CLL Flashcards by Arriane Cyrel (MTI)

B. CHRONIC LYMPHOPROLIFERATIVE DISORDERS

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

Chronic Lymphocytic Leukemia (CLL)

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● Less likely to undergo blastic transformation

Chronic Lymphocytic Leukemia (CLL)

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● Predisposition to autoimmune hemolytic anemia (AIHA)

Chronic Lymphocytic Leukemia (CLL)

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● is predominant in males (3:1 ratio)

Chronic Lymphocytic Leukemia (CLL)

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● CLL Cytogenetic abnormality:

➢ Extra Ch12

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

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

Chronic Lymphocytic Leukemia (CLL)

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Chronic, and involves mature cells

Chronic Lymphocytic Leukemia (CLL)

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Types of AIHA:

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

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 Duplicated Ch 12

Extra Ch12

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

Extra Ch12

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 predicts progression of disease

Extra Ch12

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common cell that is involved is the B-lymphocyte

B-CLL

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

B-CLL

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Dormant B-cells

B-CLL

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

Dormant B-cells

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o Cannot produce Ab even with the presence of Ag

Dormant B-cells

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B-CLL or T-CLL

Rare

T-CLL

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disseminated in the circulation/does not accumulate

T-CLL

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

T-CLL

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Enlarged lymph nodes, spleen and liver

Chronic Lymphocytic Leukemia (CLL)

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Pruritus

Chronic Lymphocytic Leukemia (CLL)

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: due to skin infection due to Herpes zoster

Pruritus

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Affects more of males; 50-60 years old

Chronic Lymphocytic Leukemia (CLL)

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

Chronic Lymphocytic Leukemia (CLL)

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

Chronic Lymphocytic Leukemia (CLL)

General symptoms of T-CLL:

erythroderma and pruritus

Median survival rate for patients with CLL:

3-4 years

Chronic Lymphocytic Leukemia (CLL) Lymphocyte count:

10-150 x 109/L

Presence of many SMUDGE CELLS

Chronic Lymphocytic Leukemia (CLL)

Hypogammaglobulinemia

Chronic Lymphocytic Leukemia (CLL)

Severe itching of the skin

Pruritus

: one of the first indication of CLL

Herpes zoster

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

SMUDGE CELLS

➢ Often confused with BASKET CELLS, but without vacuolation

SMUDGE CELLS

➢ Because of the decrease in the normal B-cell

Hypogammaglobulinemia

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

Chronic Lymphocytic Leukemia (CLL)

PROGNOSIS: 3-4 years from diagnosis

Chronic Lymphocytic Leukemia (CLL)

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

Chronic Lymphocytic Leukemia (CLL)

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

larger clumped or condensed very prominent

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).

tiny little clefting

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

Chronic Lymphocytic Leukemia (CLL)

➢ Glycogen = (+) PAS

Chronic Lymphocytic Leukemia (CLL)

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

>30% of lymphocyte in the BM.

Chronic Lymphocytic Leukemia (CLL) Treatment

1. LEUKAPHERESIS 2. GAMMA GLOBULIN INJECTIONS 3. RADIATION 4. CHEMOTHERAPY

Reduces the number of abnormal lymphocyte.

1. LEUKAPHERESIS

high lymphocyte in the PB = viscous blood

1. LEUKAPHERESIS

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

1. LEUKAPHERESIS

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

2. GAMMA GLOBULIN INJECTIONS

treat enlarged lymph nodes and spleen

3. RADIATION

reduce the tumor and abnormal lymphocyte in the PB

4. CHEMOTHERAPY

Aim: to reduce the tumor and abnormal lymphocyte

4. CHEMOTHERAPY

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

2. Pro-Lymphocytic Leukemia

▪ poorer prognosis than HCL and CLL

2. Pro-Lymphocytic Leukemia

● Rare variant of CLL (not common)

2. Pro-Lymphocytic Leukemia

● Increased in prolymphocyte, total replacement of BM

2. Pro-Lymphocytic Leukemia

● Decreased gamma globulins and T cells

2. Pro-Lymphocytic Leukemia

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

2. Pro-Lymphocytic Leukemia

2. Pro-Lymphocytic Leukemia ● Mean survival rate:

1 yr (usually less than a year)

2. Pro-Lymphocytic Leukemia ● Leukocyte count:

25-1000 x 109/L

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

2. Pro-Lymphocytic Leukemia ● Prolymphocyte

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

2. Pro-Lymphocytic Leukemia

● Rare (2%)

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

3. Hairy Cell Leukemia ● Otherwise known as

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

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis ● due to the growth and accumulation of hairy cell in the

spleen, bone marrow and PB

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis ● Mean survival rate:

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

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

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

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

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

HCL CHARACTERISTICS

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

HC Cytoplasm:

scant to abundant, agranular, light grayish blue

HC Plasma membrane:

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

Nucleus: round to oval, folded/ bilobed

HC Chromatin:

loose and lacy (like monocyte/mononuclear)

HC B-Cell Marker:

present

HCL LABORATORY DIAGNOSIS

Bone marrow aspiration

Usually results to DRY TAP (due to fibrotic bm)

Bone marrow aspiration

● Increase in reticulin fiber

Bone marrow aspiration

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

Bone marrow aspiration

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

ACP isoenzyme 5

HCL TREATMENT

● Alkylating agents ● Corticosteroid ● Splenectomy

: reduce tumor burden but makes cytopenia worse

● Alkylating agents

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

alkylating agents

: causes serious infection (used before)

● Corticosteroid

: treatment of choice/ best treatment for HCL

● Splenectomy

 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

HCL

 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

HCL

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

LYMPHOMAS

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

LYMPHOMAS

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

LYMPHOMAS

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

LYMPHOMAS

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

LYMPHOMAS

▪ presence of small lymphocytes with many fine cytoplasmic extensions

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

▪ with most consistent splenomegaly (splenectomy is often considered)

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

▪ laboratory diagnosis: TRAP (+)

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

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

3. Hairy Cell Leukemia/Leukemic Reticuloendotheliosis

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

BURKITT LYMPHOMA

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

BURKITT LYMPHOMA

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

BURKITT LYMPHOMA

Variable/pleomorphic  can be cancer cells or normal

HODGKIN DISEASE/HODGKIN LYMPHOMA

Uniformly neoplastic  only one cellular characteristic

NON-HODGKIN LYMPHOMA

Multinucleated neoplastic cell (Reedsternberg cell)

HODGKIN DISEASE/HODGKIN LYMPHOMA

B lymphocyte , T lymphocyte

NON-HODGKIN LYMPHOMA

Unifocal

HODGKIN DISEASE/HODGKIN LYMPHOMA

 It starts at one point only and spreads out.

HODGKIN DISEASE/HODGKIN LYMPHOMA

 It is predictable and easily controlled.

HODGKIN DISEASE/HODGKIN LYMPHOMA

Multifocal

NON-HODGKIN LYMPHOMA

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

NON-HODGKIN LYMPHOMA

 Less predictable

NON-HODGKIN LYMPHOMA

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.

HODGKIN LYMPHOMA

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

HODGKIN LYMPHOMA

Leukocytosis and lymphocytopenia are observed in advance cases.

HODGKIN LYMPHOMA

HODGKIN LYMPHOMA • Diagnosis:

lymph node biopsy

Reed-Sternberg cell is considered as hallmark finding

HODGKIN LYMPHOMA

CAUSE: Unknown

HODGKIN LYMPHOMA

HODGKIN LYMPHOMA PREDISPOSITION FACTORS (PROPOSED):

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

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

HODGKIN LYMPHOMA

● Mediastinal mass in between the lung chamber

HODGKIN LYMPHOMA

● Enlarged cervical nodes

HODGKIN LYMPHOMA

● Enlarged lymph nodes

HODGKIN LYMPHOMA

● Fever, night sweats and weight loss

HODGKIN LYMPHOMA

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

● A

: patient has one or more symptoms

● B

HODGKIN LYMPHOMA LABORATORY DIAGNOSIS

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

HODGKIN LYMPHOMA DEFINITIVE DIAGNOSIS:

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

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

INCREASED: MONOCYTE AND EOSINOPHIL

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

INCREASED IN WBC

● Lymphocytopenia

INCREASED IN WBC

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

INCREASED IN WBC

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

INCREASED IN WBC

usually Reed-Sternberg cell

PLASMA CELLS

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

PLASMA CELLS

● Large monocytes with vacuoles

PLASMA CELLS

● Large lymphocyte with deeply basophilic cytoplasm

PLASMA CELLS

HODGKIN LYMPHOMA Blood picture:

normocytic and normochromic (anemic)

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

BONE MARROW

● Decreased: Iron, TIBC

HODGKIN LYMPHOMA

: due to the presence of hemolytic anemia

HODGKIN LYMPHOMA ● DAT (+)

● Multinucleated

REED STERNBERG CELLS

REED STERNBERG CELLS  Nuclear membrane:

demarcated and thick (not smooth)

REED STERNBERG CELLS  Nuclei:

usually eosinophilic (orange) with a distinct halo

● 4 to 8x size of normal lymphocyte

REED STERNBERG CELLS

● Can be isolated and cultured

REED STERNBERG CELLS

● Can be used to diagnose the disease

REED STERNBERG CELLS

● Resembles an owl eyed appearance

REED STERNBERG CELLS

● 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.

REED STERNBERG CELLS

based on the extent of infiltration and abundance of RS cells

RYE CLASSIFICATION

RYE CLASSIFICATION Observed patterns are the presence of:

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

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

nodular sclerosis

(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).

lymphocyte depletion

: Abundant Lymphocytes; No fibrosis

1. Lymphocyte Predominant

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

2. Nodular Sclerosis

: Moderate lymphocytes in diffuse pattern

3. Mixed Cellularity

: Few lymphocytes w/ diffused fibrosis

4. Lymphocyte Depleted

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

ANN ARBOR STAGING SYSTEM

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

ANN ARBOR STAGING SYSTEM

Single lymph node/extralymphatic organ

Stage I

Two or more lymph nodes/contiguous extralymphatic organ

Stage II

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

Stage II

Lymph nodes on both sides of diaphragm Splenic/ extralymphatic involvement

Stage III

 Both sides of lymph nodes are affected

Stage III

Diffuse one or more extralymphatic organ

Stage IV

 Other organs are also affected

Stage IV

TREATMENT OF HODGKIN DISEASE

chemotherapy , radiation and myelosuppresive

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

Chemotherapy

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)

Chemotherapy

Example: release of High Phosphate (Hyperphophatemia)

Chemotherapy

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

Chemotherapy

effect of phosphate =

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

A more common type than Hodgkin lymphoma.

NON-HODGKIN LYMPHOMA

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

NON-HODGKIN LYMPHOMA

NON-HODGKIN LYMPHOMA BY VIRCHOW:

 Leukemic  Aleuemic

: otherwise known as lymphosarcoma

Aleuemic NON-HODGKIN LYMPHOMA

Occurs in Male

2. NON-HODGKIN LYMPHOMA

Congenital immunodeficiency

2. NON-HODGKIN LYMPHOMA

Immune diseases: RA, Sjorgen`s Syndrome, SLE

2. NON-HODGKIN LYMPHOMA

AIDS

2. NON-HODGKIN LYMPHOMA

EBV

2. NON-HODGKIN LYMPHOMA

HTLV1

2. NON-HODGKIN LYMPHOMA

ex: Ataxia, Telangiectasia, Wiscott Aldrich, IgA deficiency

Congenital immunodeficiency

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

Congenital immunodeficiency

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

Immune diseases: RA, Sjorgen`s Syndrome, SLE

: causative agent of infectious mononucleosis

EBV

causes also the African Burkitt Lymphoma

EBV

: Acute T cell Leukemia and Lymphoma

HTLV1

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

2. NON-HODGKIN LYMPHOMA

DAT positive

2. NON-HODGKIN LYMPHOMA HODGKIN LYMPHOMA

Autoimmune thrombocytopenia (not common)

2. NON-HODGKIN LYMPHOMA

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

2. NON-HODGKIN LYMPHOMA

NON-HODGKIN LYMPHOMA CLASSIFICATIONS

LOW GRADE INTERMEDIATE GRADE HIGH GRADE

45-60 y/o

LOW GRADE

Slow growing lymphoma

LOW GRADE

Small cell lymphoma

LOW GRADE

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

LOW GRADE

Survival: 5-7 years

LOW GRADE

Rapid lymph node enlargement and extranodal disease

INTERMEDIATE GRADE

BM is not involved

INTERMEDIATE GRADE

Large cell lymphoma

INTERMEDIATE GRADE

Cell involved: large lymphocytes (worse prognosis)

INTERMEDIATE GRADE

Survival: 1.5 – 3 years

INTERMEDIATE GRADE

Most rapid enlargement of LN (fastest developing malignancy)

HIGH GRADE

HIGH GRADE Subclassifications:

a. Immunoblastic lymphoma b. Lymphoblastic lymphoma c. Small noncleaved cell lymphoma

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

C1. Burkitt C2. Non burkitt

Occurs in more than 50 years old

a. Immunoblastic lymphoma

Arises in the CNS

a. Immunoblastic lymphoma

Short survival:: months to a year

a. Immunoblastic lymphoma

Occurs in teens to 20`s

b. Lymphoblastic lymphoma

Presence of mediastinal mass

b. Lymphoblastic lymphoma

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

b. Lymphoblastic lymphoma

Occurs in children to 30 years of age

c. Small noncleaved cell lymphoma

With cytogenetic abnormality

C1. Burkitt

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

C1. Burkitt

No cytogenetic abnormality

C2. Non burkitt

NON-HODGKIN LYMPHOMA DIAGNOSIS:

Lymph node biopsy

NON-HODGKIN LYMPHOMA TREATMENT

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

: Stage I and II low grade lymphoma

● Radiation

: all stages

● Chemotherapy

Various type of malignant cells:

1. Small lymphocytes 2. Small cleaved cell 3. Small noncleaved cell 4. Large cell (cleaved/non cleaved) 5. Immunoblastic large cell 6. Lymphoblastic cell

- associated with low grade small lymphocytic lymphoma

1. Small lymphocytes

1. Small lymphocytes- Microscopic examination:

diffuse pattern of small lymphocytes

- Small but actually slightly larger than normal lymphocyte

2. Small cleaved cell

- Cytoplasm is non visible

2. Small cleaved cell

- Misnamed (not really small, but actually larger; intermediate between small and large)

3. Small noncleaved cell

- Seen in burkitt and non-burkitt

3. Small noncleaved cell

: uniform size and shape

- Burkitt

: heterogeneous size and shape

- Non burkitt

: malignant cell can be seen in a high grade

- Small noncleaved cell lymphoma

- 2-3x larger than normal lymphocyte

4. Large cell (cleaved/non cleaved)

- Spotty chromatin condensation and thin rim of cytoplasm around the nucleus

4. Large cell (cleaved/non cleaved)

- Present in high grade

5. Immunoblastic large cell

- A lot bigger; 4-8x larger than normal lymphocyte

5. Immunoblastic large cell

- Cytoplasm is abundant (but faint when stained)

5. Immunoblastic large cell

- Usually large and round with convoluted nucleus

6. Lymphoblastic cell

This affects the mature T cells.

MYCOSIS FUNGOIDES

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

MYCOSIS FUNGOIDES

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

MYCOSIS FUNGOIDES

● Early onset: pruritus (severely itching skin)

MYCOSIS FUNGOIDES

MYCOSIS FUNGOIDES ● Progression:

demarcated reddened plaques (thickening of skin)

: plaques and desquamation of large flakes in the skin

MYCOSIS FUNGOIDES Generalized erythroderma

● Appearance of “Pautrier’s microabscess”

MYCOSIS FUNGOIDES

● Mycosis fungoides: ● Sezary syndrome:

skin lymph node and visceral involvement (spleen, liver)

● Lymphocytes: larger, with a cleft in the nucleus

MYCOSIS FUNGOIDES

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

MYCOSIS FUNGOIDES

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

SEZARY SYNDROME

Wider dissemination of mycosis fungoides

SEZARY SYNDROME

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

SEZARY SYNDROME

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

“Pautrier’s microabscess”

PLASMA CELL DYSCRASIAS

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

• Chemistry: Bence Jones Protein (BJP)

• Urinalysis: Many hyaline casts and positive BJP

• 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)

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

-Flame cells

intranuclear crystalline structures of abnormal IgG

-Dutcher bodies

(accumulations of IgG)

-Russel bodies

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

-Grape cell/Mott cell, Morula cell

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

2. Waldenstrom Macroglobulinemia

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

2. Waldenstrom Macroglobulinemia

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

3. Heavy Chain Disease (HCD)

CLL Flashcards

(257 cards)