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Oncology-Hematology > Leukemias and Lymphomas > Flashcards

Leukemias and Lymphomas Flashcards

1
Q

Labs required for diagnosis of leukemia ?

A

peripheral blood smear + bone marrow biopsy

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2
Q

type of leukemia by age ? (roughly)
newborn-14

A

ALL

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3
Q

type of leukemia by age ? (roughly)
40-60

A

AML or CML

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4
Q

type of leukemia by age ? (roughly)
>60

A

CLL

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5
Q

what is the percentage of blasts in the acute leukemia ?

A

> 20%

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6
Q

What are the lymphomas ?

A

Solid tumors of the the immune system

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7
Q

Is normal cell division/ proliferation is poly/mono clonal ?

A

Polyclonal

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8
Q

Definition of Leukemia ?

A

White blood cell malignancy originating in the bone marrow and going to the blood

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9
Q

What are the blast cell types we can have in Leukemia?

A

Myeloid blasts
Monoblasts
Lymphoblasts

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10
Q

Important histologic characteristic of AML ?

A

Auer rods

peroxidase positive

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11
Q

Acute leukemia morphology of the cells ?

A

Large, immature cells (blasts)

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12
Q

Lymphadenopathy in acute leukemias is painfull or painless?

A

Painless

in infections it’s painfull

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13
Q

What type of anemia we usually see in Acute leukemias?

A

Normocytic, can be also Macrocytic

Macro because of the Folic acid deficiency, because of high cell turn ov

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14
Q

What is the platelets count in acute leukemias ?

A

Low, <100,000

Normal is 150,000-400,000

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15
Q

Blasts percentage in Acute leukemias in a bone marrow biopsy?

A

blasts >20%

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16
Q

cell morphology we see in Chornic leukemias?

A

Small, mature cells, but non functioning

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17
Q

How do we consider Myelodysplasia in hematology ?

A

Pre-leukemic

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18
Q

What causes Sideroblastic anemia ?

A

Defect in Protoporphyrin

protoporphyrin—>Heme—->Hemoglobin

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19
Q

How do you define Myelodysplasia ?

A

Problem in maturation of the bone marrow, especially in the myeloid lineage

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20
Q

Do we have cytopenia in Myeloproliferative disorders?

A

No

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21
Q

Do we have cytopenia in Myelodysplastic disorders?

A

Yes

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22
Q

ALL stands for

A

Acute Lymphoblastic Leukemia

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23
Q

CLL stands for

A

Chronic Lymphocytic Leukemia

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24
Q

Important findings on Immunohistochemistry of ALL ?

A

positive for: TdT and PAS

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25
Q

Some studies suggest that giving ________________ to the pregnant mother, can decrease the incidence of ALL in the newborn

A

Folic Acid

“Give me Folic, don’t be such an alcoholic”

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26
Q

What are the main phases in the ttt of ALL ?

A

1.Remission-Induction phase
2.Consolidation*—->maintenance
3.Prophylaxis for CNS and testes

*Consolidation is needed because relapse occurs in 100% of the cases

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27
Q

AML stands for

A

Acute Myelogenous Leukemia

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28
Q

Which subtype of AML we see gingival hyperplasia/gum infiltration ?

A

M5

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29
Q

What subtype of AML is the most common?

A

M2

Myeloblastic with maturation t (8:21), good prognosis

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30
Q

What is the translocation of M3 subtype of AML ?

A

t (15;17)

Good prognosis

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31
Q

AML-M3 also known as

A

Acute promyelocytic anemia

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32
Q

AML-M5 also known as

A

Monocytic
has gum infiltration

“Mouth” has 5 letters

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33
Q

AML-M3 is strongly associated with

A

DIC

DIC has 3 letters

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34
Q

How can we treat AML-M3 ?

A

Vitamin A

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35
Q

What can we see on the smear of AML-M3 ?

A

Numerous auer rods

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36
Q

Common complication of AML M3 ?

A

DIC

Occures at diagnosis, or shortly after chemo

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37
Q

What is one of the main problems of giving a patient chemotherapy?

A

Bone marrow suppression

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38
Q

What is the advantage of giving Vitamin A to a AML-M3 patient ?

A

No bone marrow suppression

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39
Q

How does Vitamin A cure AML-M3 ?

A

By inducing maturation of primitive promyelocytes into mature Neutrophils

then the Neutrophils undergo apoptosis

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40
Q

What type of cancer can be treated with antibiotics?

A

MALTomas caused by H. pylori can be treated with antibiotics aimed at eradicating H. pylori.

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41
Q

What is the fusion gene we see in t(15:17) ?

A

PML-RAR-α

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42
Q

What is the consequence of fusion gene of PML-RAR-α ?

two things

A
  1. Arrest of differentiation
  2. Abnormal retinoic acid metabolism

That is why Vitamin A helps (vitamin A A.K.A retinoic acid)

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43
Q

What is the best initial therapy for AML-M3 ?

A

Retinoic acid

Later we can proceed to Arsenic

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44
Q

What is the translocation of CML ?

A

t(9:22)

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45
Q

What is the initial step in the pathophysiology of CML ?

A

Reciprocal translocation betweenchromosome 9 and chromosome 22

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46
Q

What is the result of BCR-ABL gene ?

A

inhibits physiologic apoptosis and increases mitotic rate

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47
Q

what is the prognosis for ALL patients with philadelphia chromosome?

A

Bad prognosis

48
Q

what is the prognosis for CML patients with philadelphia chromosome?

A

Good prognosis

note the difference in prognosis with ALL

49
Q

TTT for CML ?

A

TKI

Imatinib

50
Q

Is the Philadelphia chromosome specific for CML ?

A

No

It’s present also in ALL

but it is sensitive, 100% of patients have it

51
Q

What does LAP stands for ?

A

Leukocyte alkaline phosphatase

An enzyme found in mature leukocytes.

A high LAP score is associated with an increased number of mature white blood cells (e.g., from leukemoid reaction or myeloproliferative disorders); a low LAP score is associated with an increased number of immature white blood cells (e.g., from CML).

52
Q

A high LAP score is associated with ?

A

An increased number of mature white blood cells

(e.g., from leukemoid reaction or myeloproliferative disorders)

53
Q

A low LAP score is associated with

A

An increased number of immature white blood cells

(e.g., from CML).

54
Q

Labs of Platelets in CML ?

A

Thrombocytosis (especially in the accelerated and the blast phase)

55
Q

What type of leukemic cells can we see in CML ?

A

Evidance of maturation, “All stages of development”

Different from AML, where we had lots of blasts, and no maturation

56
Q

Results in a definitive diagnosis by bone marrow biopsy for CML ?

A
  1. Hypercellular with myeloid hyperplasia
  2. blasts <10%
57
Q

What can be a side effect of using ATRA for AML-M3 patients?

All trans retinoic acid

A

Differentiation syndrome

58
Q

What are the main characteristics of Differentiation syndrome?

A
  1. Fever
  2. Volume overload
59
Q

How do we treat differentiation syndrome ?

A
  1. Stop ATRA
  2. High dose Dexamethasone

When doctors don’t have a clue, they will give steroids to you

60
Q

What labs do we see in Blast Crisis in CML ?

A

-Blasts >20%
-Basophilia

61
Q

Two phases of treatment we see in each type of Acute leukemia ?

A
  1. Induction phase
  2. Consolidation phase
62
Q

What is the induction phase of AML treatment ?

A

High dose chemotherapy

Suppress all cell lines–> px becomes susceptible to infections

63
Q

When can we pass to the consolidation phase when treating AML ?

A

When cell counts normalize

64
Q

What is the definition of CLL ?

A

Lymphoproliferative disorder

65
Q

In CLL we have accumulation of ?

A

Lymphocytes

66
Q

Describe the morphology and functionality of lymphocytes in CLL

A

-Morphologically mature
-Functionaly incompetent

67
Q

What is CLL with a solid lymph nodal mass ?

A

SLL

Starts as leukemia and becomes lymphoma

68
Q

Peripheral smear of CLL we will see

A

Smudge cells

69
Q

Do we need bone marrow biopsy for the dx of CLL ?

70
Q

CLL on Flow cytometry, what do we see ?

A

CD-5 +
CD-23 +

71
Q

What is the result for a CLL patient on Coomb’s test ?

A

Positive

Direct coombs test !!!!

72
Q

Is leukamoid reaction malignant or benign?

73
Q

Which leukemia is mostly associated with leukostasis?

74
Q

definition of leukostasis ?

A

It is characterized by an extremely elevated blast cell count and symptoms of decreased tissue perfusion.

75
Q

What are the most common symptoms of Leukostasis?

A

Dyspnea and hypoxia

76
Q

How does leukostasis affects the blood ?

A

Increases it’s viscosity

77
Q

Count of WBC in Leukostasis?

78
Q

What is the function of Kinases ?

A

Adding Phosphate group

79
Q

What is the function of phosphorylated proteins?

A

They aid in signal transduction

“like on-off switch of the cell”

80
Q

Humor meaning ?

81
Q

What does “Phlebotomy” means?

A

Phlebo- Vein
Tomy- To cut

in greek

82
Q

Anatomy meaning ?

A

Ana- up
tomy- Cut

To cut up

83
Q

“Onkos” meaning

A

Masses

Roman

84
Q

What are the B-cell indolent lymphomas? (Mnemonic)

A

Marginal zone lymphoma
Waldenstorm lymphoma
Hairy cell leukemia
Follicular lymphoma

״מזל שוולדנסטורם נהיה שעיר בכלל השתלת הפוליקל״

85
Q

What is the translocation of Marginal zone lymphoma?

86
Q

What is the translocation of follicular lymphoma?

87
Q

What are the aggressive B-cell lymphoms? (mnemonic)

A

“If you are aggressive you are DMB”

DLBCL
Mantle cell lymphoma
Burkitt lymphoma

88
Q

What is the translocation in mantle cell lymphoma ?

89
Q

what is the translocation of burkitt lymphoma?

90
Q

What are the etiologies for Non-hodgkin lymphomas?

A

CIA-E
Chromosomal translocations
Infections
Autoimmune diseases
Environmental factors

91
Q

Indolent T-cell lymphoma

A

Mycosis fungoides

92
Q

Aggressive T-cell lymphoma?

A

Sezary syndrome

93
Q

B symptoms include ?

A

Weight loss
Fever
Night sweats

94
Q

Most important clinical feature for Non-hodgkin lymphoma?

A

Painless lymphadenopathy associated with fatigue and weakness

95
Q

Important clinical feature for high grade NHL ?

A

B symptoms

96
Q

Important clinical feature for Low grade NHL ?

A

Hepatosplenomegaly

97
Q

What is the most common tx regimen for NHL ?

A

CHOP-R

Cyclophosphamide
Hydroxidaunorubicin
Oncovin
Prednisolone
rituximab

98
Q

What is the only way to confirm lymphoma? and which one do we prefer?

A

A biopsy is the only way to confirm a person has NHL.

Excisional or incisional biopsy:

This is the preferred and most common type of biopsy if lymphoma is suspected, because it almost always provides enough of a sample to diagnose the exact type of NHL.

99
Q

What is the prognosis for NHL ?

A

Worse than that of HL

100
Q

What is the pathognomic sign for HL ?

A

Reed-sternberg cells

101
Q

important features of reed-sternberg cells?

A

Owl-eye/binuclear-bilobed nuclei

CD 15/30 positive

102
Q

DD for HL ?

A

CD 20 - positive in mononucleosis

103
Q

what are the classical HL rated from worst prognosis to best ?

A

depleted mixer תקע nod ונהיה עשיר rich

Lymphocyte depleted
Mixed cellularity
Nodular sclerosing
Lymphocyte rich

104
Q

What is the most common subtype of HL ?

A

Nodular sclerosing

105
Q

What are the Non-classical HL ?

A

Nodular lymphocyte predominant HL

106
Q

What are the characteristics of Nodular lymphocyte predominant HL? (non classical HL)

A

Pop-corn cells
cd20+
cd45+
cd79a+

NEGATIVE: CD15 and CD30

107
Q

What is the imaging used for HL ?

A

PET, with the lugano classification

108
Q

Diagnosis for HL is made with

A

Medical history and clinical features
and confirmed with lymph node biopsy

109
Q

what is the most widely used chemo approach in HL ?

A

ABVD

Adriamycin
Bleomycin
Vinblastine
Dacarbazine

110
Q

progression in HL ?

111
Q

progression in NHL ?

112
Q

Area mainly affected in HL ?

A

Cervical, Axillary, Chest

113
Q

Area mainly affected in NHL ?

A

Throughout the body

114
Q

from what cells NHL originates?

115
Q

from what cells HL originates?

116
Q

What is a pathognomic sign of CLL ?

A

Smudge cells

Oncology-Hematology (11 decks)

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