associated with previous exposure to cytotoxic agents. (B)</p> Signup and view all the answers

Which of the following acute myeloid leukemia subtypes has the poorest prognosis?

<p>AML with t(6;9)(p23;q34.1) (D)</p> Signup and view all the answers

A Prussian stain is performed on a bone marrow sample to identify ring sideroblasts. This finding is MOST relevant in diagnosing which subtype of acute myeloid leukemia (AML)?

<p>Pure Erythroid Leukemia (A)</p> Signup and view all the answers

Cutaneous infiltration and bleeding disorders are MOST commonly associated with which subtype of acute myeloid leukemia (AML)?

<p>Acute Monoblastic and Monocytic Leukemia (A)</p> Signup and view all the answers

Which of the following features is characteristic of acute megakaryoblastic leukemia?

<p>More than 50% of blast cells are of megakaryocytic origin. (D)</p> Signup and view all the answers

A patient is diagnosed with Myeloid Sarcoma. What is the defining characteristic of this condition?

<p>Extramedullary proliferation of blasts with tissue architecture disruption. (D)</p> Signup and view all the answers

Flashcards

Acute Leukemia

Rapid proliferation of leukocyte precursors in bone marrow, leading to precursors prematurely entering circulation, suppressing normal hematopoiesis.

Acute Leukemia: WBC Count

Excess accumulation of immature cells in the bone marrow and peripheral blood.

Chronic Leukemia: WBC Count

Proliferation and accumulation of mature cells of a specific lineage, developing gradually.

General Characteristics of Leukemia

Cancers with mutations from external factors (carcinogens, radiation) or inherited gene mutations, leading to rapid division and failure to mature properly.

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Acute Myeloid Leukemia (AML)

Acute Myeloid Leukemia, affects all ages, resembles acute infection, requires 20% blasts for diagnosis. Key antigens: MPO, CD13, CD33, CD177.

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AML: Infiltration effects

Disseminated Intravascular Coagulation: Malignant cells infiltrate the gums and other mucosal sites, leading to bleeding.

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Hyperuricemia in AML

Hyperuricemia in AML, especially during chemotherapy, occurs due to tumor lysis syndrome as cells release purines, overwhelm kidneys.

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Tumor Lysis Syndrome (TLS)

Rapid cancer cell breakdown releases intracellular contents like potassium, phosphate, purines, leading to hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia.

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AML with t(8;21)(q22;q22.1)

Core Binding Factor Leukemia. ≥20% blasts, large blasts with basophilic cytoplasm, Auer rods in myelocytes, nuclear dysplasia. CD13, CD33, CD117, CD19, CD34.

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AML with inv(16)

Proliferation of myeloid and monocytic precursors; increased eosonophils. inv(16)(p13.1q22) or t(16;16)(p13.1;q22), Granulocytic Markers: CD13, CD15, CD33, CD65, MPO.

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APL with t(15;17)(q22;q11-12)

Fusion of retinoid acid receptor gene-α with PML gene. Auer rods frequently found. Risk for disseminated intravascular coagulation. Treat with ATRA.

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AML with t(9;11)

Monocytic differentiation; gingival/skin involvement. Blasts large with abundant cytoplasm and fine nuclear chromatin. CD33, CD65, CD4, HLA-DR..

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Therapy-Related Myeloid Neoplasms

Complex karyotypes, TP53 mutations. Develops secondary to prior cytotoxic therapy (alkylating agents or topoisomerase II inhibitors)

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Acute Myeloid Leukemia with Minimal Differentiation

Accounts for <5% of AML; is generally either infants or older adults; large agranular blasts; FAB Classification M0, MPO = NEGATIVE; SBB = NEGATIVE

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Acute Myelomonocytic Leukemia

Elevated WBC Count; presence of both myeloid and monocytoid cells; BM is of monocytic lineage, MPO = POSITIVE, Specific Esterase in granulocytic cells, Non-Specific Esterase = POSITIVE

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Myeloid Sarcoma

EXTRAMEDULLARY PROLIFERATION OF BLASTS of one or more myeloid lineages; skin, G.I. tract, lymph nodes

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Study Notes

  • Rapid proliferation of leukocyte precursors (myeloid or lymphoid) occurs in acute leukemias
  • Excessive proliferation of precursors causes them to leak into circulation prematurely
  • Abnormal precursor clones overcrowd the bone marrow, preventing normal cells from maturing
  • Symptoms of acute leukemia indicate suppressed normal hematopoiesis
  • Anemia and infection result from normal hematopoiesis being suppressed

Acute vs. Chronic Leukemia

  • Acute characteristics: sudden onset, rapid progression, often fatal if untreated
  • Chronic characteristics: insidious onset, slower progression, longer survival
  • Acute leads to excess accumulation of precursor or blast cells in the bone marrow and peripheral blood
  • Chronic displays proliferation and accumulation of mature cells of a specific lineage
  • Manifestations of acute leukemia include bleeding, fever, and fatigue
  • Chronic leukemia may be asymptomatic

General Characteristics

  • Cancers, including hematologic cancers, involve mutations that result from external factors or inherited gene mutations
  • Mutations give cells a proliferation advantage and differentiation arrest
  • Normal hematopoietic stem cells transform into leukemic stem cells leading to suppressed normal hematopoiesis

Acute Myeloid Leukemia (AML)

  • AML affects all ages, but increases with older age, median age is >60 years

  • AML may resemble acute infection upon presentation

  • Classification is made by morphology, cytogenetics, flow cytometry, and cytochemistry

  • Diagnosis requires 20% blasts in bone marrow

  • The clinical presentation is nonspecific but suppresses of normal hematopoiesis

  • Hyperuricemia in AML occurs due to tumor lysis syndrome during chemotherapy

  • Rapid death of leukemia cells releases intracellular contents overwhelming the kidneys.

  • Tumor lysis syndrome is common during chemotherapy, abnormal cells are killed, releasing disruptive metabolites in patients

  • Hyperkalemia, hyperphosphatemia, hyperuricemia, hyperuricosuria, and hypocalcemia occurs in tumor lysis syndrome.

  • Rapid breakdown releases intracellular contents into the bloodstream

Additional Notes

  • CNS involvement is rare in AML (and better than ALL)
  • Conditions: Hyperuricemia, Hyperphosphatemia, Hypocalcemia, Hypokalemia
  • Tumor Lysis Syndrome involves metabolic conditions from dying cancer cells

AML with Recurrent Genetic Abnormalities

  • The following subtypes are characterized by specific genetic abnormalities:
  • AML with t(8;21)(q22;q22.1); RUNX1-RUNX1T1 (Core Binding Factor Leukemia)
  • AML with inv(16)(p13.1q22) or t(16;16)(p13.1;q22), CBFB-MYH11
  • Acute Promyelocytic Leukemia (APL) with t(15;17)(q22;q11-12)
  • AML with t(9;11)(p21.3;q23.3); KMT2A-MLLT3

AML Cell Morphology

  • Abnormal morphology in cell type, >20% blasts etc
  • Monoblasts and Promonocytes are seen with AML (t9:11)

AML inv16

  • Myelomonocytic in nature; myeloid and monocytic precursors proliferate abnormally

M3V APL

  • cytoplasmic granules appear sparse or reduced. Auer rods, "butterfly" or "coin-on-coin" nucleus are clues
  • History of Myelodysplasia
  • Dysplasia is abnormal in morphology in cells lineage, with various morphological symptoms
  • Complex karyotypes relating to Short and Long arm of chromosomes.
  • Has similar morphologies, and occurs following prior procedures or treatments

M0 FAB

  • Less than 5% AML. Occurs in infants / older adults.
  • Peripheral blood, bone marrow - large agranular blasts

M1 FAB

  • Less than 5% AML.
  • Blasts are similar to minimally differentiated.
  • Comprise 90% Non-erythroid cells in the bone marrow.
  • Less than 10% of leukocytes show maturation beyond promyelocytic stage

M2 FAB

  • Less than 90% non-erythroid blasts

  • 10% maturation beyond promyelocytic stage

AML, Not Otherwise Specified

  • This encompasses various AML subtypes that don't fit into the defined genetic or morphological categories, there are genetic markers

M5 Acute Monoblastic and Monocytic Leukemia ( FAB Classifications)

  • Extramedullary involvement: gingival and cutaneous infiltration, bleeding disorders.
  • 80% Marrow cells are monocytic

Acute Megakaryoblastic Leukemia

  • Blasts must be over 20%, and 50% must be of megakaryocytic origin

Pure Erythroid Leukemia remains as M6 pure erythroid linage

  • 80% Marrow cells are Erythroid and over 30% are proerythroblasts

Myeloid sarcoma

  • Proliferation of blasts which causes tissue disruption in locations like skin, GI tract, and lymph nodes

Blastic Plasmacytoid Dendritic Cell Neoplasm

  • Tumour from precursors of plasmacytoid dendritic cells
  • Aggressive, presents as skin lesions, spreads to PB/BM

Acute Leukemias of Ambiguous Lineage

  • "Undifferentiated"
  • These leukemias show no clear evidence of differentiation along a single line
  • Demonstrate a multiplicity of antigens in which it is not possible to determine a specific lineage

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