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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
marrow suppressive agents
"taxels", cisplatin, etc
26
Myeloid stimulating agents | When should CSFs be given?
Filgrastrin (GCSF), stim marrow to produce more neutros - pegfilgrastim - sargramostim (GMCSF) - Should be given BEFORE chemo to prevent neutropenia, not with (toxic) or after
27
What can giving CSFs WITH chemo cause?
major toxicity (all the -stims, ARDS, pain, rash, feber, etc)
28
Dont use EPO drugs for anemia--why?
dont work and can cause tumor progression
29
What are CSFs used for
to mediate anticipated neutropenia!
30
Most common estro receptor targets
tamoxifen, anastrazole
31
Andro receptor targets
GNRH analogs
32
Bcr/abl targets
Imatinib
33
EGFR
erlotinib
34
VEGF target
bevacizumab
35
Immunologic therapies: | PD-1.PDL-1 monoclonals
nivolumab
36
CTLA-4 tx
ipilimumab
37
TAMOXIFEN TOX
incr risk of endomet cancer, thrombus, depr/menopause sx
38
ANASTRAZOLE (AI) toxicity???
very safe
39
andro depriv tx (GNRH agonists) tox???
no sxe
40
IMATINIB (TKI against bcr-abl) TOX?
well tolerated but some hepatotoxicity
41
ERLOTINIB (TKI against EGFR) TOX?
same as prev
42
NIVOLUMAB (anti PD-1 checkpoint blockade) TOX?
ab tx: some fatigue, flu sx, allergic rxn | rare: low blood cell, skin rxns, bleeding
43
IPILIMUMAB (anti CTLA-4 checkpoint) TOX?
SAME AS PREV
44
SIPULCEL-T (dendritic cell vaccine) TOX?
no sxe
45
CAR-T CELLS TOX?
cytokine storm, | toxicities related to spec ag used
46
What can prophylatic tamoxifen prevent
BC in high risk women
47
What is Tamox assoc with
DVTs and UTERINE CANCeR
48
what is better to use in post menopausal women than tamox
aromatase inhibts
49
what tx should all BC women with ER/PR + BC receive
antiestrogen tx
50
What are 4 types of MOLECULAR INHIBITORS avail to tx cancer
Endocrine tx TKIs CDK inhibs PARP inhibs
51
What are 4 types of immunotherapies against cancer?
Monoclonal abs Dendritic Cell therapy Immune checkpoint blockade Adoptive T cell Tx
52
Why is targeted tx better than chemo
doesnt kill all cells, only some are cytotoxic, specific, many agents are oral instead of IV
53
what do targeted cancer tx generally do?
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
What does ER do in cancer
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
What do SERMs do? main example
eg TAMOXIFEN! | Selective ER modulator: binds to ER, reducing transcr, bloks G1phase progression, cytostatic (wont kill cells)
56
When are SERMs used?
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
Ancillary benefits and toxicities of SERMs (tamox)? | How can tamox resistance occur?
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
Aromatase inhibitors (AIs)
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
Aromatase inhibs generations and main gen III drug? | The 2 types of aromatase inhbits?
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
Impt anti-estrogen drug
FULVESTRANT
61
LHRH (GnRH) agonists
decr prod of estro thru neg feedback on HPA
62
Ideal treatmetns for ER+ cancers?
Tamox and AIs
63
Androgen deprivation tx
VERY successful in men with advanced prostate cancer (ADT) ablate androgen sources and synth etc
64
What drugs are involved in ADT
GNRH agonists mostly, GnRH antagonists, adrenal ablating durgs, andro rec antagonists, 4-a-reudctase inhibts
65
How do GnrH agnosits work
lots of gnrh, body responds by down reg pit gnrh receptors, so less LH rel, so less test prod
66
What are the 3 ways BC and PC can be resistant to endocrine tx?
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
suffix for TKIs?
"NIB"
68
what do TKIs do? | Tox?
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
Which drug targets BCR-ABL
IMATINIB (aka gleevec) binds to fused gene and decr activitity (use for CML/ALL)
70
What tx do we use for EGFR targeting?
ERlotinib (and gefitinib) | prevents overactive epidermal growht factor receptor activity
71
CDK inibts
CDK4 and CDK6 are most common targets | inhib overactive CDKs so inhib overactive cell cycle
72
PARP inhibs
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
Antibody therapy
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
2 drugs that are ab therapies for cancer
NIVOLUMAB (PD-1/PDL1 mab) | BEVACIZUMAB (anti-VEGF mab, prevents blood supply to tumors)
75
side effects of ab tx?
fatigue, flu like sx, allergic rx to ab (rarely low blood count, skin issues, infusion rxn)
76
First tumor vaccine
SIPULEUCEL-T - remove dendritic cells, then activated by tumor ags and then returned to body (vaccine made of pts own DCs!) - active
77
Immune checkpoint blockade
interaxn bn APC and T cell
78
What does NIVOLUMAB do?
anti-PD-1 mab | -used for PD-L1 + tumors, binds PD-1 so that PD-1 doesnt deactivate T cells
79
What does IPILIMUMAB do?
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
What does tx with CAR T-CELLS DO?
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
Toxicity of CAR T-cells? Tx for toxicity?
- toxicity: cytokine storm: elevates pro inflamm cytos causing shock and death - tx this to with anti-IL6 and steroids
82
What procedures can we do if we know someone has BRCA
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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