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4th Year Sem II > Exam 5 Pt 1 > Flashcards

Exam 5 Pt 1 Flashcards

(38 cards)

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1
Q

Methotrexate (MTX)
1. Drug class? What cell cycle phase?
2. Analog of?
3. Reversible Inhibitor of?
4. Inhibit syn of?
5. ADR? ***
6. MAO of resistance?

Leucovorin
1. Also called?
2. Opposes which med
3. MOA
4. When prescribed? Why?

A
  1. Anti-metabolite: Inhibitors of folate metabolism, S phase
  2. DHF
  3. DHFR
  4. THF
  5. induces abortion ***
  6. Overexpress DHFR
  7. folinic acid
  8. Methotrexate
  9. Directly make THF
  10. 1 day after Methotrexate therapy so norm cells can make DNA
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2
Q

Capecitabine
1. Drug class? What cell cycle phase?
2. prodrug of what?
3. Analog of?
4. Complexes with who?
5. Inhibits who?
6. inhibits synthesis of?
7. MAO of resistance?
8. Give in combo with which med?

A
  1. Anti-metabolite: Inhibitors of TS, S phase
  2. 5-Fluorouracil which converts to
    F-dUMP
  3. dUMP
  4. 5-fdUMP + TS + MTHF
  5. TS
  6. dTMP directly (DHF indirectly)
  7. overexpress TS
  8. Leucovorin
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3
Q

Azathioprine
1. Drug class? What cell cycle phase?
2. prodrug of what?
3. Activated by what?
4. Analog of?
5. Inhibit who?
6. Prevent the synthesis of?
7. Metabolized by?
8. Don’t combo with which med? Why?
9. MAO of resistance?

Thioguanine
1. Activated by who?
2. MOA?
3. Can Allopurinol be coadmin?

A
  1. Anti-metabolite, Inhibitors of purine metabolism, S phase
  2. 6- Mercaptopurine (6-MP)
  3. HGPRT to 6-TIMP
  4. IMP
  5. IMPDH
  6. AMP & GMP > downstream
  7. XO into inactive
  8. Allopurinol, bc it inhibits XO, so there is less metabolism of 6-MP and Azathioprine, now med is at toxic levels
  9. overexpress XO, underexpress HGPRT, overexpress IMPDH
  10. HGPRT into 6-TGMP
  11. gets incorporated into DNA causing strand break
  12. yes
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4
Q

Hydroxyurea
1. Drug class? What cell cycle phase?
2. Inhibits who?
3. Inhibits the formation of who? ***
4. Also used in the treatment of?
5. ADR?
6. MAO of resistance?

A
  1. Anti-metabolite, Inhibitors of ribonucleotide reductase, S phase
  2. ribonucleotide reductase
  3. deoxyribonucleotide
  4. sickle cell disease
  5. Long term use > LEUKOGENIC, along w/ top 3 ADR (hair loss, N/V, immunosuppression) ***
  6. overexpress Ribonucleotide reductase
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5
Q

Cladribine
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA

A
  1. Chlorafabine
  2. Anti-metabolite, Purine (adenosine) analogues, S phase
  3. replaces A which makes the DNA unstable
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6
Q

Cytarabine
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA

A
  1. Gemcitabine
  2. Anti-metabolite, Pyrimidine (cytidine) analogues, S phase
  3. replaces C which makes the DNA unstable
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7
Q

Vincristine
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA?
4. MOA of resistance?

A
  1. Vinblastine
  2. Anti-mitotic, Vinca alkaloids, M phase
  3. bind to b-tubulin and inhibits the microtubules from elongating
  4. overexpress b-tubulin or changes b-tubulin structure so drug can’t bind
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8
Q

Paclitaxel
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA?
4. MOA of resistance?
5. ADR ***

A
  1. Docetaxel, Nab-paclitaxel (Abraxane)
  2. Anti-mitotic, Taxanes, M phase
  3. bind to b-tubulin and promote microtubule growth (can’t shrink)
  4. overexpress b-tubulin or changes b-tubulin structure so drug can’t bind
  5. acute hypersensitivity- except nab-paclitaxel ***
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9
Q

Mechlorethamine
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA
4. Unique abt each drug

Cyclophosphamide
1. Prodrug activated by what?
2. admin
3. ADR ***

Bendamustine
1. MOA

A
  1. Melphalan, Chlorambucil
  2. Alkylating agents, Nitrogen mustards, no specific phase
  3. Alkylation of guanine
    • Mechlorethamine: oral unstable, reconstitute right before inj
      - Melphalan, Chlorambucil: stable so taken orally and less toxic
  5. CYP450
  6. PO
  7. creates a toxic byproduct called ACROLEIN which accumulates in the bladder causing, HEMORRHAGIC CYSTITIS, treated with MESNA ***

1.
- Extensive DNA damage +
- insufficient DNA repair +
- inhibition of mitotic checkpoint control (mitotic catastrophe) +
- apoptosis

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10
Q

CisPLANTIN
1. which other med does this?
2. Drug class? What cell cycle phase?
3. MOA
4. ADR ***

A
  1. CarboPLANTIN, OcaliPLANTIN
  2. Alkylating agents, Platinum Compounds, no specific phase
  3. add platinum into DNA structure
    - Formation of DNA adducts
    - Crosslinking of DNA strands
  4. Cisplatin: Nephrotoxicity and Neurotoxicity > bc unstable and short t1/2 ***
    Carboplatin: less nephrotoxicity
    Oxaliplantin: neurotoxicity exacerbation by cold temp
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11
Q

Bleomycin
1. Drug class? What cell cycle phase?
2. MOA
3. ADR
4. Unique bc?
5. Metabolized by?

A
  1. Alkylating agents, Natural compound, no specific phase
  2. Chelates iron to form an unstable complex > incr in reactive oxygen species > ss and dsDNA breaks
  3. Pulmonary fibrosis and skin ulcerations (IRREVERSIBLE & CUMULATIVE ***
  4. Lifetime max dose: 400 units
  5. Bleomycin hydrolase- low levels in the lung and skin reason why we have these ADR
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12
Q

Irinotecan
1.Water soluble prodrug of
2. Drug class?
3. MOA
4. ADR **
5. Unique **

A
  1. cleaved to release active lipophilic metabolite SN-38
  2. Topo 1 Inhibitor, Camptothecins
  3. prevents resealing step of DNA
  4. Severe GI toxicity/ life-threatening diarrhea/ bone marrow depression ***
  5. UGT1A1 metabolizes SN-38 into SN38G (inactive), but UGT1A1 is polymorphic and UGT1A128 has decr metabolism activity which incr the med, issue is it creates toxic levels > ADR: NEUTROPENIA(severe form of bone marrow depression) diarrhea **
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13
Q

Etoposide
1. Drug class
2. MOA
3. ADR ***
4. Note:

A
  1. Topo 2 Inhibitor, Epipodophyllotoxins
  2. DNA double-strand scission > inhibit ligation (reseal)
  3. Bone marrow suppression ***
  4. combo with direct DNA damaging agents for synergy
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14
Q

Doxorubicin
1. which other med does this?
2. Drug class
3. MOA
4. Excreted?
5. ADR **
6. Unique **
7. Coadmin with? ***

A
  1. Daunorubicin
  2. Topo 2 Inhibitors, Anthracyclines
  3. MOA: React with iron to produce reactive free radicals > oxidative stress > lipid peroxidation
  4. In bile so dose adj in liver dysfunction
  5. Cardiotoxicity (IRREVERSIBLE & CUMULATIVE) ***
  6. Lifetime max dose: 550 mg/m^2 ***
  7. Dextrazoxane (iron chelating agent) for cardioprotective ***
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15
Q

Leuprolide
1. MOA
2. Use

A
  1. MOA: Continuous GnRH agonist > inhibits testosterone synthesis
  2. Male: prostate cancer, Female: breast and uterine cancer
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16
Q

Degarelix
1. MOA
2. Use

Study These Flashcards
A
  1. MOA: GnRH Receptor Antagonist> inhibits testosterone synthesis
  2. Male: prostate cancer, Female: breast and uterine cancer
17
Q

Dutasteride
1. MOA
2. Use

Study These Flashcards
A
  1. 5a-reductase (type II) inhibitor >inhibits conversion of testosterone to DHT
  2. Male: Prostate cancer
18
Q

BicLUTAMIDE
1. Which other med does this?
2. MOA
3. Use

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A
  1. EnzaLUTAMIDE
  2. Androgen receptor antagonists
  3. Male: Prostate cancer
19
Q

Abiraterone
1. MOA

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A
  1. Steroidogenesis inhibitors that are highly selective for CYP17 inhibitors > oppose testosterone syn > less effective
20
Q

Anastrozole
1. Which other med does this?
2. MOA
3. Use

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A
  1. Letrozole, Exemestane
  2. Aromatase Inhibitor > inhibits conversion of testosterone into estrogen
  3. breast and uterine cancer
21
Q

Fluvestrant
1. MOA
2. Use

Study These Flashcards
A
  1. SERD
  2. breast and uterine cancer
22
Q

Tamoxifin
1. prodrug of
2. MOA
3. Use
4. Note:
5. Unique ***

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A

1converted by CYP2D6 into Endoxifen
2. SERM
3. breast cancer
4. Partial agonist at bone and endometrial tissues (poss uterine cancer)
5. CYP2D6 is polymorphic, so if ultrarapid/ extensive (normal) metabolizers (metabolized into Endoxifen) > GIVE and ONLY ultrarapid can get SSRI (CYP2D6 inhibitors) for hotflashes ***

23
Q

Ertolinib
1. Which other med does this?
2. MOA
3. Difference
4. ADR ***

Study These Flashcards
A
  1. Afatinib
  2. EGFR inhibitor
    • Ertolinib: reversible
      - Afatinib: irreversible > overcome resistance> better
  4. Acneiform rash & diarrhea ***
24
Q

Lapatinib
1. MOA
2. ADR ***

Study These Flashcards
A
  1. EGFR-HER2 dual Inhibitor
  2. Acneiform rash & diarrhea ***
25
Cetuximab 1. Which other med does this? 2. MOA 3. Resistance 4. ADR***
1. Panitumumab 2. EGFR inhibitor 3. activates mutation in kRAS so it's always on (constitutive activation) > bypass upstream EGFR blockade > proliferation 4. Acneiform rash & diarrhea ***
26
TrasTUZUMAB 1. Which other med does this? 2. MOA 3. ADR ***
1. PerTUZUMAB 2. HER2 inhibitors 3. Severe cardiotoxicity ***
27
BeVAcizumab 1. MOA 2. ADR ***
1. VEGF/VEGFR inhibitor > bind to VEGF (ligand)> inhibits angiogenesis/cell survival 2. Vessel injury/ bleeding/ proteinuria/HTN ***
28
Sunitinib 1. Which other med does this? 2. MOA 3. ADR ***
1. Sorafenib/ Regorafenib/ Dasatinib/ Ponatinib 2. Multi-kinase inhibitor 3. *** - hair & skin depigmentation (bc cKIT blocked) - vessel injury/ bleeding/ proteinuria/ HTN (bc block VEGFR)
29
Alectinib 1. Which other med does this? 2. MOA 3. Use 4. Resistance
1. Ceritinib/ Crizotinib 2. EML4-ALK tyrosine kinase inhibitor 3. EML4-ALK positive lung cancer 4. Overexpress the fusion protein (EML4-ALK)
30
Bosutinib 1. Which other med does this? 2. MOA 3. Use 4. Resistance
1. Asciminib/ Nilotinib/ Dasatinib/ Ponatinib/ Imatinib 2. BCR-ABL inhibitor 3. chronic myelogenous leukemia (CML) 4. Overexpress the fusion protein (BCR-ABL)
31
Palbociclib 1. MOA
1. CDK Inhibitor > stops the cell cycle at G1
32
Everolimus 1. MOA 2. ADR ***
1. mTOR inhibitor 2. Severe hyperglycemia !!! ***
33
AcalaBRUTinib 1. Which other med does this? 2. MOA
1. IBRUTinib/ ZanuBRUTinib 2. BTK (Bruton's tyrosine kinase) Inhibitor> inhibits B-cell receptor signaling > decr B-cell activation > cause apoptosis
34
IdelaLISIB 1. Which other med does this? 2. MOA
1. CopanLISIB/ DuveLISIB 2. PI3K inhibitor > stops kinase activity
35
Rituximab 1. Which other med does this? 2. MOA 3. Use 4. ADR 131I Tositumomab 90Y Ibritumomab Loncastuximab
1. Obinutizimab 2. binds to CD20 antigen > CDC (complement dependent cytotoxicity) + ADCC (antibody dependent cellular cytotoxicity > kills B-cells 3. Non-Hodgkin lymphoma (CD20 antigen are overexpressed in B cells) 4. immunosuppression - radioactive portion is the B-cell killing part. - mab portion is to bring it to the specific B-cell - 131I Tositumomab: ADR- immunosuppression/ hypOthyroidism Loncastuximab- Anti-CD19 antibody
36
Brentuximab 1. MOA 2. Use 3. Unique ***
1. Anti-CD30 mAB conjugated w/ MMAE (antimitotic agent) = ADC (antibody-drug conjugate) 2. Hodgkin lymphoma (in b-cells) 3. ***Black box warning: PML (progressive mutifocal leukoencephalopathy)
37
Nivolumab 1. Which other med does this? 2. MOA 3. Use 4. ADR ***
1. Pembrolizumab 2. bind to PD-1 receptor (on T-cell) > interfere w/ PD-L binding (on tumor cell) > T-cell attack > cell death 3. lung cancer 4. skin rash ***
38
BiTE (Bi-specific T-cell engagers) 1. MOA
1. fragment + flexibile linker + fragment, one fragment binds to a T-cell (CD3 section) and the other binds to the tumor cell > T-cell activates killing the tumor cell and cytokine production

4th Year Sem II (6 decks)

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