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Oncology > 4 - Acute Lymphoblastic Leukemia and Chronic Lymphocytic Leukemia > Flashcards

4 - Acute Lymphoblastic Leukemia and Chronic Lymphocytic Leukemia Flashcards

1
Q

ALL

A 
Acute LymphoBLASTic Leukemia
Focuses on very early immature cells
Aggressive
Requires immediate treatment
Curable
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2
Q

CLL

A

Chronic LymphoCYTic Leukemia
Often indolent
May not need treatment for years
Incurable

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3
Q

ALL - Detected but not treated

A

You could die within days to weeks

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4
Q

Malignant lymphocytes mainly in the lymph nodes

A

Lymphoma

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5
Q

Malignant lymphocytes mainly in the blood and bone marrow

A

Leukemia

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6
Q

Lymphocytic Leukemia - Arrested a mature state

A

CLL

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7
Q

Lymphocytic Leukemia - Arrested at an immature state

A

ALL

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8
Q

2 Types of ALL

A

B Cell

T Cell

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9
Q

ALL - Incidence

A

Rare

~1000 cases per year

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10
Q

ALL - Prognosis

A

Pediatrics - Curable, even at relapse

Adults - Often fatal

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11
Q

ALL - Risk Factors

A

Radiation exposure

Trisomy 21

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12
Q

ALL - Patient Presentation

A

Acute complications of cytopenias (Bleeding, Infection, Fatigue, Dyspnea, Dizziness)
Fever
Bone Pain
Rarely lymphadenopathy

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13
Q

Acute complications of cytopenias

A 
Bleeding
Infection
Fatigue
Dyspnea
Dizziness
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14
Q

ALL - Microscopic

A 
Large redundant lymphocytes
Open chromatin
Prominent nucleoli
Light purple cytoplasm
No granules
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15
Q

ALL - Physical Exam

A 
Signs of anemia
Ecchymosis, petechiae
Lymphadenopathy (rare)
Splenomegaly (rare)
Rash (from an infection)
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16
Q

ALL - Diagnosis

A 
Bone Marrow Tests:
Core biopsy
Flow cytometry
Aspirate slides
Cytogenetics

Source for core biopsy: Superior iliac crest (feel through the skin)

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17
Q

Flow Cytometry

A

Critical test for all lymphoid malignancies
Less critical for myeloid malignancies

Suck fluid out of bone marrow, or take blood
Label the cells with fluorescent antibodies
Shoot cells down a channel
Hit them with a laser and see what lights up

Therapeutic implications:
Once you know which surface markers are on a cancer cell, you can target those cells using that surface marker.

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18
Q

B Cell ALL - Diagnosis on Flow Cytometry

A 
TdT
CD19 (can be therapeutic target)
CD22
CD79
Immunoglobulin
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19
Q

T Cell ALL - Diagnosis on Flow Cytometry

A

TdT
CD7
CD2
CD3

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20
Q

CD19

A

B Cell ALL Marker

Can be therapeutic target

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21
Q

T Cell ALLs often present with

A

Large mediastinal mass

When it disappears, it means you’ve given good chemotherapy and it’s worked

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22
Q

Components of Therapy - ALL

A

Induction
CNS Therapy
Intensification
Maintenance

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23
Q

ALL Therapy - Induction

A 
Prednisone
Dexamethasone
Vincristine
Doxorubicin
Cyclophosphamide
Asparaginase
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24
Q

ALL Therapy - CNS Therapy

A

Craniospinal irradiation
Intrathecal Methotrexate and Cytarabine

This is important because ALL spreads to the CNS through the CSF

Maybe don’t radiate kids though if you can avoid it. Check CSF to see if there’s any cancer in there.

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25
ALL Therapy - Intensification
Similar to Induction: ``` Prednisone Dexamethasone Vincristine Doxocubicin Cyclophosphamide Asparaginase ```
26
ALL Therapy - Maintenance
Prednisone Mercaptopurine Methotrexate
27
ALL Therapy - Time Course
2+ years
28
Chemotherapy - Dexamethasone
Directly toxic to lymphocytes
29
Chemotherapy - Prednisone
Directly toxic to lymphocytes
30
Chemotherapy - Vincristine
Inhibits microtubule polymerization
31
Chemotherapy - Doxorubicin
Inhibits Topoisomerase II | Used in lymphoma, leukemia, breast cancer, etc
32
Chemotherapy - Cyclophosphamide
Alkylating agent - Induces bulky DNA lesions
33
Chemotherapy - Asparaginase
Depletes asparagine ALL cells are particularly sensitive to this. Most other tumors are not.
34
Chemotherapy - Methotrexate
Folate antagonist
35
Complications of ALL
DIC | Tumor Lysis Syndrome
36
DIC Labs
``` PT ↑ aPTT ↑ Fibrinogen ↓ (sometimes "spuriously" normal) D-Dimer ↑ Platelets ↓ Schistocytes +/- ```
37
DIC - Treatment
Cryoprecipitate
38
Tumor Lysis Syndrome Labs
K+ ↑ (from lysed cells and reduced renal clearance) Creatinine ↑ (from acute renal failure due to Uric Acid) Uric Acid ↑ (from DNA breakdown) Phosphorous ↑ (from lysed cells) LDH ↑ (from lysed cells) Calcium ↓ (it binds to phosphorous)
39
How do you prevent the complications of Tumor Lysis Syndrome?
Allopurinol (prevent Uric Acid formation) | Rasburicase (break down Uric Acid)
40
Allopurinol
Prevents breakdown from xanthine to uric acid | Doesn't help the problem if the patient already has high levels of uric acid.
41
Rasburicase
Recombinant enzyme Breaks down Uric Acid into Allantoin (white stuff in bird poop) Costs more than $10,000
42
ALL - Adverse Prognostic Factors
``` Younger than 1 year old Older than 10 years old Adults - Increasing age, especially over 60 WBC > 30K (B-Cell) WBC > 100K (T-Cell) Adverse cytogenetics B-Cell Phenotype Presence of minimal residual disease ```
43
Minimal Residual Disease
Detect DNA left over from leukemia cells when in apparent remission Test: PCR Indicates likelihood of relapse
44
ALL - Adverse Cytogenetic Risk Factors
t(9;22) "Philadelphia Chromosome" - Poor Prognostic Marker, more common in adults t(4;11) "Mixed Lineage Leukemia" - Poor Prognostic Marker, more common in infants Hyperdiploidy - Favorable Prognostic Marker, more common between ages 1 and 10
45
ALL - Allogeneic Bone Marrow Transplant
Young patients with adverse cytogenetics in first remission Standard treatment for relapsed ALL in young patients Important factors in other scenarios: Patient Age Presence of HLA-matched sibling
46
2 new therapies for ALL
Blinatumomab | CART therapy
47
Blinatumomab
Bispecific T-Cell engaging Ab (BiTE) Redirects T cells to lyse CD19+ malignant and nonmalignant B cells It's essentially an adaptor, hooking up T Cells and CD19 B Cells Effective in patients who have not responded well to standard therapy Costs $200,000
48
CART Cells
Chimeric Antigen Receptor T Cells Take T Cells out of the body, transfect them with DNA that causes them to express a novel T Cell receptor specifically looking for CD19 Effective in getting rid of refractory ALL They may never make antibodies again, though.
49
CLL - Incidence
Most common form of leukemia Only form of leukemia with NO increased incidence with a-bomb survivors Disease of the elderly
50
CLL - Microscopic Smear
Small redundant lymphocytes (around the size of an RBC) Clumped chromatin Absent nucleoli Light purple cytoplasm Smudge cells (not pathognomonic, but frequently seen)
51
CLL - Patient Presentation
Asymptomatic Lymphocytosis Lymphadenopathy (Common) Chronic complications of cytopenias (recurrent sino-pulmonary infections, gradual fatigue, dyspnea, dizziness) Chronic weight loss
52
Chronic complications of cytopenias
Recurrent sino-pulmonary infections | Gradual fatigue, dyspnea, dizziness
53
CLL - Diagnosis on Flow Cytometry
``` Predominance on lymphocytes of: CD5 CD19 CD20 (can be therapeutic target) CD23 ``` Adverse prognosis: High expression of CD38 & ZAP-70 Look for "light chain restriction" meaning only kappa or lambda light chains are expressed, not both (which would indicate normal light chains)
54
CLL Diagnosis
No bone marrow needed. Can do flow cytometry on the blood
55
CLL - Cytogenetics order of prognosis (Worst-to-best)
``` 17p Deletion (lose p53) 11q Deletion 12q Trisomy Normal 13q Deletion as SOLE abnormality ```
56
CLL - Heavy Chain Hypervariable Region Mutations
If you see mutations in the hypervariable region of the heavy chains on surface Ab, it is a FAVORABLE prognosis. Wild type hypervariable regions indicate POOR prognosis.
57
CLL - Stage 0
Monoclonal lymphocytosis | >6,000/μL
58
CLL - Stage 1
Lymphadenopathy
59
CLL - Stage 2
Hepatosplenomegaly
60
CLL - Stage 3
Hemoglobin
61
CLL - Stage 4
Platelets
62
If a patient has asymptomatic CLL, when do we treat?
At Stage 3!
63
Immune Dysregulation due to CLL
``` Immune Thrombocytopenic Purpura (ITP) Autoimmune Hemolytic Anemia (AIHA) Hypogammaglobulinemia Pure Red Cell Aplasia (PRCA) Other auto-immune diseases ```
64
Venn Diagram of Mechanisms of Thrombocytopenia
ITP (platelets low, out of proportion to the hemoglobin) Splenic sequestration Marrow involvement
65
CLL - Indications for treatment
``` Stage 3/4 CLL Rapid lymphocyte doubling time (faster than every 6 months) Symptomatic lymphadenopathy Fevers, night sweats, weight loss Transformation to high grade lymphoma ```
66
CLL Treatment - Agents
``` Cyclophosphamide (C) Fludarabine (F) Rituximab (R) Bendamustine (B) Alemtuzumab Ofatumumab Chrlorambucil ```
67
CLL Treatment - Regimens
FCR: Fludarabine Cyclophosphamide Rituximab FR: Fludarabine Rituximab BR: Bendamustine Rituximab
68
Chemotherapy - Fludarabine
Nucleoside Analogue
69
Chemotherapy - Rituximab
Monoclonal Ab to CD20 Partially humanized, but synthesized in mouse ovaries Opsonizes CLL B Cells
70
Chemotherapy - Ofatumumab
Monoclonal Ab to CD20
71
Chemotherapy - Obinotuzumab
Monoclonal Ab to CD20
72
Chemotherapy - Alemtuzumab
Monoclonal Ab to CD52
73
Chemotherapy - Chlorambucil
Alyklating agent - Induce bulky DNA lesions
74
Chemotherapy - Bendamustine
Aklylating agent - Induce bulky DNA lesions
75
Idelalisib
New Therapy for CLL. Blocks PI3kδ PO therapy Small molecular inhibitors of growth pathways in CLL cells B cell receptors aren't just important in recognizing antigen. They also trigger proliferation. Poison that pathway with these drugs.
76
Ibrutinib
New Therapy for CLL. Blocks BTK PO therapy Small molecular inhibitors of growth pathways in CLL cells B cell receptors aren't just important in recognizing antigen. They also trigger proliferation. Poison that pathway with these drugs.
77
Idelalisib & Ibrutinib
``` Oral Monotherapy Highly effective in relapsed CLL Effective in 17p- Disease Effective in the infirm Induce transient lymphocytosis ```
78
Only cure for CLL
Allogeneic Bone Marrow Transplant | Carries a high mortality rate (10 - 40%)

Oncology (23 decks)

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