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Neoplasia Block > PHARM 2 lectures (treatment of cancer complications, targeted therapy) > Flashcards

PHARM 2 lectures (treatment of cancer complications, targeted therapy) Flashcards

1
Q

aspirin, acetominophen, ibuprofen, ketorolac are

A

NSAIDS

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2
Q

morphine, hydromorphine, fentanyl, oxycodone, codeine are all

A

opioids

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3
Q

Adjuncts for neuropathic pain

A 
antidepressants (tricyclic)
anticonvulsants
local anesthetics
bisphosphonates (for bone pain)
psycostimulants (eg methylphenidate for fatigue)
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4
Q

drugs for treating nausea and vomiting

A

5-HT3 antagonists (eg ondansetron)
steroids (eg dexamethasone)
antidopaminergics (eg metoclopramide, haloperidol)
neurokinin 1 antagonists (eg aprepitant

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5
Q

nausea/vomiting adjuncts

A

benzos (eg lorazepan for anticipatory nausea)
H2 antagonists and proton pump inhibs (diphenhydramine and omeprazole)
cannabinoids (eg dronabinol)
antipsychotics/phenothiazines (eg promethazine)

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6
Q

Examples of colony stimulating factors (CSFs)

A

Filgrastim (GCSF), pegfilgrastim, sargramostim

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7
Q

What types of N/V can cisplatin cause

A

chemo-induced (min to hours), delayed (after a day), anticipatory (v highly emetic agent)

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8
Q

Most emetogenic compound known?

A

CISPLATIN!

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9
Q

Drug combos for highly emetic tx

A
  • 5HT3 antagonists (ONDANSETRON)
  • steroids (DEXAMETHASONE)
  • Neurokinin-1 antagonists (AREPITANT) and adjuncts (benzos, PPIs such as OMEPRAZOLE)
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10
Q

Drug combos for low emetic tx

A

steroids, benzos, PPIs

-ANtidopaminergics (metoclopramide, prochloroperazine for motion sickness aka composine, haloperidol)

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11
Q

What are metoclopramide and haloperidol used for/ what type of drug?

A

antidopaminergic, for low emetic tx

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12
Q

Drugs for breakthru emesis

A

ADD, dont remove
-antipsychotics (olanzapine), cannabinoids (such as DRANABINOL aka marinol), phenothiazines (PROCHLORPERAZINE, PROMETHAZINE), 5ht3 antagonists, steroids

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13
Q

Tx for anticipatory nausea

A

BENZOS (lorazepam, also anti-anxiety)

acupuncture/pressure, behavioral

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14
Q

3 types of pain to be treated

A

SOMATIC (most common, well localized, paine from bone metas, PGs sensitive nociceptors)
VISCERAL (deep, squeezing, colicky aka waves, often from obstufction, hard to localize)
NEUROPATHIC (second most common, tumor eroding into nerve, or chemo causing neuro dmg, burning/electrical paroxysmal aka sudden/short/freq)

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15
Q

How do NSAIDS treat pain

A

inhib PGs which sensitize nociceptors, no tolerance/dependency issues, some GI/liver/nephrotoxicity

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16
Q

NSAIDs examples

A

ASA/acetominophen
Ibuprofen, naproxen
Salsalate (doesnt affect platelets)
Ketorolac (can be given IV)

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17
Q

Weak opiate examples (2)

A

Codeine (must be conv to morphine in liver by p450, some ppl cant make conversion)
Oxycodone

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18
Q

Strong opiates

A

Morphine
Hydromorphone
Methadone
Fentanyl (avail as topical patch)

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19
Q

Why shouldnt meperidine be used?

A

causes seizures

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20
Q

Drug examples for neuropathic pain

A

not opiates
tricyclics, antidepressants, anticonvulsants, local anesthetics (eg gapapentin, lyrica) (for neuropathic pain NOT general pain!)

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21
Q

What is bone pain treated with

A

bisphosphonates (pamidornate, zoledronic acid)

INHIBITS OSTEOCLASTS

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22
Q

Morphine side effects

A

CONSTIPATION (tx with lactulose or senna, NOT stool softeners), morphine causes gut not to move, so use a stimulate laxative

  • itching: tx with H1 antagonist
  • somnolence (sleepy) use psychostimulants
  • nausea (usu gets better)
  • resp depression
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23
Q

How to treat fatigue induced by cancer tx

A

Methylphenidate (or caffiene/beh tx)

Erythropoeisis stimulating agents have no effect “poeitin”

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24
Q

How to treat marrow suppression

A

can get neutropenia etc so more sus to bacterial infxn, put on antibiotics, and CSFs for anticipation of febrile neutropenia (filgrastim,peg, sagro, etc)

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25
Q

marrow suppressive agents

A

“taxels”, cisplatin, etc

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26
Q

Myeloid stimulating agents

When should CSFs be given?

A

Filgrastrin (GCSF), stim marrow to produce more neutros

  • pegfilgrastim
  • sargramostim (GMCSF)
  • Should be given BEFORE chemo to prevent neutropenia, not with (toxic) or after
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27
Q

What can giving CSFs WITH chemo cause?

A

major toxicity (all the -stims, ARDS, pain, rash, feber, etc)

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28
Q

Dont use EPO drugs for anemia–why?

A

dont work and can cause tumor progression

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29
Q

What are CSFs used for

A

to mediate anticipated neutropenia!

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30
Q

Most common estro receptor targets

A

tamoxifen, anastrazole

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31
Q

Andro receptor targets

A

GNRH analogs

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32
Q

Bcr/abl targets

A

Imatinib

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33
Q

EGFR

A

erlotinib

34
Q

VEGF target

A

bevacizumab

35
Q

Immunologic therapies:

PD-1.PDL-1 monoclonals

A

nivolumab

36
Q

CTLA-4 tx

A

ipilimumab

37
Q

TAMOXIFEN TOX

A

incr risk of endomet cancer, thrombus, depr/menopause sx

38
Q

ANASTRAZOLE (AI) toxicity???

A

very safe

39
Q

andro depriv tx (GNRH agonists) tox???

A

no sxe

40
Q

IMATINIB (TKI against bcr-abl) TOX?

A

well tolerated but some hepatotoxicity

41
Q

ERLOTINIB (TKI against EGFR) TOX?

A

same as prev

42
Q

NIVOLUMAB (anti PD-1 checkpoint blockade) TOX?

A

ab tx: some fatigue, flu sx, allergic rxn

rare: low blood cell, skin rxns, bleeding

43
Q

IPILIMUMAB (anti CTLA-4 checkpoint) TOX?

A

SAME AS PREV

44
Q

SIPULCEL-T (dendritic cell vaccine) TOX?

A

no sxe

45
Q

CAR-T CELLS TOX?

A

cytokine storm,

toxicities related to spec ag used

46
Q

What can prophylatic tamoxifen prevent

A

BC in high risk women

47
Q

What is Tamox assoc with

A

DVTs and UTERINE CANCeR

48
Q

what is better to use in post menopausal women than tamox

A

aromatase inhibts

49
Q

what tx should all BC women with ER/PR + BC receive

A

antiestrogen tx

50
Q

What are 4 types of MOLECULAR INHIBITORS avail to tx cancer

A

Endocrine tx
TKIs
CDK inhibs
PARP inhibs

51
Q

What are 4 types of immunotherapies against cancer?

A

Monoclonal abs
Dendritic Cell therapy
Immune checkpoint blockade
Adoptive T cell Tx

52
Q

Why is targeted tx better than chemo

A

doesnt kill all cells, only some are cytotoxic, specific, many agents are oral instead of IV

53
Q

what do targeted cancer tx generally do?

A

turn off division signals, change prots in cell so they undergo apop, stop neoangiogenesis, trigger immuns sys to destroy cells, deliver toxin to cancer cell only

54
Q

What does ER do in cancer

A

estro signaling causes cancer to prolif

estro receptor binds to estro in cyto, dimeraizes with another, head to nucl to activate TF for gene transcr

55
Q

What do SERMs do? main example

A

eg TAMOXIFEN!

Selective ER modulator: binds to ER, reducing transcr, bloks G1phase progression, cytostatic (wont kill cells)

56
Q

When are SERMs used?

A

Gold standard for adjuvant tx (tx after tumor removal) in ER + BCs, esp POST-menopausal (DONT use if cancer is ER -) bc will be ineffective

57
Q

Ancillary benefits and toxicities of SERMs (tamox)?

How can tamox resistance occur?

A

ancillary benefits: less CV issues, less bone fractures

  • toxicity: INCR RISK OF ENDOMETR CANCER, THROMBOEMBOLISM, depr/menopause sx
  • resistance: many paths, eg aromatase (producing estrogen anyway thru alternative signalign), eg ER mutation or Her-2 signaling
58
Q

Aromatase inhibitors (AIs)

A

aromatase conv andro to estro in periph (usu in post-meno)

  • use as 2nd line tx when tamox not suff, instead of steroid
  • v safe
59
Q

Aromatase inhibs generations and main gen III drug?

The 2 types of aromatase inhbits?

A

1st-3rd gen, main gen III is ANASTRAZOLE (also extremestane and letrozole)
-2 types: I enzyme inactivators (steroidal), and II competitive antagonists (no steroidal)

60
Q

Impt anti-estrogen drug

A

FULVESTRANT

61
Q

LHRH (GnRH) agonists

A

decr prod of estro thru neg feedback on HPA

62
Q

Ideal treatmetns for ER+ cancers?

A

Tamox and AIs

63
Q

Androgen deprivation tx

A

VERY successful in men with advanced prostate cancer
(ADT)
ablate androgen sources and synth etc

64
Q

What drugs are involved in ADT

A

GNRH agonists mostly, GnRH antagonists, adrenal ablating durgs, andro rec antagonists, 4-a-reudctase inhibts

65
Q

How do GnrH agnosits work

A

lots of gnrh, body responds by down reg pit gnrh receptors, so less LH rel, so less test prod

66
Q

What are the 3 ways BC and PC can be resistant to endocrine tx?

A

1 subversion: mutation in receptor causes abnormal phosphorylation patterns
2 opportunity: cell signal interrupted so creates more receptors (eg if her2/neu blocked with drugs, might overexpress receptor)
3 redundancy: mutation/deletion in rec can make it const active so doesnt need bound ligand to cause growht

67
Q

suffix for TKIs?

A

“NIB”

68
Q

what do TKIs do?

Tox?

A

target tyroskine kinases to target prolif
well tolerated but some hepatotox
-not used by selves
-antiVEGF can cause HTN bc limits blood vessel growth

69
Q

Which drug targets BCR-ABL

A

IMATINIB (aka gleevec) binds to fused gene and decr activitity (use for CML/ALL)

70
Q

What tx do we use for EGFR targeting?

A

ERlotinib (and gefitinib)

prevents overactive epidermal growht factor receptor activity

71
Q

CDK inibts

A

CDK4 and CDK6 are most common targets

inhib overactive CDKs so inhib overactive cell cycle

72
Q

PARP inhibs

A

Poly ADP-Ribose polymerase inhibs (DNA repair enzyme by cancer cells to go thru cell cycle fast) (BRCA 1/2 fxn similarly)

  • best suited for BRCA - tumors (if no BRCA oncogene, PARP is responsible for DNA repair)
  • prevents repair and leads to tumor cell death
  • long half life, bbb penetration, some liver issues like others
73
Q

Antibody therapy

A

monoclonal antibodies against cancer ags, bind and kill cells thru complement act, ADCC, neutralize, oposonize, etc etc
-conjugated is attached to radioactive cpd or toxin

74
Q

2 drugs that are ab therapies for cancer

A

NIVOLUMAB (PD-1/PDL1 mab)

BEVACIZUMAB (anti-VEGF mab, prevents blood supply to tumors)

75
Q

side effects of ab tx?

A

fatigue, flu like sx, allergic rx to ab (rarely low blood count, skin issues, infusion rxn)

76
Q

First tumor vaccine

A

SIPULEUCEL-T

  • remove dendritic cells, then activated by tumor ags and then returned to body (vaccine made of pts own DCs!)
  • active
77
Q

Immune checkpoint blockade

A

interaxn bn APC and T cell

78
Q

What does NIVOLUMAB do?

A

anti-PD-1 mab

-used for PD-L1 + tumors, binds PD-1 so that PD-1 doesnt deactivate T cells

79
Q

What does IPILIMUMAB do?

A

Anti-CTLA-4 (CTLA-4 usu inhibs T cells and binds ot B7 on APCs), ipilimumab binds CTLA-4 but doesnt signal, so it wont bind B7 (instead, b7 can now bind more to CD28 and excite T cells)

80
Q

What does tx with CAR T-CELLS DO?

A

cell based gene tx
T cells removed and tarnsudced with CAR (chimeric antigen receptor)
-adv: live drug, engineers NK and CD8 cells to kill tumor

81
Q

Toxicity of CAR T-cells? Tx for toxicity?

A
  • toxicity: cytokine storm: elevates pro inflamm cytos causing shock and death
  • tx this to with anti-IL6 and steroids
82
Q

What procedures can we do if we know someone has BRCA

A

reduce risk of cancer thru prophylactic oophorectomy and mastectomy
(with high risk cancer, can even use tamox prophylactically)

Neoplasia Block (16 decks)

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