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Hematology 2 Lec > CLL > Flashcards

CLL Flashcards

1
Q

B. CHRONIC LYMPHOPROLIFERATIVE DISORDERS

A
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2
Q

● Proliferation of lymphocytes which are abnormal because they are unresponsive to antigenic stimuli.

A

Chronic Lymphocytic Leukemia (CLL)

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3
Q

● Less likely to undergo blastic transformation

A

Chronic Lymphocytic Leukemia (CLL)

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4
Q

● Predisposition to autoimmune hemolytic anemia (AIHA)

A

Chronic Lymphocytic Leukemia (CLL)

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5
Q

● is predominant in males (3:1 ratio)

A

Chronic Lymphocytic Leukemia (CLL)

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6
Q

● CLL Cytogenetic abnormality:

A

➢ Extra Ch12

➢ t(14q)  Translocation on the long arm of Ch14

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7
Q

B cell: produces antibodies due to presence of antigen (normally increases in synchrony)

A

Chronic Lymphocytic Leukemia (CLL)

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8
Q

Chronic, and involves mature cells

A

Chronic Lymphocytic Leukemia (CLL)

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9
Q

Types of AIHA:

A

Warm AIHA (IgA and IgG) and Cold AIHA(IgM)

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10
Q

 Duplicated Ch 12

A

Extra Ch12

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11
Q

 marker for Lymphocytic Leukemia (all Lymphocytic Leukemia have this)

A

Extra Ch12

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12
Q

 predicts progression of disease

A

Extra Ch12

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13
Q

common cell that is involved is the B-lymphocyte

A

B-CLL

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14
Q

B-lymphocyte is unresponsive to antigenic stimuli = do not function well (abnormal)

A

B-CLL

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15
Q

Dormant B-cells

A

B-CLL

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16
Q

o Due to proliferation (useless), they accumulate but stay dormant in the peripheral blood, bone marrow or in the lymph nodes

A

Dormant B-cells

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17
Q

o Cannot produce Ab even with the presence of Ag

A

Dormant B-cells

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18
Q

B-CLL or T-CLL

Rare

A

T-CLL

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19
Q

disseminated in the circulation/does not accumulate

A

T-CLL

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20
Q

Key features: appearance of rash (skin and CNS is involved)

A

T-CLL

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21
Q

Enlarged lymph nodes, spleen and liver

A

Chronic Lymphocytic Leukemia (CLL)

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22
Q

Pruritus

A

Chronic Lymphocytic Leukemia (CLL)

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23
Q

: due to skin infection due to Herpes zoster

A

Pruritus

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24
Q

Affects more of males; 50-60 years old

A

Chronic Lymphocytic Leukemia (CLL)

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25
Q

Common (early onset): fatigue, reduced tolerance to exercise

A

Chronic Lymphocytic Leukemia (CLL)

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26
Q

Advanced (progressive): bruising (thrombocytopenia), pallor (anemia), jaundice (anemia, iron loss), weight loss, obstruction of the lymph node

A

Chronic Lymphocytic Leukemia (CLL)

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27
Q

General symptoms of T-CLL:

A

erythroderma and pruritus

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28
Q

Median survival rate for patients with CLL:

A

3-4 years

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29
Q

Chronic Lymphocytic Leukemia (CLL) Lymphocyte count:

A

10-150 x 109/L

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30
Q

Presence of many SMUDGE CELLS

A

Chronic Lymphocytic Leukemia (CLL)

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31
Q

Hypogammaglobulinemia

A

Chronic Lymphocytic Leukemia (CLL)

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32
Q

Severe itching of the skin

A

Pruritus

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33
Q

: one of the first indication of CLL

A

Herpes zoster

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34
Q

➢ lymphocytes that appear normal but are very fragile when doing the smear preparation

A

SMUDGE CELLS

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35
Q

➢ Often confused with BASKET CELLS, but without vacuolation

A

SMUDGE CELLS

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36
Q

➢ Because of the decrease in the normal B-cell

A

Hypogammaglobulinemia

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37
Q

CAUSE: same causes as other leukemia (except ionizing radiation)

A

Chronic Lymphocytic Leukemia (CLL)

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38
Q

PROGNOSIS: 3-4 years from diagnosis

A

Chronic Lymphocytic Leukemia (CLL)

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39
Q

NOTE: The appearance of lymphocytes can also determine what stage of disease the patient is already in

A

Chronic Lymphocytic Leukemia (CLL)

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40
Q

Chronic Lymphocytic Leukemia (CLL)
● Mild Diseases: lymphocytes are usually (?) and they have (?) chromatin with (?) nucleoli.

A

larger

clumped or condensed

very prominent

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41
Q

Chronic Lymphocytic Leukemia (CLL)
● Aggressive diseases: lymphocytes appear (?) with (?) cytoplasm (almost non-visible) (?) of nuclei represents the course of the disease is follicular (origin: thyroid).

A

tiny

little

clefting

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42
Q

➢ Cytopenia – causes anemia and thrombocytopenia; the bone marrow is already filled with lymphoid tissues; 50% of the bone marrow is replaced by lymphoid tissue

A

Chronic Lymphocytic Leukemia (CLL)

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43
Q

➢ Glycogen = (+) PAS

A

Chronic Lymphocytic Leukemia (CLL)

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44
Q

Chronic Lymphocytic Leukemia (CLL)
Diagnostic (percentage of B cell):

A

> 30% of lymphocyte in the BM.

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45
Q

Chronic Lymphocytic Leukemia (CLL) Treatment

A
  1. LEUKAPHERESIS
  2. GAMMA GLOBULIN INJECTIONS
  3. RADIATION
  4. CHEMOTHERAPY
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46
Q

Reduces the number of abnormal lymphocyte.

A
  1. LEUKAPHERESIS
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47
Q

high lymphocyte in the PB = viscous blood

A
  1. LEUKAPHERESIS
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48
Q

Aim: to make blood thin (leukopheresis can not reduce tumor burden, unlike chemotherapy; NOT for tumor)

A
  1. LEUKAPHERESIS
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49
Q

Since you have hypogammaglobulinemia, this is meant to raise the B cell count

A
  1. GAMMA GLOBULIN INJECTIONS
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50
Q

treat enlarged lymph nodes and spleen

A
  1. RADIATION
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51
Q

reduce the tumor and abnormal lymphocyte in the PB

A
  1. CHEMOTHERAPY
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52
Q

Aim: to reduce the tumor and abnormal lymphocyte

A
  1. CHEMOTHERAPY
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53
Q

▪ an increase in prolymphocytes, with almost total replacement of the bone marrow

A
  1. Pro-Lymphocytic Leukemia
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54
Q

▪ poorer prognosis than HCL and CLL

A
  1. Pro-Lymphocytic Leukemia
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55
Q

● Rare variant of CLL (not common)

A
  1. Pro-Lymphocytic Leukemia
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56
Q

● Increased in prolymphocyte, total replacement of BM

A
  1. Pro-Lymphocytic Leukemia
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57
Q

● Decreased gamma globulins and T cells

A
  1. Pro-Lymphocytic Leukemia
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58
Q

● Poorer prognosis than CLL or HCL (Hairy Cell Leukemia)

A
  1. Pro-Lymphocytic Leukemia
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59
Q
  1. Pro-Lymphocytic Leukemia
    ● Mean survival rate:
A

1 yr (usually less than a year)

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60
Q
  1. Pro-Lymphocytic Leukemia
    ● Leukocyte count:
A

25-1000 x 109/L

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61
Q

: large, with oval to round nucleus, coarse chromatin and 2 large vesicular nucleoli with condensation of chromatin (abnormal)

A
  1. Pro-Lymphocytic Leukemia

● Prolymphocyte

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62
Q

 Abnormal cells: Prolymphocytes
 Normal lymphocyte: small and no condensed chromatin

A
  1. Pro-Lymphocytic Leukemia
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63
Q

● Rare (2%)

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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64
Q
  1. Hairy Cell Leukemia
    ● Otherwise known as
A

“Leukemic reticuloendotheliosis” “Reticulosis”, “Aleukemic reticuloendotheliosis” and “Reticulum cell leukemia”

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65
Q
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
    ● due to the growth and accumulation of hairy cell in the
A

spleen, bone marrow and PB

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66
Q
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
    ● Mean survival rate:
A

5 yrs (slower than CLL: 3-4 years)

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67
Q

● Most affected here are men with an average age of 55 years old

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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68
Q

● Presence indicate that there is pancytopenia, predominantly granulocytes and monocytes (granulocytopenia and monocytopenia).

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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69
Q

HCL CHARACTERISTICS

A
  1. Large spleen (similar to other diseases)
  2. Mononuclear cells with cytoplasmic projection ( “HAIRY CELL”)
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70
Q

HC Cytoplasm:

A

scant to abundant, agranular, light grayish blue

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71
Q

HC Plasma membrane:

A

irregular with hairlike or ruffled projections (irregularity can be seen under phase microscopy or electron microscopy)

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72
Q

Nucleus: round to oval, folded/ bilobed

A

HC

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73
Q

HC Chromatin:

A

loose and lacy (like monocyte/mononuclear)

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74
Q

HC B-Cell Marker:

A

present

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75
Q

HCL LABORATORY DIAGNOSIS

A

Bone marrow aspiration

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76
Q

Usually results to DRY TAP (due to fibrotic bm)

A

Bone marrow aspiration

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77
Q

● Increase in reticulin fiber

A

Bone marrow aspiration

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78
Q

HCL = (+) TRAP (Tartrate Resistant Acid Phosphatase)

A

Bone marrow aspiration

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79
Q

HCL contains the [?] which is usually detected by your TRAP

A

ACP isoenzyme 5

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80
Q

HCL TREATMENT

A

● Alkylating agents

● Corticosteroid

● Splenectomy

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81
Q

: reduce tumor burden but makes cytopenia worse

A

● Alkylating agents

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82
Q

are not selective of the cells that it kills, so it makes the count lower and lower

A

alkylating agents

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83
Q

: causes serious infection (used before)

A

● Corticosteroid

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84
Q

: treatment of choice/ best treatment for HCL

A

● Splenectomy

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85
Q

 Remember that one of the characteristics is large spleen. So with the removal of spleen (splenectomy), it allows the volume of the cell which was previously sequestered by the spleen to remain in the circulation and it raises the cell count

A

HCL

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86
Q

 So the only way that we can raise the cell count to prevent decreased levels of B cells in circulation is to remove the spleen. Because the larger the spleen, the more it sequesters the cells

A

HCL

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87
Q

cancers of the lymph nodes characterized by uninhibited growth of cellular elements normally found in lymphatic tissues resulting to lymph node enlargement.

A

LYMPHOMAS

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88
Q

● Are uninhibited growth of cellular elements which is found in the lymphatic tissue

A

LYMPHOMAS

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89
Q

● The cells inside the lymphatic tissue (T cell and B cells), it grows uninhibited and unregulated

A

LYMPHOMAS

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90
Q

● Characterized by abnormal lymph node enlargement with disruption or replacement of the normal histologic structures

A

LYMPHOMAS

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91
Q

● Because of the growth of cellular elements in that tissue, disruption and replacement occurs of the normal tissues making the structure abnormal.

A

LYMPHOMAS

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92
Q

▪ presence of small lymphocytes with many fine cytoplasmic extensions

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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93
Q

▪ with most consistent splenomegaly (splenectomy is often considered)

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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94
Q

▪ laboratory diagnosis: TRAP (+)

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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95
Q

▪ prognosis:
• quite good (benign)
• can be longer than 10 years

A
  1. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
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96
Q

This is a B-cell neoplasm associated with EBV and HIV infections.

A

BURKITT LYMPHOMA

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97
Q

It is endemic among African children (observed as jaw mass).

A

BURKITT LYMPHOMA

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98
Q

Cytogenic abnormality involves a translocation of c-myc gene on chromosome regions (Ch 8:14)

A

BURKITT LYMPHOMA

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99
Q

Variable/pleomorphic  can be cancer cells or normal

A

HODGKIN DISEASE/HODGKIN LYMPHOMA

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100
Q

Uniformly neoplastic  only one cellular characteristic

A

NON-HODGKIN LYMPHOMA

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101
Q

Multinucleated neoplastic cell (Reedsternberg cell)

A

HODGKIN DISEASE/HODGKIN LYMPHOMA

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102
Q

B lymphocyte , T lymphocyte

A

NON-HODGKIN LYMPHOMA

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103
Q

Unifocal

A

HODGKIN DISEASE/HODGKIN LYMPHOMA

104
Q

 It starts at one point only and spreads out.

A

HODGKIN DISEASE/HODGKIN LYMPHOMA

105
Q

 It is predictable and easily controlled.

A

HODGKIN DISEASE/HODGKIN LYMPHOMA

106
Q

Multifocal

A

NON-HODGKIN LYMPHOMA

107
Q

 It involves multiple lymph nodes and even non-lymphatic tissues.

A

NON-HODGKIN LYMPHOMA

108
Q

 Less predictable

A

NON-HODGKIN LYMPHOMA

109
Q

This is characterized by painless enlarged lymph node usually in the neck and/or in some, the cervical nodes that spreads in an orderly fashion.

A

HODGKIN LYMPHOMA

110
Q

Signs & symptoms include fever, night sweats or 10% weight loss in 6 months, or a combination of both.

A

HODGKIN LYMPHOMA

111
Q

Leukocytosis and lymphocytopenia are observed in advance cases.

A

HODGKIN LYMPHOMA

112
Q

HODGKIN LYMPHOMA
• Diagnosis:

A

lymph node biopsy

113
Q

Reed-Sternberg cell is considered as hallmark finding

A

HODGKIN LYMPHOMA

114
Q

CAUSE: Unknown

A

HODGKIN LYMPHOMA

115
Q

HODGKIN LYMPHOMA PREDISPOSITION FACTORS (PROPOSED):

A
  1. Genetic influence
  2. Environmental hazards
  3. Infectious agent (EPSTEIN BARR VIRUS)
116
Q

● Painless enlarged lymph node (but if the enlargement is rapid it becomes painful)

A

HODGKIN LYMPHOMA

117
Q

● Mediastinal mass in between the lung chamber

A

HODGKIN LYMPHOMA

118
Q

● Enlarged cervical nodes

A

HODGKIN LYMPHOMA

119
Q

● Enlarged lymph nodes

A

HODGKIN LYMPHOMA

120
Q

● Fever, night sweats and weight loss

A

HODGKIN LYMPHOMA

121
Q

: no symptoms, the peripheral blood has abnormality but it doesn’t present symptoms

A

● A

122
Q

: patient has one or more symptoms

A

● B

123
Q

HODGKIN LYMPHOMA LABORATORY DIAGNOSIS

A

PERIPHERAL BLOOD (INCREASED: MONOCYTE AND EOSINOPHIL , INCREASED IN WBC, PLASMA CELLS)

BONE MARROW

OTHERS:
● Decreased: Iron, TIBC
● DAT (+): due to the presence of hemolytic anemia

124
Q

HODGKIN LYMPHOMA DEFINITIVE DIAGNOSIS:

A

● Lymph node biopsy (if bone marrow biopsy is not available; primary organ involved)
● Confirmatory: Reed Sternberg cells

125
Q

● Presence of large abnormal lymphocyte w/ little cytoplasm and irregular nucleus

A

INCREASED: MONOCYTE AND EOSINOPHIL

126
Q

(This stage stage mimics leukemoid reaction usually seen in leukemia; confused as leukemia instead of lymphoma)

A

INCREASED IN WBC

127
Q

● Lymphocytopenia

A

INCREASED IN WBC

128
Q

● Presence of large bizarre platelets (seen during progression of disease)

A

INCREASED IN WBC

129
Q

● Granulocytosis (↑basophil, eosinophil and neutrophil [granulocytes]; ↓lymphocytes [agranulocytes])

A

INCREASED IN WBC

130
Q

usually Reed-Sternberg cell

A

PLASMA CELLS

131
Q

This stage occurs when there is predisposition of viral infection [Ex. EBV]

A

PLASMA CELLS

132
Q

● Large monocytes with vacuoles

A

PLASMA CELLS

133
Q

● Large lymphocyte with deeply basophilic cytoplasm

A

PLASMA CELLS

134
Q

HODGKIN LYMPHOMA Blood picture:

A

normocytic and normochromic (anemic)

135
Q

● Seldom involved except in stage IV (not a common basis due to fibrotic bm, unlike in leukemia with blast cells)

A

BONE MARROW

136
Q

● Decreased: Iron, TIBC

A

HODGKIN LYMPHOMA

137
Q

: due to the presence of hemolytic anemia

A

HODGKIN LYMPHOMA
● DAT (+)

138
Q

● Multinucleated

A

REED STERNBERG CELLS

139
Q

REED STERNBERG CELLS  Nuclear membrane:

A

demarcated and thick (not smooth)

140
Q

REED STERNBERG CELLS  Nuclei:

A

usually eosinophilic (orange) with a distinct halo

141
Q

● 4 to 8x size of normal lymphocyte

A

REED STERNBERG CELLS

142
Q

● Can be isolated and cultured

A

REED STERNBERG CELLS

143
Q

● Can be used to diagnose the disease

A

REED STERNBERG CELLS

144
Q

● Resembles an owl eyed appearance

A

REED STERNBERG CELLS

145
Q

● It cannot be distinguished as B lymphocyte, T lymphocyte and monocyte because it shares common features with those three cells but it does not have the antigenic markers, which is unique in B and T lymphocytes, and monocytes.

A

REED STERNBERG CELLS

146
Q

based on the extent of infiltration and abundance of RS cells

A

RYE CLASSIFICATION

147
Q

RYE CLASSIFICATION

Observed patterns are the presence of:

A

 lymphocyte dominance
 nodular sclerosis
 mixed cellularity
 lymphocyte depletion

148
Q

(RS is located on the lacuna of the lymph node)

A

nodular sclerosis

149
Q

(fibrosis is diffused; lymphocyte cannot produce nor proliferate because the bone marrow is fibrotic; lymphocyte still comes in the bone marrow and it only matures in the spleen and lymph node).

A

lymphocyte depletion

150
Q

: Abundant Lymphocytes; No fibrosis

A
  1. Lymphocyte Predominant
151
Q

: Moderate lymphocytes with nodulating collagen bands; RS in clear zones

A
  1. Nodular Sclerosis
152
Q

: Moderate lymphocytes in diffuse pattern

A
  1. Mixed Cellularity
153
Q

: Few lymphocytes w/ diffused fibrosis

A
  1. Lymphocyte Depleted
154
Q

Roman numbers I - IV indicate the region of lymph node affected

A

ANN ARBOR STAGING SYSTEM

155
Q

Suffixes A and B and subscripts E and S indicate
A = no symptoms
B = presence of symptoms
E = extralymphatic involvement
S = spleen involvement

A

ANN ARBOR STAGING SYSTEM

156
Q

Single lymph node/extralymphatic organ

A

Stage I

157
Q

Two or more lymph nodes/contiguous extralymphatic organ

A

Stage II

158
Q

 Same side as the lymph node (either left only or right only)

A

Stage II

159
Q

Lymph nodes on both sides of diaphragm Splenic/ extralymphatic involvement

A

Stage III

160
Q

 Both sides of lymph nodes are affected

A

Stage III

161
Q

Diffuse one or more extralymphatic organ

A

Stage IV

162
Q

 Other organs are also affected

A

Stage IV

163
Q

TREATMENT OF HODGKIN DISEASE

A

chemotherapy , radiation and myelosuppresive

164
Q

: causes rapid tumor lysis/targets tumor burden of the body

A

Chemotherapy

165
Q

if tumor is rapidly lyse it releases intracellular substances (tumor is made up of tissues and tissues contain cells; each cell contains intracellular substances such as: Uric Acid, Potassium and Phosphate)

A

Chemotherapy

166
Q

Example: release of High Phosphate (Hyperphophatemia)

A

Chemotherapy

167
Q

may helpin Hodgkin Diseases in removing the tumor but can cause complications

A

Chemotherapy

168
Q

effect of phosphate =

A

lower down the calcium (hypocalcimia); renal failure (accumulation of Blood Urea Nitrogen due to Uric Acid)

169
Q

A more common type than Hodgkin lymphoma.

A

NON-HODGKIN LYMPHOMA

170
Q

It is a B-cell lymphoma characterized by painless lymph node enlargement (cervical nodes are most often involved).

A

NON-HODGKIN LYMPHOMA

171
Q

NON-HODGKIN LYMPHOMA BY VIRCHOW:

A

 Leukemic
 Aleuemic

172
Q

: otherwise known as lymphosarcoma

A

Aleuemic NON-HODGKIN LYMPHOMA

173
Q

Occurs in Male

A
  1. NON-HODGKIN LYMPHOMA
174
Q

Congenital immunodeficiency

A
  1. NON-HODGKIN LYMPHOMA
175
Q

Immune diseases: RA, Sjorgen`s Syndrome, SLE

A
  1. NON-HODGKIN LYMPHOMA
176
Q

AIDS

A
  1. NON-HODGKIN LYMPHOMA
177
Q

EBV

A
  1. NON-HODGKIN LYMPHOMA
178
Q

HTLV1

A
  1. NON-HODGKIN LYMPHOMA
179
Q

ex: Ataxia, Telangiectasia, Wiscott Aldrich, IgA deficiency

A

Congenital immunodeficiency

180
Q

effect: increases the risk to non-hodgkin lymphoma 10,000x

A

Congenital immunodeficiency

181
Q

effect: increases the risk to non-hodgkin lymphoma 3-40x

A

Immune diseases: RA, Sjorgen`s Syndrome, SLE

182
Q

: causative agent of infectious mononucleosis

A

EBV

183
Q

causes also the African Burkitt Lymphoma

A

EBV

184
Q

: Acute T cell Leukemia and Lymphoma

A

HTLV1

185
Q

Blood counts are normal (in some cases there is hemolytic anemia)

A
  1. NON-HODGKIN LYMPHOMA
186
Q

DAT positive

A
  1. NON-HODGKIN LYMPHOMA

HODGKIN LYMPHOMA

187
Q

Autoimmune thrombocytopenia (not common)

A
  1. NON-HODGKIN LYMPHOMA
188
Q

Some abnormalities such as alkaline phosphatase, LD, and uric acid (due to the accumulation/lysis of tumor)

A
  1. NON-HODGKIN LYMPHOMA
189
Q

NON-HODGKIN LYMPHOMA CLASSIFICATIONS

A

LOW GRADE

INTERMEDIATE GRADE

HIGH GRADE

190
Q

45-60 y/o

A

LOW GRADE

191
Q

Slow growing lymphoma

A

LOW GRADE

192
Q

Small cell lymphoma

A

LOW GRADE

193
Q

Cell involved: small cell lymphocytes, however with a progression it can evolve to large cell lymphoma

A

LOW GRADE

194
Q

Survival: 5-7 years

A

LOW GRADE

195
Q

Rapid lymph node enlargement and extranodal disease

A

INTERMEDIATE GRADE

196
Q

BM is not involved

A

INTERMEDIATE GRADE

197
Q

Large cell lymphoma

A

INTERMEDIATE GRADE

198
Q

Cell involved: large lymphocytes (worse prognosis)

A

INTERMEDIATE GRADE

199
Q

Survival: 1.5 – 3 years

A

INTERMEDIATE GRADE

200
Q

Most rapid enlargement of LN (fastest developing malignancy)

A

HIGH GRADE

201
Q

HIGH GRADE Subclassifications:

A

a. Immunoblastic lymphoma

b. Lymphoblastic lymphoma

c. Small noncleaved cell lymphoma

202
Q

c. Small noncleaved cell lymphoma Two subtypes (classification depends on the lymph node biopsy – If it is disseminated to bone marrow and CNS)

A

C1. Burkitt

C2. Non burkitt

203
Q

Occurs in more than 50 years old

A

a. Immunoblastic lymphoma

204
Q

Arises in the CNS

A

a. Immunoblastic lymphoma

205
Q

Short survival:: months to a year

A

a. Immunoblastic lymphoma

206
Q

Occurs in teens to 20`s

A

b. Lymphoblastic lymphoma

207
Q

Presence of mediastinal mass

A

b. Lymphoblastic lymphoma

208
Q

Chemotherapy: subjected to relapse (not successful; prognosis becomes poorer and poorer)

A

b. Lymphoblastic lymphoma

209
Q

Occurs in children to 30 years of age

A

c. Small noncleaved cell lymphoma

210
Q

With cytogenetic abnormality

A

C1. Burkitt

211
Q

Translocation in the C-MYC gene located in t(Ch8:14)

A

C1. Burkitt

212
Q

No cytogenetic abnormality

A

C2. Non burkitt

213
Q

NON-HODGKIN LYMPHOMA DIAGNOSIS:

A

Lymph node biopsy

214
Q

NON-HODGKIN LYMPHOMA TREATMENT

A

● Radiation: Stage I and II low grade lymphoma
● Chemotherapy: all stages

215
Q

: Stage I and II low grade lymphoma

A

● Radiation

216
Q

: all stages

A

● Chemotherapy

217
Q

Various type of malignant cells:

A
  1. Small lymphocytes
  2. Small cleaved cell
  3. Small noncleaved cell
  4. Large cell (cleaved/non cleaved)
  5. Immunoblastic large cell
  6. Lymphoblastic cell
218
Q
  • associated with low grade small lymphocytic lymphoma
A
  1. Small lymphocytes
219
Q
  1. Small lymphocytes- Microscopic examination:
A

diffuse pattern of small lymphocytes

220
Q
  • Small but actually slightly larger than normal lymphocyte
A
  1. Small cleaved cell
221
Q
  • Cytoplasm is non visible
A
  1. Small cleaved cell
222
Q
  • Misnamed (not really small, but actually larger; intermediate between small and large)
A
  1. Small noncleaved cell
223
Q
  • Seen in burkitt and non-burkitt
A
  1. Small noncleaved cell
224
Q

: uniform size and shape

A
  • Burkitt
225
Q

: heterogeneous size and shape

A
  • Non burkitt
226
Q

: malignant cell can be seen in a high grade

A
  • Small noncleaved cell lymphoma
227
Q
  • 2-3x larger than normal lymphocyte
A
  1. Large cell (cleaved/non cleaved)
228
Q
  • Spotty chromatin condensation and thin rim of cytoplasm around the nucleus
A
  1. Large cell (cleaved/non cleaved)
229
Q
  • Present in high grade
A
  1. Immunoblastic large cell
230
Q
  • A lot bigger; 4-8x larger than normal lymphocyte
A
  1. Immunoblastic large cell
231
Q
  • Cytoplasm is abundant (but faint when stained)
A
  1. Immunoblastic large cell
232
Q
  • Usually large and round with convoluted nucleus
A
  1. Lymphoblastic cell
233
Q

This affects the mature T cells.

A

MYCOSIS FUNGOIDES

234
Q

This is an early stage of Sezary syndrome and is characterized by pruritus, eczematoidal psoriasiform non-specific exfoliative dermatitis.

A

MYCOSIS FUNGOIDES

235
Q

Diagnostic evaluation of the skin reveals Pautrier’s microabscesses (clusters of lymphocytes forming on the skin) accompanied by parakeratosis.

A

MYCOSIS FUNGOIDES

236
Q

● Early onset: pruritus (severely itching skin)

A

MYCOSIS FUNGOIDES

237
Q

MYCOSIS FUNGOIDES
● Progression:

A

demarcated reddened plaques (thickening of skin)

238
Q

: plaques and desquamation of large flakes in the skin

A

MYCOSIS FUNGOIDES

Generalized erythroderma

239
Q

● Appearance of “Pautrier’s microabscess”

A

MYCOSIS FUNGOIDES

240
Q

● Mycosis fungoides:

● Sezary syndrome:

A

skin

lymph node and visceral involvement (spleen, liver)

241
Q

● Lymphocytes: larger, with a cleft in the nucleus

A

MYCOSIS FUNGOIDES

242
Q

● Special test: monoclonal ab reacting to surface markers → presence of CD4+ (T cell) subtype of helper cell

A

MYCOSIS FUNGOIDES

243
Q

This stage manifests infiltration of the lymph nodes and viscera, characterized by band-like infiltrates of lymphocytes with cerebriform nuclei called Sezary cells

A

SEZARY SYNDROME

244
Q

Wider dissemination of mycosis fungoides

A

SEZARY SYNDROME

245
Q

Pautrier’s microabscess is seen (band-like infiltrate of lymphocytes)

A

SEZARY SYNDROME

246
Q

Band like infiltrate of lymphocytes in cluster in the epidermis that infiltrated the epidermis

A

“Pautrier’s microabscess”

247
Q

PLASMA CELL DYSCRASIAS

A
  1. Multiple Myeloma
  2. Waldenstrom Macroglobulinemia
  3. Heavy Chain Disease (HCD)
248
Q

• Chemistry: Bence Jones Protein (BJP)

A
249
Q

• Urinalysis: Many hyaline casts and positive BJP

A
250
Q

• Hematology:
-Elevated ESR
-Rouleaux formation
-Flame cells (plasma cell with red to pink cytoplasm associated with increase in IgA)
-Dutcher bodies intranuclear crystalline structures of abnormal IgG)
-Russel bodies (accumulations of IgG)
-Grape cell/Mott cell, Morula cell (plasma cell that contains small colorless or blue/pink protein vacuoles that appear like grapes)

A
251
Q

(plasma cell with red to pink cytoplasm associated with increase in IgA)

A

-Flame cells

252
Q

intranuclear crystalline structures of abnormal IgG

A

-Dutcher bodies

253
Q

(accumulations of IgG)

A

-Russel bodies

254
Q

(plasma cell that contains small colorless or blue/pink protein vacuoles that appear like grapes)

A

-Grape cell/Mott cell, Morula cell

255
Q

This is the second most common type of plasma cell dyscrasia.

A
  1. Waldenstrom Macroglobulinemia
256
Q

Malignant plasma cells show increase production of IgM (>3 g/dL).

A
  1. Waldenstrom Macroglobulinemia
257
Q

This shows an abnormal synthesis of heavy chains (Gamma HCD; Alpha HCD)

A
  1. Heavy Chain Disease (HCD)

Hematology 2 Lec (29 decks)

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