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Emma Heme/Onc > Detailed Pharm (Chemo/Alkylating&Hormones/Anti-Metabolites) > Flashcards

Detailed Pharm (Chemo/Alkylating&Hormones/Anti-Metabolites) Flashcards

(85 cards)

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1
Q

5-HT antagonist

anti-emetic MOA

A

bind serotonin receptors in GI tract and chemoreceptor trigger zone

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2
Q

5-HT antagonist toxicities

A

HA
hiccups
cardiotoxicity (QT prolong)
constipation

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3
Q

aprepitant

anti-emetic MOA

A

blocks substance P action at NK1 receptor

aprepitant NK1 antagonist

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4
Q

aprepitant

toxicities

A

multiple drug interactions (P450)
hiccups
fatigue

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5
Q

corticosteroids

anti-emetic MOA

A

unknown

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6
Q

corticosteroids

toxicities

A

glucose intolerance

insomnia
agitation

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7
Q

3 drug prophylaxis plan for chemo-induced N/V

A

aprepitant
palonosetron
dexamethasone

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8
Q

olanzapine

anti-emetic MOA

A

atypical antipsychotic

-modulates central dopaminergic and serotonergic activity

very sedating

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9
Q

DA antagonists

anti-emetic MOA

A

bind D1 and D2 receptors in CTZ

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10
Q

DA antagonists toxicities

A

extrapyramidal side effects

sedation

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11
Q

benzos

anti-emetic MOA

A

act on limbic/thalamic/hypothalamic areas of CNS

action mediated by GABA

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12
Q

benzos AE

A

sedation

retrograde amnesia

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13
Q

EPO stimulating agents

A

lack of response correlates w/ high pretreatment EPO level

concurrent Fe admin

some agents found to dec survival

AE: HTN, rash, arthralgias

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14
Q

absolute neutrophil count

A

WBC (%bands + %neutrophils)/100

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15
Q

adverse effects of myeloid gfacs

A

fever
bone pain
inc uric acid, LDH, alkaline phosphatase
splenic infarct (rare)

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16
Q

pegfilgrastim

A

long-acting myeloid gfac

single injection after chemo

large molecule, dec Cl

self-regulating Cl (inc as neutrophils recover)

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17
Q

alkylating agents

general toxicities

A 
BM suppression
N/V/D
anorexia
sterility
amenorrhea
secondary malignancy
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18
Q

alkylating agents

MOA

A

alkylation of DNA by subst alkyl group for active H atom

reactive intermediates –> attack nucleophilic sites on DNA –> covalent linkages –> DNA damage

inter/intra strand crosslinks

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19
Q

platinum agents

MOA

A

bind DNA, RNA

forms 2 stable bonds under physiologic conditions

–> covalent cross-links

  • Cl replaced by H2O
  • bind to N7 (guanine/adenine)
  • RNA>DNA>proteins
  • resistance: inc glutathione-S-transferase, augmented DNA repair/cellular transport etc.
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20
Q

cisplatin

AE

A

DELAYED N/V
nephrotoxicity
neurotoxicity

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21
Q

cisplatin nephrotoxicity

A
  • LOH, DCT, CD
  • risks: hypOalbuminemia, hypERuricemia
  • inactiv of renal brush border enzymes

acute:
- dec Mg/Ca/K, GFR
- inc BUN, serum creatinine
- can reverse w/ discontinuation

chronic:

  • stable, reduced GFR
  • normal/inc serum creatinine

anemia (dec EPO)

prevention: hydration, hypERtonic saline, 24 hr infusions

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22
Q

cisplatin neurotoxicity

A
  • axonal degeneration
  • peripheral neuropathy
  • auditory impairment (high freq hearing loss)
  • visual disturbances
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23
Q

cisplatin uses

A

testicular
ovarian
lung

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24
Q

oxaliplatin

MOA

A

DNA adducts between purine/pyrimidine bases

inhibit DNA synthesis

induce apoptosis

synergistic in vitro w/ 5-FU

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25
oxaliplatin toxicity
- neurotoxicity (peripheral sensoru neuropathy, distal paresthesias, COLD TRIGGERS) - myelosuppression (anemia>thrombocytopenia>neutropenia) - hepatotoxicity - asthenia
26
oxaliplatin uses
colorectal | GI
27
carboplatin toxicities
- HS rxn - N/V - neurotoxicity (pts prev tx w/ cisplatin) - ? inc tox if admin prior to taxane
28
carboplatin drug interactions
need to administer taxane FIRST before carboplatin can also cause neurotoxicity if pt was previously treated w. cisplatin
29
which drug/s is synergistic in vitro w/ 5-FU?
oxaliplatin leucovorin
30
cyclophosphamide
Nitrogen mustard - binds to nucleophiles - inter*/intrastrand DNA cross linking @ guanine - inactivation of DNA template - cessation of DNA synthesis
31
cyclophosphamide is activated by oxidases in ____
LIVER
32
cyclophosphamide is cleared how?
RENALLY
33
two mojo metabolites of cyclophosphamide
1. phorsphoramide mustard (ative alkylating species) | 2. acrolein (UROTOXIC)
34
hemorrhagic cystitis
cyclophosphamide ifosfamide ^--> metabolite=acrolein
35
Due to the immunosuppressive effect of _____ it is also use to tx rheum/AI diseases
cyclophosphamide
36
cyclophosphamide toxicity
``` delayed N/V hemorrhagic cystitis cardiotoxicity immunosuppression neutropenia ```
37
cyclophosphamide | uses
breast leukemia lymphoma BMT
38
ifosfamide activation
requires p450 mixed function oxidases for activation
39
which has longer half-life, cyclophosphamide or ifosfamide?
ifosfamide (slower activation rate)
40
ifosfamide toxicities
- neurotoxicity (crosses BBB): lethargy, confusion, seizure, encephalopathy - hemorrhagic cystitis - neutropenia - nephrotoxicity
41
mesna use/AE
admin w/ ifosfamide binds acrolein in bladder shorter half-life than ifosfamide AE: flushing N/V/D altered taste HS/anaphylaxis
42
ifosfamide
sarcomas lymphoma uterine
43
glucocorticoid uses
- immunosuppressive effects | - lymphocytic
44
androgen uses
- NHL, leukemia, testicular | - myeloplastic, BM failure
45
anti-androgens MOA/toxicities
MOA: bind androgen receptor, inhibit uptake/binding in nucleus AE: hot flashes, dec libido, gynecomastia, transient LFT abnormalities
46
anti-estrogens
- compete w/ estrogen for binding to estrogen receptor - cell cycle SPECIFIC; blocks cell in mid-G1 phase - stim TGF-b --> inhibits TGF-a and IGF-1 --> dec proliferation
47
anti-estrogen toxicities
- menopoausal sx (hot flashes, sweats, vaginal dryness) - fluid retention, peripheral edema - tumor flare - DVT, PE - endometrial hyperplasia
48
Aromatase inhibitors
competitive inhibitors of aromatase block conversion of adrenal androgens --> estrogens no effects on adrenal corticosteroid production
49
aromatase inhibitors AE
``` estrogen deprivation (hot rashes, night sweats, vaginal dryness) arthralgias HA fatigue elevations in serum lipids diarrhea/constipation) dec bone density ```
50
LH-RH agonists
- initial release of FSH/LH - ultimate suppression of gonadotropin bc of feedback inhibitors of GRH - dec LH/FSH from pituitary
51
LH-RH toxicities
- hot flashes, gynecomastia - tumor flare - elevated serum CHL - peripheral edema - asthenia
52
methotrexate (MTX) MOA
S-phase specific binds reversibly to dihydrofolate reductase - inhib conversion FH2-->FH4 - depletes reduced folate necessary for 1 C transfers -dec FH2 cannot work w/ TS to form dTTP --> no purines
53
MTX absorption/distribution
poor PO - 50% bound to plasma proteins (albumin) - 3rd SPACING (ascites, edema, pleural effusions)
54
methotrexate transport
carrier mediated active transport @ low concentration passive diffusion @ high doses
55
MTX metabolism
- formation of DAMPA by intestinal bacteria - hydroxylation to 7-OH methotrexate - POLYGLUTAMATION
56
MTX - most imp metabolism step
polyglutamation by FPGS - formed intracellular;y - inhib DHFR and TS - inc synthesis w/ inc dose and duration of MTX - RETAINED IN CELL
57
MTX ELIMINATION
>90% RENAL <10% BILIARY
58
MTX toxicity
myelosuppression nephrotoxicity (precipitates in renal tubules at high doses) -chronic leukoencephalopathy (rare:lethargy, dementia, seizures, spasticity) pneumonitis
59
Before admin of MTX, be sure to
drain effusion if present (MTX can accumulate in 3rd space) maintain adequate hydration, alkalinize urine, maintain urine output @ 100-150ml/hr, monitor serum creatinine
60
Risk fx for high dose MTX toxicity
- poor hydration - acidic urine pH - dehydration from N/V - dec creatinine Cl - intestinal obstruction - 3rd spacing - methotrexate level >5microM
61
leucovorin rescue
- bypasses blockade of DHFR - started 24 hr after MTX - competes w/ MTX active transport - continue leucovorin until MTX <0.05microM
62
Time until MTX causes irreversible cell damage
48 hr
63
other MTX reversal agents besides leucovorin
- hemodialysis - glucarpidase - charcoal hemoperfusion
64
giving ______ 9-10d prior or immediately after MTX may reduce toxicity
L-asparaginase | via protein inhibition; prevents cells from entering S phase
65
MTX uses
acute lymphoid leukemias NHL may be given intrathecally
66
cytarabine MOA
(Ara-C) - S-phase - metab by deoxycytidine kinase - forms phosphorylated nucleotide - falsely incorporates into DNA - chain elongation terminated - most active on proliferating cells
67
cytarabine absorption/clearance
- not effective orally (gut deamination) | - biphasic elimination (hepatic deamination/renal Cl)
68
cytarabine toxicity w/ conventional dose
myelosuppression flu-like syndrome mucositis hand-foot syndrome
69
cytarabine toxicity w/ high dose
cerebellar (nystagmus, dysarthria, ataxia, slurring of speech) ocular (xs tearing, chemical conjunctivitis) noncardiogenic pulm edema (tachypnea, hypoxemia, pulm infiltrates)
70
cytarabine uses
acute myeloid/lymphoid leukemias chronic myeloid leukemias NHL may be given intrathecally
71
5-fluorouracil MOA
- S-phase specific - require activation to cytotoxic metabolite - incorporation of FUTP into RNA, FdTUP into DNA and inhibition of thymidylate synthase by FdUMP - synergistic w/ LEUCOVORIN
72
5-FU elimination
5_FU undergoes enzymatic degradation intracellularly to toxic metabolite *can be used in pts w/ mild/mod hepatic/renal fxn
73
5-FU toxicity
- myelosuppression - mucositis/diarrhea - hand-foot syndrome - neurotoxicity - CP, EKG changes (coronary vasospasm) - metallic taste - phlebitis
74
5-FU uses
COLORECTAL GI head and neck topical basal cell CA
75
Gemcitabine
- S-phase specific - intracellular activation by deoxycitidine kinase - incorporation into DNA, RNA - inhib DNAP, ribonucleuotide reductase
76
Gemcitabine pharmacokinetics
metabolism by deamination
77
Gemcitabine toxicity
``` myelosuppression N/V flu-like sx infusion rx proteinuria, hematuria maculopapular skin rash ```
78
gemcitabine interactions
potent radiosensitizer
79
_______ enhances cytotoxicity of cisplatin
gemcitabine
80
gemcitabine uses
pancreatic NSCLC bladder cancer sarcoma
81
catheter system for intrathecal administration
lumbar puncture or ommaya reservoir
82
drugs typically associated w/ cardiotoxicity
high dose cyclophosphamide and anthracyclines
83
drugs most highly associated w/ N/V
platinum agents
84
______ are begun prior to initiation of GnRH analogs specifically to block “tumor flare” induced by the initial increase in androgen synthesis.
Androgen receptor inhibitors (bicalutamide, flutamide)
85
ocular toxicity
cytarabine

Emma Heme/Onc (16 decks)

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