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Fall 2018/P3 Year' > Therapeutics Exam 2 Pt. 2 (Weddle) > Flashcards

Therapeutics Exam 2 Pt. 2 (Weddle) Flashcards

1
Q 
Prostate Cancer:
Main etiologies?
Hormonal:\_\_\_\_\_\_\_\_
\_\_\_\_\_\_\_ receptor alterations
Enzyme \_\_\_\_\_\_\_ is key to synthesis of the hormone
can be genetic (small % tho)
A

testosterone hormone….
Androgen receptor alterations (amplification/overexpression; mutations; splice variants)

enzyme: CYP17A1

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2
Q

Prostate Cancer: Risk Factors:
Age: increases with increasing age
Race: more common in ______ (thought to be due to differences in androgen receptors and testosterone production)
Family Hx: increased risk with first degree relative
Others: ?

A

race: African Americans

Others:
Diet - high fat = higher risk
Occupation - textile and other industrial workers = increased risk
(long term vasectomy– but like no because maybe they are been screened more/have an urologist)

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3
Q

Prostate Cancer:

what things may have a Protective effect?

A

Vit. E
selenium
soy
lycopenes

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4
Q

screening options for Prostate Cancer?

A

DRE (direct rectal exam) (nose feeling = normal; chin = more of concern)
PSA (prostate specific antigen)

(TRUS - transrectal ultrasonography = bad specificity and sensitivity)

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5
Q

PSA levels:
normal: ______
needs evaluation: ______
Highly suspicious of malignancy: _______

OR is PSA velocity (change in a year) is _______

A

normal: 0 - 4 ng/mL

eval: > 4
suspic for malignancy: > 10

PSA velocity: > 0.75

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6
Q

Factors of PSA levels:

what will decrease PSA

A

finasteride and dutasteride

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7
Q

Factors of PSA levels:

what will increase it

A

ejaculation/prostatic manipulation or biopsy
BPH
prostatitis

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8
Q

ACS Screening Guidelines for Prostate Cancer:

Men > _____ y.o should get a PSA +/- DRE

A

50 years old!

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9
Q

ACS Screening Guidelines for Prostate Cancer:
once a man gets a PSA:
if his PSA is < _____ they should get the PSA checked every 2 years
or
if his PSA is > _____ they should get the PSA checked every annually

A

if < 2.5 - Q 2 years

if > 2.5 - then yearly

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10
Q

Discussion of screening of prostate cancer should happen earlier in high risk patients —
who is high risk and when to start screening

A

if african american - higher chance - start at age 45

if several first degree relatives - maybe start at 40 y.o

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11
Q

T or F: Finasteride but not dutasteride is approved for prostate cancer prevention

A

FALSE! neither of them are

there were trials for them but like not FDA approved

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12
Q

Finasteride trial finding in relation to prostate cancer prevention?

A

did reduce risk BUT people who did get prostate cancer had disease with a higher GLEASON score (aka more aggressive and less differentiated)

but maybe because prostate had shrunk – they could get better biopsies and diseases looked worse..?

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13
Q

what is the current recommendation for prostate cancer prevention?

A

there is not one :’(

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14
Q

Prostate Cancer Pathophys:

the _______ passes through the prostate and prostatic hypertrophy may compress it

A

urethra

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15
Q

Prostate Cancer Pathophys:

compressing on the urethra may lead to what things related to urination?

A 
increaesd frequency
inability to start and stop flow
dysuria
hematuria
nocturia
incomplete bladder emptying
dribbling
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16
Q

Signs and Symptoms of Prostate Cancer:

A 
asymptomatic early on...
but advanced disease:
alterations in urinary habits
impotence
lower extremity edema
weight loss
anemia
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17
Q

Prostate Cancer:

Metastasis to the ______ is most common but can also go to liver and lung

A

bone

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18
Q

99% of Prostate Cancer is ______

what kind of histology

A

adenocarcinoma

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19
Q

Explain Gleason Score

A

can be 2 - 10
get 2 diff scores (1 -5) from the primary and secondary growth patterns then add them together
higher score = higher risk of exracapsular spread

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20
Q

Gleason Score:
scores of _____ = slow growing and well differentiated
scores of ____ = aggressive and poorly differentiated

A

2 - 4 = slow

8 - 10 = aggressive

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21
Q

TNM staging for prostate:

T is referring to the _____ of the tumor

A

the spread of it/how extended it is (like if on both lobes or not)
T is not referring to size per se

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22
Q

what are the overall possible treatment options for prostate cancer

A

observation
active surveillance
Radiation therapy - external beam = ERBT
brachytherapy - implantable radiation therapy
Radical Prostatectomy + PLND (pelvic lymph node dissection)
ADT (androgen deprivation therapy)

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23
Q

How to do observation treatment for prostate cancer pts

A

PSA and DRE Q 6 mos
just monitor the course of disease - expect to deliver palliative therapy for development of sxs or change in the monitoring

(usually someones heart will kill them before prostate cancer will…. so like we dont have to freak if we suspect something)

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24
Q

Pros and Cons of observation therapy of prostate cancer pts

A

pros: avoids immediate morbidity assoc. w/ treatment
cons: risk of disease complications such as urinary retention or fractures

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25
Q

complications of radiation therapy of the prostate cancer pts?

A

bladder/rectal sxs
erectile dysfunction
radiation proctitis

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26
Q

idea behind active surveillance of prostate cancer pts

A

monitor PSA, DRE, Sxs

tx is initiated with any rising PSA or development of sxs….

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27
Q

radical prostatectomy and PLND:
is ________ therapy
use this method in men who _______

A

definitive curative therapy

men who have life expectancy > 10 years

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28
Q

Androgen Deprivation therapy for Prostate Cancer:

Goal is to induce ______ levels of testosterone

A

castrate levels

aka < 50 ng/dL after 1 month of therapy

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29
Q

ways to induce andgrogen deprivation therapy in prostate cancer

A

surgically: orchiectomy (remove da testis)
medically: LHRH agonists
antiandrogens (-tamides) - block androgen receptor

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30
Q

LHRH Agonists Toxicities of Prostate Cancer:

Acute Toxicities?

A

tumor flare, gynecomastia, hot flashes, erectile dysfunction, edema, injection site reaction

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31
Q

LHRH Agonists Toxicities of Prostate Cancer:

Long term Toxicities?

A

Osteoporosis/fracture!! obesity
insulin resistance
changes in lipids
increased risk in diabetes and CV events

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32
Q

since LHRH agonists can cause a flare at the beginning of the therapy and this can be really bad (esp in metastatic disease) - what can we do to help

A

give antiandrogens first!! for like 7 days..

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33
Q

Symptoms of tumor flare in prostate cancer due to LHRH agonists

A 
Bone pain (bc metastasis)
Increased urinary symptoms
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34
Q

what is the most common anti-androgen therapy (anti androgen receptor) and why

A

biclutamide

b/c QD and less ADEs

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35
Q

what drug is a LHRH antagonist

A

degarelix

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36
Q

why is degarelix better than LHRH agonists (leuprolide or goserelin)

A

drops testosterone very fast - 7 days – and NO tumor FLARE!!!

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37
Q

CAB in metastatic prostate cancer?

A

CAB = combined androgen blockade

using two diff androgen related therapies (anti-androgen and LHRH agonists) — this will lead to more toxicities

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38
Q

what is the standard of care for chemo combo treatment options for metastatic prostate cancer

A

docetaxel and ADT

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39
Q

use the docetaxel and ADT combo in metastatic prostate cancer when??

A

when pt has high volume disease!!

aka visceral or 4+ bone metastases

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40
Q

idea behind intermittent androgen deprivation

A

monitor PSA and when they return to a pre-specified baseline (ex: < 4) then stop the androgen suppression and keep monitoring PSA and when at another high level (ex: >10) - start the meds again

good because decreasing exposure/ giving pts a break - decreased cost and decreased side effects

intermittent seen to be as effective…

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41
Q

what is metastatic CRPC?

A

CRPC = castrate recurrent prostate cancer

even though hormone free pt is still progressing
all pts become hormone refractory

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42
Q

what is Sipuleucel? and what is it used for

A

Sipuleucel used for metastatic CRPC (asymptomatic or minimally symptomatic)
it is where you take out APCs then give the PAP-GM-CSF

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43
Q

1st line for metastatic disease regimen for prostate cancer

what is 2nd line?

A

docetaxel and prednisone

2nd: cabazitaxel (it is PGP resistant!!)

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44
Q

Abiraterone MOA?

A

irreversibly inhibits CYP17

an enzyme involved in androgen synthesis

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45
Q

Abiraterone: must be given with ______ and why

A

prednisone

to prevent adrenal insufficiency

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46
Q

Abiraterone: take with or without food?

A

without food!

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47
Q

Abiraterone: CYP interaction

A

CYP3A4

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48
Q

Enzalutamide: MOA?

A

androgen binding is blocked

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49
Q

Enzalutamide:

caution in pts with ______ history

A

seizure

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50
Q

when is Enzalutamide used?

A

when pts have failed doxetaxel

used in metastatic CRPC

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51
Q

Enzalutamide: give with prednisone?

A

NO!! (give prednisone with abiraterone)

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52
Q

Toxicities of Enzalutamide?

A

fatigue/falls/weakness!

diarrhea/hot flashes/ muscoskeleteal pain, HA, HTN

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53
Q

Metastatic prostate cancer — what is 1st line for pts that are castration NAIVE

A

abiraterone + prednisone

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54
Q

Radium 223 Dichloride:

forms complexes with _____ areas with increased _____ turnover

A

bone; bone

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55
Q

Radium 223 Dichloride:

use by itself or with chemo too?

A

by itself!! b/c ADE’s would be too wild

ADEs - anemia,neutropenia, thrombocytopenia

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56
Q

Radium 223 Dichloride:

approved for what related to prostate cancer?

A

related to symptomatic bone metastases for CRPC

but no known visceral metastatic disease

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57
Q

Current recommended screening for lung cancer:

A

low dose CT scan for pts age 55- 75 who have 30 pk hx of smoking and still smoking or quit w/in past 15 years

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58
Q

there was a trial that showed that ______, a supplement/herbal increased lung cancer risk

A

beta carotene

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59
Q

4 main mutations seen in EGFR? which one is seen in smokers?

A

EGFR, ALK, ROS-1
K-RAS (seen in smokers)

also check for BRAF and PDL-1….?

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60
Q

PD-L1 Status:

Testing is not recommended for NSCLC or SCLC?

A

not recommended for SCLC

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61
Q

NSCLC vs SCLC:

has a clear relationship to smoking?

A

SCLC

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62
Q

NSCLC vs SCLC:

has slower growth fraction

A

NSCLC

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63
Q

NSCLC vs SCLC:

rapid cell growth fraction

A

SCLC

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64
Q

NSCLC vs SCLC:

highly sensitive to chemo/radiation

A

SCLC

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65
Q

NSCLC vs SCLC:

moderately sensitive to radiation/chemo

A

NSCLC

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66
Q

NSCLC vs SCLC:

commonly see paraneoplastic syndromes

A

SCLC

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67
Q

what are some paraneoplactic syndromes?

*typically seen in SCLC

A

overall they are nonmetastatic systemic effects that accompany malignant disease

ex: cushing’s syndrome, hypercalcemia, SIADH

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68
Q

T or F: In lung cancer: pts who have EGFR mutations, ALK or ROS-1 rearrangements typically do not have PD-1 expression

A

True!!!

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69
Q

____ testing is not recommended for SCLC
_____ is recommended to test in first line metastatic setting for NSCLC

(what types of mutations)

A

do not test for PDL1 in SCLC

BRAF V600E: recommended fro NSCLC

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70
Q

Histology/pathology Subcategories of NSCLC and SCLC

A

NSCLC: adenocarcinoma, squamous, large cell

SCLC: small cell…

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71
Q

NSCLC Histology Subcategories: (adenocarcinoma, squamous, large cell)
which one of them is related to smoking, which one is related to non smokers and which one is usually located peripherally to the lung

A

smoking: squamous
adenocarcinoma: non smokers
peripheral: large cell

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72
Q

staging of SCLC?

A

limited or extensive….

extensive = metastasis

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73
Q 
SCLC
will progress (slowly or quickly) and is (resistant or sensitive) to chemo/radiation
A

progress quickly;

is sensitive

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74
Q

Treating SCLC Limited stage disease:
Combined treatment of ______ is used but maintenance chemo is not valuable

Prophylactic _____ radiation should be considered because lots of ppl form metastases here

A

radiation and PLATINUM based combo chemo

brain

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75
Q

Treating SCLC extensive stage disease:

_____ based combo chemo (with or without) radiation is preferred

A

platinum
without

*like limited stage but no radiation

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76
Q

Treating SCLC extensive stage disease:
if brain metastases are present — do what?

maintenance therapy - yay or nay?

A

metastases = brain radiation therapy

nay to maintenance

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77
Q

Commonly used chemo regimens for SCLC?

A

platinum dublets!!

EP, EC, Cisplatin/Irinotecan, Carboplatin/Irinotecan

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78
Q

what is the EP chemo regimen

A

cisplatin

etoposide

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79
Q

what is the EC chemo regimen

A

carboplatin

etoposide

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80
Q

cisplatin based regimens - biggest complications:

________ failure

A

renal

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81
Q

NSCLC:

______ is the most efficacious modalities for treating

A

surgery

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82
Q

NSCLC:

T or F: adjuvant chemo has benefits

A

true!
surgery and chemo is dope for NSCLC

(Surgery is SCLC - not as dope)

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83
Q

T or F: NSCLC does not get maintenance therapy just like SCLC

A

false!!

NSCLC can get maintenance but SCLC extensive does not…

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84
Q

if pt has NSCLC and it is a IIIB/IV cancer - what was the treatment option?

A

IIIB/IV is unresectable and thus do the platinum dublet

carboplatin less toxic than cisplatin!!

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85
Q

if treating metastatic NSCLC: consider what for therapy

A

if adenocarcinoma/squamous

and consider mutations!!

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86
Q

what agents are for EGFR

A

afatinib
erlotinib
gefitinib
osimeritinib

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87
Q

what agents are for ALK

A

alectinib
certinib
brigatinib
criozitinib

88
Q

what drugs are for ROS-1

A

crizotinib

certinib

89
Q

what drugs are for BRAF V600E

A

dabrafenib + trametinib

tram - is actually MEK but used with BRAF therapy!!

90
Q

Tyrosine Kinase Inhibitors Review:

EGFR mutations are in exons ____ and ____

A

19 and 21

91
Q

Tyrosine Kinase Inhibitors Review:

________ is used for the T790M mutation

A

osimertinib

92
Q

A pt does not have the t790M mutation but does have an EGFR mutation – can you use osimertinib?

A

yes!

93
Q

what ALK targeting therapy is first line?

A

alectinib

94
Q

for the ROS-1 therapies what is 1st line and what is 2nd line

A

1 - Crizotinib

2 - Ceritinib

95
Q

For treating metastaic lung cancer: if no mutation or chemo has been exhausted…
check _______
if it is > 50% give -______

A

check PD-L1

give pembrolizumab

96
Q

Pembrolizumab or nivolizumab is 1st line?

A

pembro

97
Q

immunotherapy toxicities? (from drugs of PDL1 and CTLA4..)

A

-itis

pneumotitis, hepatitis, nephritis (THESE ARE DELAYED REACTIONS!!)

98
Q

what are the genetic factors related to melanoma

A

FAMMS (familia atypical multiple mole syndrome)

HDNS (hereditary dysplastic nevus syndrome)

99
Q

Sunlight is obvs a risk factor for melanoma - but which UV is especially damaging

A

UV B

A may play a role as well tho..

100
Q

Melanoma:

ADA recommends ____ self exams

A

monthly!

101
Q

melanoma types:

superficial spreading melanoma?

A

appears flat but becomes irregular and asymmetrical

102
Q

melanoma types:

nodular?

A

vertical growth only - more aggressive!!

103
Q

melanoma types:

lentigo maligna?

A

BROWN or black lesion (like tan spot on face of the elderly)

104
Q

melanoma types:

acral lentiginous?

A

in weird places:

on palms, soles, under nail beds

105
Q

melanoma types:

uveal melanoma?

A

on da eye

106
Q

where does uveal melanoma typically metastasis in?

A

the liver!

the one on the eye goes to the liver??

107
Q

Melanoma:
_____ is curative therapy
______ is only used in palliative setting

A

surgery

radiation

108
Q

Treatment overview for melanoma:
IB/IIA

or IIB/IIC

or III

Or unresectable

A

IB/IIA: clinical trial or observation

IIB/IIC: clinical trial, observation or INTERFERON

III: observation, immunotherapy!!!(nivolumab or HD ipilumimab /dabraf/tram) /interferons

unresectable: T-VEC!

109
Q

symptom management of ipilumimab toxicities

if grade 1?

A

symptom control - NO STEROIDS - keep on the anti CTLA4 therapy

110
Q

symptom management of ipilumimab toxicities

if grade 2?

A

symptom control - NO STEROIDS - wait on the anti CTLA4 therapy til back to grade 1 toxicity

if it does not get back to grade 1 - treat like grade3/4

111
Q

symptom management of ipilumimab toxicities

if grade 3/4?

A

hold anti CTLA4 therapy!
give high dose steroids!!!! then taper of steroids for a long ass time.. may give infiximab if no response from steroids in 2 -3 days

112
Q

interferon alpha used to be the only immunotherapy option for melanoma — but it sucked - why?

A

suuuuuper toxic and at high doses but not super effective

toxicities: Depression/suicidal ideation; hepatic/hematologic toxicity; fever/flu-like sxs; severe fatigue

113
Q

what are the first line metastatic melanoma options?

A

nivolumab; nivolumab/ipilimumab
pembrolizumab
dabrafenib/tramietinib
vemuraf/cobimeti

aka NO CHEMO DRUGS
do immunotherapy

114
Q

Melanoma treatment:
deciding on treatment:
always start with ______ for a quicker set of action

_______ can take weeks to see effect

A

start with targeted oral - it is faster

immunotherapy_ can take weeks

115
Q

unique toxicity vemurafenib and dabrafenib?

A

may develop squamous cell carcinoma!!

116
Q

Trametinib is good with dabrafenib - why?

A

will decrease time til resistance develops b/c tram. works downstream from BRAF

also it will decrease squamous cell carcinoma

117
Q

IL-2:

can be used in melanoma ——–but we dont but why tho

A

toxic af and hella high dose
and LIFE THREATENING CAPILLARY LEAK SYNDROME

if they get it - they get it in the ICU

118
Q

Histology of Testicular Cancer:

Most (95%) of testicular cancers are ______ tumors and are divided into 2 major histology types: ______ and ______

A

germ cell;

seminoma; non-seminoma

119
Q 
Histology of Testicular Cancer:
Seminoma or Non-Seminoma -
which one resembles primordial germ cell tumor
common in4th decade of life
secretes b-HCG ONLY
A

seminoma

120
Q 
Histology of Testicular Cancer:
Seminoma or Non-Seminoma -
has 4 histopathologic subtypes (embryonal, yolk sac, choriocarcinoma, teratome)
common in 3rd decade of life
may secrete b-HCG and a-FP (fetoprotein)
A

non-seminoma

121
Q

Histology of Testicular Cancer:
Seminoma or Non-Seminoma -
which one is more aggressive

A

non-seminoma

122
Q

Risk factors of testicular cancer?

A

cryptorchidism (undescended testicle)

maybe kleinfelters syndrome

123
Q

signs/sxs of testicular cancer
________ mass
_______ to antibiotics
ultrasound will reveal a ______ mass

A

painless testis
NOT responding to abx
hypoechioc mass

124
Q

Testicular cancer:

is _______ growing (slow or rapid)

A

rapid!! - treat ASAP!

125
Q

Testicular cancer:

T or F: best method for diagnosis is needle biopsy of da scrot

A

false!!!

never do this! it can contaminate lynphnodes and lead to metastatic disease!!

126
Q

Testicular cancer:

what are tumor markers to look at post-orchiectomy and with metastatic therapy?

A

AFP and beta-HCG can be increased by testicular cancer!!

127
Q

what are some other factors that may increase beta-HCG

A

prostate, bladder, ureteral cancers and MARIJUANA absue

128
Q

T or F:

Chemo penetrates the testis super well and is first line for early stages of testicular cancer

A

FALSE!
chemo doesnt get to the testis well
1st line is radical orchiectomy

129
Q

what are the common testicular cancer regimens (just initials listed as answer)

A

BEP
VIP
VeIP

130
Q

what does the BEP regimen consist of

this is used notably in testicular cancer

A

bleomycin(b)
cisplatin (p)
etoposide (e)

131
Q

what does the VIP regimen consist of

this is used notably in testicular cancer

A

cisplatin (p)
ifosphamide (I)
etoposide (the V because of whatever its brand name is)

MESNA! bc ifosphamide

132
Q

what does the VeIP regimen consist of

this is used notably in testicular cancer

A

cisplatin (P)
ifosphamide (I)
vinsblastine (Ve)
MESNA! bc ifosphamide

133
Q

If a patient relapses their testicular cancer —-

what is the main treatment option/salvage therapy

A

high dose chemo + stem cell transplant!!!

134
Q

what are the steps of salvage therapy/ high dose chemo for relapsing testicular cancer (some flow chart pic in the notes)

A

collect blood stem cells? (PBSC and give G-CSF)

then give 1 cycle of chemo (Caroplatin and etoposide days before transplant!) “Day -5, -4 -3”

then PBSC re-infusion and filgrastim “Day 0”

do more PBSC collecting if needed
then do cycle 2 of HD chemo

135
Q

late effects of toxicities of testicular cancer treatments

A 
sterility
neuropathy (vinblastine!!)
nephrotoxicity (platins!!)
pulmonary fibrosis!! (BLEOMYCIN bish)
vascular toxicities 
secondary malignancies
136
Q

Ovarian Cancer:

possible etiology?

A

“incessant ovulation”

more ovulation = more disruption and epithelial fixing in the ovaries

137
Q

things that will increase ovarian cancer risk?

A

early menarche/late menopause - aka more time for ovulation
increased age
nullparity (aka constant ovulation no break because not pregnant)
in-vitro fertilization (bc given ovulation stimulating factors)
2 + 1st degree relatives with ovarian cancer
genetic factors: BRACA and p53
HPNCC
caucasian race

138
Q

what is HPNCC and how does it relate to cancers?

A

HPNCC = hereditary nonpolyposis colorectal cancer

this is a familial predisposition and increases endometrial cancer and ovarian cancer

139
Q

things that will decrease ovarian cancer risk?

A

multiple pregnancies
prolonged use of oral contraceptives ( >50% risk reduction if used for over 5 years)
prophylactic ooporectomy

140
Q

Ovarian cancer:

screening options?

A

no effective screening tool :’(
(known as the silent killer!!!)

just do prevention (like oral contraceptives 5+ years and have kids….)
or do prophylactic ooprhrorectomy if pt has BRCA mutations

141
Q

Biggest con with ovarian cancer presentation/

A

usually asymptomatic and then when they do have symptoms they are very general/non-specific and are like similar to PMS/period symptoms…

142
Q

what is the typical first line treatment for ovarian cancer?

A

surgery + adjuvant chemo!!

usually can cure easily but relapse is typically quite quick

143
Q

Ovarian cancer surgery is called _______ surgery

A

debulking!

lots of things removed! the peritoneal is messed with because apparently the cancer likes to go there

144
Q

Surgical outcomes of ovarian cancer:
patients are either _______ or ______
and which one is related to poorer prognosis

A

either: optimally debulked or sub-optimally debulked

sub-optimal = poorer prognosis duh

145
Q

optimally debulked and sub-optimally debulked:

how are the two differentiated

A

optimal = < 1 cm of disease left

sub - optimal = > 1 cm of disease left

146
Q

current standard chemo for ovarian cancer?

A

carboplatin and paclitaxel Q 3wk
and get like 6 cycles of chemo

also seen that carboplatin Q3 weeks and paclitazel dose dense weekly was effective too!!!

147
Q

Ovarian Cancer dosing of Carboplatin:
elimination of carboplatin closely mirrors _____
and then the dosing uses the _____ equation

A

mirrors GFR

Calvert equation

148
Q

what is the calvert equation?

A

used for carboplatin dosing in ovarian cancer –
carboplatin dose = AUC x (GFR +25)

*AUC is decided by the Dr (5 - 7.5)

149
Q

what is IP chemo?

A

intraperitonieal chemo

used in ovarian cancer!!!

150
Q

why use IP chemo?

A

increase tumor exposure but decrease systemic toxicity

151
Q

bad things about IP chemo?

A

grade 3/4 toxicities were worse vs IV only chemo
v. toxic
dumping 2 L of fluid into da abdomen = discomfort

152
Q

who will probably not handle IP chemo well?

A

poor performance status pts
Stage IV disease! (used in Stage III ovarian cancer tho!!)
> 65 y.o

153
Q

Metastatic Disease - Ovarian Cancer:
Recurrence definitions
Platinum sensitive vs platinum resistant vs platinum progressive?

A

sensitive = relapses > 6 mos after completing initial platinum regimen

resistant = relapse < 6 mos after completing initial platinum regimen

progressive = no response or progressed during primary therapy…

*if sensitive – use the regimen again!!!

154
Q

3 PARP agents approved in ovarian cancer?

A

olaparib
rucaparib
niraparib

155
Q

indications for all the PARP inhibitors?
olaparib
rucaparib
niraparib

A

ola: BRCA mutation ovarian cancer and tried 3+!!! agents
OR maintenance of complete or partial response to pt based therapy

ruca: BRCA mutation ovarian cancer and tried 2+!!! agents
OR maintenance of complete or partial response to pt based therapy

nira: maintenance only!!

156
Q

must monitor what with Niraparib?

A

CBC, BP and HR!!

b/c ADE’s = myleosuppression and HTN and HTN crisis

157
Q

Pathophys of HCM? (hypercalcemia of malignancy)

A 
increased PTHrP (parathyroid related protein)
increased calcitriol
increased resorption
decreased elimination
bone metastases
158
Q

HCM etiologies

A 
humoral!!! (because PTHrP)
local osteolytic hypercalcemia
Vit. D secreting lymphomas
ectopic hyperparathyroidism
renal
159
Q

Signs and Symptoms of HCM:
Mild:
Moderate:
Severe:

A

mild: polyuria/polydipsia
Moderate: dehydration/lethargy/confusion/EKG changes
severe: seizures, coma, arrhythmias

160
Q

corrected calcium eqn?

A

Serum calcium + 0.8(4-albumin)

161
Q

normal calcium levels?

A

8.5 - 10 mg/dL

162
Q

what levels of corrected calcium is mild, moderate, or severe

A

mild: <12
moderate: 12 - 14
Severe: > 14

163
Q

HCM treatment algorithim:
if less than 12
for mild sxs:

for moderate sxs:

A

mild: drink 3L/day - repeat Ca level in 4 weeks; d/c meds that increase Ca2+
moderate: consider alternate cause; give hydration (200 - 400 mL/hr 0.9% NS) and bisphosphonate (may repeat 7 days after if needed)

164
Q

HCM treatment algorithim:
if greater than 12
no life threatening symptoms or severe symptoms

A 
either one is treated the sameeeeeeee
zoledronic acid 4 mg 
or 
pamidronate 60 to 90 mg
can give calcitonin - but only works for 48 hours before tachyphylaxis
165
Q

T or F: when treating HCM -you MUST adjust for renal dysfunction

A

false!
for HCM - you do not!!!
it is the Ca2+ that is causing the renal dysfunction

needs

166
Q

when do you use loop diuretics for HCM pts?

A

if the fluids are too much and the pts get fluid overload — then use loop diuretics

167
Q

what drugs can be used for REFRACTORY HCM

A

phosphates
gallium nitrate
denosumab

168
Q

phosphates and refractory HCM:
use in caution to severe _______
may induce metastatic ______
nausea/diarrhea

A

hypercalcemia

induce metastatic calcification

169
Q

Zoledronic acid 4 mg IV over _______ monthly (for chronic HCM)

A

15 minutes

170
Q

Pamidronate 90 mg IV over _______ monthly (for chronic HCM)

A

2 - 4 hours

171
Q 
SREs (skeletal related events) are defined as:
Pathological \_\_\_\_\_\_
need for \_\_\_\_\_\_ or \_\_\_\_\_\_
\_\_\_\_\_\_ compression
Hyper\_\_\_\_\_\_\_\_
A

pathological FRACTURE
need for bone radiotherapy or surgery
spinal cord compression
hyperCALCEMIA

172
Q

SRE morbidity and mortality:
bone pain and structural damage leads to what two things?
reduces in quality of life by limiting ______ and decreased social function

A

leads to radiotherapy ad bone surgery

limits mobility

173
Q

treatment options of bone metastases?

A 
goal - palliate symptoms
radiation - localized
chemo - systemic
IV bone modifying agents
radioisotopes
174
Q

Women with breast cancer: fracture risk factors?

A 
bone mineral density
Aromatase inhibitor treatment
Age (> 65 y.o)
corticosteroid use ( > 6 mos)
BMI < 20 kg/m2
family hx of hip fracture
hx of fracture before age 50
smoking
175
Q

Men with prostate cancer: fracture risk factors?

A

androgen deprivation therapy

176
Q

Radiation therapy works well and acts (slow or fast)

A

slow! 1 - 2 weeks for pain relief

great response rate tho

177
Q

IV bisphosphonates for SRE:

options?

A

Pamidronate 90 mg IV over 2 - 4 hours q 3 -4 weeks
or
Zoledronic acid 4 mg IV over 15 minutes every 3 - 4 weeks

(RENAL DOSE ADJUST, YO!)

178
Q

when treating SREs with bisphosphonates what is good contaminant therapy?

A

supplmentation of calcium 500 mg and vit. d 400 IU bid!!!

179
Q

denosumab - has approved indications for what?

A

bone metastases from solid tumors (Xgeva q4wks)
osteopenia from breast cancer (prolia Q6mos)
and now indicated for hypercalcemia of malignancy when refractory to bisphosphonate therapy

180
Q

denosumab:
should have _____ corrected prior to initiation
supplement: _________
yay or nay - renal dosage adjustments in package insert?
Very $$$$

A

correct hypocalcemia
supplement calcium 1000 mg and vit D QD

no renal dosage

181
Q

V bad ADE of denosumab and bisphosphonates?

A

OSTEONECROSIS of the jaw!! (ONJ)

182
Q

what makes osteonecrosis occur at a higher risk?
IV or PO

and

Monthly or yearly agent

A

IV is worse

monthly is worse

183
Q 
what makes osteonecrosis occur at a higher risk?
which drugs are worse??
pamidronate
denosumab
zoledronic acid
A

zoledronic acid and denosumab are worse

184
Q

possible causes of ONJ

A

invasive dental procedures
poor oral hygiene
use of dental appliances
(do dental procedure before these agents if you can!!)

185
Q

Renal Dysfunction and bone drugs

rank the drugs from most to least affect on kidneys

A

zoledronic acid > pamidronate&raquo_space; denosumab

186
Q

Renal Dysfunction and bone drugs

Bisphosphonate should not be used if CrCl < _____ or pts taking ______ meds

A

< 30 mL/min

nephrotoxic meds

187
Q

Renal Dysfunction and bone drugs
Denosumab:
renally eliminated - yes or no

A

no!

188
Q

common ADEs of the bone drugs

A 
hypocalemia!! (bigger in denosumab)
bone pain
Nausea
diarrhea
fatigue
189
Q 
Colorectal Cancer:
Risk Factors ----
Age
Family Hx of Colon cancer
Dietary: \_\_\_\_ fat and \_\_\_\_ fiber
\_\_\_\_: small % will turn into cancer
A

high fat/low fiber

polyps

190
Q

Colorectal Cancer:

what are the two hereditary syndromes?

A

FAP (familial adenomatous polyposis)

HNPCC (hereditary nonpolyposis colorectal cancer)

191
Q

If pt has FAP - start screening for colon cancer at age _____

A

10 - 12!

192
Q

If pt has HNPCC - start screening for colon cancer at age _____

A

20 - 25

193
Q

if pt has family hx of colon cancer - start screening at age ____

A

40 or 10 years before when family member had diagnosis

194
Q

General age to start getting colon cancer screenings?

A

45

50 y.o FOR SURE

195
Q

common screening for colon cancer is _____ and is done every ______

A

colonoscopy every 10 years

196
Q

Colorectal Cancer:

what are some lifestyle things that are risk factors

A

alcohol
smoking
obesity

197
Q

Screening tests for Colorectal Cancer:

Which ones primarily detect cancer only?

A

FOBT (fecal occult blood test)

FIT (fecal immunohistochemical test)

198
Q

Screening tests for Colorectal Cancer:

which ones can detect cancer and advanced lesions

A

Endoscopic and radiologic exams

199
Q

Screening tests for Colorectal Cancer:

How to avoid false positives with FOBT?

A

avoid red meat and raw veggies with peroxidase activity (turnips, broccoli, cauliflower, and radishes)
3 DAYS PRIOR TO TESTING

200
Q

Screening tests for Colorectal Cancer:

How to avoid false negatives with FOBT?

A

Avoid vitamin C in excess for 3 days prior to testing

201
Q

Screening tests for Colorectal Cancer:

Medical restrictions for FOBT? (good counseling points!)

A

Avoid enemas/rectal meds for 3 days prior
avoid ASA/NSAID for up to 7 DAYS prior
avoid testing if blood from hemorrhoids is present
Delay testing until 3 days after menstrual bleeding has ended

202
Q

Which endoscopy procedure is the gold standard for detecting colon cancer and why

A

colonoscopy! bc it can see the entire bowel

flexible sigmoidoscopy lets you only 60% of the bowel

203
Q

What is an important mutation to detect during the work up of colorectal cancer?

A

dMMR - defective mismatch repair

will influence which kind of chemo can be used!!!

204
Q

If a pt has dMMR or MSI-H and has stage II disease - what does that mean?

A

do NOT use adjuvant 5-FU because it predicts a decreased benefit!

205
Q

If a pt has dMMR or MSI-H and has stage III disease - what does that mean?

A

use adjuvant 5-FU they will have benefit from that therapy!

206
Q

pMMR vs dMMR?

A 
p = proficient
d = defective
207
Q

what is the preferred chemo adjuvant therapy in colorectal cancer?

A

FOLFOX

5-FU, leucovorin, oxaplatin

208
Q

what does FOLFIRI chemo consist of?

A

5-FU, leucovorin, irinotecan

209
Q

A _____ deficiency will lead to increase toxicities in 5-Fu

A

DPD

210
Q

mutations/deficiencies in _____ will lead to toxicities of irinotecan

A

UGT1A1

211
Q

Irinotecan ADE’s:
early or late onset _______
could be fatal….

A

diarrhea

212
Q

Irinotecan can have _______ syndrome - should be treated with _____

A

cholinergic

atropine

213
Q

what drug has an unique toxicity of cold intolerance and the sensation of not being able to breathe
(they can breathe just feel that way)

A

oxaliplatin

seen in FOLFOX for colorectal!!

214
Q

what drug has an unique dose limiting toxicity of hand-foot syndrome

A

capecitabine (5- Fu prodrug)

215
Q

what are some antibody drugs to use in colorectal cancer - and what are the targets?

A

Cetuximab - EGFR
Bevacizumab - VEGF
Panitumumab - EGFR

216
Q

cannot use cetuximab and panitumumab for colorectal cancer if the pt is ________

A

pt is KRAS mutant

pt MUST be KRAS wild to use these drugs

217
Q

Significant toxicities of bevacizumab?

A

HTN! and bleeding

Fall 2018/P3 Year' (16 decks)

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