Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Reproductive > PHARM: Testicular Cancer > Flashcards

PHARM: Testicular Cancer Flashcards

1
Q

What is the most common type of testicular cancer?

A

germ cell tumors (seminoma or nonseminoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which type of testicular germ cell tumor grows slowly and does not spread rapidly?

A

seminomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do non-seminomas spread?

A

liver, lungs, and brain (via blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is stage 1 testicular cancer?

A

cancer only in testicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is stage 2 testicular cancer?

A

cancer has spread to lymph nodes in the abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is stage 3 testicular cancer?

A

cancer has spread beyond the LNs in the abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What markers can be used to monitor seminomas in the follow-up period after treatment?

A

AFP, LDH, β-hCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you manage organ-confined testicular cancer?

A

surgery (removal of one of the testes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you manage stage 2 testicular cancer?

A

radiotherapy (treatment is repeated five days per week for approximately five to six weeks) and or chemotherapy are used in an adjunctive manner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a common factor in ALL chemotherapeutic therapies for testicular cancer?

A

CISPLATIN (platinum agent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 4 major divisions of the manners in which testicular cancer can become resistant to cisplatin?

A

Pre-Target Alterations
On-Target Alterations
Post-Target Alterations
Off-Target Alterations

(usually multifactoral!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some pre-target alterations that render testicular cancer resistant to cisplatin?

A

o Decreased influx
o Sequestration
o Increased efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some on-target alterations that render testicular cancer resistant to cisplatin?

A

o Increased DNA repair

o Increased tolerance to lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some post-target alterations that render testicular cancer resistant to cisplatin?

A

Defective activation and/or execution of cell death/ senescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some off-target alterations that render testicular cancer resistant to cisplatin?

A

Pro-survival antagonizing signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the 3 top first line chemo combinations for testicular cancer?

A

1) Etoposide + Cisplatin
2) Bleomycin + Etoposide + Cisplatin
3) Etoposide + Mesna + Ifosfamide + Cisplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What may be added to some “high dose” chemotherapy regimens?

A

peripheral stem cell infusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOA: Binds DNA in presence of iron with ferrous oxide-mediated DNA strand breakage

A

Bleomycin

19
Q

MOA: Binds with high affinity to nuclear DNA (N7 sites) as well as interacting with mitochondrial DNA and proteins→Nuclear and mitochondrial damage + redox stress→ activation of pro-apoptotic BCL-2 members (BAK1 and KAB), opening of VDAC1, activating p53→ cell death and senescence

A

Cisplatin

Carboplatin (slower RXN with nuclear DNA)

20
Q

MOA: Stabilizes DNA and topo II complexes resulting in strand breakage

A

Etoposide

21
Q

MOA: Promotes microtubule assembly and stabilizes their formation by inhibiting depolymerizaiton

A

Paclitaxel

22
Q

MOA: Binds to low affinity sites on tubulin, resulting in splitting of the microtubules into spiral aggregates or protofilaments—leading to the disintegration of the microtubule

A

Vinblastin

23
Q

MOA: Alkylating agent that produces intra-and inter-strand DNA cross- links

A

Ifosfamide

24
Q

MOA: Forms acrolein-mesna thioester complexes that are inactive and eliminated in the urine

A

Mesna

25
Q

What drug is mesna used with? Why?

A

Ifosfamide (to prevent hemorrhagic cystitis)

26
Q

TOXICITY: Pulmonary Fibrosis and late-developing skin toxicities

A

Bleomycin

27
Q

TOXICITY: Renal toxicity, ototoxic (higher doses damage cochlea—via ROS), neurotoxic;

A

Cisplatin

28
Q

TOXICITY: Thrombocytopenia, less neruotox/ototox than other drug in class

A

Carboplatin

29
Q

TOXICITY: Leukopenia; hepatic toxicity after high dose treatment

A

Etoposide

30
Q

TOXICITY: Bone marrow suppression, peripheral neuropathy

A

Paclitaxel

31
Q

TOXICITY: Neuropathy

A

Vinblastine

32
Q

TOXICITY: Myelosuppression, neurotoxicity, Hemorrhagic Cystitis

A

Ifosfamide

33
Q

TOXICITY: Dysgeusia, soft stools and headache

A

Mesna

34
Q

What drug is given with paclitaxel to protect against bone marrow suppression?

A

Filgrastim

35
Q

What drugs is given with cisplatin to buffer adverse effects?

A

Amifostine

36
Q

True or false: cisplatin is actively pumped into renal and cochlear cells.

A

TRUE–cause of the nephrotoxicity and ototoxicity

37
Q

How does the accumulation of cisplatin in renal and cochlear tissues lead to adverse effects?

A

cellular stress causes a rise in ROS and depletion of cytoprotective oxidants

38
Q

What transporter takes cisplatin up into both normal and tumor cells?

A

Ctr1

39
Q

What transporter is expressed on only renal, cochlear, and nervous cells (with down-regulation on tumors)?

A

OCT2

40
Q

How might we prevent uptake of cisplatin into renal, cochlear and nervous cells?

A

specific inhibition of OCT2

41
Q

How does bleomycin injure lung epithelial cells?

A

produces ROS, chemokines and cytokines that enhance recruitment of leukocytes to sites of tissue injury

42
Q

How might you detect lung epithelial injury caused by bleomycin?

A

measuring NALP3

43
Q

What is the role of IL-1β in epithelial lung injury from bleomycin?

A

activates ROS-expressing neutrophils to cause damage and promotes TGF-β1

44
Q

What is the role of TGF-β1 in lung epithelial injury from bleomycin?

A

an important profibrotic cytokine that triggers fibroblast proliferation and activation (induces EMT and the formation of ECM producing myofibroblasts) and stimulates differentiation of Th17 cells

Reproductive (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions