Brainscape's Knowledge GenomeTM

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


See full index

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

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

1
Q

5-HT antagonist

anti-emetic MOA

A

bind serotonin receptors in GI tract and chemoreceptor trigger zone

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

5-HT antagonist toxicities

A

HA
hiccups
cardiotoxicity (QT prolong)
constipation

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

aprepitant

anti-emetic MOA

A

blocks substance P action at NK1 receptor

aprepitant NK1 antagonist

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

aprepitant

toxicities

A

multiple drug interactions (P450)
hiccups
fatigue

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

corticosteroids

anti-emetic MOA

A

unknown

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

corticosteroids

toxicities

A

glucose intolerance

insomnia
agitation

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

3 drug prophylaxis plan for chemo-induced N/V

A

aprepitant
palonosetron
dexamethasone

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

olanzapine

anti-emetic MOA

A

atypical antipsychotic

-modulates central dopaminergic and serotonergic activity

very sedating

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

DA antagonists

anti-emetic MOA

A

bind D1 and D2 receptors in CTZ

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

DA antagonists toxicities

A

extrapyramidal side effects

sedation

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

benzos

anti-emetic MOA

A

act on limbic/thalamic/hypothalamic areas of CNS

action mediated by GABA

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

benzos AE

A

sedation

retrograde amnesia

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

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

absolute neutrophil count

A

WBC (%bands + %neutrophils)/100

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

adverse effects of myeloid gfacs

A

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

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

pegfilgrastim

A

long-acting myeloid gfac

single injection after chemo

large molecule, dec Cl

self-regulating Cl (inc as neutrophils recover)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

alkylating agents

general toxicities

A 
BM suppression
N/V/D
anorexia
sterility
amenorrhea
secondary malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cisplatin

AE

A

DELAYED N/V
nephrotoxicity
neurotoxicity

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cisplatin neurotoxicity

A
  • axonal degeneration
  • peripheral neuropathy
  • auditory impairment (high freq hearing loss)
  • visual disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cisplatin uses

A

testicular
ovarian
lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

oxaliplatin

MOA

A

DNA adducts between purine/pyrimidine bases

inhibit DNA synthesis

induce apoptosis

synergistic in vitro w/ 5-FU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

oxaliplatin

toxicity

A
  • neurotoxicity (peripheral sensoru neuropathy, distal paresthesias, COLD TRIGGERS)
  • myelosuppression (anemia>thrombocytopenia>neutropenia)
  • hepatotoxicity
  • asthenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

oxaliplatin uses

A

colorectal

GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

carboplatin

toxicities

A
  • HS rxn
  • N/V
  • neurotoxicity (pts prev tx w/ cisplatin)
  • ? inc tox if admin prior to taxane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

carboplatin drug interactions

A

need to administer taxane FIRST before carboplatin

can also cause neurotoxicity if pt was previously treated w. cisplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

which drug/s is synergistic in vitro w/ 5-FU?

A

oxaliplatin

leucovorin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

cyclophosphamide

A

Nitrogen mustard

  • binds to nucleophiles
  • inter*/intrastrand DNA cross linking @ guanine
  • inactivation of DNA template
  • cessation of DNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

cyclophosphamide is activated by oxidases in ____

A

LIVER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

cyclophosphamide is cleared how?

A

RENALLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

two mojo metabolites of cyclophosphamide

A
  1. phorsphoramide mustard (ative alkylating species)

2. acrolein (UROTOXIC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

hemorrhagic cystitis

A

cyclophosphamide
ifosfamide
^–> metabolite=acrolein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Due to the immunosuppressive effect of _____ it is also use to tx rheum/AI diseases

A

cyclophosphamide

36
Q

cyclophosphamide

toxicity

A 
delayed N/V
hemorrhagic cystitis
cardiotoxicity
immunosuppression
neutropenia
37
Q

cyclophosphamide

uses

A

breast
leukemia
lymphoma
BMT

38
Q

ifosfamide activation

A

requires p450 mixed function oxidases for activation

39
Q

which has longer half-life, cyclophosphamide or ifosfamide?

A

ifosfamide (slower activation rate)

40
Q

ifosfamide

toxicities

A
  • neurotoxicity (crosses BBB): lethargy, confusion, seizure, encephalopathy
  • hemorrhagic cystitis
  • neutropenia
  • nephrotoxicity
41
Q

mesna

use/AE

A

admin w/ ifosfamide

binds acrolein in bladder

shorter half-life than ifosfamide

AE: flushing
N/V/D
altered taste
HS/anaphylaxis

42
Q

ifosfamide

A

sarcomas
lymphoma
uterine

43
Q

glucocorticoid uses

A
  • immunosuppressive effects

- lymphocytic

44
Q

androgen uses

A
  • NHL, leukemia, testicular

- myeloplastic, BM failure

45
Q

anti-androgens

MOA/toxicities

A

MOA: bind androgen receptor, inhibit uptake/binding in nucleus

AE: hot flashes, dec libido, gynecomastia, transient LFT abnormalities

46
Q

anti-estrogens

A
  • 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
Q

anti-estrogen

toxicities

A
  • menopoausal sx (hot flashes, sweats, vaginal dryness)
  • fluid retention, peripheral edema
  • tumor flare
  • DVT, PE
  • endometrial hyperplasia
48
Q

Aromatase inhibitors

A

competitive inhibitors of aromatase

block conversion of adrenal androgens –> estrogens

no effects on adrenal corticosteroid production

49
Q

aromatase inhibitors

AE

A 
estrogen deprivation (hot rashes, night sweats, vaginal dryness)
arthralgias
HA 
fatigue
elevations in serum lipids
diarrhea/constipation)
dec bone density
50
Q

LH-RH agonists

A
  • initial release of FSH/LH
  • ultimate suppression of gonadotropin bc of feedback inhibitors of GRH
  • dec LH/FSH from pituitary
51
Q

LH-RH

toxicities

A
  • hot flashes, gynecomastia
  • tumor flare
  • elevated serum CHL
  • peripheral edema
  • asthenia
52
Q

methotrexate (MTX) MOA

A

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
Q

MTX

absorption/distribution

A

poor PO

  • 50% bound to plasma proteins (albumin)
  • 3rd SPACING (ascites, edema, pleural effusions)
54
Q

methotrexate transport

A

carrier mediated active transport @ low concentration

passive diffusion @ high doses

55
Q

MTX metabolism

A
  • formation of DAMPA by intestinal bacteria
  • hydroxylation to 7-OH methotrexate
  • POLYGLUTAMATION
56
Q

MTX - most imp metabolism step

A

polyglutamation by FPGS

  • formed intracellular;y
  • inhib DHFR and TS
  • inc synthesis w/ inc dose and duration of MTX
  • RETAINED IN CELL
57
Q

MTX ELIMINATION

A

> 90% RENAL

<10% BILIARY

58
Q

MTX

toxicity

A

myelosuppression
nephrotoxicity (precipitates in renal tubules at high doses)
-chronic leukoencephalopathy (rare:lethargy, dementia, seizures, spasticity)
pneumonitis

59
Q

Before admin of MTX, be sure to

A

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
Q

Risk fx for high dose MTX toxicity

A
  • poor hydration
  • acidic urine pH
  • dehydration from N/V
  • dec creatinine Cl
  • intestinal obstruction
  • 3rd spacing
  • methotrexate level >5microM
61
Q

leucovorin rescue

A
  • bypasses blockade of DHFR
  • started 24 hr after MTX
  • competes w/ MTX active transport
  • continue leucovorin until MTX <0.05microM
62
Q

Time until MTX causes irreversible cell damage

A

48 hr

63
Q

other MTX reversal agents besides leucovorin

A
  • hemodialysis
  • glucarpidase
  • charcoal hemoperfusion
64
Q

giving ______ 9-10d prior or immediately after MTX may reduce toxicity

A

L-asparaginase

via protein inhibition; prevents cells from entering S phase

65
Q

MTX uses

A

acute lymphoid leukemias
NHL

may be given intrathecally

66
Q

cytarabine

MOA

A

(Ara-C)

  • S-phase
  • metab by deoxycytidine kinase
  • forms phosphorylated nucleotide
  • falsely incorporates into DNA
  • chain elongation terminated
  • most active on proliferating cells
67
Q

cytarabine

absorption/clearance

A
  • not effective orally (gut deamination)

- biphasic elimination (hepatic deamination/renal Cl)

68
Q

cytarabine

toxicity w/ conventional dose

A

myelosuppression
flu-like syndrome
mucositis
hand-foot syndrome

69
Q

cytarabine

toxicity w/ high dose

A

cerebellar (nystagmus, dysarthria, ataxia, slurring of speech)

ocular (xs tearing, chemical conjunctivitis)

noncardiogenic pulm edema (tachypnea, hypoxemia, pulm infiltrates)

70
Q

cytarabine uses

A

acute myeloid/lymphoid leukemias

chronic myeloid leukemias

NHL

may be given intrathecally

71
Q

5-fluorouracil

MOA

A
  • 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
Q

5-FU

elimination

A

5_FU undergoes enzymatic degradation intracellularly to toxic metabolite

*can be used in pts w/ mild/mod hepatic/renal fxn

73
Q

5-FU

toxicity

A
  • myelosuppression
  • mucositis/diarrhea
  • hand-foot syndrome
  • neurotoxicity
  • CP, EKG changes (coronary vasospasm)
  • metallic taste
  • phlebitis
74
Q

5-FU uses

A

COLORECTAL
GI
head and neck
topical basal cell CA

75
Q

Gemcitabine

A
  • S-phase specific
  • intracellular activation by deoxycitidine kinase
  • incorporation into DNA, RNA
  • inhib DNAP, ribonucleuotide reductase
76
Q

Gemcitabine pharmacokinetics

A

metabolism by deamination

77
Q

Gemcitabine

toxicity

A 
myelosuppression
N/V
flu-like sx
infusion rx
proteinuria, hematuria
maculopapular skin rash
78
Q

gemcitabine

interactions

A

potent radiosensitizer

79
Q

_______ enhances cytotoxicity of cisplatin

A

gemcitabine

80
Q

gemcitabine

uses

A

pancreatic
NSCLC
bladder cancer
sarcoma

81
Q

catheter system for intrathecal administration

A

lumbar puncture or ommaya reservoir

82
Q

drugs typically associated w/ cardiotoxicity

A

high dose cyclophosphamide and anthracyclines

83
Q

drugs most highly associated w/ N/V

A

platinum agents

84
Q

______ are begun prior to initiation of GnRH analogs specifically to block “tumor flare” induced by the initial increase in androgen synthesis.

A

Androgen receptor inhibitors (bicalutamide, flutamide)

85
Q

ocular toxicity

A

cytarabine

Emma Heme/Onc (16 decks)

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