Brainscape's Knowledge GenomeTM

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


See full index

Drug Mech > Anti-cancer: natural products > Flashcards

Anti-cancer: natural products Flashcards

1
Q

What are the drugs in the vinca alkaloids class?

A

vinblastine, vincristine, vinorelbine

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

Vinca alkaloids are cell cycle…

A

specific

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

What is the mechanism of action of the vinca alkaloids?

A

bind to the microtubule protein tubulin in dimeric form and form a drug-tubulin complex. this complex adds to the forming end of the microtubules to terminate assembly and cause depolymerization of the microtubules.

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

Depolymerization of microtubules results in

A

mitotic arrest at the M phase, dissolution of the mitotic spindle and interference with chromosome segregation

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

What are the toxicities of vinblastine?

A

nausea/vomiting, myelosuppresion, alopecia

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

What are the toxicities of vincristine?

A

neurotoxicity, myelosuppresion (not as bad as vinblastine)

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

What are the toxicities of vinorelbine?

A

just myelosuppresion

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

Where are each of the vinca alkaloids derived from?

A

vinblastine and vincristine - periwinkle plant. Vinorelbine is semisynthetic

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

The epipodophyllotoxins include

A

etoposide and teniposide

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

The epipodophyllotoxins are cell cycle

A

specific

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

What is the MoA of the epopodophyllotoxins?

A

they block cell division in the late S-G2 phase by inhibiting topoisomerase II, resulting in DNA damage through strand breakage (because of the formation of a DNA, drug and enzyme complex)

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

What is the toxicity of etoposide and teniposide?

A

nausea/vomiting, alopecia, myelosuppression

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

Where are etoposide and teniposide derived from?

A

an extract of the mayapple root, podophyllotoxins

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

The camptothecins are cell cycle

A

non-specific (CCNS)

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

the camptothecins include

A

topotecan and irinotecan

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

What is the MoA of the camptothecins?

A

they inhibit topoisomerase I, which is the key enzyme in cutting and religating single DNA strands, resulting in DNA damage

17
Q

What is the toxicity of the camptothecins?

A

nause/vomiting/diarrhea, myelosuppression, anthralgias (joint pain)

18
Q

Where are the camptothecins derived from?

A

a tree! camtotheca acuminata

19
Q

Taxanes are cell cycle

A

specific

20
Q

Taxanes include

A

paclitaxel, docetaxil, cabazitaxel

21
Q

What is the MoA for the taxanes?

A

through high affinity binding to microtubules, they poison mitotic spindles and enhance tubulin polymerization. This leads to arrest of cells in G2-M and inhibition of cell division. induces apoptosis

22
Q

Toxicities of taxanes

A

Paclitaxel - arrythmias, myelosuppression, peripheral sensory neuropathy. Doxetaxel - neurotoxicity and neutropenia

23
Q

Where do the taxanes come from?

A

Paclitaxel is the only totally natural of the three - comes from the pacific yew tree. The other two are semisynthetic

24
Q

Anthracyclines are cell cycle

A

non-specific (CCNS)

25
Q

Anthracyclines include

A

Daunorubicin and Doxorubicin

26
Q

What is the MoA of the anthracyclines?

A

4 mechanisms: inhibition of topoisomerase II, inhibition of DNA and RNA synthesis due to high affinity binding by intercalation, binding to cellular membranes to alter transport, generation of semiquinone free radicles and oxygen free radicals (cardiac toxicity)

27
Q

What are the side effects of the anthracyclines?

A

myelosuppression, neutropenia, cardiotoxicity

28
Q

Cardiotoxicities are variable during use of anthracyclines. How is this characterized?

A

acute occures within the first 2-3 days of use - arrhythmias and myocarditis. Chronic is dose dependent, associated with heart failure.

29
Q

What is Dexrazoxane used for with anthracyclines?

A

reduction of cardiotoxicity

30
Q

Mitomycin is cell cycle

A

non-specific (CCNS)

31
Q

The mitomycins include

A

mitomycin C

32
Q

What is the MoA of mitomycin?

A

after it’s metabolically activated by an enzymatic reduction reaction, an alkylating electrophillic species is produced that is capable of cross-linking DNA

33
Q

What are the toxicities of mitomycin C?

A

thrombocytopenia, leucopenia

34
Q

Bleomycin is part of what class?

A

it is its own class

35
Q

Bleomycin is cell cycle

A

specific

36
Q

What is the MoA of bleomycin?

A

it binds to DNA and results in single and double strand breaks following free radical formation - a complex can also be formed (DNA-Bleomycin-iron) that can fragment DNA. Causes accumulation of cells in G2

37
Q

What are the toxicities of bleomycin?

A

pulmonary toxicity

Drug Mech (29 decks)

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