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Therapeutics > EXam 2 lecture 7 > Flashcards

EXam 2 lecture 7 Flashcards

1
Q

What are the diseases of myeloid cell lines?

A

Myelodysplastic syndrome (MDS)
chronic myeloid leukemia (CML)
acute myeloid leukemia (AML)

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2
Q

What are lymohoid cell line diseases

A

Hodgkin lymphoma (HD)
non-hodgkin lymphoma (NHL)
chronic lymphocytic leukemia (CLL)
acute lymphocytic leukemia (ALL)
multiple myeloma (MM)

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3
Q

What are the 2 major types of lymphomas? what is the backbone of tx?

A

hodgkin lymphoma (HL)
non-hodgkin lymphoma

Chemo is backbone of therapy

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4
Q

risk factors for HL

A

Epstein-barr virus (EBV)
impaired immune function

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5
Q

symptoms of HL

A

Painless rubery enlarged lymph node.

B symptoms (25%-50%)
-fever
drenching sweats
unintentional weightloss

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6
Q

How is HL diagnosed

A

Excisional biopsy is gold standard

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7
Q

staging of HL

A

stage I-II without unfavorable factors
STage I-II with unfavorable factors
stage III-IV

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8
Q

How to treat IA, IIA favorable HL

A

ABVD + RT
Stanford V + RT
ABVD
ABVD + escelated BEACOPP

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9
Q

How to treat I-II unfavorable HL

A

ABVD + RT
STanford + RT
Escalated BEACOPP x 2 + ABVD x 2 + RT

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10
Q

stage III/IV HL treatment

A

ABVD +/- RT
AAVD
Stanford + RT
Escelated BEACOPP +/- RT (IPS>or=3)

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11
Q

What does ABVD stand for? toxicities?

A

Doxorubicin (adriamycin)
Bleomycin
Vinblastine
Dacarbazine

toxicities
- cardiotoxicity (from doxorubicin)
- pulmonary toxicity (from bleomycin)

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12
Q

What does AAVD stand for

A

Doxorubicin
Brentuximab vendotin
Vinblastine
Dacarbazine

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13
Q

How to treat relapsed HL? When is early relapses time frame?

A

Early relapse is less than 1 year after tx

AUTOLOGOUS stem cell transplant and high dose chemo used with brentuximab as maintenance therapy following transplant

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14
Q

Which one occurs earlier, HL or NHL? which one occurs more?

A

HL

NHL occurs more

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15
Q

What happens in NHL

A

malignant cells proliferate and replace normal cells in lymph nodes and/or bone marrow

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16
Q

What cells do NHL primarily affect

A

85% B cell and 15% t cell

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17
Q

risk factors for NHL

A

EBV, infections and other viruses, immunodeficiency states (autoimmune)

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18
Q

How does NHL present

A

presentation depends on tumor location,

B cell: Lymph nodes, spleen, bone marrow (40% of patients)
T cell: Extra nodal sites (skin and lung) 10-35% of patients)

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19
Q

DO we give chemo even if the patient is neutropenic in HL

A

yes

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20
Q

What are the B symptoms associated with NHL presentation?

A

Fever
drenching sweats
unintentional weight loss

21
Q

Diagnosis of NHL

A

Excisional biopsy

22
Q

What are the different types of B cell lymphomas?

A

Indolent (25=40%)
Aggressive (60-75%)
Highly aggressive

23
Q

among indolent, aggressive and highly aggressive, which ones are curable? Which ones arent? Why?

A

Indolent is usualy incurable due to how slow it grows.

aggressive and highly aggressive are usually curable

24
Q

In general, what are the different treatment approaches to NHL

A

Radiation therapy
multi agenttherapy
immunotherapy
high dose chemo with stem cell rescue
CAR-T
T cell engagers

25
What is the name of the 2nd most common NHL? HOw to treat it?
follicular lymphoma treated if symptomatic or patient preference with chemotherapy
26
What is richters transformation? How to treat? What can we expect after tx?
FOllicular lymphoma can transform into an aggressive NHL Chemo yields 40% Complete remission, but still have underlying follicular lymphoma (Treat like DLBCL)
27
What is DLBCL? genetic abnormalities to identify? How does it present?
DLBCL is 30% of NHL cases. 30-40% present with extranodal disease (head/neck, GI tract, skin, bone) genetic abnormalities to identify- double hit/ triple hit (BCL translocation)
28
What are the multi agent chemotherapies we can use in NHL
R-CHOP- rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone DA-EPOCH- Etoposide, prednisone, vincristine, doxorubicin, cyclophosphamide POLA+R+CHP- Polatuzumab, rituximab, cyclophosphamide, doxorubicin, prednisone
29
How to treat the dufferent stages of DLBCL
Stage I-II- 3 cycles RCHOP + Rituximab or 6 cycles R-CHOP Stage III-IV (+bulky stage II)- 6 cycles R-CHOP or 6 cycles pola + R + CHP (IPI> or = 2)
30
R-CHOP toxicities
neutropenia thrombocytopenia infection anemia
31
What is seen with rituximab use? How to avoid this?
Hepatitis B reactivation seen. Treatment with pre emptive therapy- entecavir late neutropenia also seen. Treat with growth stimulating factors. (IVIG if GSF do not work)
32
How to treat relapsed DLBCL/ aggressive NHL
two rounds of salvage chemo followed by autologous stem cell rescue if they respond well to chemo another option can be CART therapy Another option can be Palliative chemo (bendamusine, rituximab+polatuzumab) another option cane be BITEs (epcoritamab, glofitamab)
33
MOA of CART cell
take CART cell out of body modify them so that they recognize the cancer then we give back the t cells back into body this poses a lot of risk for side effects (CD-19 is a target)
34
What are the names of the different CART cells used in NHL? What diseases do they specifically treat? MOA of CAR T
Tisagenlecucel- treats ALL, follicular lymphoma, NHL Axicaptagine- treats follicular lymphoma, NHL Lisocaptagine treats NHL rememeber that T cell therapy targets CD 19. They activate T cell immune response to cause T cell destruction of the lymphome by genetically modifying patients T cells
35
What do we treat patients that did not reposnd to CAR T or stem Cell transplants (i.e 3rd line NHL)
BITE 1. epocritamab 2. glofitamab
36
MOA of BITE
They take patient T cell and and takes it to CD 19 lymphoma. and forces T cell to turn on to start destructing
37
BITE and CART unique toxicities
Cytokine release syndrome (CRS) Immune effector cell associated neurotoxicity syndrome (ICANS)
38
how to handle CRS caused by BITE or CART
tocilizumab (anti IL-6 antibody) is used for CART cells- decreases cytokine storm (for grade 2) corticosteroids for grade 3 or higher
39
How to handle ICANS associated with CART and BITE
treatment must be with corticosteroids (IL6 does not cross BBB) Higher risk for ICANS with CART therapy compared to BITEs
40
What are the tests we do before starting RCHOP
hepatitis B surface antigen and hepatitis core antibody
41
what cells do MM affect?
Plasma cells (they produce antibodies)
42
What goes wrong in MM
Abnormal clone plasma cells in bone marrow (they usually should not be in marrow) plasma cells and MM cells are produced from differentiated B cells after antigen stimulation. Normal plasma cells die after a few days, MM plasma cells are long luved and they slowly proliferate. They secrete 60% igG, 20% igA and are secreted in urine
43
what are the preceding cells before MM
MGUS and smoldering MGUS-> MM rate 1% per year smoldering MM-> MM rate 10% per years for 1st five years
44
When do we know when to treat MM
CRAB
45
What does CRAB stand for? What is its use?
Calcium >11.5 Renal dysfunction Scr > 2 mg/dr or CrCL <40 Anemia <10 g/dl or 2 g/dl below normal bone frcature or osteolytic lesions USed to see whether or not to treat MM
46
MM treatment overview
It is incurable but we wanna control disease Induction followed by consolidation followed by maintenance therapy
47
Induction therapy in MM
If transplant candidate do high dose chemotherapy followed by stem cell rescue. If they are not a transplant candidate- 3 drug regimen
48

Therapeutics (38 decks)

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