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John's Cards > Chemo basic > Flashcards

Chemo basic Flashcards

0
Q

Gompertzian tumor growth

A

pattern of exponential growth with exponential growth retardation.

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1
Q

What are the 3 cell growth types?

A

1) Static – neurons, striated muscle, oocytes
2) Expanding (normally quiescent except under stress/injury a proliferative burst is followed by return to quiescence)- hepatocytes, bile duct epithelium, vascular endothelium
3) Renewing (continuous proliferation) – bone marrow, epithelium, GI epithelium, sperm

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2
Q

Tumor doubling curve

A

-As tumor mass increases the time to double the tumor volume decreases.
-At later stages of tumor growth a small # of doublings produce a marked change in tumor size w/ increased potential for adverse clinical consequences.
-In general metastases have faster doubling times than their corresponding primary lesions.
Average doubling time for human cancers is 50 days.

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3
Q

1 cm mass ~ X number of doubling

A

30

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4
Q

Growth Fraction

A

The proportion of tumor cells that are actively cycling.
Usually those cells near small blood vessels.
Variable by tumor type – 25-95%
Cell loss in tumors is high…70-95%

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5
Q

First order Cell Kill Kinetics

A

A constant fraction of exposed cells are killed, rather than a constant number.
For curative chemotherapy, log cell kill (% of cells killed each cycle) must be very large (>99%) and repetitive.

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6
Q

Cure or prolonged survival achieved when…

A

cell pop reduced to 10 ^1 and 10^ 4 (not clinically detectable.

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7
Q

Hepatic metabolism (ICE VAT)

If you don’t take the liver into account, you’ll need an ice vat

A
  • Vinca alkaloids (vincristine, vinblastine, vinorelbine)
  • Ifos, Cytoxan, etoposide (hepatically metabolized, renally cleared)
  • Taxanes (Taxol, Taxotere)
  • Anthracycylines (doxil, doxorubicin)
  • VEGF inhibitors (cleared)
  • dose reduce MTX bc can cause hepatic fibrosis (Renault cleared)
  • 5 FU
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8
Q

Renal clearance (Top BMI Promotes Cancer)

A 
Platinums
Bleomycin
MTX
Topotecan
Ifos
Cytoxan
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9
Q

Alkylating agents (contain + charged alkyl groups that bind neg charged DNA)

A
  • Direct DNA damage (X-link, free radical, strand breakage) G1, S, G2 arrest
  • RT, platinum
  • Nitrogen mustards(cytoxan, ifos, melphalan)
  • Temodar
  • Bleomycin (not exactly alkylating agent, produces ROS-> DNA breaks)
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10
Q

Antimetabolites

A
  • Inhibition of nucleotide synthesis. G1, S arrest

- Antifolates(MTX, pemextred), nucleoside analogs (5FU, gemzar), hydroxyurea

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11
Q

Microtubule

A

M arrest
Taxanes (taxol, doxetaxol) promote tubulin polymerization
Vinka alkaloid inhibit polymerization

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12
Q

Topoisomerases

A
  • Topo II inhibitors :anthracyclines (doxorubicin, doxil),etoposide, actinomysin D
  • Topo I inhibitors: Topotecan
  • S phase
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13
Q

Signal transduction

A
  • Growth factor blockade: Trastuzumab, cetuximab, bevicizumab, pertuzumab
  • Inhibition of Tyr kinase signal transduction: erlotinib, gefitinib, imitanib, sorafenib, sunitinib, lopatinib
  • Hormonal inhibition
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14
Q

RECIST = Response Evaluation Criteria in Solid Tumors

A

At least one 2cm (one dimension) target lesion
Other non target lesions
CR – disappearance of all target & nontarget
PR – disappearance of all target, without progression of nontarget & no new, at least 30% decrease in sum LD
PD – 20 % increase sum LD of targets
SD – BTWN PR and PD
CR: complete response, PR: partial response, LD: longest diameter, PD: progressive disease, SD: stable disease

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15
Q

Bone Marrow Toxicity

A
  • Neutropenia #1 manifesting 7-14 days from tx, lasting 3-10 days
  • RT, alkylating agents,DNA damaging agents (nitrosoureas, mitomycin C) can have cumulative effects
16
Q

Emetogenicity

A

High: Cisplatin, carboplatin, Cytoxan, dactinomycin
Low: Bleomycin, taxanes, vinca alkaloids, 5FU, MTX, doxil, gemzar, topotecan

17
Q

Which chemotherapies cause Alopecia?

TEA CUP

A

Worst: Taxanes, doxorubicin/doxil, IV etoposide
Possible: platinums, Cytoxan, 5FU

18
Q

Which chemotherapies cause Neurotoxicity?

A

Cisplatin*, taxanes, hexalen,

-cisplatin sx’s come on later and continue after stopping tx

19
Q

What dugs cause PPE?

A

Oral etoposide, 5 FU, Doxil, bleomycin, docetaxel, MTX

FU Doxil Making Beautiful Toes Erythematous

20
Q

Which chemotherapies are vesicants (can cause extravasion necrosis)?

A

Doxorubicin, dactinomycin, Taxotere, vincristine, mitomycin C

21
Q

Genitourinary complication of chemotherapy

A
  • Cisplatin: AKI if UOP not maintained. Mg and K loss known

- Hemorrhagic cystitis: Ifos-use mesna to bind acrolein. Can also happen with cytoxan

22
Q

What EXACTLY is cremephor??

A
  • Carrier of paclitaxel

- Mixture of polyoxyethylated castor oil and dehydrated alcohol (leads to mast cell degranulation and clinical HSR)

23
Q

Timing of hypersensitivity reactions

A
  • Platinum: second cycle of second course (~eighth)

- Taxol: 1st or 2nd cycle

24
Q

Treatment of hypersensitivity reactions

A
  • Platinum
  • Taxol
25
Q

What are the 3 phases of clinical trials?

A
  • Phase 1: determine max tolerated dose & dose limiting toxicity
  • Phase 2: determine efficacy (e.g. RR) and toxicity. Done for a specific dx
  • Phase 3: RCT comparing new agent to standard therapy
26
Q

How is body weight used in chemo?

A
  • Actual: measured body weight
  • Adjusted (ABW) = ideal body weight (IBW) + 0.4(ABW - IBW). Used for obese patients (e.g BMI >25)
  • ASCO recommends using ACTUAL
  • GOG calculator uses adjusted
27
Q

Infertility

A
  • High risk: cytoxan, ifos, melphalan
  • Medium risk: cisplatin, doxorubicin
  • Low risk: MTX, 5FU, bleomycin, vincristine, dactinomycin
  • taxane risk unclear due to limited studies
  • should wait 6months after chemo to try to get preg
  • ovarian suppression effectiveness controversial

Whole abdominal or pelvic radiation doses
> 6 Gy in adult
> 15 Gy in pre-pubertal girls
> 10 Gy in post -pubertal girls

Ref: American Cancer Society and Breast Cancer.org

28
Q

What is an AUC?

A
  • AUC: the area under the curve is a plot of concentration of drug in plasma against time. (correlates with anti-tumor activity)
  • The amount eliminated by the body = clearance (volume/time) * AUC (mass*time/volume).
  • Calvert Formula: Carboplatin dose (mg) = (Target AUC) x (GFR + 25)

-GFR about equivalent to the estimated creatinine clearance (Ccr). Calculated with Cockcroft-Gault:
Ccr (ml/min) = ([140 - Age(years)] x Weight (kg) x 0.85) /72 x Serum Creatinine (mg/dl)

29
Q

platinum drugs

A

Gain access to intracellular compartment by passive diffusion and carrier mediated uptake; resistance MOA include increased efflux, reduced influx, intracellular detoxification by glutathione and metallothionenines, changes in DNA repair, defective apoptosis

30
Q

Goldie Coldman hypothesis

A

treatment should begin as soon as possible to treat the smallers amt of bulk; multiple non cross resistant agents should be used to avoid selection of resistant clones; use drugs often and at highest possible doses

31
Q

mechanisms of chemotherapy resistance

A

alteration of drug movement across cell membrane; increased DNA repair, defective apoptosis ; alterations of drug targets

32
Q

Prodrugs

A 
o	Hexamethylamine (liver demethylation)
o	Cyclophosphamide (liver P450)
o	Xeloda(capecitabine) gets transformed to 5-FU (cells via dihydropyrimidine reductase)
o	Gemzar (cells via deoxycitidine kinase)
o	Ifos (liver microsomal enzymes)
o	Irinotecan (liver to active SN-38)
o	Mitoycin (reduction to alkylating agent)
33
Q

Chemo dosing adjustments

A
  • Cr capped w/ carbo for < 0.7?

John's Cards (8 decks)

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