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3.4b WBC Patholoy II Flashcards

0
Q

What is the main difference between acute and chronic leukemia?

A

Number of blasts seen in PBS

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1
Q

Malignant neoplasms of hematopoietic cells characterized by REPLACEMENT of BM by neoplastic cells, which eventually SPILL INTO BLOOD

A

Leukemia

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2
Q

Subtypes of Leukemia (4)

A
  1. Chronic Lymphocytic Leukemia (CLL)
  2. Acute Lymphocytic Leukemia (ALL)
  3. Chronic Myelogenous Leukemia (CML)
  4. Acute Myelogenous Leukemia (AML)
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3
Q

What disorders often accompany leukemia? (2)

A
  1. Thrombocytopenia

2. Anemia

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4
Q

Lab test used to diagnose leukemia

A

Biopsy of BM

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5
Q
  1. Most common cancer of children (F

3. Whites > Blacks

A

ALL

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6
Q

Pathology in ALL

A

Mutation of genes required for B-cell development -> Blocked maturation

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7
Q

Immunohistochemical marker for ALL: Immature cells (pre-B and pre-T lymphoblasts)

A

(+) Tdt

an immunomarker for immature cells :. all precursor cells would be Tdt+

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8
Q

Immunohistochemical marker for ALL: Mature “late pre-B” ALL

A

(+) CD10, 19, 20

IgM heavy chain

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9
Q

70% of T-ALLs have a mutation in?

A

NOTCH1, which is required in T-cell development

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10
Q

In B-ALLs, there is mutation in? (4)

A

PAX5
E2A
EBF
t(12:21)

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11
Q

Mass effect of ALL

A

Bone Pain
-Caused by neoplastic infiltration and marrow expansion of subperiosteum leading to bone resorption

Testicular enlargement

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12
Q

Symptoms in ALL that are related to DEPRESSION OF MARROW FUNCTION (3)

A
  1. Fatigue d/t anemia
  2. Fever d/t infections secondary to neutropenia
  3. Bleeding d/t thrombocytopenia
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13
Q

Complications seen in T-ALL are related to what?

A

Compression of larger vessels and airways in the mediastnum

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14
Q

The ff indicate a favorable prognosis for which disease?

  1. 2-10 year olds
  2. Low white cell count
  3. Hyperploidy
  4. Trisomy of chromosomes 4,7,10
  5. Presence of a t(12:21)
A

ALL

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15
Q

Low grade chronic B cell leukemia characterized by the presence of fine hair-like projections on the lymphocytes

A

Hairy Cell Leukemia

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16
Q

What is the basis of leukemia in Hairy Cell Leukemia?

A

Proliferation of lymphocytes in the BM (decreased WBC in peripheral blood)

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17
Q

Important to know about Hairy Cell Leukemia (3)

A

Massive splenomegaly
(+) TRAP
Middle-aged

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18
Q

Pathology in Hairy Cell Leukemia

A

Proliferation of WBC (particularly lymphocytes) in BM enmeshed in a network of reticulum -> hard to pass through peripheral blood -> cytopenia -> splenomegaly

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19
Q

Hairy cell leukemia typically expresses which markers? (3)

A
  1. Pan B-cell markers: CD19,20

2. Surface Ig, usually IgG

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20
Q

Common manifestation in Hairly cell leukemis

A

massive splenomegaly

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21
Q

What lab diagnosis is specific for hairy cell leukemia?

A

(+) TARP: Tartarate Resistant Acid Phosphatase

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22
Q

Microscopic features of Hairy Cell Leukemia (2)

A
  1. Fried egg or honeycomb appearance

2. Fine hair-like projections on lymphocyte

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23
Q

Which of the myeloid series:

  1. Contains large primary granules
  2. Nucleus is 50-60% of the cell size
A

Promyelocyte

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24
Q

Which of the myeloid series:

  1. Sunset appearance (a clearing near the nucleus)
  2. Nucleus is 50% of the size
  3. First cell in the series to contain specific granules
A

Myelocyte

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25
Q

Which of the myeloid series:

  1. Appearance with a slight indentation of the nucleus
  2. Also with sunset appearance
A

Metamyelocyte

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26
Q

Which of the myeloid series:

1. Indentation reaches 50% of the nucleus

A

Stab cell

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27
Q

Myeloid disorders (3)

A
  1. Acute myelogenous leukemia (AML) - malignant
  2. Myelodysplastic syndrome (MDS) - premalignant
  3. Chronic Myeloproliferative Disorders (4)
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28
Q

In Chronic myeloproliferative disorders, there is the presence of all types of myeloid series (4)

A

Malignant

  1. CML
  2. Polycythemia vera

Premalignant

  1. Essential Thrombocytosis
  2. Myelofibrosis
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29
Q

Myeloid disorder caused by the accumulation of immature myeloid forms in the BM

A

AML

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30
Q

Myeloid disorder where

  1. stem cells are destroyed
  2. ineffective hematopoiesis -> cytopenias
A

Myelodysplastic Syndrome (MDS)

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31
Q

Pathology in AML

A

Block in maturation of myeloid stem cell -> impede differentiation

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32
Q

Most cases of ALL are due to translocations between which two chromosomes?

A

Chromosome 12 and 21

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33
Q

DIC is unique for which classification of AML that are NOS (M0-M7)?

A

M3 (acute promyelocyte)

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34
Q

If both Auer rods (coalescent granules) and enzymes (myeloperoxidase) are present, it is classified under which classification of AML that are NOS?

A

M2 (mature)

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35
Q

What is the specific genetic abnormality seen in M3?

A 
RARA gene (Retinoic Acid Receptor Alpha)
-located on chromosome 17
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36
Q

Absence of this gene leads to a block in the maturation of promyelocyte to myelocyte

A

RARA gene

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37
Q

Treatment for M3 (2)

A
  1. Retinoid acid treatment

2. Chemotherapy

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38
Q

The ff are laboratory diagnoses for?

  1. Elevated WBC counts
  2. Low platelet and RBC count (d/t BM suppression)
  3. > 20% blast cells in WBC differential count
  4. Special stains:
    - Nonspecific esterase: monoblasts
    - Myeloperoxidase: myeloblasts
    - PAS: lymphoblasts
A

AML

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39
Q

Which classification of AML that are NOS is being described?

  1. (+) myelocytes with les granules
  2. Abundant cytoplasm
A

M2: AML with maturation

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40
Q

Which classification of AML that are NOS is being described?

  1. (+) promyelocytes with Auer rods (look like dark scratches)
  2. (+) primary granules in cytoplasm
A

M3: Acute promyelocyte

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41
Q

M0 or M5 (Myeloid without differentiation or acute monocytic leukemia) can be differentiated using what test?

A

Esterase Test

-Monocytic cells are esterase (+) and have nuclei that are more irregular and cerebroid

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42
Q

Which classification of AML that are NOS is being described?
(+) RBC presursors
Royal blue cytoplasm

A

M6: Acute Erythroid Leukemia

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43
Q

What stain is used for cells of myeloid linease?

A

Peroxidase

√positive result: fine brown dots in cytoplasm

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44
Q

Which stain is used for lymphoblasts?

A

PAS (Periodic Acid Schiff)

√(+) result: large pink dots in cytoplasm

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45
Q

Which stain is used for monoblasts?

A

Nonspecific esterase

√(+) result: red stain

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46
Q

Treatment for AML

A

BM transplant

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47
Q

s/sx for AML that are common for all forms (3)

A
  1. Anemia
  2. Decreased platelet
  3. Neutropenia
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48
Q

(S/SX) What specific change can be seen in M3?

A

DIC

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49
Q

(S/SX) What specific change can be seen in M1 and M2?

A

Granulocytic sarcoma (chloroma) - tumurous infiltration of soft tissue and bones

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50
Q

(S/SX) What specific change can be seen in M4 and M5?

A

Infiltration of gums and skin (leukemic cutis)

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51
Q

In the case of granulopoiesis, the stage before the occurrence of anaplasia is?

A 
Myelodysplastic Syndrome (MDS)
√myeloid stem cell is damaged
√can still produce cells but they're all abnormal -> maturation defects -> ineffective hematopoiesis
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52
Q

Pathology in Myelodysplastic Syndrome (MDS)

A

Stem cell damage -> maturation defects associated with ineffective hematopoiesis

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53
Q

Deletions and monosomy 5 &7 are seen in?

A

Myelodysplastic Syndrome (MDS)

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54
Q

Treatment of Myelodysplastic Syndrome (MDS)

A

BM transplant for younger patients

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55
Q

In which disease can the ff cellular abonrmalities that affect all nonlymhpoid cells be seen?

  1. Ringed sideroblasts
  2. Megaloblastoid maturation
  3. Pawn ball megakaryocytes
  4. Nuclear budding
  5. Abnormal granulation
  6. Pseudo Pelger-Huet cells
56
Q

Disease in which a lot of different cells are produced but dies before entering peripheral blood

A

Myelodysplastic Syndrome (MDS)

57
Q

What is the picture of the BM in MDS?

A

Hypercellular

58
Q

PBS in MDS

59
Q

In this disease, blast cells can be present. In inflammation, shift to the left occurs until myelocytes.

60
Q

In this disease, the changes seen are so diverse that it affects RBCs, platelets, WBC, all of which results from STEM CELL DAMAGE :. it can lead to production of myelogenous leukemia.

61
Q

In which disease can this be seen?

+) Pseudo Pelger-Huet nuclei (2 lobes

62
Q

In ___, there is abnormal deposition of iron in the the perinuclear portion of the red cell (normally, iron must be evenly distributed)

63
Q

It is the result of an increased production of one or more types of blood cells

A

Myeloproliferative Disorders (MPD)

64
Q

Myeloprolifeative Disorders (4)

A
  1. Chronic Myelogenous Leukemia
  2. Polycythemia Vera
  3. Essential Thrombocytosis
  4. Myelofibrosis of BM
65
Q

It is the neoplastic transformation of multipotent progenitor cells capable of giving mostly to mature myelogenous cells

66
Q

It is caused by a continuous stimulatory effect to multipotent or pluripotent progenitor cekks -> these cells lose normal proliferative control

67
Q

In MPD, the abnormality is due to?

A

Mutated Tyrosine Kinase -> stem cell circumvents normal control -> growth factor-indepent proliferation and survival of marrow progenitors

68
Q

Due to its mutation in MPD, this enzyme becomes “constitutively activated” but DOES NOT lead to impaired differentiation

A

Tyrosine Kinase

69
Q

Normally, tyrosine kinase is activated by?

A

Hematopoietic growth factors

70
Q

Variable transformation in MPD is characterized by? (2)

A
  1. BM fibrosis
  2. Peripheral blood cytopenias

Exhaustion from constant proliferation leads to a stop -> BM fibrosis -> cytopenia -> malignancy -> acute leukemia

71
Q

Which disease involves the ff?

  1. Involves large volumes of cells from the BM and
  2. Homing of neoplastic cells from the BM to secondary hematopoietic organs (liver and spleen aka Extramedullary hematopoiesis) -> hepatosplenomegaly
72
Q

What disease causes the ff pathology?

Causes a neoplastic transformation of pluripotent GRANULOCYTIC stem cells with NO BLOCK in maturation

A

Chronic myelogenous leukemia (CML)

73
Q

What is the chromosomal abnormality in CML?

A

Translocation of ABL and BCR gene t(9:22) -> Philadelphia chromosome

74
Q

Treatment of CML

75
Q

Preferentially drive MEGAKARYOCYTIC progenitors and causes abnormal release of immature granulocytic forms from the BM to blood

76
Q

What enzyme is absent in WBC as seen in CML?

A

Alkaline phosphatase
√ kills bacteria
√ increased during infections

77
Q

What is used to differentiate leukemoid reaction from CML?

A

Alkaline phosphatase

REMEMBER:
CML: (+) blast cells
Leukemoid reaction: (-) blast cells

78
Q

PBS of?

  1. Thrombocytosis
  2. High platelet count
  3. All stages of maturation are present
A

CML

*High platelet count indicates that it is chronic

79
Q

Clinical features of?

  1. First symptom
    - dragging sensation in the abdomen d/t massive splenomegaly OR
    - upper quadrant abdominal pain d/t splenic infarction
  2. Hypermetabolism d/t increased cell turnover
  3. Fatigability, weakness, weight loss, anorexia
  4. Mild to medium anemia
80
Q

Stem cell disorder CONFINED to MEGAKARYOCYTE

A

Essential Thrombocytosis

81
Q

What clinical characteristics seen in Essential Thrombocytosis are seen due to a large number of dysfunctional platelet? (2)

A
  1. Thrombosis

2. Hemorrhage

82
Q

PBS seen in?

  1. Giant platelets with very high count
  2. Mild leukocytosis
  3. Modest degrees of extramedullary hematopoiesis -> organomegaly
A

Essential Thrombosis

83
Q

Obliterative marrow fibrosis is the hallmark sign of?

A

Myelofibrosis: replacement of BM by fibrosis -> extensive extramedullary hematopoiesis -> hepato and splenomegaly

84
Q

Its chief pathologic feature is: extensive deposition of collagen in the marrow by non-neoplastic fibroblasts

-> marrow failure

A

Myelofibrosis

85
Q

Changes in the BM:
Hypercellular d/t increases in maturing cells of all lineages
-> becomes more hypocellular and diffusely fibrotic -> osteosclerosis (fibrotic marrow space is converted into bone)

A

Myelofibrosis

86
Q

Sites of extramedullary hematopoiesis in Myelofibrosis (3)

A

spleen
liver
LNs

87
Q

PBS of?

  1. Leukoerythroblastosis
    - d/t premature release of nucleated erythroid and early granulocytic progenitors
  2. Dacrocytes (tear-drop shaped cells)
A

Myelofibrosis

88
Q

Clinical characteristics of?

  1. Progressive anemia: moderate to severe normochromic normocytic anemia
  2. Splenomegaly
  3. Abdominal enlargement
  4. Hyperuricemia and gout
  5. Fatigue, weight loss, night sweats
A

Myelofibrosis

89
Q

Cells that results from B-cell proliferation that synthesize or secrete Ig or its fragments

A

Plasma cells

90
Q

Plasma Cell Dyscrasias and Disorders (5)

A
  1. Myeloma
  2. Waldenstorm Macroglobulinemia
  3. Heavy Chain Release
  4. Primary/Immunocyte-associated amyloidosis
  5. Monoclonal Gammopathy of Undetermined Significance
91
Q

Benign counterpart of multiple myeloma

A

Plasmacytoma

92
Q

What is the most common plasma cell gammopathy?

A

Multiple Myeloma

93
Q

What protein is present in the urine of patients with Multiple Myeloma?

A

Bence Jones Protein

94
Q

Pathology in MM? (2)

A
  1. Increased M-protein
  2. Multifocal destructive bone lesion throughout skeletal system
    - affects central > long bones
95
Q

What is seen in the xray of those with MM?

A

Soap bubble appearance

96
Q

What is seen in the BM biopsy in MM? (3)

A
  1. Replacement of marrow cells with plasma cells
  2. Russel bodies (in cytoplasm)
  3. Dutcher bodies (in nucleus)
97
Q

Describe the morphology of normal plasma cells (2)

A
  1. Clock-face nuclei

2. Eccentrically located nuclei

98
Q

Clinical s/sx of?

  1. Infiltration of bones
  2. Recurrent infection d/t suppression of normal Ig
  3. s/sx of renal insufficiency: Bence Jones Proteinuria
99
Q

Complications in MM (3)

A
  1. Myeloma nephrosis
  2. Myeloma nephropathy
  3. Systemic amyloidosis
100
Q

In the diagnosis of MM, what is seen in the urine sample? (1)

A

Bence Jones Protein, which is specific to MM

101
Q

Rouleaux formation is present in __ d/t increased erythrocyte sedimentation rate

102
Q

In the lab diagnosis of MM, what is seen in blood or urine?

A

(+) M protein spike

103
Q

Proliferation of IMMATURE DENDRITIC CELLS (Langerhans histiocytes)

A

Histiocytosis

104
Q

The ff are microscopic characteristics of which cells seen in histiocytosis?

  1. Folded/grooved nuclei
  2. Moderately abundant pale cytoplasm, often vacuolated
  3. Mixed with a few eosinophils
A

Langerhans cells

105
Q

In histiocytosis, the proliferation of which cells is MONOCLONAL and is thus likely to be neoplastic in origin

A

Langerhans cell

106
Q

Birbeck granules are characteristic of which disorder?

A

Histiocytosis

107
Q

These are pentilaminar tubules often with a dilated terminal end producing a tennis racket-like appearance, which contain the protein langerin

A

Birbeck granules

108
Q

It is also known as UNIFOCAL and multifocal unisystem Langerhans cell histiocytosis

A

Eosinophilic granuloma

109
Q

Types of Histiocytosis (4)

A
  1. Eosinophilic granuloma
  2. Hand-Schuller-Christian Disease
  3. Letterer-Siwe Syndrome
  4. Pulmonary Langerhans Cell Histiocytosis
110
Q

It is characterized by proliferation of langerhans cells admixed with variable numbers of EOSINOPHILS, lymphocytes, plasma cells, neutrophils

A

Eosinophilic granuloma

111
Q

Where do eosinophilic granulomas usually arise?

A

Medullary cavities of bones

  • calvarium
  • ribs
  • femur
112
Q

In eosinophilic granuloma:
√ this most commonly affects the skeletal system in older children or adults
√ Indolent
√ may heal spontaneousl or cured by excision

A

Unifocal lesions

113
Q

In eosinophilic granuloma:
√ usually affects young children
√ present with multiple erosive bony masses that sometimes expand to adjacent soft tissue

A

multifocal unisystem disease

114
Q

It is aka Multifocal Unisystem Langerhans cell histiocytosis

A

Hand-Schuller-Christian Disease

115
Q

Its symptoms include a combination of:
√ calvarial bone defects (skull)
√ diabetes insipidus
√ exophthalmos

A

Hand-Schuller-Christian Disease

note: the three symptoms is collectively known as the Hand-Schuller-Christian triad

116
Q

What comprises the Hand-Schuller-Christian triad?

A

√ calvarial bone defects (skull)
√ diabetes insipidus
√ exophthalmos

117
Q

If exophthalmos are present in adults, rather than in children, the disease is now known as?

A

Grave’s disease

118
Q

It is also known as Multifocal Multisystem Langerhans cell histiocytosis

A

Letterer-Siwe Syndrome

119
Q

What is the dominant clinical feature in Letterer-Siwe Syndrome?

A

Development of cutaneous lesions that resemble a seborrheic eruption

120
Q

Extensive infiltration of the marrow -> anemia, thrombocytopenia, predisposition to recurrent infections such as otitis media and mastoiditis

this is seen in?

A

Letterer-Siwe Syndrome

121
Q

Who are affected in Letterer-Siwe Syndrome?

A

Infants

Young children

122
Q

The ff are symptoms of?

  1. Fever
  2. Concurrent hepatosplenomegaly, lymphadenopathy, pulmonary lesions, destructive osteolytic bone lesions (bone will have soft parts)
A

Letterer-Siwe Syndrome

123
Q

This represents a special category of disease most often seen in adult smokers and usually comprises a polyclonal population of langerhans cells (which suggests that it is a reactive hyperplasia rather than a true neoplasm)

A

Pulmonary langerhans cell histiocytosis

124
Q

It is a diversity of neoplasms that may arise from the thymus

125
Q

Most thymomas arise from which region?

A

Superior mediastinum

126
Q

Who are affected with thymomas?

A

Adults >40 years old. rare in children

127
Q

What are thymomas?

A

Tumors of thymic epithelial cells

128
Q

What are the (3) histologic subtypes of thymomas?

A
  1. Benign, noninvasive
  2. Benign, invasive/metastatic
  3. Malignant
129
Q

The ff are microscopic features of?

  1. neoplastic epithelial cells arranged in a swirling pattern and have bland oval to elongated nuclei with inconspicuous nucleoli
  2. only a few reactive lymphoid cells are interspersed
A

Benign thymoma (medullary type)

130
Q

The ff are microscopic features of?

  1. neoplastic epithelial cells are polygonal and have round to oval, bland nuclei with inconspicuous nucleoli
  2. Numerous reactive lymphoid cells are interspersed
A

Malignant thymoma

131
Q

The ff describe the morphology of?

  1. lobulated, firm, white-gray masses
  2. areas of cystic necrosis and calcification
  3. emcapsulated
132
Q

they are composed of medullary-type epithelial cells (Elongated or spindle-shaped) or a mixture of medullary- and cortical-type epithelial cells.

A

Noninvasive thymoma

133
Q

There is a mixture of polygonal cortical-type epithelial cells and a denser infiltrate of thymocytes

A

Mixed thymoma

134
Q

Refers to a tumor that is cytologically benign but locally invasive

A

Invasive thymoma

135
Q

Macroscopically, they are usually fleshy, invasive masses, sometimes accompanied by metastases to sites like the lungs

A

thymic carcinoma

136
Q

Microscopically, most are squamous cell carcinomas

A

Thymic carcinoma

137
Q

a tumor composed of sheets of cells with distinct borders that bear a close histologic resemblance to nasopharyngeal carcinoma

A

Lymphoepithelioma-like carcinoma

138
Q

Myasthenia gravis is a symptom of?

Pathology (10 decks)

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