Hematology/Oncology (WBC,s) Flashcards
What is the diffrence between leukemia and lymphoma?
Leukemia- cancer of wbc in blood (abnormal wbc in blood)
lymphoma - cancer of wbc in the ymph nodes (abnormal wbc in lymphnodes)
Lymphoma is a solid tissue mass (lemon)
leukemia is liquid (in blood,lemonade)
lemon can be made into lemonade and lemonade seed in lemon
so lymphoma can give rise to leukemia and leukemia to lymphoma.
Explain lymphocytes.
Lineage-lymphoid
agranulocytes
1) NK cells
2) T cells ( form in BM, mature in thymus)
3) B cells( form in BM, mature in MALT/ GALT (peyer patches)
circulation/bone marrow - leukemia
lymph nodes / maturing organs - lymphoma
Can you diffrentiate between T and B cell under the microscope?
No, its impossible.
We diffrentiate by flow cytometry (Detection of cluster of diffrentiation) (CD - basically the ID of the cell)
NK cells- CD16, CD56
T cells- Helper- CD3, 4
killer- CD3, 8
B cells - MHC2 CD19 and 20
What are some Benign Leucocyte reactions? (Reactions that are not diorders)
Eosinophilia neutrophilic leucocytosis basophilia monocytosis etc
What is the diffrence between normal division and neoplastic division/
Neoplasia on its own doesn’t mean malignancy. Neoplasia can be benign or malignant
Neoplasia is monoclonal (a single cell decides to go bezerk)
it is irregular and not reversible
normal division is regular, reversible and include many cells (polyclonal)
Name the Hematological Malignancies (all the malignancies related to the hematology) (high WBC)
Leukemia ( in the blood/BM)
1) Acute Lymphoblastic Leukemia (ALL) (newborn to 14 years)
2) Acute Myeloblastic Leukemia(AML) (14-60)
3) Chronic Lymphocytic leukemia (CLL) (>60)
4) Chronic myelocytic Leukemia (CML) (14-60)
Lymphomas (in the LN)
Hodgkins and Non-Hodgkins
Myeloma (multiple Myeloma)
What are the main diffrences between Acute and Chronic leukemias?
Acute-
young patients
Cells are immature (blasts)
cell lose ability to diffrentiate byt retains ability to divide
chronic
older patients
mature cells (cytes)
for example
ALL- since its lymphoblastic (lymphoid lineage) we know that when maturing they will form lymphocytes (T and B cells)
but the immature cells will lose diffrentiating abilitya and we will have a lot of immature lymphoid lineage cells
These will be Medium sized
agranular (lymphoid lineage doesn’t form any granulocytes so obviously immature cells will also not have granules)
Scanty cytoplasms (because mature T and B cells also doesn’t have much cytoplasms)
AML- Myeloid lineage so they are the immature forms of the Granulocytes
They are larger. Granules present and more cytoplasm
now chronic-
CLL- Lymphocytes will be seem (Chronic=mature)
smudge cells
CML - Myelocytes,neutrophils and basophils high
Explain Acute Leukemias :)
We will have BLASTS.
Reasons for development of leukemias- Both genetic and environmental Antineoplastic agents radiation Hodgkin lymphoma benzene multiple myeloma
Acute Leukemias asre MONOCLONAL disorders of early stem cells of either MYELOID or LYMPHOID origin
these Myeloblasts and Lymphoblasts Replicate and
1) Replace most of the bone marrow cells, crowding out normal haematopoesis
this will result in pancytopenia (BM wll have trouble doing normal haematopoesis as the abnormal one is crowding)
due to pancytopenia
RBC low-anaemia
WBC low-INfections
Patelets low-Bleeding
2) Then they Enters the peripheral blood
3) metastasize throughout the body (further lead to splenomegaly, Hepatomegaly, Lymphomas,bone pain)
platelets less than 100,000
WBC less than 10,000 or more than 100,000
Explain the clinical features of the acute leukemias
1) painless LN enlargement
2) testicular enlagment in ALL
3) bone pain
How can leukemias / lymphomas or other cancer leads to megaloblastic anaemias?
Due to high cell turnover (a lot of dividing and forminf cells) a lot of FOLATE is consumed by these cells leading to the high demand of folate and not enough for the RBC DNA synthesis.
What are auer Rods?
Seen in the Blast cells Of AML (acute myeloid Leukemia) Myeloid are Granulocyte lineage
-in myeloblasts not monoblasts
Auer rods are clumps of azurophilic granular material that form elongated needles and can be seen in the cytoplasm of leukemic blasts under microscopic examination. They are composed of fused lysosomes and contain peroxidase, lysosomal enzymes, and large crystalline inclusions.
Immature Myeloid lineage cells will contain auer rods (myeloblasts not monoblasts)
Explain Chronic Leukemias :)
MONOCLONAL disorders of the LATE cells Mature and smaller can be identified easily in older persons Blasts cells are not seen or less than 10%
Onset of signs and symptoms are usually slower
lypadenopathy still seen
hepato and aplenomegaly also seen
platelets less than 100,000
WBC less than 10,000 or more than 100,000
basophilia can be seen
Explain Acute Lymphoblastic Leukemia :) (ALL)
F
What do you mean by secondary AML?
CML can cause AML that means chronic myelocytic leukemia (meloid lineage ) (mature) can give rise to Acute one (immature)
in this case it is called secondary AML.
What are the risk factors for the Acute Myelocyitic anaemia?
Acute ML means immature myeloid lineage cells
high cytoplasm and granular
Myeloid lineage —-1) Myeloblasts (have Auer rods that are peroxidase posiitive)
2) monoblasts
primary AML occurs due to Radiation, Bemzene, or antineoplastic agents
if nn of these agents then we call it the seconary AML that can be due to Myelodysplastic Syndrome Aplastic Anaemia PNH Myeloproliferative Disorders Fanconi anaemia
AML will have gum Infilteration )M5 variant
all other symtoms are the same of the leukemia
Classification of AML?
M0 to M7
most Important to learn
M2- Myeloblastic with Maturation t(8;22)
M3- Acute promyelocytic leukemia
M5 - monocytic gum infiltration
What is good and Bad prognosis?
A bad prognosis means there is little chance for recovery. Someone with a good or excellent prognosis is probably going to get better.
Explain Acute Promyelocytic leukemia. (aPML)
Specific subtype of AML
M3
The problem is not with the BLASTS cells (Myeloblasts)
but with promyeloblasts (one step further before division not Neuto mono baso)
auer rods present
t(15:17)
Complication- DIC syndrome
very good prognosis as it can be treated with Vitamin A (ATRA- All Trans Retinoic Acid) or Arsenic
vitamin A induces maturation of primitive promyelocytes- from neutrophils that will go apoptosis and will not continue to diffrentiate
however Vit A can cause Diffrentiaton syndrome]
Vitamin A also does not cause myelosuppresion (other cancer drugs do)
Explain Some clinical used of Vitamin A.
- Treatment of Acne (but can cause abortion)
- treatment of measles and low risk of blindness
- Treatment of aPML (acute promyelocytic leukenmia)
- treatment of Hairy Leukoplakia
- retinitis pigmentosa
What is Diffrentiation Syndrome?
Previously known as retinoic acid syndrome
Differentiation syndrome (DS; originally called “retinoic acid syndrome”) is a potentially fatal complication of treatment of acute promyelocytic leukemia (APL) with all-trans retinoic acid and/or arsenic trioxide
treatment- Give high dose of Dexamethasone (when doctors have no clue,they give corticosteroids)
stopping the ARTA
What are the treatment for Acute lymphoblastic Leukemia? (ALL)
First we should stabilize the symptoms of the patient to make them ready for the chemotherapy
for example if patient have
thrombocytopenia- do a platelet tranfusion
fever and granulocytopenia- blood culture+antibiotics
leucostasis- do leucopharesis
1) remission induction- Prednisone + Vincristine
2) consolidation- (maintainence)
high dose methotrexate
bone marrow transplant is the last resort
If the patient have a philadelphia chromosome translocation in ALL t(9:22) then we will give
Tyrosine Kinase Inhibitor.