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antineoplastics Flashcards

1
Q

Drugs in Nitrogen-mustards

A

cyclophosphamide, Ifosfamide and chlorambucil

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2
Q

MOA of Nitrogen-mustards

A

Binds to Guanines and will either cross-link or bind to single strain. Alkylates the DNA and causes strand breakage. cellular replication is affected causing cells apoptosis
non-specific

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3
Q

S/E of nitrogen mustards (cyclophosphamide and ifosfamide)

A

myelosuppression, alopecia, Haemorrhagic cystitis due to metabolic byproduct of acrolein - give MESNA and fluid

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4
Q

s/e of chlorambucil (alkylating agent)

A

the usual but may cause seizures

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5
Q

MOA of Dacarbazine

A

alkylating agent - not specific
analogue of step 8 in purine de-novo
also alkylating agent that affects guanine. pro-drug forms methyltriazenoimidazole

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6
Q

A/E of Dacarbazine (Alkylating agent)

A

Neutropenia, thrombocytopenia, pain from injected vein, flu syndrome, facial flushing

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7
Q

MOA of Busulfan

A

Not specific

Alkylating agent. forms cross-links between DNA causes a disruption in cellular replication

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8
Q

A/E of Busulfan (Alkylating agent)

A

Myelosupression, hyperpigmentation, seizures, tachycardia and pulmonary fibrosis

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9
Q

MOA of Platinum Complexes

A

Not specific
Cisplatin, Carboplatin and Oxaliplatin
Are activated within the cell by displacement of chloride ions, instead leaving positively charged molecules that are able to react with DNA. Inhibition of DNA replication, transcription, and cell division results in apoptosis. Able to bind to DNA via intra and inter strand cross-links.

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10
Q

A/E of Platinum complexes

A

Emetic - Cisplatin>Oxaliplatin>Carboplatin
Myelosuppression (especially carboplatin), hypersensitivity, N&V, elevation in liver enzymes, electrolyte imbalance, Myalgia

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11
Q

Name of PARP inhibitors

A

poly ADP-ribose polymerase enzyme

Olaparib/Veliparib/Niraparib

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12
Q

MOA of PARP inhibitors

A

Not specific
the enzyme is able to repair single strand damage. Inhibiting PARP will cause double-strand breaks. Tumour cells with mutated non-functional BRCA1 and 2 genes are unable to repair these DNA breaks, resulting in cell death

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13
Q

A/E of PARP Inh

A

Taste disturbances, reduced appetite, NVD, oral mucositis, anaemia, Neutropenia

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14
Q

MOA of 5-Fluorourical (5-FU)

A

non-specific, Pyrimidine analogue, antimetabolite
inhibits synthesis of pyrimidine nucleotides by 3 MOA
1. locks thymidylate synthase in inhibited state.
2. RNA incorporation of 5-F-UTP
3. DNA-base pair mismatching (faulty mismatching)

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14
Q

MOA of 5-Fluorourical (5-FU)

A

non-specific, Pyrimidine analogue, antimetabolite
inhibits synthesis of pyrimidine nucleotides by 3 MOA
1. locks thymidylate synthase in inhibited state.
2. RNA incorporation of 5-F-UTP
3. DNA-base pair mismatching (faulty mismatching)

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15
Q

A/E of 5-FU

A

Myelosuppression (especially IV bolus)
hand-foot syndrome
angina-like chest pain
NVD

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16
Q

drug interactions of 5-FU

A
  • cisplatin - increases DNA strand breaks
  • methotrexate - increases effect
  • metronidazole - decreases clearance
  • leucovorin - increases cytotoxic effect
17
Q

MOA of Capecitabine

A

pro-drug of 5-FU

Converted to fluorouracil by a 3‑step process in which the final step is more active in malignant than normal cells

18
Q

other pyrimidine analogues

A

Cytarabine - blocks elongation and temple function by competing for space in DNA
Gemcitabine - analogue of deoxy-cytidine
Azacitidine - hypomethylation of cytosine in DNA (mis-match error)

19
Q

MOA of Vinca Alkaloids

A

non-specific
Vinblastine, Vincristine, Vinorelbine
binds to tubulin and blocks the assembly of tubulin. Cells kept in metaphase - apoptosis

20
Q

A/E of Vinca Alkaloids

A 
Haematological neoplasms
myelosuppresion
P-gp substrate
Peripheral neuropathy
urinary retentions - hypertension
hyperuricaemia.
oral mucositis
21
Q

MOA of taxanes

A

non-specific

promotes microtubule formation and inhibits disassembly leading to cell cycle arrest in late G2 and M phase.

22
Q

A/E of Taxanes

A

hypersensitivity, peripheral neuropathy, neutropenia, increase liver enzymes, bradycardia, fluid retention, increased tears, changes to nails

23
Q

MOA of Etoposide

A

non-specific - Epipodophyllotoxin
Inhibits topoisomerase II resulting in DNA strand breaks and inhibition of cell division in the late S and G2 phases of the cell cycle

24
Q

A/e of Etoposide

A

hypersensitivty, hypotension, NVD, taste disturbances, myelosuppression, alopecia

25
Q

MOA of Topoisomerase Inhibitors

A

Irinotecan/topotecan
only causes single stranded breaks unlike Topo II. Interfering with coiling and uncoiling of DNA during replication, which inhibits nucleic acid synthesis. Actions are specific for S‑phase

26
Q

A/E of Topo II inhibitors - irinotecan and topotecan

A

less damaging to cells
myelosuppression, NVD, oral mucositis
Irinotecan - cholinergic effects exacerbating ASTHMA, CVD and IBD, do not use with these.

27
Q

MOA of Dactinomycin (Antibiotic)

A

non-sepcific
1. binds double strand dna (intercalates) and inhibits RNA polymerase
2. topoisomerase 11 induced DNA strand breakage
Pg-substrate - no CNS entry

28
Q

A/E of Dactinomycin

A

myelosuppression, NVD, stomatitis, alopecia, extravasation

29
Q

MOA Anthracyclines (-rubicin)

A

non-specific
1. intercalates DNA base pairs
2. inhibits topoisomerase II preventing DNA repair
3.Free radical production may also contribute to cytotoxicity
4.. cell membrane binding
P-gp substrates

30
Q

A/E of anthracyclines

A

cardiomyopathy, myelosuppression, extravasation (posssible necrosis)

31
Q

MOA Bleomycin (antibiotic)

A

non-specific
Inhibits DNA and to a lesser extent RNA synthesis, produces single and double strand breaks in DNA possibly by free radical formation

32
Q

A/E of bleomycin

A

pulmonary toxicity, NVD, skin reactions, hypersensitivity.

33
Q

MOA of Selective Oestrogen Receptor Modulators (SERMs)

A

Specific - Tamoxifen and toremifene
competes with oestrogen for receptor (ER). Induces tertiary structure change and ER stops binding to ER element on DNA. Stops TGF-b production. Inhibiting tumour growth.

34
Q

A/E of SERMs

A

hot flushes, NV, fluid retention, vaginal discharge, irregular menstrual cycle
Tamoxifen - Hypercalcaemia - avoid thiazides

35
Q

Drug interactions of SERM

A

Increase metabolism - carbamazepine, phenytoin, phenobarb

Decrease metabolism - erythromycin and ketoconazole

36
Q

MOA of Aromatase Inhibitors

A

Anastrozole and letrozole - specific
Exemestase - irreversable inh
inhibiting this enzyme stops the production of Oestrogen as Aromatase generates oestriol and oestradiol.

37
Q

A/R of Aromatase Inhibitors

A

similar to Tamoxifen

more bone issues, add vit D to diet and calcium due to bone mineral density loss.

38
Q

MOA of GnRH - Goserelin/Leuprorelin/triptorelin

A

Specific
suppresses ovarian and testsicular steroidogensis. GnRH initially stimulates synthesis of FSH, LH, increasing serum testosterone, serum estrogen. Continuous administration of GnRH agonists inhibits gonadotrophin production, and inhibiting the growth of certain hormone-dependent tumours

39
Q

MOA of Colaspase

A

specific
Asparaginase breaks down L‑asparagine; certain types of leukaemic cells cannot synthesise this essential amino acid and are therefore unable to grow and survive

40
Q

A/E of GnRH inhibitors

A

altered glucose tolerance, anaemia, weight gain, muscle atrophy, loss of body hair.

41
Q

A/E of colaspase

A

hypersensitivity, liver damage, prolonged clotting time, increase hypergylcaemia

Antineoplastics (1 decks)

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