CLL Flashcards
B. CHRONIC LYMPHOPROLIFERATIVE DISORDERS
● Proliferation of lymphocytes which are abnormal because they are unresponsive to antigenic stimuli.
Chronic Lymphocytic Leukemia (CLL)
● Less likely to undergo blastic transformation
Chronic Lymphocytic Leukemia (CLL)
● Predisposition to autoimmune hemolytic anemia (AIHA)
Chronic Lymphocytic Leukemia (CLL)
● is predominant in males (3:1 ratio)
Chronic Lymphocytic Leukemia (CLL)
● CLL Cytogenetic abnormality:
➢ Extra Ch12
➢ t(14q) Translocation on the long arm of Ch14
B cell: produces antibodies due to presence of antigen (normally increases in synchrony)
Chronic Lymphocytic Leukemia (CLL)
Chronic, and involves mature cells
Chronic Lymphocytic Leukemia (CLL)
Types of AIHA:
Warm AIHA (IgA and IgG) and Cold AIHA(IgM)
Duplicated Ch 12
Extra Ch12
marker for Lymphocytic Leukemia (all Lymphocytic Leukemia have this)
Extra Ch12
predicts progression of disease
Extra Ch12
common cell that is involved is the B-lymphocyte
B-CLL
B-lymphocyte is unresponsive to antigenic stimuli = do not function well (abnormal)
B-CLL
Dormant B-cells
B-CLL
o Due to proliferation (useless), they accumulate but stay dormant in the peripheral blood, bone marrow or in the lymph nodes
Dormant B-cells
o Cannot produce Ab even with the presence of Ag
Dormant B-cells
B-CLL or T-CLL
Rare
T-CLL
disseminated in the circulation/does not accumulate
T-CLL
Key features: appearance of rash (skin and CNS is involved)
T-CLL
Enlarged lymph nodes, spleen and liver
Chronic Lymphocytic Leukemia (CLL)
Pruritus
Chronic Lymphocytic Leukemia (CLL)
: due to skin infection due to Herpes zoster
Pruritus
Affects more of males; 50-60 years old
Chronic Lymphocytic Leukemia (CLL)
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
- LEUKAPHERESIS
- GAMMA GLOBULIN INJECTIONS
- RADIATION
- CHEMOTHERAPY
Reduces the number of abnormal lymphocyte.
- LEUKAPHERESIS
high lymphocyte in the PB = viscous blood
- LEUKAPHERESIS
Aim: to make blood thin (leukopheresis can not reduce tumor burden, unlike chemotherapy; NOT for tumor)
- LEUKAPHERESIS
Since you have hypogammaglobulinemia, this is meant to raise the B cell count
- GAMMA GLOBULIN INJECTIONS
treat enlarged lymph nodes and spleen
- RADIATION
reduce the tumor and abnormal lymphocyte in the PB
- CHEMOTHERAPY
Aim: to reduce the tumor and abnormal lymphocyte
- CHEMOTHERAPY
▪ an increase in prolymphocytes, with almost total replacement of the bone marrow
- Pro-Lymphocytic Leukemia
▪ poorer prognosis than HCL and CLL
- Pro-Lymphocytic Leukemia
● Rare variant of CLL (not common)
- Pro-Lymphocytic Leukemia
● Increased in prolymphocyte, total replacement of BM
- Pro-Lymphocytic Leukemia
● Decreased gamma globulins and T cells
- Pro-Lymphocytic Leukemia
● Poorer prognosis than CLL or HCL (Hairy Cell Leukemia)
- Pro-Lymphocytic Leukemia
- Pro-Lymphocytic Leukemia
● Mean survival rate:
1 yr (usually less than a year)
- 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)
- Pro-Lymphocytic Leukemia
● Prolymphocyte
Abnormal cells: Prolymphocytes
Normal lymphocyte: small and no condensed chromatin
- Pro-Lymphocytic Leukemia
● Rare (2%)
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
- Hairy Cell Leukemia
● Otherwise known as
“Leukemic reticuloendotheliosis” “Reticulosis”, “Aleukemic reticuloendotheliosis” and “Reticulum cell leukemia”
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
● due to the growth and accumulation of hairy cell in the
spleen, bone marrow and PB
- 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
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
● Presence indicate that there is pancytopenia, predominantly granulocytes and monocytes (granulocytopenia and monocytopenia).
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
HCL CHARACTERISTICS
- Large spleen (similar to other diseases)
- 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
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
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
▪ with most consistent splenomegaly (splenectomy is often considered)
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
▪ laboratory diagnosis: TRAP (+)
- Hairy Cell Leukemia/Leukemic Reticuloendotheliosis
▪ prognosis:
• quite good (benign)
• can be longer than 10 years
- 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):
- Genetic influence
- Environmental hazards
- 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
- Lymphocyte Predominant
: Moderate lymphocytes with nodulating collagen bands; RS in clear zones
- Nodular Sclerosis
: Moderate lymphocytes in diffuse pattern
- Mixed Cellularity
: Few lymphocytes w/ diffused fibrosis
- 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
- NON-HODGKIN LYMPHOMA
Congenital immunodeficiency
- NON-HODGKIN LYMPHOMA
Immune diseases: RA, Sjorgen`s Syndrome, SLE
- NON-HODGKIN LYMPHOMA
AIDS
- NON-HODGKIN LYMPHOMA
EBV
- NON-HODGKIN LYMPHOMA
HTLV1
- 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)
- NON-HODGKIN LYMPHOMA
DAT positive
- NON-HODGKIN LYMPHOMA
HODGKIN LYMPHOMA
Autoimmune thrombocytopenia (not common)
- NON-HODGKIN LYMPHOMA
Some abnormalities such as alkaline phosphatase, LD, and uric acid (due to the accumulation/lysis of tumor)
- 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:
- Small lymphocytes
- Small cleaved cell
- Small noncleaved cell
- Large cell (cleaved/non cleaved)
- Immunoblastic large cell
- Lymphoblastic cell
- associated with low grade small lymphocytic lymphoma
- Small lymphocytes
- Small lymphocytes- Microscopic examination:
diffuse pattern of small lymphocytes
- Small but actually slightly larger than normal lymphocyte
- Small cleaved cell
- Cytoplasm is non visible
- Small cleaved cell
- Misnamed (not really small, but actually larger; intermediate between small and large)
- Small noncleaved cell
- Seen in burkitt and non-burkitt
- 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
- Large cell (cleaved/non cleaved)
- Spotty chromatin condensation and thin rim of cytoplasm around the nucleus
- Large cell (cleaved/non cleaved)
- Present in high grade
- Immunoblastic large cell
- A lot bigger; 4-8x larger than normal lymphocyte
- Immunoblastic large cell
- Cytoplasm is abundant (but faint when stained)
- Immunoblastic large cell
- Usually large and round with convoluted nucleus
- 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
- Multiple Myeloma
- Waldenstrom Macroglobulinemia
- 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.
- Waldenstrom Macroglobulinemia
Malignant plasma cells show increase production of IgM (>3 g/dL).
- Waldenstrom Macroglobulinemia
This shows an abnormal synthesis of heavy chains (Gamma HCD; Alpha HCD)
- Heavy Chain Disease (HCD)
