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Spring 2018 Pharm Exam 3 > Lecture 4: Chemo Drugs > Flashcards

Lecture 4: Chemo Drugs Flashcards

1
Q

Alkylating Agents

- what are the 2 drugs in this class? and what are each of their subclasses?

A

Alkylating Agents

  1. Cyclophosphamide - Nitrogen Mustard
  2. Cisplatin - Platinum Analog
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2
Q

Alkylating Agents:

  1. what is their MAJOR MOA?
  2. what are the 2 types of alkylating agents (reactive groups)
A

Alkylating Agents

  1. major MOA - alkylate DNA at N7 position of guanine
  2. 2 types
    - mono-fxnal (1 reactive group)
    - bi-fxnal (2 reactive groups)
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3
Q

Alkylating Agents: mono-fxnal (1 reactive group)

  1. what does the alkylated guanine abnormally base pair with
  2. what is the result of this
A

Alkylating Agents: mono-fxnal (1 reactive group)

  1. alkylated guanine abnormally base pair w/ Thymine
  2. Result = protein miscoding + apoptosis
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4
Q

Alkylating Agents: bi-fxnal (2 reactive groups)

  1. what drug is in this category
  2. what type of cross linking occurs
  3. what is the result of this
  4. easier or harder to repair damage by these agents vs mono-fxnal
A

Alkylating Agents: bi-fxnal (2 reactive groups

  1. drug = cyclophosphamide
  2. INTERstrand cross linking
  3. Result = inhib of DNA replic/transcription + DNA breaks
  4. harder to repair damage by bi-fxnal alkylating agents (vs mono-fxnal)
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5
Q

Alkylating Agents: Cisplatin

  • how does its MOA differ from Cyclophosphamide (what also occurs)
A

Alkylating Agents: Cisplatin

MOA: also has INTRAstrand crosslinking of G bases (in addition to interstrand cross linking)

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6
Q

Alkylating Agents: Cyclophosphamide (prodrug)

  1. what does the active form of the drug produce that is cytotoxic
  2. why is liver (site of activation) protected from the effects of this
A

Alkylating Agents: Cyclophosphamide (prodrug)

  1. active form produces acrolein (cytotoxic)
  2. liver (site of activation) protected d/t formation of inactive metabolites
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7
Q

Alkylating Agents: Cyclophosphamide AEs

  1. what is the dose limiting toxicity
  2. what AE does acrolein (active metabolite) cause
    - what drug can be coadmin to prevent this

Other: how was it used in WWI

A

Alkylating Agents: Cyclophosphamide AEs

  1. major dose limiting toxicity = immunosupp
  2. Acrolein –> hemorrhagic cystitis
    - prevent by coadmin MESNA (mercaptoethane sulfonate)

Other: used in WWI as chemical warfare agent –> myeloid+ lymphoid suppression

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8
Q

Alkylating Agents: Cisplatin

  1. what is the unique dose limiting toxicity
    - what drug can be given to prevent this & other non-pharm Tx
  2. other 2 AEs
A

Alkylating Agents: Cisplatin

  1. what is the unique dose limiting toxicity = IRREV/cumul damage to renal tubules
    - prevent w/admin of mannitol (diuresis) + hydration
  2. other 2 AEs
    - otoxic (tinnitus, HL)
    - moderate myelosuppression
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9
Q
  1. incr capacity of tumor cell to repair DNA lesions
  2. decr transport of drug into the CA cell
  3. incr production of glutathione
  4. incr activity of glutathione S-transferase

what are these examples of

A

Mechanisms of resistance of Alkylating Agent drugs

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10
Q

Alkylating Agents + Antimetabolites

  • which is CCNS drug (usu more active in G0) and which is CCS drug (usu more active in S phase)
A

Alkylating Agents + Antimetabolites

CCNS drug = Alkylating Agents
- but can have greatest anti-CA activity in S

CCS drug = Antimetabolites

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11
Q

Antimetabolites

  1. what is the common dose limiting toxicity of all 3 drugs in this class
  2. what are the 3 drugs in this class
  3. what are the antagonists of
A

Antimetabolites

  1. common dose limiting toxicity = myelosupp
  2. 3 drugs = MTX, Mercaptopurine, Fluorouracil
  3. antagonists of biosynthethic pathway
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12
Q

Antimetabolites: #1 MTX (MC USED ANTI-CA AGENT)

  1. what is MTX an analog of
  2. binds to active site of ______
  3. by binding what does it prevent the formation of (2 things)
  4. overall what is the result of this (interrupts what 3 things)
A

Antimetabolites: #1 MTX

  1. analog of folic acid
  2. binds to active site of DHFR
  3. binding –> prevents formation of THF/THF cofactors
  4. result = interrupt DNA, RNA, & protein syn
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13
Q

Antimetabolites: #1 MTX

  1. what are the 3 drugs that have Drug interactions w/MTX d/t inhibiting renal excretion of it
  2. 2 major AEs
    - how to prevent 1 of those toxicities
  3. what is given for accidental MTX OD or w/high dose therapy of MTX (& why)
A

Antimetabolites: #1 MTX

  1. 3 drug interactions = PCN, cephalosporins, NSAIDs
  2. major AEs
    - severe GI disturbances
    - Renal toxicity (prevent w/hydration)
  3. Leucovorin (folinic acid)
    - given for accidental MTX OD or
    - w/high dose therapy of MTX to rescue normal cells from toxicity
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14
Q
  1. decr drug transport
  2. decr polyglutamate addition (glycine residues)/decr activity of FPGS (folypolyglutamate synthase)
  3. amplified DHFR gene
  4. mutant DHFR gene w/decr activity for the drug
  5. incr DR1

mechanisms of resistance for which drug

A

mechanisms of resistance of MTX

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15
Q

Antimetabolites: #2 Mercaptopurine

  • what is the name of the prodrug & active metabolite
  • what type of analog is it
A

Antimetabolites: #2 Mercaptopurine

  • prodrug = Azathioprine –> active metabolite TIMP (by HGPRT)
  • purine analog
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16
Q

Antimetabolites: #2 Mercaptopurine

  1. what does TIMP incorp itself into
  2. What 2 products does it utimately form
  3. what is the result of this
  4. what does TIMP prevent the formation of (2 things), which ultimately prevents formation of what 2 other things
A

Antimetabolites: #2 Mercaptopurine

  1. TIMP incorp into de novo purine syn pathway
  2. 2 products = Thio-dGTP + ThioGTP
  3. products cause DNA/RNA damage, inhib translation, & lysis of CA cells
  4. TIMP prevents formation of AMP + GMP –> prevent formation of dATP + dGTP
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17
Q

Antimetabolites: #2 Mercaptopurine

  • major drug interaction
A

Antimetabolites: #2 Mercaptopurine

drung interaction = Allopurinol

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18
Q

Antimetabolites: #2 Mercaptopurine drug interaction w/Allopurinol

  • what does allopurinol prevent during Tx of leukemias w/MP
  • but what is the problem admin of allopurinol causes? & what must be done to dose of MP
A

Antimetabolites: #2 Mercaptopurine drug interaction w/Allopurinol

  1. allopurinol prevents hyperuricemia during Tx of leukemias w/MP
  2. problem: allopurinol –> incr 6-MP levels –> toxicity/myelosuppression –> decr dose of 6-MP
19
Q

Antimetabolites: #3 Fluoruracil

  1. what type of analog is it
  2. name of its 3 active metabolites
A

Antimetabolites: #3 Fluoruracil

  1. pyrimidine analog
  2. 3 active metabolites: 5-FUTP, 5-FdUTP, 5-dUMP
20
Q

Antimetabolites: #3 Fluoruracil

  1. what do the active metabolites incorp into? (2 things)
  2. what is the result of this
  3. what does 5-dUMP inhibit?
A

Antimetabolites: #3 Fluoruracil

  1. active metabolites incorp into DNA + RNA
  2. result = RNA + DNA damage
  3. 5-dUMP inhibits TS
21
Q

Antimetabolites: #3 Fluoruracil

5-dUMP inhibits TS
- what is TS needed for? therefore what is the result of inhibiting this

A

Antimetabolites: #3 Fluoruracil

5-dUMP inhibits TS

  • TS needed for de novo pyrimidine syn
  • result of inhibiting TS –> slow CA cell replication
22
Q

What is resistance of Fluoruracil d/t ?

A

Resistance of Fluoruracil d/t amplification of TS gene

23
Q

Antimetabolites: #3 Fluoruracil

Other than GI disturbances what is the major toxicity

A

Antimetabolites: #3 Fluoruracil AEs

  • GI (N/V/D
  • Neurotoxicity
24
Q

Plant Alkaloids

  1. What are the names of the 4 classes of drugs?
  2. What types of drugs are all of these: CCS or CCNS drugs?
  3. What are all the drugs resistance d/t
A

Plant Alkaloids

  1. 4 classes = Vinca alkaloids, Taxanes, Epipodophyllotoxins, Camptothecins
  2. all are CCS drugs (one is also CCNS drug)
  3. All the drugs resistance is d/t incr MDR1 gene expression
25
Q

Plant Alkaloids: #1 Vinca Alkaloids

what 2 drugs are in this class

MOA:

  • what do these drugs bind to
  • what does this prevent & then block
  • what part of the cell cycle do cells get arrested in?
  • what does this cause?
A

Plant Alkaloids: #1 Vinca Alkaloids

2 drugs = VinBlastine, VinCristine

MOA:

  • bind to b-tublin –> prevent polymerization of microtubules
  • block mitotic spindle formation during M phase
  • mitotic arrest in M phase –> apoptosis/tumor cell death
26
Q

Plant Alkaloids: #1 Vinca Alkaloids

  1. Major AE a/w Vinblastine
  2. how does Vincristine differ from Vinablastine AEs
  3. What is the dose limiting toxicity of Vinacristine
    - what is the other AE
A

Plant Alkaloids: #1 Vinca Alkaloids

  1. VinaBlastine AE = Bone marrow suppression
  2. Vincristine spares bone marrow
  3. dose limiting toxicity of Vinacristine = periph neuritis/neuropathy
    - other AE = muscle weakness
27
Q

Plant Alkaloids: #2 Taxanes

- what is the drug in this class

A

Plant Alkaloids: #2 Taxanes

- drug = Paclitaxel

28
Q

Plant Alkaloids: #2 Taxanes (Paclitaxel) MOA

  1. what does it bind to & what is the result of this
  2. what does it prevent
  3. what phases of the cell cycle are cells blocked at & what does this prevent the formation of

(how is the MOA sim and diff from Vinca Alkaloids)

A

Plant Alkaloids: #2 Taxanes (Paclitaxel) MOA

  1. bind to b-tublin –> stabilizes microtubule formation
  2. prevents DEpolymerization of microtubules (diff from vinca alkaloids)
  3. cell blocked at G2/M phase –> cant form norm mitotic spindle
29
Q

Plant Alkaloids: #2 Taxanes (Paclitaxel)

  • what are the 2 dose limiting toxicities

(how are they similar to Vinca alkaloids)

A

Plant Alkaloids: #2 Taxanes (Paclitaxel)

  • dose limiting toxicites = myelosupp + periph neuropathies (combo of Vinca alkaloids)
30
Q

Plant Alkaloids: #3 Epipodophyllotoxins

- drug in this class?

A

Plant Alkaloids: #3 Epipodophyllotoxins

- drug = Etoposide

31
Q

Plant Alkaloids: #3 Epipodophyllotoxins (Etoposide) MOA

  1. what enzyme does it inhibit –>
  2. what phase of the cell cycle are tumor cells stopped in–>
  3. what does this ultimately cause

2 AEs = myelopsuppression (common) and Alopecia

A

Plant Alkaloids: #3 Epipodophyllotoxins (Etoposide)

inhibit topoisomerase II —> blocks tumor cells in late S/G2 –> DNA strand breakage

32
Q

Plant Alkaloids: #3 Camptothecins
- what drug in this class?
- this drug is CCS + CCNS drug
(when is it a CCNS drug)

A

Plant Alkaloids: #3 Camptothecins

  • irinotecan
  • CCNS drug at higher conc
33
Q

Plant Alkaloids: #3 Camptothecins (Irinotecan) MOA

  1. what enzyme does it inhibit? (how is this diff from Etoposide)
  2. therefore what does it cause
A

Plant Alkaloids: #3 Camptothecins (Irinotecan) MOA

  1. inhibits topo I (etoposide inhibits topo II)
  2. causes DNA breakage/apoptosis
34
Q

Plant Alkaloids: #3 Camptothecins (Irinotecan)

prodrug

  • what liver enzyme converts it to active metabolite?
  • what is name of active metabolite?
A

Plant Alkaloids: #3 Camptothecins (Irinotecan)

  • carboxylesterase converts it to active metabolite (SN-38)
35
Q

Plant Alkaloids: #3 Camptothecins (Irinotecan) AEs

2 dose limiting toxicites (common + uncommon)

A

Plant Alkaloids: #3 Camptothecins (Irinotecan)

2 dose limiting toxicites = myelosupp + diarrhea

36
Q

Plant Alkaloids: #4 ABXs

  • what are the 2 drugs in this class
A

Plant Alkaloids: #4 ABXs

  1. Doxorubicin (Anthracycline)
  2. Bleomycin (CCS)
37
Q

Plant Alkaloids: #4 ABXs

  1. what are they both isolated from
  2. in general what is their MOA (where do they insert/name of this MOA)
A

Plant Alkaloids: #4 ABXs

  1. isolated from Streptomyces
  2. gen MOA = intercalation (insert themselves b/t DNA base pairs) –> DNA strand breakage
38
Q

Plant Alkaloids: #4 ABXs (Doxorubicin)

  1. what does it inhibit that causes DNA strand breakage
  2. what 2 bad things does it generate, & what type of toxicity results d/t this
A

Plant Alkaloids: #4 ABXs (Doxrubicin)

  1. inhibits topoisomerase II –> DNA strand breakage
  2. generates semiquinone + O2 free radicals –> cardiac toxicities
39
Q

Plant Alkaloids: #4 ABXs, Doxorubicin AEs

  1. what are the Reversible AEs (2)
  2. what is the IRREV/chronic AE
A

Plant Alkaloids: #4 ABXs, Doxorubicin AEs

  1. reverisble - acute arrhythmias + conduction abn
  2. IRREV chronic cardiac myopathies
40
Q
  1. incr MDR1 expression
  2. incr glutathione peroxidase activity
  3. mutations of topo II

Resistance mechanisms for what drug?

A

resistance mechanisms for Doxorubicin

41
Q

Plant Alkaloids: #4 ABXs, Bleomycin

  1. what type of rxn causes intercalation & DNA strand breakage
  2. what part of the cell cycle does it inhibit
    (only ABX that is cycle specific)
A

Plant Alkaloids: #4 ABXs, Bleomycin

  1. oxidation rxn –> intercalation & DNA strand breakage
  2. inhibits G2 of cell cycle
42
Q

Plant Alkaloids: #4 ABXs, Bleomycin AEs

  1. what is the dose limiting toxicity
  2. what are the 2 other AEs (what organ systems involved)
A

Plant Alkaloids: #4 ABXs, Bleomycin AEs

  1. dose limiting toxicity = pulm fibrosis
  2. other AEs
    - cutaneous toxicity
    - anaphylactic like rxn (HoTN + CV collpase)
43
Q
  1. incr levels of (drug name) hydrolase and DNA repair activity

Resistance mechanisms for what drug?

A

resistance mechanisms for Bleomycin

Spring 2018 Pharm Exam 3 (4 decks)

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