Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

WILLIAM'S HEMATOLOGY > 82 Classification and Clinical Manifestations of the Clonal Myeloid Disorders > Flashcards

82 Classification and Clinical Manifestations of the Clonal Myeloid Disorders Flashcards

1
Q

Refers to the relationship of the disease in question to normal cellular differentiation and maturation and the regulation of cell population homeostasis (birth and death rates)

A

Deviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Preclinical and Minimally-Deviated Clonal Myeloid Diseases

A
  • A. Clonal hematopoiesis of indeterminate potential (CHIP)
  • B. Clonal hematopoiesis of oncogenic potential (CHOP)
  • C. Clonal cytopenias of unknown significance (CCUS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Moderate-deviation neoplasms (no increase in blast cells [<2%] are evident in marrow)

A

A. Underproduction of mature cells is prominent
* 1. Clonal anemia
* 2. Clonal bi- or tricytopenia
* 3. Paroxysmal nocturnal hemoglobinuria

B. Overproduction of mature cells is prominent
* 1. Polycythemia vera
* 2. Essential thrombocythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Moderately-severe-deviation neoplasms (very small percentage of leukemic blast cells present in marrow [usually ≤6%])

A

A. CML
* 1. Philadelphia (Ph) chromosome–positive, BCR rearrangement–positive (~90%)
* 2. Ph chromosome–negative, BCR rearrangement–positive (~6%)
3. Ph chromosome–negative, BCR rearrangement–negative (~4%)

B. Primary myelofibrosis (chronic megakaryocytic leukemia)

C. Chronic eosinophilic leukemia
* 1. PDGFR rearrangement–positive
* 2. FGFR1 rearrangement–positive

D. Chronic neutrophilic leukemia
* 1. CSF3R rearrangement–positive
* 2. CSF3R and SETBP1 rearrangement–positive
* 3. JAK2V617F rearrangement–positive

E. Chronic basophilic leukemia

F. Systemic mastocytosis (chronic mast cell leukemia)
* 1. KITD816V mutation–positive (~90%)
* 2. KITV560G mutation–positive (rare)
* 3. FILIPI-PDGFRα

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Severe-deviation neoplasms (usually moderate
concentration of leukemic blast cells present in marrow)

A

A. Oligoblastic myelogenous leukemia (myelodysplastic syndrome)

B. Chronic myelomonocytic leukemia
* 1. PDGFR rearrangement–positive (rare)
*
C. Atypical myeloproliferative disease (syn. atypical CML)

D. Juvenile myelomonocytic leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Very-Severe-deviation neoplasms (leukemic blast or early progenitor cells frequent in the marrow and blood)

A

A. Phenotypic variants of AML
* 1. Myeloblastic (granuloblastic)
* 2. Myelomonocytic (granulomonoblastic)
* 3. Promyelocytic
* 4. Erythroid
* 5. Monocytic
* 6. Megakaryocytic
* 7. Eosinophilic
* 8. Basophilic
* 9. Mastocytic
* 10. Histiocytic or dendritic

B. Higher-frequency genotypic variants of AML [t(8;21), Inv16 or t(16;16), t(15;17), or (11q23)]

C. Myeloid sarcoma

D. Acute biphenotypic (myeloid and lymphoid markers) leukemia

E. Acute leukemia with lymphoid markers evolving from a prior clonal myeloid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clonal hematopoiesis as a result of a somatic mutation in a clone of marrow cells, but marrow and blood cells without any phenotypic evidence of a blood cell disorder, that is, normal marrow and blood cell morphology and normal blood cell counts.

A

CLONAL HEMATOPOIESIS OF INDETERMINATE POTENTIAL (CHIP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A somatic mutation in which an unequivocally abnormal cytopenia is or cytopenias are present

A

Clonal cytopenia of unknown significance (CCUS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Definition of cytopenias in clonal cytopenia of unknown significance (CCUS)

Hemoglobin :
Absolute neutrophil count :
Platelet count :

A

Hemoglobin : <100 g/L
Absolute neutrophil count : <1.8 × 10 9 /L
Platelet count : <100 × 10 9 /L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A somatically mutated clonal disorder without a phenotype but with more concerning somatic mutations

A

Clonal hematopoiesis of oncogenic potential (CHOP)

In the case of CHOP, the mutations are disease-related or even disease-specific mutations and have a higher propensity to undergo clonal evolution to a progressive neoplasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TRUE OR FALSE

In the cases of CHIP and CHOP, the definition includes absence of evidence of paroxysmal nocturnal hemoglobinuria or clonal lymphocytosis or cytologic dysmorphia.

A

TRUE

In the cases of CHIP and CHOP, the definition includes absence of evidence of paroxysmal nocturnal hemoglobinuria or clonal lymphocytosis or cytologic dysmorphia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most frequent specific gene mutations which make up about 75% of CHIP

A

DNMT3A, TET2, ASXL1, and JAK2

12 specific gene mutations so far identified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mutations that are more frequently detected in secondary AML, following MDS or CMML

A

TET2
ASXL1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Associated with deletions in the long arm of chromosome 11 and with the presence of ring sideroblasts in MDS.

A

SF3B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The variant allele frequency (VAF) by definition is above ____ %

A

Above 2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

TRUE OR FALSE

Age-related clonal hematopoiesis (ARCH) is in essence a synonym for CHIP but denotes the effect of aging

A

TRUE

Age-related clonal hematopoiesis (ARCH) is in essence a synonym for CHIP but denotes the effect of aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The rate of progression of CHIP to a clinically evident neoplasm is approximately 0.75% of affected persons per year, of which the majority are __________ neoplasms

A

Myeloid neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TRUE OR FALSE

A coexisting significant finding in patients with CHIP is a predisposition to cardiovascular morbidity and mortality.

A

TRUE

A coexisting significant finding in patients with CHIP is a predisposition to cardiovascular morbidity and mortality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The vascular occurrences in CHIP may relate to the mutations of genes such as __________

A

TET2 and JAK 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Defined as an idiopathic cytopenia(s) without a detectable somatic mutation.

A

Idiopathic cytopenias of undetermined significance (ICUS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diseases include one group in which late precursor apoptosis (ineffective myeloproliferation) is characteristic (the clonal cytopenias) and one group in which proliferation is exaggerated and cellular maturation approximates normal (effective myeloproliferation)

A

MODERATE-DEVIATION CLONAL MYELOID DISEASES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Essential characteristic of moderate-deviation clonal myeloid diseases

A

Cytopenias resulting from exaggerated apoptosis of marrow late precursors (referred to as “ineffective hematopoiesis”)

Variable dysmorphogenesis of blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The blood cell abnormalities, characteristic of the clonal cytopenias and oligoblastic myelogenous leukemia, include abnormalities of:

A

(a) red cell size (macrocytosis, anisocytosis), shape (poikilocytosis), and cytoplasm (basophilic stippling, pathologic sideroblasts);

(b) neutrophil nuclear or organelle structure (cytoplasmic hypogranulation, nuclear hypolobulation or hyperlobulation, and condensation)

(c) platelet variation in size (megathrombocytes) and granulation (hypogranulation or abnormal granulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Blast percentage in:

AML:
MDS:

A

Blast percentage in:

AML: 20% or more
MDS:5%–20%

The use of an arbitrary boundary of 20% blasts has no pathobiologic basis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

TRUE OR FALSE

In severe inflammatory states with leukemoid reactions, the marrow myeloblast percent is usually increased .

A

FALSE

In severe inflammatory states with leukemoid reactions, the marrow myeloblast percent is usually DECREASED because in this circumstance, precursor cell expansion in the myelocyte pool is far greater, such that the percent of blast cells decreases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

TRUE OR FALSE

Three percent or 4% blast cells in the marrow at the time of presentation, after therapy, or suspected relapse should not be considered “normal” and is evidence of leukemic hematopoiesis.

A

TRUE

Three percent or 4% blast cells in the marrow at the time of presentation, after therapy, or suspected relapse should not be considered “normal” and is evidence of leukemic hematopoiesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TRUE OR FALSE

Polycythemia vera and essential thrombocythemia show morphologic evidence of leukemic hematopoiesis

A

FALSE

Polycythemia vera and essential thrombocythemia DO NOT show morphologic evidence of leukemic hematopoiesis

The proportion of blast cells in the marrow is never increased above normal, and blast cells are never present in the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Percentage of Janus kinase 2 (JAK2) gene mutation in:

PV:
ET:

A

PV: 95%
ET: 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Other mutations in ET aside from JAK2

A

Wild-type JAK2 gene
Calreticulin (CALR) gene
Myeloproliferative leukemia virus gene (MPL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The most constant feature in primary myelofibrosis

A

Abundance of neoplastic, dysmorphic megakaryocyte

Predisposition to marrow reticulin and collagen fibrosis, osteosclerosis, extramedullary fibrohematopoietic tumors, splenomegaly, and teardrop-shaped red cells (dacryocytes) in virtually every oil immersion field

The megakaryocytic abnormalities are so dominant and consistent in this disorder that it could be considered chronic megakaryocytic leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Gene mutations in PMF

A

JAK2 gene (50%)
CALR gene (30%)
MPL mutation (10%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Percentage with “triple negative” mutation in PMF

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Cause of fibrosis in PMF

A

Cytokines released by neoplastic (leukemic) megakaryocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Gene mutation in CML

A

Translocation t(9;22) (q34;q11)(BCR-ABL1 [Abelson murine leukemia viral oncogene homologue 1])

Philadelphia chromosome, now called the Ph chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Percentage of patients with CML with t(9;22) mutation

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Percentage of CML patients do not have the rearrangement

A

4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Primary myelofibrosis terminates in acute leukemia in approximately _____% of patients.

A

15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

TRUE OR FALSE

Therapy is required in all cases of CML and primary myelofibrosis at the time of diagnosis.

A

FALSE

Therapy is required in all cases of CML, and in most, but not all, cases of primary myelofibrosis at the time of diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Gene mutation in Chronic neutrophilic leukemia

A

Colony-stimulating factor 3 receptor gene (CSF3R) 30%
CSF3R and a SET binding protein gene (SETBP1) mutation 60%
JAK2 V617F mutation 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Previous name of Chronic eosinophilic leukemia

A

Hypereosinophilic syndrome with evidence of clonal hematopoiesis involving eosinopoiesis

41
Q

Gene mutation in Chronic eosinophilic leukemia

A

PDGFR-β gene
PDGFR-α gene (FIP1L1–PDGFR-α fusion gene)

42
Q

Treatment for Chronic eosinophilic leukemia

A

Imatinib mesylate (or a congener)

43
Q

FIP1L1–PDGFR-α fusion gene mutation is inferred by

A

Deletion in the CHIC2 gene

detected during FISH

44
Q

TRUE OR FALSE

A clonal myeloid syndrome that includes eosinophilia and a translocation between 8p11, at the site of the tyrosine kinase domain of the fibroblast growth factor receptor-1 (FGFR1) gene, and several different partner chromosomes, is responsive to imatinib mesylate

A

FALSE

A clonal myeloid syndrome that includes eosinophilia and a translocation between 8p11, at the site of the tyrosine kinase domain of the fibroblast growth factor receptor-1 (FGFR1) gene, and several different partner chromosomes, is NOT responsive to imatinib mesylate

45
Q

Gene mutation in Systemic mastocytosis

A

KIT gene mutation

46
Q

KIT V560G or KIT D816V

is sensitive to imatinib mesylate

A

KIT V560G

KIT D816V is insensitive to imatinib but may be responsive to second-generation tyrosine kinase inhibitors.

47
Q

These disorders fall into a group that progresses less rapidly than acute leukemia and more rapidly than CML; have a predisposition to develop with a granulocytic and monocytic phenotype, either morphologically or cytochemically

A

SEVERE-DEVIATION CLONAL MYELOID DISEASES

Include oligoblastic myelogenous leukemia (formerly designated refractory anemia with excess blasts), chronic myelomonocytic leukemia, and juvenile myelomonocytic leukemia

48
Q

Characteristics of atypical myeloproliferative disease or atypical CML (aCML)

A
  • Seen in older patients (>65 years)
  • Low myeloblast percentage in marrow (<5%) and blood
  • Never have a rearrangement in the BCR gene
  • Not responsive to tyrosine kinase inhibitors
  • Have a poor prognosis (median survival of 5–20 months)
49
Q

Atypical myeloproliferative disease (aCML) has a relatively high frequency of ______ gene mutations

A

CSF3R

50
Q

TRUE OR FALSE

In AML, knowing the cytogenetic alteration is useful for estimating the probability of entering a sustained remission (risk category)

A

TRUE

In AML, knowing the cytogenetic alteration is useful for estimating the probability of entering a sustained remission (risk category)

51
Q

Cytogenetics in AML with favorable outcome; more likely to enter a prolonged remission or be cured with therapy

A

t(8;21)
t(15;17)
t(16;16)
inv(16)

52
Q

Treatment for patients with t(15;17) AML

A

All-trans-retinoic acid and arsenic trioxide

53
Q

Useful for determining subclinical (minimal) residual disease and monitoring therapy in cases in which an appropriate genetic marker is available, such as the t(8;21) or t(15;17)

A

Polymerase chain reaction

54
Q

Gene expression studies in AML are important because:

A

(a) identify genes that cooperate or interact to result in a fully malignant phenotype,
(b) provide potential new targets for therapy,
(c) help identify patients who might benefit from early hematopoietic stem cell transplantation,
(d) may be used to measure minimal residual disease, and
(e) may permit analysis of the mutational evolution from the earliest neoplastic cell without malignant potential to cells with additional mutations capable of developing lethal clones

55
Q

TRUE OR FALSE

Currently, prognostic group stratification of AML has value, principally in assessing the utility of using allogeneic hematopoietic stem cell transplantation as an early therapy.

A

TRUE

Currently, prognostic group stratification of AML has value, principally in assessing the utility of using allogeneic hematopoietic stem cell transplantation as an early therapy.

56
Q

Likelihood of clonal myeloid disases progressing to florid (polyblastic) AML (a very-severe-deviation neoplasm)

PNH:
Clonal anemia:
Clonal bi- or tricytopenia:
Oligoblastic myelogenous leukemia:
ET:
PV:
PMF:

A

PNH: less than 1%
Clonal anemia: 10%
Clonal bi- or tricytopenia: 35%
Oligoblastic myelogenous leukemia: 66%
ET: 5% (rises to 10% over 25 years)
PV: 12%
PMF: 20%

Virtually all patients with CML have the potential to progress to acute leukemia of any subtype, including in about a quarter of cases to lymphoid phenotypes

57
Q

Likelihood of polycythemia vera evolving to a syndrome indistinguishable from primary myelofibrosis

A

15%

58
Q

Term used for exposures that result in the development of AML, presumably without a preexisting predisposing mutation, such as exposure to chemotherapy or radiation therapy

A

Secondary AML

59
Q

Term used for AML that results from clonal evolution of a less advanced neoplasm (eg, CHIP, CHOP, CCUS, MDS, CMML, CNL, or a MPN)

A

ceAML (clonal evolution to AML)

60
Q

TRUE OR FALSE

A severe block in maturation is characteristic of AML, whereas a high proportion of leukemic primitive multipotential cells mature into terminally differentiated cells of all lineages in patients with CML.

A

TRUE

A severe block in maturation is characteristic of AML, whereas a high proportion of leukemic primitive multipotential cells mature into terminally differentiated cells of all lineages in patients with CML.

61
Q

AML associated with tissue infiltration, including into the CNS

A

Monocytic leukemia

62
Q

AML associated with disseminated intravascular coagulation, fibrinolysis, and hemorrhage

A

Promyelocytic leukemia

*Monocytic leukemia (to lesser extent)

63
Q

AML associated with hepatosplenomegaly

A

Eosinophilic leukemia

64
Q

AML associated with mediator-release syndromes

A

Basophilic or mast-cell leukemia

65
Q

AML associated with predisposition to myeloid sarcomas

A

AML with t[8;21] or inv[16] cytogenetic abnormalities

66
Q

AML associated with intense marrow fibrosis

A

Megakaryocytic leukemia

67
Q

Identification of markers unique for erythroid cells

A

CD 71

68
Q

Identification of markers unique for megakaryocytic cells

A

CD41, CD42, or CD61

69
Q

Gene mutation in Paroxysmal nocturnal hemoglobinuria

A

PIG-A gene on the active X chromosome

The mutation causes a highly specific alteration in blood cell membranes, a deficiency in the glycosylphosphatidylinositol anchor, with decreased cell-surface CD59, rendering the blood cells exquisitely sensitive to complement lysis.

70
Q

Discrete tumors of leukemic cells that form in skin and soft tissues, breast, periosteum and bone, lymph nodes, mediastinum, lung, pleura, gastrointestinal tract, gonads, urinary tract, uterus, central nervous system, and virtually any other site

A

Myeloid (granulocytic) sarcomas (also called chloromas or myeloblastomas)

71
Q

One of four histopathologic patterns usually is evident by immunocytochemistry in Myeloid (granulocytic) sarcomas

A

Myeloblastic, monoblastic, myelomonoblastic, or megakaryoblastic

72
Q

AML with these cytogenetics has a predisposition to form myeloid sarcomas

A

t(8;21) and inv(16)

73
Q

Patients with this type of AML has more diffuse collections of leukemic promonocytes or monoblasts can invade the skin, gingiva, anal canal, lymph nodes, CNS, or other tissues

A

Monocytic subtype

74
Q

AML with features of microvascular thrombosis

A

Acute promyelocytic
Acute monocytic
Acute myelomonocytic leukemia

75
Q

A very rare presenting feature or complication of leukemia but has occurred in the setting of hyperleukocytosis and as a presenting feature of acute promyelocytic leukemia.

A

Large-vessel arterial thrombosis

76
Q

Proportion of patients with AML and CML that manifest extraordinarily high blood leukocyte counts.

A

AML (5%–15%)
CML (10%–20%)

77
Q

Hyperleukocytic Syndromes occur when counts are greater than:

AML: _____________
CML: ______________

A

AML:100 × 109/L
CML:300 × 109/L

78
Q

In AML with hyperleukocytosis, _________________ and _________________ are the most serious manifestations in predicting early death

A

Intracerebral hemorrhage and the impairment of pulmonary function

79
Q

TRUE OR FALSE

In CML, there is a very close negative correlation of hematocrit with leukocrit, preventing an increase in bulk viscosity.

A

TRUE

In CML, there is a very close negative correlation of hematocrit with leukocrit, preventing an increase in bulk viscosity.

80
Q

Initial management of hyperleukocytosis

A

Hydration, leukapheresis, and/or cytotoxic therapy

81
Q

A consequence of rapid cell lysis, usually as a result of cytotoxic therapy, and the resultant release of potentially toxic intracellular contents, resulting in hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia

A

Tumor Lysis Syndrome

82
Q

It has been proposed that the risk of tumor lysis syndrome can be predicted most accurately by the ______________ level

A

Serum uric acid

83
Q

Another marker of high tumor burden

A

Serum lactic dehydrogenase

84
Q

The major vascular manifestations of thrombocythemia

A

Arterial vascular insufficiency and venous thromboses

85
Q

Patients with essential thrombocythemia who have the _________ mutation have a significantly lower risk of thrombotic disease

A

CALR mutation

86
Q

Thrombotic complications occur in approximately _____% of patients with polycythemia vera.

A

40%

87
Q

Erythrocytosis and thrombocytosis may interact and cause hypercoagulability, especially in the _________________ circulation.

A

Abdominal venous circulation

88
Q

Nearly ____________ of patients with paroxysmal nocturnal hemoglobinuria have thrombosis, especially in the venous system.

A

Half

89
Q

TRUE OR FALSE

Thrombosis is more common in patients with paroxysmal nocturnal hemoglobinuria–aplastic anemia hybrid than in those with the paroxysmal nocturnal hemoglobinuria with the classical hemolytic syndrome

A

FALSE

Thrombosis is more common in patients with paroxysmal nocturnal hemoglobinuria with the classical hemolytic syndrome than in those with the paroxysmal nocturnal hemoglobinuria–aplastic anemia hybrid

90
Q

TRUE OR FALSE

Fever during cytotoxic therapy, when neutrophil counts are extremely low, is nearly always a sign of infection

A

TRUE

Fever during cytotoxic therapy, when neutrophil counts are extremely low, is nearly always a sign of infection

91
Q

Acid–base disturbances occur in approximately 25% of patients, the majority having _______________.

A

Respiratory or metabolic alkalosis

92
Q

FACTITIOUS LABORATORY RESULTS in leukemia

A

High K
Low glucose
Low arterial blood oxygen

93
Q

TRUE OR FALSE

In AML, palpable splenomegaly is present in approximately one-third of cases, but usually is slight in extent.

A

TRUE

In AML, palpable splenomegaly is present in approximately one-third of cases, but usually is slight in extent.

94
Q

Percentage of splenomegaly in MPNs:

PV:
CML:
PMF:
ET:

A

PV: 80%
CML: 90%
PMF: 100%
ET: 30%

95
Q

TRUE OR FALSE

Extensive marrow necrosis, an uncommon event, can occur in any clonal myeloid disease, especially AML, and less often, primary myelofibrosis, CML, essential thrombocythemia, and polycythemia vera.

A

TRUE

Extensive marrow necrosis, an uncommon event, can occur in any clonal myeloid disease, especially AML, and less often, primary myelofibrosis, CML, essential thrombocythemia, and polycythemia vera.

96
Q

Most common symptoms in marrow necrosis

A

Bone pain and fever

Anemia and thrombocytopenia are very common, as are nucleated red cells and myelocytes in the blood (leukoerythroblastic reaction)

97
Q

Findings in marrow necrosis

A

Hypocellularity with loss of marrow cell structural definition (blurred staining of residual cells), evidence of cell necrosis, gelatinous transformation of marrow, and, often, an amorphous eosinophilic material throughout

98
Q

The mechanism in marrow necrosis

A

Microvascular dysfunction

WILLIAM'S HEMATOLOGY (109 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions