Questions

Normal Ranges
Normal % of Myeloblasts
Normal range for ANC
Normal range for WBC
Normal range for Platelets
Anemia
Sickle cell disease patients up to age 5 need are given what
prophylaxis?
Leukemia
AML is a cancer of which type?
What is leukostasis?
Least common leukemia in children:
Most common leukemia in children:
2nd most common?
Lymphoma is a cancer of a ___________.
What is a lymphocytic leukemia?
All lymphomas can have a leukemic phase.
Which leukemia has these 3 stages:
- Chronic
- Accelerating
- Blast crisis
What blood malignancy is associated with autoimmune
hemolytic anemia (AIHA)?
Lymphoma
Treatment for (Diffuse Large B-Cell Lymphoma) DLBCL?
Clinical/Labs
If patient has impressive cerival adenopathy, get CXR
because they might have a mediastinal mass.
Burkitt's Lymphoma often has acute abdominal symptoms
and can be mistaken for appendicitis.
What does the Coomb's test check for?
What might you check for in a lab for:
Hemolytic anemia
Patient has:
Elevated LDH
Elevated bilirubin
Low Hb
Low haptoglobin
Probably cause?
Treatments
Chemo has a maximum effect 2 weeks after starting
treatment.
It takes 2 weeks for blood cell count to bounce back.
Total of 4 weeks.
What is the treatment for leukostasis?
Class of drugs that end in "ib"
i.e. Imatinib (Gleevac)
Answers Notes
5%
1.5 to 8 (1000's)
4,500 to 10,000
150,000 to 400,000
Penicillin for susceptibility to infection
Myeloblasts
Myeloblasts aggregating in the peripheral blood ->
Sludging *Seen in advanced AML (and others)
CLL (<1%)
Most common: ALL (80%)
2nd most common: AML
Lymphocytes *Not a cancer of lymph node!
Cancer of circulating lymphocyte
CML
CLL
R-CHOP
Autoimmune Hemolytic Anemia
Elevated LDH
Elevated bilirubin
Low Hb
Low haptoglobin
Hemolytic anemia
Luekopheresis
Hydroxyurea -> myelosuppression
Questions
Acute Myeloid Leukemia (AML)
AML is a...
Neoplastic accumulation of myeloblast (cell).
AML:
Age Group: ?
AML:
Dx: ?
Secondary AML can arise from the following: (3)
Treatment for AML:
Symptoms of AML:
Which blood malignancy is associated with MDR as a bad
prognostic factor?
Bad prognostic genetics for AML:
Good prognostic genetics for AML:
In which blood malignancy does having a translocation have a
better prognosis than having normal cytogenetics?
Which genetic syndromes increase the likelihood of AML?
Acute Promyelocytic Leukemia (APL)
Age range for APL:
This blood malignancy has a disrupted Retinoic Acid Receptor
(RAR).
Which blood malignancy?
Chronic Lymphocytic Leukemia
Definitive diagnosis for CLL:
CLL patient has thrombocytopenia:
How can you tell if it's from immune-mediated
thrombocytopenia (ITP) or Stage 4 CLL disease?
What is Richter's transformation?
Answers Notes
Older (50's and 60's)
Bone marrow biopsy -> Myeloblasts -> 20 % (Auer Rods)
Lineage confirmation w/ FLOW if needed -> MPO+
- Prior chemo
- Radiotherapy
- MDS
Induction: "7+3+3" or "7+3"
Cytarabine - 7 days
Daunorubicin - 3 days
(Etoposide) - 3 days
Consolidation (Booster)
3 boosters
Bone marrow transplant *85% relapse after remission
Anemia -> fatigue and dyspnea
Thrombocytopenia -> pethechia and bleeding
Neutropenia -> infection
Diffuse bone pain -> microscopic periosteal stretching
AML
-5, -7
11q23 (MLL gene)
Inversion with Chromosome 16
t(8,21)
*Better to have translocation than have normal
cytogenetics
AML
Down's and Neurofibromatosus
23's and 30's
APL
Peripheral blood FLOW cytometry:
CD5 (abberrant T-cell marker) plus CD5,19,20 (normal B-
cell marker)
Bone marrow biopsy -> Look for megakaryocytes
CLL progression to Diffuse Large B-Cell Lymphoma
Questions
140811.1 Intro and Normal Hematopoiesis
Infants have hematopoiesis in which bones?
As we mature, hematopoiesis gets restricted to these bones:
(3)
When does hematopoeisis start in utero?
Where does hematopoeisis take place at 3 weeks?
Where does hematopoeisis take place at 12 weeks?
Where does hematopoeisis take place at 27 weeks?
Where does hematopoeisis take place at 34 weeks?
Where does hematopoeisis take place 3 weeks after birth?
Where does hematopoeisis take place 12 weeks post-
partum?
6 stages of RBC development:
Mean diameter of RBC
Central pallor of RBC should be _____ of cell diameter
What are the 3 granulocytes?
Which granulocytes have pink granules?
Which granulocytes have blue granules?
What are the 6 stages of neutrophil development?
How many lobes in a normal neutrophil?
How many lobes in a normal eosinophil?
High eosinophil count might indication what type of
infection?
Allergens can bind to IgE on a basophil, which leads to a
release of histamines.
Monocytes circulate in the blood for 24 hours.
Monocytes are white blood cells that are like "vacuum
cleaners" because they eat up fungi, pyogenic bacteria,
mycobacteria, and old or defective RBCs.
2 morphological stages for lympocytes:
The nucleus of a lymphocyte is about the same size as a RBC.
NK cell surface markers:
B-cell surface markers:
T-cell surface markers:
Plasma (memory) cell surface marker:
Megakaryocytes rarely get out into peripheral circulation,
but if they do, they get caught up.
Where?
What is the largest collection of lymphoid tissue in a person?
25% of our lymphocytes are where in the body?
T cells form PALS (Periarterial lymphatic sheaths) around the
central arteries of the spleen.
The red pulp of the spleen is composed of these 2 structural
components and this very important cell:
140811.3 Laboratory Evaluation of hematologic parameters
If a patient's WBC count is too high or too low, what should
you look at next?
When in life is RBC (red blood count) the highest?
At what age does HbF decrease to a normal level?
Normal % for HbF:
# of RBCs decreases with age.
T/F?
MCV tells you:
What is MCH and MCHC?
Normal range for MCV:
Normal range for RDW:
Reticulocyte morphology:
Basophilic stippling in RBCs is actually the precipitation of
undegraded RNA and seen in (condition) lead toxicity.
You see basophilic stippling in a patient's peripheral blood
smear:
Immediately think: --> (Dx)
You see Target cells in a patient's peripheral blood smear:
Possible Dx's (4):
You see Schistocytes (helmet cells) in a patient's peripheral
blood smear:
You should think these Dx's: (2)
You see Acanthocytes (thorn cells) in a patient's peripheral
blood smear:
Immediately think: --> (Dx)
In Rouleaux, RBCs abnormally adhere to each other due to
increased plasma protein production.
You see Rouleaux in a patient's peripheral blood smear:
Immediately think: --> (Dx)
Howell Jolly Bodies are remnants of nuclear chormatin
normally removed by macrophages in the spleen.
You see Howell Jolly Bodies in a patient's peripheral blood
smear:
Immediately think: --> (Condition)
You see Spherocytes in a patient's peripheral blood smear:
Immediately think: --> (Dx)
What part of the body do you take a bone marrow biopsy?
What is the normal range for myeloblast percentage?
What do you do with a bone marrow aspirate? (Tests)
What do you use from a patient to run a metabolic panel?
What is SPEP?
What is a sickle cell screen?
140811.4 Synthesis & catabolism of Normal Hemoglobin
Heme molecules have a ring structure called:
What is the charge of iron in a heme molecule?
Globin chains:
Alterations in the amino acid sequences result in different
globin chains.
Globin genes:
The alpha genes are on chromosome 16.
Globin genes:
The beta, delta, and gamma genes are on chromosome 11:
Humans have 2 copies of these hemoglobin chains per
chromosome: (2)
Hemoglobin A:
Which globin chains?
Hemoglobin A2:
Which globin chains?
Hemoglobin F:
Which globin chains?
Normal % range for:
- HbA2
- HbF
What is hemoglobin A1C?
Bohr Effect:
Low pH (acidic environment) shifts oxygen curve L/R?
Higher relative levels of 2,3-BPG (bisphosphoglycerate) shifts
oxygen curve L/R?
Fever and acidosis:
Oxygen curve shifts L or R?
Hb values for newborns:
Higher or Lower? Why?
What is the Embden-Meyerhof pathway?
What are 2 important functions of 2,3-BPG for RBCs?
What is methemoglobin?
Without the enzyme, G6PD, no NADPH is formed, which is
needed for to metabolize glutathione.
This enzyme deficiency, which can cause hemolysis, is the
most common enzye deficiency in the world.
G6PD deficiency puts the patient at risk for hemolysis when
his cells are exposed to oxidative stress.
What 3 important things should you know about the Embden-
Meyerhof Pathway?
Causes of Hemolysis:
Intracorpuscular Hemolysis VS Extracorpuscular Hemolysis
(Just Click and Read)
Free hemoglobin binds to haptoglobin and the complex is
removed by the liver.
Hemosiderin in the urine can indicate what type of
hemolysis?
Which cells break down RBCs in the spleen (extravascularly)?
Within the splenic macrophage cytoplasm, RBC hemoglobin
is broken down into 3 parts:
Globin: --> Explain
Iron: --> Explain
Protoporphyrin --> Explain
Evaluating for Hemolysis:
Increase of Decrease?
LDH (Lactate Dehydogenase):
Haptoglobin:
Reticulocyte Count:
Total Bilirubin:
Indirect Bilirubin:
Coomb's Test: (+/-)?
Nutritional requirements for Chronic Hemolysis:
What is the purpose of a Direct (or Indirect) Coomb's Test?
Answers Notes
All of them
- breast bones
- pelvic bones
- proximal part of long bones
3 weeks *When the yolk sac develops
Yolk sac *First 6 weeks
Liver *6-18 weeks
Liver and Spleen *18-30 weeks
Liver, Spleen, and Bone Marrow *30 weeks - 8 weeks after birth
Liver, Spleen, and Bone Marrow *30 weeks - 8 weeks after birth
Bone marrow only *After 10 weeks after birth
- Pronormoblast
- Basophilic normoblast
- Polychromatophilic normoblast
- Orthochromatic normoblast
- Reticulocyte
- RBC
8 um
1/3
Neutrophils, eosinophils, and basophils
Eosinophils
Basophils
- Myeloblast
- Promyelocyte
- Myelocyte
- Metamyelocyte
- Band
- Neutrophil
3 to 6 lobes
2 lobes (bi-lobed)
Parasite or helminth infection
*Could also be season allergies or allergic
reaction
Lymphoblast and lymphocyte
*Cell surface markers need to be identified to
further differentiate
** Can't do it morphologically
CD 16
CD 56
CD 10
CD 19
CD 20
CD 79a
sIg k/d
CD 3
CD 4
CD 5
CD 7
CD 8
CD 38
Lung microvasculature *Smallest capillaries
Spleen
White pulp of the spleen
- Sinusoids
- Splenic Cords ("Billroths" cords)
- Monocytes/macrophages
*Dark alley analogy where new cells can squeeze
through small windows to escape monocytes but
old cells get stuck and are destroyed
**Extensive RBC damage leads to blood getting
trapped in spleen
WBC differential
Check "NLMEB" and make sure percentages are okay.
At birth
3 months
2%
FALSE *Anemia is not a normal finding in the elderly
Mean corpuscular volume
Tells you the size of the RBC
MCH - Mean corpuscular hemoglobin
- Avg. Weight of Hb / Cell
MCHC - Mean corpuscular hemoglobin concentration
- Avg. Concentration of Hb / Cell
60-80 fL
Less than 12%
- Larger than an RBC
- Less central pallor (Giemsa stain)
- Pricipitated RNA (methylene blue stain)
*Reticulocyte count not part of CBC - Need to
order separately
*It's a sign of ineffective hematopoiesis
Lead toxicity
*Basophilic stippling in RBCs is actually the
precipitation of undegraded RNA and seen in
(condition) lead toxicity.
Anything that results in extra membrane or decreased cell
volume
- Hemoglobinopathies/Thalassemias
- Iron deficiency anemia
- Drug-induced hemolytic anemia
- Liver disease
Conditions w/ increased fibrin:
- DIC / MAHA
- TTP
Liver disease
(Or something else that would affect the membrane
morphology)
*Liver dysfunction -> decreased synthesis of
cholesterol, which is needed for normal cell
membrane
Multiple myeloma
Patient is functionally/surgically asplenic.
Heriditary spherocytosis
(Can also be acquired: physical damage of RBCs)
Flatter part of Posterior Superior Iliac Crest
Less than 5%
Smear, FLOW, Cytogenetics (karyotype), FISH
Serum
Serum Protein Electrophoresis
RBCs are mixed with a reducing agen in a tube
Turbidity = Hemolysis = Sickle Cell Add picture
Protoporhyrin IX
2+ (ferrous state)
Alpha and gamma
(Hemoglobin A and Hemoglobin F) *Because they are more important
2 alpha
2 beta
2 alpha
2 delta
2 alpha
2 gamma
HbA2: 3.5%
HbF: 1-2%
Glycated (Glycosylated) hemoglobin as a result of glucose
being added to the beta chain
*Used to monitor diabetic patients
**Example of post-translational modification of
hemoglobin
Shifts right (Oxygen more easily released into tissues)
*Oxygen saturation (y-axis) is decreasing for any
given partial pressure (x-axis)
**Think lactic acid build up in muscles -> Want
more oxygen unloaded
Shifts right (Oxygen more easily released into tissues)
*2,3-BPG causes Hb molecule to tense up and
deoxygenate
Shifts right (Oxygen more easily released into tissues)
Higher
Because they have fetal hemoglobin, which binds oxygen
more tightly. Therefore need higher concentrations to
unload oxygen to tissues.
Anaerobic glycolytic pathways for RBCs
- Glucose gets metabolized to lactic acid
- Input 2 ATP to get 4 ATP = Net gain of 2 ATP *Also generates 2,3-BPG!
- Shifts oxygen curve right -> better oxygen delivery to
tissues
- Reduces methemoglobin (Fe3+) to hemoglobin (Fe2+)
Hemoglobin with iron in a Fe3+ state
*CAN'T Bind Oxygen!
*Glutathione converts H202 (damaging oxidant),
to water
G6PD deficiency
*G6PD is essential to prevent oxidative stress,
cell death, and lysis.
*Example: Antibiotics
- Energy (Input 2 ATP to get 4 ATP = Net 2 ATP
- 2,3-BPG reduces methemoglobin into hemoglobin
- G6PD from hexose monophosphate shunt prevents
oxidative damage (hemolysis)
Intra:
RBC membrane disorders
- heriditary spherocytosis or elliptocytosis
RBC enzyme disorders
- G6PD deficiency
- Pyruvate kinase deficiency
Hemoglobin Disorders
- Methemoglobinemia
- Thalassemia
- Sickle Cell Disease
Extra:
- Antibodies
- Sludging, trapping, destruction in spleen
- Trauma (prosthetic valces, DIC, etc)
- Chemicals (w/ oxidant properties)
- Infectious destruction (malaria, babesiosis, etc)
Intravascular Hemolysis
- Hb breaks down into alpha-beta dimers, which are small
enough to be filtered by the glomerulus.
- Some dimers are taken up into the renal tubular cells
and the iron is stored as hemosiderin.
- Renal tubular cells slough off into urine -> can be
detected.
Macrophages
Globin: --> Amino Acids (recycled)
Iron: --> Binds to Transferrin -> Goes to Liver, Spleen,
Bone Marrow (recycled)
Protoporphyrin --> Unconjugated Bilirubin -> Binds to
Albumin and sent to Liver -> Eventually excreted
LDH (Lactate Dehydogenase): Increase
Haptoglobin: Decrease
Reticulocyte Count: Increase
Total Bilirubin: Increase
Indirect Bilirubin: Increase
Coomb's Test: (+/-)? Positive
Folic Acid: Supplementation required
Vitamin B12: Usually not required (Body has 10 yr store)
Iron: Not required (iron gets recycled and stored)
Test for Autoimmune Hemolytic Anemia
- Agglutination = Positive Test
Direct test uses patient's RBCs (antigen already stuck on
them)
Indirect uses store bought RBCs and patient's serum
(which should have antibodies in it)
Questions
140818.4 Myeloid Disorders - Beaty
Answers Notes
What protein is iron bound to when stored intracellularly? Ferritin
What protein is iron bound to when traveling in the blood? Transferrin
Enterocytes transport iron into the bloodstream via
ferroportin.
Sequesters iron into storage sites, preventing
use by erythroid precursors
Suppresses EPO production
The congenital defect that causes sideroblastic anemia most
commonly involves the enzyme Aminolevulinic synthase
(ALAS)
What are the lab findings for sideroblastic anemia?
Ferratin
TIBC
Serum Iron
% Saturation
Ferratin - Increase
TIBC - Decrease
Serum Iron - Increase
% Saturation - Increase
What is the role of the acute phase reactant, hepcidin, when
it comes to anemia of chronic disease
Questions
Chapter 6.1 Leukopenia and Leukocytosis
CD marker for Hematopoietic Stem Cells:
Chapter 6.2 Acute Leukemia
Acute leukemia is a neoplastic proliferation of blasts (cell
type).
Acute leukemia is defined as a greater than 20% blasts in the
bone marrow.
Acute Leukemia
Why is the WBC (in the blood) high?
What is the phenotypic marker for lymphoblasts?
What is the phenotypic marker for myeloblasts?
You see Auer Rods in a blood smear.
What kind of cell are you looking at?
Presence of Auer rods indicates that your probably dealing
with which malignancy?
Acute Lymphoblastic Leukemia (ALL) most commonly arises
in:
Children of Adults
B-ALL is the most common type of ALL.
Cytogenetics (genotype) you should know for B-ALL: (2
Translocations)
Which has the better prognosis?
Patient, who is a teenager, presents with a mediastinal
(thymic mass):
Likely diagnosis?
AML is more commonly seen in which decades of life?
Acute promyelocytic leukemia is characterized by:
(translocation)
Acute promyelocytic leukemia (APL):
Pathogenesis
Acute promyelocytic leukemia (APL):
Treatment
AML risk factors:
Chapter 6.3 Chronic Leukemia
Chronic Leukemia - neoplastic proliferation of mature
circulating lymphocytes
Cells co-express CD5 and CD 20:
Likely diagnosis:
Primary cause of death in CLL patients?
CLL is a neoplasm of which cell?
CLL can progress to which condition?
CLL is associated with which autoimmune condition?
Hairy Cell Leukemia - neoplastic proliferation of mature B-
cells
Hairy Cells are positive for TRAP
Would you see lymphadenopathy in Hair Cell Leukemia?
Would you see splenomegaly in Hairy Cell Leukemia?
Hairy Cell Leukemia:
Treatment
Adult T-Cell Lymphoma Leukemia (ATLL):
Neoplastic proliferation of mature CD4+ T-Cells
ATLL is associated with which virus?
Mycosis fungoides:
Neoplastic proliferation of mature CD4+ T-Cells
Patient has aggregates of neoplastic T-cells in the epidermis
(Pautrier microabscesses):
Likely Dx?
When cancer cells in Myscosis Fungoides spreads to the
blood it's called Sezary Syndrome. The cells have a
cerebriform (characteristic) nuclei in the blood smear.
Answers Notes
Overproduction of blasts -> Leaks out into blood
TdT
*TdT is a DNA polymerase
**TdT is absent in myeloid blasts and mature
lymphcytes
Myeloperoxidase (MPO)
Myeloblast -> Probably looking at AML
*Auer Rods are crystallized MPO (seen only in
Myeloblasts)
Acute Myeloid Leukemia (AML)
Children *Associated with Down Syndrome (after age 5)
t(12;21) - Good prognosis
t(9;22) - Poor Prognosis
*t(9;22) also known as the Philadelphia
Chromosome
*t(9;22) more classically associated with CML
T-ALL
50-60 yo
t(15;17)
RAR receptor disrupted -> promyelocytes accumulate *Promyelocytes also contain auer rods
ATRA (all-trans retinoic acid)
- derivative of vitamin A
- causes blasts to mature
Preexisting dysplasia (Myelodysplastic Syndrome)
Prior exposure to alkylating agents (chemo)
Radiotherapy
CLL
Infection due to hypogammaglobulinemia
B-Cell
Diffuse Large B-Cell Lymphoma
Autoimmune hemolytic anemia
No - cells are trapped in bone marrow
Yes - expansion of red pulp
2-CDA
*Adenosine deaminase inhibitor
**Adenosine accumulates to toxic levels in neoplastic B
cells
HTLV-1
*Japan and Carribean
Mycosis fungoides
*Cells infiltrate skin producing rashes, plaques, or nodules
Add picture
Questions
140819.1 Intro to Lymphomas 2014
What is the difference between Leukemia and Lymphoma?
Primary lymphoid tissues (2):
Secondary lymphoid tissues (4):
Where are the primary and secondary follicles in a lymph
node?
Where in the lymph node does an dentritic cell present an
antigen to a T-cell?
Plasma cells and sinuses containing macrophages and
histiocytes can be found in which part of the lymph node?
What kind of cells are in the Primary follicles of a lymph
node?
Secondary follicle?
In a secondary follicle, what kinds of cells are in the dark
zone?
Light zone?
In the secondary follicle, ________________, destroy B-cells
with wrong antibodies.
Thymic epithelial cells interact with lymphocytes to help w
What are the high grade lymphomas? (4)
What are the intermediate grade lymphomas? (3)
What are some lymphomas that can have a leukemic phase?
(4)
Follicular Lymphoma:
High
Intermediate
or Low Grade?
Most common low grade non-Hodgkin lymphoma
Follicular Lymphoma:
Median age?
Histology shows "small-cleaved cells", centrocytes, and
centromeres.
Most likely dx?
Grading for Follicular Lymphoma is based on:
85% of patients with Follicular Lymphoma will have t(14;18)
(chromosomal abnormality).
If a patient has a t(14;18), what lymphoma might you
suspect? (2)
What is the most common of the intermediate grade
lymphomas?
What is the treatment for Diffuse Large B-Cell Lymphoma?
What are the 3 types of Burkitt's Lymphoma?
Burkitt's Lymphoma (especially African) is associated with an
infection by which virus?
Which lymphoma involves bones of the jaw and face?
Histology shows "a starry sky pattern".
Most likely dx?
Explain the presence of "starry sky" in histology of Burkitt's
Lymphoma
Cytogenetic abnormality necessary for Burkitt's Lymphoma:
Patient has a C-myc abnormality on chromosome 8.
What kind of cancer?
140819.2 Intro to Lymphoproliferative Disorders 2014
Which lymphoma is more common?
Non-Hodgkin or Hodgkin?
Normal age range for Hodgkin lymphoma?
Non-Hodgkin?
What type of cell is a Reed-Sternberg cell? Which kind of
malignancy is it associated with?
Patient has nodal malignancy with predictable, contiguous
spread.
What kind of lumphoma?
What kind of translocation would you see in a patient w/
Follicular lymphoma?
Answers Notes
Leukemias are cancers of the myeloid system and
Lymphomas are cancers of the lymphoid system
(lymphocytes)
Think cell type and location.
*Every lymphoma is a cancer of lymphocytes
*Lymphoma can have a leukemic phase
(lympocytes have the potential to circulate in the
blood)
Bone Marrow and Thymus
Lymph Nodes, Spleen, Tonsils, Clusters in GI tract and
pulmonary tract
Cortex
Paracortex
Medulla
*Macrophages and histiocytes (in the medullary
sinuses) capture antigen and process it
Primary: Nave B Cell
Secondary: Proliferating B Cells (after encountering
antigen)
Dark zone: Centroblasts
Light zone: Centrocytes
Tingible Body Macrophages
Burkitt's Lymphoma/Leukemia
Pre-B Cell ALL/Lymphoma
Pre-T Cell ALL/Lymphoma
Adult T-Cell Lymphoma (HTLV-1)
Diffuse Large B-Cell Lymphoma
Anaplastic Large Cell Lymphoma
Mantle Cell Lymphoma
Burkitt's Lymphoma/Leukemia
Pre-B Cell ALL/Lymphoma
Pre-T Cell ALL/Lymphoma
CLL/SLL
Low
Follicular Lymphoma
60-70 yo
Follicular Lymphoma
Centroblasts per HPF (high power field)
*Translocation (14;18) not diagnostic because it
could also be Diffuse Large B-cell Lymphoma
- Follicular Lymphoma
- Diffuse Large B-cell Lymphoma
Diffuse Large B-Cell Lymphoma
R-CHOP
----Rituximab
----Cyclophosphamide
----Hydroxy -doxorubicin
----Oncovin
----Prednisone
African, American, Immunodeficiency-associated
EBV
African Burkitt's
Burkitt's Lymphoma
*Refers to either the "white cells" (macrophages
and histiocytes) or the vacuoles
Starry sky appearance refers to either the "white cells"
(macrophages and histiocytes) or the vacuoles.
Burkitt's cells multiply so fast that they spontaneously die.
The "white cells" are macrophages and histiocytes
cleaning up the debris.
Chromosome 8: C-myc
*can happen in a variety of different ways (translocations)
Burkitt's Lymphoma
Non-Hodgkin (70% of malignant lymphomas)
*Hodgkin (30%)
Non-Hodgkin (Young Adult: 20's and 30's)
*Hodgkin (Adults)
Malignant B-Cell associated with Hodgkin Lymphoma
Hodgkin Lymphoma
t(14;18)
*Add Picture
Add picture
Questions
140820.3 Chemotherapy
Hemorrhagic Cystitis is caused by an accumulation of
Acrolein.
How do you prevent hemorrhagic cystitis?
MESNA is indicated for:
MESNA mechamism of action:
Which class of chemo drugs cause myelosuppression?
What is typically the cause of the dose limiting toxicity for
alkylating agents?
Dangerous side effect of Cisplatin
If a patient has impaired renal function, would you give him
Cisplatin or Carboplatin?
Platinum analogues:
Indications?
Side effect for Carboplatin:
Interesting side effect of Oxaliplatin:
Which class of chemo drugs causes IgE-mediated
hypersensitivity?
Common side effects for alkylating agents: (5)
Answers Notes
- Vigorous hydration
- MESNA (mercaptoethane sodium)
*MESNA must be given before chemo treatment
- Cyclophosphamide > 1g/m2/dose
- Ifosfamide (any dose) *Must be given before chemo treatment
Binds acrolein (uroprotectant)
*Preventative; Too late if hemorrhagic cystitis is
present
- Alkylating agents
Myelosuppression
- Nephrotoxic, but renally cleared
---Positive feedback cycle
- Patient must have good renal function
*Also nausea/ vomiting
"SPLAT" in Cisplatin
Carboplatin *Cisplatin is very nephrotoxic
Solid Tumors
- breast, lung, testicular, cervical/ovarian, colorectal,
bladder, lymphoma
Myelosuppresion/decreased platelet count
Cold-sensitizing peripheral neuropathy
Platinum analogues (alkylating agent)
- myelosuppression
- secondary leukemias
- infertility
- alopecia
- nausea/vomiting