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Fall 2018/P3 Year' > Therapeutics Exam 2 Pt. 3 Liquid Cancers - Griffin > Flashcards

Therapeutics Exam 2 Pt. 3 Liquid Cancers - Griffin Flashcards

1
Q

Liquid Cancers:

seen in what 3 places..?

A

blood
bone marrow
lymph nodes

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2
Q

What cancers are apart of the myeloid cell lines

A

MDS - myelodysplastic syndrome
CML - chronic myeloid leukemia
AML - acute myeloid leukemia

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3
Q

What cancers are apart of the lymhoid cell lines

A 
HD - hodkin lymphoma
NHL - non-hodgkin lymphoma
CLL - chronic lymphocytic leukemia
ALL - acute lymphocytic leukemia
MM - multiple myeloma
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4
Q

which cancer has reed sternberg cells?

A

hodgkin lymphoma

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5
Q

what is a reed sternberg cell

A

binucleated cell

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6
Q

what is lymphoma?

A

clonal disorder of HEMATOPOESIS involving malignant transformation of lymphocytes that predominate in the lymphatic system

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7
Q

Hodgkin Lymphoma- Etiology:

_______ giant cells that originate from _______

A

multinucleated giant cells

from B- lymphocytes

(aka Reed Sternberg cells)

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8
Q

Hodgkin Lymphoma:
Reed Sternberg cells overexpress _________

which leads to increased _______
and decreased _______

A

overexpress NFkB (nuclear factor Kappa B)

increased cell proliferation

decreased apoptosis

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9
Q

Hodgkin Lymphoma:
______ will upregulate NFkB

(up to 50% of hodking lymphoma cells are infected with ________)

A

infections will upregulate

EBV - epstein bar virus

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10
Q

Hodgkin Lymphoma - Clinical Presentation
Painless/rubbery - enlarged lymph node in _______ area
Mediastinal (around chest and sternum) involvement is common
______ manifestations are not common
_____ symptoms are 25 - 50 % common

A

in supradiaphragmatic area

Extranodal manifestations - not common
B symptoms

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11
Q

what are B symptoms?

A 
fever greater than 38 degrees
Drenching sweats (esp at night)
Unintentional weight loss (> 10% over a period of 6 mos or less)
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12
Q

B symptoms - leads to better or worse overall prognosis?

A

worse

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13
Q

Hodgkin Lymphoma:

______ Staging - talks about how many lymph nodes are involved

A

Ann Arbor

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14
Q 
Hodgkin Lymphoma: Ann Arbor Staging -
Stage 1?
2?
3?
4?
A

1: involvement of one lymph node area
2: 2+ lymph node ares on SAME side of diaphragm
3: lymph node involvement on both sides
4: extranodal involvement (like bone marrow)

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15
Q

Hodgkin Lymphoma:

What does IPS stand for?

A

international prognostic score

score to see who is at poorer prognosis

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16
Q

Hodgkin Lymphoma:

what factors are seen to put someone at a poorer prognosis? (IPS factors!)

A 
Albumin < 4
HgB < 10.5
Male
stage IV
45 + y.o
WBC > 15
Lymphocytopenia < 0.6
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17
Q

Hodgkin Lymphoma:

if they have ____ factors it is seen more as an unfavorable disease

A

2 + factors

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18
Q

Hodgkin Lymphoma:

What are some treatment modalities for this cancer?

A 
RT (radiation therapy)
Combo Chemo (ABVD!!!!, Standford V, BEACOPP)

or HD chemo with stem cell rescue

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19
Q

what does ABVD stand for?

A

doxorubicin (adriamycin!)
bleomycin
vinblastine
dacarbazine

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20
Q

Hodgkin Lymphoma:

for ABVD - how many cycles of it?

A

if stage I or II it is 4 cycles

if stage III or IV - then 6 cycles

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21
Q

Non-Hodgkin Lymphoma:
Symptoms are dependent on site of involvement:
if B cell lymphomas: _____, _____, _____ affected
it T cell lymphomas: ________ (_____ and _____)
Peripheral lymphadenopathy
40% of pts will have B symptoms

A

B cells: lymph nodes, spleen, bone marrow

T cells: extranodal sites (skin and lungs!)

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22
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:

which one is more often localized to a single group of nodes?

A

Hodgkin

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23
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:

has a noncontagious spread (aka a variety of lymph nodes are affected)

A

non-hodgkin lymphoma

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24
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:

which one has more frequent involvement of multiple peripheral nodes?

A

Non-Hodgkin Lymphoma

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25
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:
which one will orderly spread by contiguity?
aka spread to close lymph nodes first)

A

hodgkin

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26
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:

which one will commonly have extranodal presentation?

A

non-hodkgin

hodgkin will rarely have extranodal involvement!!

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27
Q

Non-Hodgkin Lymphoma vs Hodgkin Lymphoma:

which one will commonly have mesenteric nodes and waldeyer ring?

A

non-hodgkin

hodgkin will rarely have mesenteric or waldeyer ring!

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28
Q

what is the most common B cell lymphoma?

A

diffuse large B cell

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29
Q

what B cell lymphoma is “indolent”

aka has a relatively long survival and usually incurable?

A

follicular B cell lymphoma

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30
Q

what B cell lymphoma is “aggressive”

aka rapid growth and short survival if untreated and usually curable

A

diffuse large B cell

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31
Q

what B cell lymphoma is “highly aggressive”

aka has a doubling time around 18 h!! but also usuall curable bc super sensitive to chemo

A

burkitt B cell lymphoma

and AIDS related b cell lymphoma

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32
Q

T or F: lymphomas are steroid sensitive

A

TRUE!
why R-CHOP has prednisone!

R-CHOP is big with diffuse large B cell

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33
Q

what does R-CHOP mean?

A 
R- Ritxuimab
C - Cyclophosphamide
H - doxorubicin
O - vincristine
P - prednisone
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34
Q

why is rituximab good for B - cell lymphomas?

A

it targets CD-20! found on B cells…

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35
Q

when R-CHOP used?

A

when B cells lymphomas - part of non hodgkins lymphoma

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36
Q

Folliclular lymphoma:

use ______ to gauge risk factors

A

FLIPI (follicular lymphoma international prognostic index)

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37
Q

what are 1st line therapy options for follicular lymphoma?

A

bendamustine + rituximab (good if pt is good performance status!! - this is the BEST OPTION!)
R-CHOP
R-CVP
Rituximab (preferred if pt is elderly)

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38
Q

what does R-CVP stand for and when is it used?

A 
R - rituximab
C - cyclophosphamide
V - vincristine
P- prednisone
*used for non-hodgkin lymphoma -- follicular lymphoma
(same as R-CHOP but no doxorubicin!)
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39
Q

what is richters syndrome?

A

when indolent lymphoma (ex: follicular) transforms into more aggressive lymphoma

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40
Q

treatment options for richters syndrome?

A

doxorubicin based chemo w/ rituximab

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41
Q

Burkitt Lymphoma:
(mild or aggressive?)
Translocation involving ______ gene detected in nearly all cases

A

MYC gene

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42
Q

bone marrow in burkitt lymphoma looks like ______

A

starry sky

??

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43
Q

what are the FDA approved products for T - Cell immunology

A

Tisagenlecleucel (Kymriah)
or
Axicabtagebe ciloleucel (yescarta)

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44
Q

AIDS Related lymphoma:
Occurs (early or late) in HIV infection
Most AIDS related lymphomas are ____ neoplasms

A

late

B - cell (DLBCL or burkitt)

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45
Q

what is DLBCL mean?

A

difuse large B cell lymphoma

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46
Q

Treatment considerations of AIDS related lymphoma:
Most pts present with ______ and advanced disease
Concurrent ____ is assoc w/ higher complete remission rates
______ for all pts
_______ chemo for prophylaxis

A

present w/ B symptoms
concurrent HAART
G-CSF for all pts
intrathecal chemo

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47
Q 
Lymphoma Summary:
Treat with multi agent chemo = 5 yo overall survival
what chemos are best?
Hodgkin: \_\_\_\_\_\_
Non-Hodgkin: \_\_\_\_\_\_
A

Hodgkin: ABVD

Non-Hodgkin: R-CHOP

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48
Q

what is MM?

A

multiple myeloma

a progressive B cell disorder

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49
Q

Multiple Myeloma:

Typically have ____ symptoms

A

CRAB

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50
Q

what are CRAB symptoms for Multiple Myeloma?

A

C - Calcium corrected > 11 (albumin - for correction)
R renal dysfunction SCr > 2 or CrCl < 40
Anemia < 10 or 2 below normal
Bone - 1+ osteolytic lesions or pathologic fractures

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51
Q

Multiple Myeloma:

T or F: it has a very high cure rate

A

false

remains an incurable malignancy

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52
Q

Progression of Multiple Myeloma (?)

the flow chart of multiple myeloma

A

MGUS (monoclonal gammopathy of undetermined significance) –> Bone marrow increased angiogenesis –> lytic bone lesions –> plasma cells in blood

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53
Q

some other signs/symptoms of multiple myeloma outside of CRAB symptoms?

A

EMPs (extramedullary plasmacytomas) - plasma cell tumors arise outside the bone marrow

increased susceptibility of infections

Hyperviscosity (blood too thick b/c of myeloma proteins) (HA, blurred vision, oral bleeding etc)

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54
Q

what are the 3 phases of therapy for multiple myeloma

A

induction therapy
consolidation therapy
maintenance therapy

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55
Q 
Multiple Myeloma - Induction Therapy:
# drug regimens are preferred over # drug regimens
A

3 preferred over 2

if pt could tolerate 3 then do it!

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56
Q

Multiple Myeloma - Induction Therapy:

is the patient a ________ candidate - if so do _____ after the 3 drug regimen

A

potential transplant candidate?

do a stem cell harvest (do after 3 - 4 cycles of induction) - dont wait too long because then none will be there

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57
Q

what are some common Multiple Myeloma - Induction Therapy options

A

ALL ARE BORTEZOMIB BASED
(VRD) bortezomib/lenalidomide/dexamethasone
(CyBorD) bortezomib/cyclophosphomide/dexamethasone
bortezomib/doxarubicin/dexamethasone

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58
Q

what are common agents used in multiple myeloma (induction therapy)

(6 total)

A 
Steroids
IMiDs (immunomodulatory drugs)
Proteasome Inhibitors
Traditional Chemo (doxarubicin and cyclophosphamide)
Monoclonal Abs
Histone Deacteylase inhibitors
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59
Q

what drugs are IMiDs?

A

thalidomide, lenalidomide, pomalidomide (REMS program!!)

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60
Q

what drugs are proteosome inhibitors?

A

bortezomib, carfilzomib, ixazomib

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61
Q

what are some monoclonal antibodies used in multiple myeloma (induction therapy)

A

daratumumab

elotuzumab

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62
Q

what are some histone deacteylase inhibitor used in multiple myeloma (induction therapy)

A

panobinostat

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63
Q

Bortezomib based regimens usually have a significant comorbidity of _____

A

PN (peripheral neuropathy)

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64
Q

what is SCT

A

stem cell transplant

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65
Q

Who can get a SCT? (stem cell transplant)
____ is not a limiting factor
but
______ limits pts from becoming a SCT canidate

A

age is not

poor performance status will prevent candidacy

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66
Q

what was found to decrease rates of PN (peripheral neuropathy)
(dosing frequency, route etc)
*I think PN rates of the -zomibs..?

A

SQ admin decreased rates of PN

Weekly dosing instead of twice weekly still had same rate but there was less discontinuation — so in long run pts rcvd more of the dose

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67
Q

Stem cell transplant before or after CR (complete remission) is the better/superior outcome

A

SCT after CR!!

clear it out then give whole new system

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68
Q

Daratumumab targets _____ and is used in ______

A

CD-38

used in multiple myeloma

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69
Q

Common Complications of multiple myeloma?

A

bony manifestations
herpes zoster
thromboembolism risk

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70
Q

Common Complications of multiple myeloma:

How to treat bony manifestations…

A

bisphosphonates! (pamidronate and zoledronic acid)

use these for 2 years

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71
Q

Common Complications of multiple myeloma:
Treating bony manifestations —
monitor _____ and ______
and supplement ____

A

monitor renal function and osteonecrosis

pts should get 500 mg Ca2+ and 500 units of Vit. D

72
Q

Common Complications of multiple myeloma:

People can get herpes zoster how?

A

pts on proteasome inhibitor or monoclonal antibody are at increased risk of HSV infections

73
Q

Common Complications of multiple myeloma:

How to decrease chance of HSV infections

A

prophylactically treat with acyclovir and valacyclovir

74
Q

Common Complications of multiple myeloma:

what drugs increase risk of thromboembolism?

A

IMiDs and Dexamethasome regimens increase VTE risk

75
Q

Common Complications of multiple myeloma:

What to do to decrease thromboembolism risk with IMiD/dexamethasone regimens?

A

give ASA! or warfarin or enoxaparin… just give VTE crap

76
Q

CML (chronic myleoid leukemia)

genetics behind it?

A

Philadelphia Chromosome (BCR- ABL)

77
Q

how can you cure CML?

A

allogenic hematopoeitic stem cell transplantation (HSCT)

78
Q

what drug class is used in CML

A

TKI’s (tyrosine kinase inhibitor)

79
Q

what drugs are TKI’s used for CML

A 
imatinib
nilotinib (2nd gen)
dasatinib (2nd gen)
bosutinib (2nd gen)
ponatinib (3rd gen)
80
Q

which TKI’s produced a faster/deeper response in CML

A

nilotinib and dasatinib

81
Q

CML:

only one TKI is BID - which one?

A

Nilotinib

82
Q

CML:

which one must be taken with an empty stomach

A

Nilotinib

83
Q

CML:

main issues with TKIs?

A

DRUG INTERACTIONS CYP3A4 wit all

P-Gp for some

84
Q

Main Side Effect of Imatinib?

A

Nausea

85
Q

Main Side Effect of Dasatinib?

A

Fluid retention (pleural effusion)

86
Q

Main Side Effect of Nilotinib?

A

QTc prolongation

metabolic syndrome

87
Q

Main Side Effect of Bosutinib?

A

diarrhea

88
Q

Main Side Effect of Ponatinib

A

Ischemic reactions
Vascular occlusion
HTN

** huge in picking what therapy ppl can use!!!

89
Q

BCR-ABL can have resistance/a mutation that prevents normal TKI’s to be effective
what is the mutation and what drug overcomes it?

A

T3151

Ponatinib

90
Q

T or F: For 2nd line tx of CML - you can increase the imatinib doses and the 2nd gen doses

A

FALSE
can increase imatinib
but do NOT dose increase the 2nd gens

91
Q

T or F: since ponatanib is effective with the “gate keeper” mutation - it should be used 1st line

A

FALSE! only do it if mutation or failed other options – severe ADE’s so save it

92
Q

what is another drug for CML that tackle the T3151 mutation

A

Omacetaxine

93
Q

what are different phases of CML?

A

Chronic (most common)
accelerated
or Blast

94
Q

Goal is to get pts with CML to the ____ phase

A

chronic (not accelerated or blast)

95
Q

CLL (chronic lymphoblastic leukemia) - genetics:

which mutation leads to the biggest decrease in survival ?

A

deletion 17p

96
Q

why is the loss of 17p in CLL so devastating?

A

it reflects the loss of the key tumor supressor TP53

97
Q

CLL -

treatment usually done for what pts? (what staging)

A

only treat stages III/IV or those that are symptomatic

98
Q

what is first line tx for CLL pts - IF Young and Fit (<65 and no comorbidities)

if no del 17 or TP53 mutation - give what?

A

give FCR!!!
FCR = fludrabine
cyclophosphamide
rituximab

or maybe ibrutinib

99
Q

what is first line tx for CLL pts - old and Fit (>65 and no comorbidities)
w/ no del17/TP53 mutation

A

obinutuzumab + chlorambucil

or ibrutinib (good option for old ppl who cant tolerate FCR)

100
Q

what is first line tx for CLL pts - for frail pts?

w/ no del17/TP53 mutation

A

obinutuzumab + chlorambucil

or ibrutinib (good option for old ppl who cant tolerate FCR)

101
Q

what is first line tx for CLL pts?

w/ the del17/TP53 mutation!!

A

Ibrutinib
HDMP + Rituximab
Alemtuzumab +/- Rituximab

102
Q

what are some of the 2nd line CLL options?

A

Ventetoclax
Ibrutinib
Idealisib

103
Q

MOA of ventetoclax?

A

B -cell receptor inhibitor

104
Q

Venetoclax ADEs?

A 
Tumor lysis syndrome
Cytopenia
N/V
HA
Upper respiratory infections
105
Q

T or F: Venetoclax is best in combo therapy

A

TRUE — do not use this drug as mono therapy

106
Q

Ibrutinib ADEs?

A

transient lymphocytosis!!! (may look like failing therapy but nah - the drug is working!)
bleeding events!
A.fib
diarrhea

107
Q

Idelalisib ADEs?

A

transient lymphocytosis!!! (may look like failing therapy but nah - the drug is working!)
Increases LFTs
Diarrhea/Colitis - maybe treat w/ corticosteroids

108
Q

how to combat the transient lymphocytosis seen with idelalisib

A

give rituximab with it

109
Q

The lymphocytosis seen from Idelalisib and ibrutinib resolves by _____
and remember this transient increase in absolute ______ count does NOT signify disease progression

A

resolves by week 12

absolute lymphocyte count

110
Q

what does MDS stand for

A

myelodysplastic syndrome

111
Q

MDS has the potential to evolve into _____

we want to precent this evolution!!

A

AML

112
Q

diagnosing of MDS:
stable _____ for at least 6 mos
Specific MDS associated karyotype (____)

A

cytopenia

del5q

113
Q

MDS clinical presentation?

Since Cytopenia…. what symptoms will see what?

A

Cytopenia = low WBCs, platelets, RBCs –>
Fatigue/malaise/dyspnea on exertion (low RBCs)
cough/dysurea (low WBCs)
bleeding/bruising easily (low platelets)

114
Q

what are the main therapeutic options for MDS?

A

supportive care
low intensity therapy
high intensity therapy
enrollment in a clinical trial

115
Q

what are some supportive care options for MDS

A 
blood product transfusions
growth factor support
EPO stimulating agents
TPO receptor agonists
Managing iron overload (esp w/ frequent transfusions)
116
Q

MDS Treatment Options: If a pt is to get low intensity therapy:
if pt has Del5q - give them ______
if pt has low sEPO give them ______
if pt has normal - high sEPO give them _____ and ______

A

Del5q- Lenalidomide

low sEPO - ESA

Normal-High EPO: give IST (immuno- suppresive therapy) and 2nd line?? - hypoalkylating agents

117
Q

________ is the drug used when MDS pts have a del5q chromosome abnormality

A

lenalidomide

it causes apoptosis!

118
Q

MDS Treatment: Low Intensity Therapy
Immunosuppresive therapy goal: ______

ESA goal: ___________

A

IST: mitigate bone marrow failure

ESA: reduce symptoms of anemia and allow for transfusion independence

119
Q

MDS Treatment: Low Intensity Therapy
Response seen after how long of therapy?
Immunosuppresive therapy: _______
ESA therapy: _________

A

IST: 4 - 6 mos!!! ahhh so long

ESA: 6 - 8 weeks

120
Q

MDS Treatment: HIgh Intensity Therapy

what are the 2 options?

A

intensive AML chemo –> stem cell transplant
or
hypo-methylatying agents!

121
Q

what drugs are a part of immunosuppresive therapy in MDS

A

cyclosporine

antithymocyte globulin

122
Q

what drugs are hypo-methylatying agents

A

azacitidine

decitabine

123
Q

DNA methylation leads to the tumor suppressor gene becoming _____

A

silenced!

why HYPOalkylating agents = tumor suppressor gene is active

124
Q

MDS Summary:
Use low intensity therapy when ________
use high intensity therapy when ________

A

low: treat symptoms
high: prevent transformation to AML

125
Q

AML?

A

acute myeloid leukemia

126
Q

what gene mutation is seen as very unfavorable in AML

A

FLT3

127
Q

what drug was recently approved for FLT3 mutation in AML

A

midosautrin

128
Q

Secondary AML is common with what agents?

A

Alkylating agents

TOPO II inhibitors

129
Q

Treatment for AML

1) _______ Goal is remission
2) ______ goal is prevent relapse
3) ______ prevent relapse if high risk

A

1 - induction
2- consolidation
3 - transplant

130
Q

AML Tx:
Intensive therapy? (what drugs)

Goal = complete remission

A

cytarabine and an anthracycline
7 + 3 chemo!!!
all 7 days get cytarabine
first 3 you get anthracycline (with cytarabine)

131
Q

what are some high dose toxicities of cytarabine?

A

cerebellar side effects (look drunk..)
and
CHEMICAL CONJUCTIVITIS!!

132
Q

what is a good drug therapy to go with HD cytarabine?

A

eye drops!! (steroid or natural eyes)

HD cytarabine leads to chemical conjuctivtis

133
Q

what is the one way to cure AML

A

stem cell transplant

134
Q

APL is a type of ______

it is key to know the differences because it needs to be treated fast….?

A

type of AML

it is the better one to have

135
Q

APL:

there is a ______ of chromosomes 15/17 which is apart of the ______ receptor

A

translocation

retinoic acid receptor

136
Q

All-trans retinoic acid
ex: _______
effective in AML/APL because it disrupts the binding of _______ and restores normal _____/______ pathway

A

ex: trentinoin

disrupts gene repressor binding

normal maturation/differentiation pathway

137
Q

AML diagnosis based on _________ biopsy

A

bone marrow

138
Q

ALL -

what drug classes are staples for treatment

A

steroid
vinca alkaloid
antrhacycline

139
Q

25% of Adult ALL patients will have ______ positive disease and adding ________ inhibitors to multiagent chemo is best

A

Philadelphia positive disease (BCR-ABL!!!)

adding TKIs

140
Q

MOA of Blinatumomab and what cancer may it be used in

A

MOA: bispecific T cell engaged (CD19 and CD3)

ALL cancer (used 2nd line)

141
Q

black box warnings of blinatumomab?

A

cytokine release syndrome

neurotoxicity

142
Q

ALL:
______ plays a large role in overall prognosis

_________ plays a large role in treatment

A

Risk stratification

Maintenance therapy

143
Q

Definitions:

Autologous Transplant

A

pt serves as own donor

144
Q

Definitions:

Engraftment

A

blood cell recovery after transplant

145
Q

Definitions:

Allogeneic transplant

A

matched sibling or unrelated donor

146
Q

Definitions:

conditioning regimen

A

chemo/radiation given prior to stem cell infusion

147
Q

Definitions:

stem cell mobilization

A

process of collecting stem cells

148
Q

what type of SCT is common for AML cancer

A

allogenic

149
Q

what type of SCT is most common in the US

A

autologous

150
Q

For allogenic transplant: ______ matching is key

A

HLA (human leukocyte antigens)

151
Q

HLA is encoded by genes of the _____ which is located on chromosome 6 (the major function is regulation of __________)

A

genes of NHC (major histocompatibility complex)

major function is immune responsiveness

152
Q

what are the main sources of donor cells for SCT?

A

bone marrow
peripheral blood
umbilical cord blood

153
Q

Donor Cell Source: Bone marrow, peripheral blood, or umbilical cord blood?
invasive procedure/large volume collected/LONGER TIME TO ENGRAFT

A

bone marrow

154
Q

Donor Cell Source: Bone marrow, peripheral blood, or umbilical cord blood?
small volume collected/faster engrafment/may require multiple sessions

A

peripheral

155
Q

Stem cell mobilization must happen because there is not enough stem cells in peripheral blood – thus give ______

A

give growth factors (filgrastim +/-perixafor)

156
Q

If a healthy pt gets filgrastim – what will they typically complain of?

A

bone pain

157
Q

what is the main difference in the process of autologous and allogenic stem cell transplants?

A

must start immunosupression before giving stem cells in allogeneic

158
Q

radiation may be used in combo with chemo prior to SCT —- this is helpful when the tumor cells are hard to reach with chemo — what are examples of this?

A

CNS and testes

159
Q

what does TBI stand for

A

total body irradiation

160
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
Cyclophosphamide?

A

cardiomyopathy

161
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
melphalan

A

mucositis

162
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
busulfan

A

hepatic

163
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
TBI

A

pulmonary

164
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
Carboplatin

A

hepatic/renal

165
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
etoposide

A

mucositis

166
Q

Per Griffin Lecture: NON-hematologic dose limiting toxicities table:
carmustine

A

hepatic/pulmonary

167
Q

what does MAC mean?

A

myeloablative conditioning (AKA take out allllll of bone marrow - and must rescue with stem cells)

168
Q

what is RIC and when is it used?

A

RIC = reduced intensity conditioning
(also known as non-myleoablative conditioning)
use when pts probably wont be able to tolerate allogeneic SCT…

169
Q

what are some common myeloablative conditioning regimens?

A

busulfan and cyclophosphamide (BuCy)

cyclophosphamide and TBI (Cy/TBI)

170
Q

Engraftment occurs when
_____ and _____ are above certain levels 3 days in a row
_____ and _____ take hella lot longer to get back to normal

A

neutrophils and platelets

lymphocytes and erthocytes

171
Q

Transplant related complications?

what is seen post transplant

A

infections
graft vs host disease
organ dysfunction

172
Q

Transplant related complications?

what is seen peri transplant

A 
peri = about/around
infections
N/V/D
mucositis
graft failure 
organ dysfunction
173
Q

Acute vs chronic GVHD: how many days to be considered each?

A

< 100 days post SCT = acute

> 100 days post SCT = chronic

174
Q

how to treat both acute or chronic GVHD

A

steroids

175
Q

Grading Acute GVHD – looking at what 3 different things?

A

skin
liver
intestinal tract

176
Q

Counseling points related to SCT

  • Good _______ and limit________
  • Minimal contact with recipients of _________ for 4 weeks
  • SCT pts require _______ over 1 - 2 year period post transplant
A
  • good hand hygiene/ limit sick contact
  • avoid recipients of live vaccines for 4 weeks
  • require re-immunization over 1 - 2 year period (like childhood vaccines!)
177
Q 
Late complications of SCT?
\_\_\_\_\_\_\_\_\_\_\_ disease
\_\_\_\_\_\_\_\_ disease
\_\_\_\_\_\_\_\_ formation
\_\_\_\_\_\_\_\_ dysfunction and \_\_\_\_\_\_
\_\_\_\_\_\_\_\_\_ disease
\_\_\_\_\_\_\_\_\_\_\_\_\_
A 
restrictive and obstructive pulmonary disease
bone/joint disease
cataract formation
thyroid dysfunction/sterility
Cardiovascular disease
Secondary malignancies

Fall 2018/P3 Year' (16 decks)

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