Leukemias Flashcards by Loren Tholcke

Leukemoid rxn

Left shift (Increase in band cells)
Alk phos would be increased but not in CML!!!

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Leukemia

Low leukocyte alk phos

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Hodgkin’s lymphoma characteristics

Reed-sternberg cells
Local lymph nodes 
B symptoms
May be associated with EBV
Less reed cells, better outcome
PET scan best for staging

Brentaximab also used for advanced

Early- ABVD- Adriamycin, Bleomycin, Vinblastine and Dacarbazinefor all stages

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Non hodgkins lymphoma characteristics

Widespread lymph nodes
B symptoms not as common
May be associated with HIV
Prognosis varies widely

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Reed sternberg cell

Owl eyes
CD30/CD15 positive
CD45 negatve, only lymphoprolifrative disorder that is negative.
Lymphomas always do an excisional biopsy
Under somatic hypermutation

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Hodgkin lymphoma types

Nodular sclerosis
Mixed cellularity
Lymphocyte depletion
Lymphocyte predominance (CD 20+)

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Nodular sclerosis

Most common in women
Mediastinal, supraclavicular, and lower cervical nodes
Good prognosis (low reed sternberg count)
Can see collagen banding on biopsy

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Mixed cellularity

Intermediate prognosis
Is associated with EBV
Lymphocytes and reed sternberg about equal

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Lymphocyte predominance

Mostly men, lots of lymphocytes, good prognosis

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Lymphocyte depletion

EBV associated

Poor prognosis

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Hodgkins lymphoma staging

1) 1 LN
2) More than one LN, same side as diaphragm
3) More than one LN, both sides of diaphragm
4) Outside of LN system

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Burkitt lymphoma

B- cell
Africa- Jaw
US- abd
(8:14  2:8  8:22) c-myc translocation
Starry sky pattern

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Diffuse large well differentiated lymphocytic lymphoma

Older Patients (Most common non hodgkins)
Lymph/hepatosplenomegaly
Bone marrow almost always involved
5-7 year survival

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Mantle cell lymphoma

t(11;14) IgH to bcl-1
Lymph/hepatospleenomegaly with fever and night sweats
Poor prognosis—3 years
CD5+

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Follicular lymphoma

Slower growing
t(14;18) IgH to bcl2 so less apoptosis
May be associated with immunodificiency states

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Adult t-cell leukemia/lymphoma

Mosly japan, some africa
Lymph/hepatospleenomgaly, skin lesion, and hypercalcemia
Cause: HTLV1

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Cutaneous T-cell lymphomas

Mycosis fungoides- Inflammation, plaque, tumor

Sezary syndrome- Once its in the bloodstream.

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Multiple myeloma

Plasma cell neoplasm
CRAB- Calcium, Renal, Anemia, Bone lysis

Test: serum protein electrophoresis shows a large spike of serum or urine of monoclonal IgG or IgA

Over production of light chain gets stuck in distal renal tubule (kappa bence jones proteins) and causes necroses.
Marrow cells have Russell bodes
X-rays show punched out defects (can produce hyper calcemia because they secrete osteoclast activating factor)
Rouleaux formation shows stacked RBC’s

Staging based on serum albumin levels and B-2 microgloblulin

Waldenstrom macroglobulinemia

Like multiple myeloma only monoclonal IgM
Get thick blood, clotting
NO BONE LYSIS

Monoclonal gammopathy of undetermed significance

Also get a M spike electrophoresis without symptoms associated with waldenstrom and multiple myelomas

3 criteria
Monoclonal <10%
No end organ damage

Smoldering the same except with bone marrow plasma cells between 10-60g/dl

Acute lymphoblastic leukemia/lymphoma

ALL

Less than 15 y/o
Increased bone marrow lymphoblast
TdT and CALLA+
If t(12;21), better prognosis
t(8;14); t(8;22); t(2,8)
t(9;22) Philly!!! Really bad

Children- 60-80% cure
Adults- 30-60% cure

Responds to imitinib, also monitor kidney and use allopurinol

Small lymphocytic lymphoma and Chronic lymphocytic leukemia

SLL/CLL

Greater than 60 y/o, Men more likely
Often asymptomatic, smudge cell in PBS
Warm Ab autoimmune hemolytic anemia
CLL has more lymphocytosis than SLL

Possible:
Autoimmune hemolytic anemia
Autoimmune Thrombocytopenia
Infections due to Hypogammaglobulinemia

Grading
0- Lymphocytosis
1- with lymphadenopathy (SLL)
2- Organomegaly
3- Anemia
4- Thrombocytopenia

Deletion 11q23 and Alteration 17p is poor prognosis

Hairy cell leukemia

B cell tumor with hair like projections

Stains TRAP +

Acute myelogenous leukemia AML

Peaks at 60yo
increased myeloblasts on PBS
Auer rods present
t(15;17) 
M3 AML subtype responds to all trans retinoic acid (Vit A)
DIC common in these patients

Chronic myelogenous leukemia CML

``` 50-60 yo t(9;22) bcl-abl Ph Increased (always) neutrophils, metamyelocytes, and basophils Low leukocyte alk phos Responds to imitinib, nilotinib, dasatib ```

B cell and T cell markers

B- CD10/19/20 | T- CD2-8

Neutrophilic leukocytosis

Bacterial infection Tissue necrosis High cotrisol state (release cells from marginated pool) Early left shift cells express CD16 with decreased Fc expression

Monocytosis

Inflammation and malignancy

Eosinophilia

HODGKINS LYMPHOMA Via IL5 | Allergic/parasite

Basophilia

CML

Lymphocytic leukocytosis

CD8+ response Viral and Bordetella pertusis EBV, CMV less common

Myeldysplastic disorder

Qualitative and quantitative disorder with more immature

Myeloproliferative

See more mature cells

Fanconi's Anemia

``` Chromosomal Breakage Syndrome Autosomal Recessive(?) Constitutional Aplastic Anemia with thumb & radius malformations, hyperpigmentation & hypogonadism AMML; ~10% incidence (No ALL reported) 1 in 12 risk before age 21 years ```

Li-Fraumini Syndrome

``` Germline p53 mutation Autosomal Dominant Familial clustering of certain cancers: Acute Leukemia (usually childhood ALL) Breast/Brain/Sarcoma Adrenal Cortical Carcinomas ```

Increased risk for ALL

``` Downs Blooms Li-fraumini Radiation Alkylating Agents Topoisomerase inhibitors ```

Increased risk for AML

Benzene Blooms Alkylating agents Topoisomerase inhibitors

Tumor lysis syndrome

Look it up

CLL and MCL markers

CD5- T cell marker in both CD20 B-cell marker in both CLL also CD23 to distinguish

Polycythemia vera

Increase in all cells | Can present with blurred vision, HA, flushed

Myelofibrosis

Jak 2 | See

Juvenile myelomonocytic leukemia

Like CML but Ph chromosome negative and found in children

Chronic myelomonocytic leukemia

Myelodysplastic disorder of monocytes | No Ph chromosome

Myeloproliferative disorders

CML ET PV Primary meylofibrosis If untreated, can become AML