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SBL > Pathology of White Blood Cells, Lymph Nodes, Spleen, and Thymus (Part 4 of 4) > Flashcards

Pathology of White Blood Cells, Lymph Nodes, Spleen, and Thymus (Part 4 of 4) Flashcards

1
Q

What is acute myeloid leukemia?

A

mutations to hematopoietic stem cells or progenitor cells that allow for the development of a “leukemic stem cell”

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2
Q

What is the malignancy of in AML?

A

myeloid progenitors

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3
Q

what is the diagnostic criteria for AML?

A

> 20% BLASTS in bone marrow

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4
Q

How does AML present? (5)

A

fever, fatigue, bleeding/bruising, and pancytopenia

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5
Q

how does the peripheral blood look in AML patients?

A

normal/ no blasts in peripheral smear- you have to go to the bone marrow

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6
Q

what is the bone marrow full of in AML patients?

A

myeloblasts

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7
Q

What are the 4 ways AML can be classified?

A

AML with genetic aberrations, AML with MDS-like features, AML-therapy related, and AML not otherwise specified

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8
Q

What are the two different genetic aberrations associated with AML?

A

t(8;21) and t(15;17)

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9
Q

what does AML with t(8;21) usually show? and what are the characteristics of AML with t(8;21)

A

neutrophilic maturation- you can actually see the granules in the blasts; often younger patients and they have a good prognosis

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10
Q

What is AML with a t(8;21) genetic aberration sometimes called?

A

CBF leukemia

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11
Q

What occurs in the t(8;21) genetic aberration?

A

the RUNX-1-RUNX1T1 fusion product disrupts the core binding factor-mediated hematopoietic differentiation and maturation

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12
Q

what is AML with t(15;17) genetic aberration often referred to as?

A

acute promyelocytic leukemia

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13
Q

What is characteristic of AML with t(15;17)?

A

Auer rods are seen in the cytoplasm of the promyelocyte

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14
Q

What is the function of normal RAR?

A

it helps drive neutrophilic differentiation forward

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15
Q

what happens to the RAR in AML patients with t(15;17)?

A

the retinoic acid that binds and drives this forward is no longer liked by the receptor, so the fusion product creates a distaste for RA

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16
Q

What is the treatment for AML t(15;17)?

A

all trans RA

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17
Q

what are individuals with t(15;17) AML at risk for?

A

DIC

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18
Q

why are individuals with AML t(15;17) at risk for DIC?

A

the leukemic cells express tissue factor, which activates factor X; high levels of annexin II receptors on plasma cells convert plasminogen into plasmin

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19
Q

What are unusual presentations of AML?

A

acute monocytic leukemia (morphologic (M5) and extranodal involvement is common (including gingival and leukemia cutis)) and soft tissue mass formation

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20
Q

What is the soft tissue mass formation named as in a patient with AML?

A

granulocytic sarcoma/myeloid sarcoma/ “chloroma”

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21
Q

what stain is used to diagnose a granulocytic sarcoma/myeloid sarcoma/ “chloroma”?

A

myeloperoxidase stain

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22
Q

What is myelodysplastic syndrome?

A

a clonal disorder with morphologic manifestations that can range through many cell lineages

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23
Q

what is MDS considered to be a precursor to?

A

AML

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24
Q

transformation of MDS into AML is most likely when?

A

if MDS is due to prior cytotoxic therapy/radiation (t-MDS)

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25
Q

how do patients with myelodysplastic syndrome present?

A

cytopenias (most commonly anemia)

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26
Q

What is classification of MDS based on?

A

dysmorphic features in one or more lineages, chromosomal analysis, and if blast count is increased (but not quite to the point of AML)

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27
Q

What percentage of blasts gives you MDS RAEB-1?

A

5-9%

28
Q

what percentage of blasts gives you MDS RAEB-2?

A

10-19%

29
Q

When looking at dysmorphic features in MDS patients, what are 4 potential morphologies?

A

dyserythropoiesis, ring sideroblasts, pseudo pelger-huet cells, dysmegakaryopoiesis

30
Q

which classification of MDS is likely to turn into AML?

A

RAEB II- moving closer to the 20% blast count in the bone marrow is needed for an outright diagnosis of AML

31
Q

what type of disorders are myelodysplastic syndromes?

A

clonal disorders with driver mutations

32
Q

what are some of the driver mutations of myelodysplastic syndromes?

A

epigenetic mutations, RNA splicing factor mutations, Transcription factor mutations

33
Q

What are myeloproliferative neoplasms driven by?

A

mutated kinases that are constitutively active

34
Q

what happens in myeloproliferative neoplasms?

A

something in the bone marrow proliferates, neoplastic stem cells travel to other sites (like the spleen) causing extramedullary hematopoiesis, fibrosis can be apart of the disease progression

35
Q

what is chronic myeloid leukemia?

A

proliferation of predominantly mature myeloid cells

36
Q

how does chronic myeloid leukemia present?

A

peripheral leukocytosis

37
Q

what genetic aberration causes chronic myeloid leukemia?

A

the 9;22 translocation forming the BCR ABL product

38
Q

What will you see in CML patients? (3)

A

marked leukocytosis (WBC count> 100K), an increased buffy coat, splenomegaly

39
Q

What can happen to CML over time? / what are the different stages of CML?

A

chronic phase–> accelerated phase–> blastic phase

40
Q

what classifies CML being in the chronic phase?

A

when the circulating blasts are less than 10%

41
Q

what classifies CML being in the accelerated phase?

A

circulating blasts 10-19%

42
Q

what classifies CML being in the blastic phase?

A

circulating blasts >20%

43
Q

what is the myeloproliferative neoplasm of white cells called?

A

chronic myeloid leukemia

44
Q

what is the myeloproliferative neoplasm of red cells called?

A

polycythemia vera

45
Q

what is the myeloproliferative neoplasm of platelets called?

A

essential thrombocythemia

46
Q

what is the myeloproliferative neoplasm of stroma called?

A

primary myelofibrosis

47
Q

What mutations are primary myelofibrosis associated with?

A

JAK2 kinase mutations- they are the drivers for growth

48
Q

what is the effect of myelofibrosis?

A

depletion of marrow elements puts increased pressure on the spleen

49
Q

what medication is used to treat splenomegaly in a patient with myelofibrosis?

A

Ruxolitnib

50
Q

What is langerhans cell histiocytosis?

A

clonal proliferations of immature dendritic cells called langerhans cells

51
Q

what are the different forms of langerhans cells histiocytosis? (3)

A

multifocal multisystem LCH, unisystem LCH, Pulmonary LCH (smokers)

52
Q

What is the appearance of LCH?

A

grooved nuclei of the Langerhans cells: tennis-racket-shaped Birbeck granules

53
Q

What can you stain for to help identify langerhans cells?

A

S-100 and CD1a

54
Q

Where are most of the lymphocytes in the spleen located?

A

germinal centers (white pulp)

55
Q

What are four functions of the spleen?

A

phagocytosis of blood cells and blood-borne matter, antibody production, hematopoiesis, and sequestration of blood cells

56
Q

What two things could cause splenomegaly?

A

reactive splenitis and congestive splenomegaly

57
Q

what is hypersplenism and what could cause it?

A

enlargement associated with cytopenias; may be due to an issue with circulating cells themselves or due to a primary/secondary splenic disorder

58
Q

What disorders could cause splenic enlargement?

A

hereditary spherocytosis, sickle cell anemia, and idiopathic thrombocytopenic purpura (ITP)

59
Q

what occurs in hereditary spherocytosis that leads to splenic enlargement?

A

stiff red cells get stuck in sinuses

60
Q

what occurs in sickle cell anemia?

A

sickled cells are trapped

61
Q

what occurs in idiopathic thrombocytopenic purpura (ITP)?

A

platelets are opsonized, spleen clears them

62
Q

what splenic disorder could cause splenic enlargement?

A

congestive splenomegaly

63
Q

Which splenic neoplasia is more commonly seen?

A

hematologic malignancies rather than primary tumors

64
Q

What could cause splenic infarct?

A

outgrowth or clog

65
Q

What could cause Myasthenia gravis?

A

autoantibodies produced in either thymic hyperplasia or thymoma

66
Q

What are two different types of thymic pathology?

A

hyperplasia and thymoma

SBL (14 decks)

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