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Clinical Pharmacology > Cancer drugs > Flashcards

Cancer drugs Flashcards

1
Q

Cancer treatment depends on what 5 things

A

Type of cancer, Grade, Stage
Known biological behavior
Other factors

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2
Q

Type of cancer

A 
Cytology/biopsy
Radiographic appearance (i.e. OSA)
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3
Q

Grade

A

Degree of differentiation (histopath)
Mitotic index
Other markers (i.e. AgNor score)

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4
Q

Mitotic Index

A

Number of mitoses seen in 10 high powered fields

Higher MI= higher liklihood metastasis

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5
Q

Special way of scoring mast cell tumors

A

AgNor scores (Argyrophilic) is silver staining for nucleolar organizing regions within individual nuclei

higher AgNor score = higher likelihood metastasis

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6
Q

Stage **on exam

A

Is there metastasis present? Or is it local? What is the overall tumor LOAD?

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7
Q

Known biological behavior – example= OSA

A

OSA thoracic rads- most have no visible pulmonary metastasis at TIME of diagnosis

90% of canine OSA patients will die within 1 year of diagnosis (pulmonary metastasis)

CONSIDER SYSTEMIC DISEASE treatment

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8
Q

What are “other factors” that cancer treatment depends on

A

Oncogenes
receptors
anatomic location
mdr1 status etc

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9
Q

Three primary methods of cancer treatment

A

Localized Disease- Surgery, radiation therapy

Systemic Disease- Chemotherapy

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10
Q

What are characteristics of cancer cells not shared by normal cells?

A

Rapid proliferation (enzymes, substrates related to DNA synth/structure/fxn)
Angiogenesis (cancer cells need blood supply)
Ability to manipulate immune cells and microenvironment

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11
Q

Stages of the Cell Cycle

A

M, G1 (if not dividing go into cell G0), S, G2

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12
Q

how long does M stage take

A

1-7 hours (small % of cell cycle)

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13
Q

M stage- what drug works here

A

Vinca alkaloids

give once a week

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14
Q

how long does G1 stage take

A

7-170 hours

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15
Q

What happens in G1 phase (1st gap phase)

A 
RNA transcription (produce mRNA)
Protein synthesis (required for DNA replication)
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16
Q

What drugs work in G1 phase

A

not that many ..

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17
Q

How long does S phase take

A

8-30 hours

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18
Q

What happens in S phase

A

DNA synthesis in preparation for chromosomal duplication (8-30 hours)

Making DNA so have big nuclei, high metabolic rate and energy requirements

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19
Q

What drugs work in S phase

A

Antimetabolites

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20
Q

how long does G2 phase last

A

1-4 hours

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21
Q

what happens in G2 phase

A

2nd gap phase

It is a pause prior to mitosis - likely organization of proteins and cellular machinery required for mitosis

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22
Q

G0 phase- how long

A

variable, can be years

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23
Q

G0 phase– what cells do not re-enter cell cycle?

A

Neurons, muscle cells do not re-enter cell cycle
Hepatocytes normally do not re-enter after maturity, but can readily do so! (can sit there for years, then start to grow)

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24
Q

Chemotherapy and cell cycles

A

Can be cell cycle non specific (kills non replicating cells as easily as replicating cells), Cell cycle specific, and phase specific ?

not very phase specific ?

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25
Q

Fractional cell kill- define

A

Chemotherapy kills a constant FRACTION of cells, not a constant NUMBER of cells
Can be 10% to 99.9%

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26
Q

small tumor vs tumor at time of dx

A 
small tumor (1 gram) has 1 billion cells (10^9)
tumor at time of dx is about 10 grams (10 billion cells)
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27
Q

how many cells = incompatible with human lfie

A

1 kg tumor = 10^12 cells

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28
Q

1 gram tumor has undergone ___ doubling times if it started from 1 cell

A

30

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29
Q

To get from 10 grams (Diagnosis) to 1 kg (Incompatible with life), only ___ more double times required

A

10

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30
Q

1 gram of tumor is how many cells

A

1 billion

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31
Q

Dr Mealey’s drug for fractional cell kill

A

Mealeymicin, theoretical antineoplastic agent would have 90% cell kill fraction

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32
Q

Mealeymicin Fractional cell kill – see charts

A

..

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33
Q

Chemotherapy is limited by what

A

By host toxicity
**Dose and interval

By development of drug resistant cells

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34
Q

Chemo– what interval is best

A

3 week intervals at best, allows repopulation of tumor cells

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35
Q

What are four ways of Chemo resistance?

A

Altered Target
Inactivation of drug
Failure to reach target
Failure to undergo apoptosis

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36
Q

How does the target get altered?

A 
Chemo drugs(such as Doxorubicin)  target DNA topoismerase enzymes (essential for DNA replication) 
MUTATIONS in enzyme can occur in tumor cells
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37
Q

How do chemo drugs get inactivated?

A

Detoxifying mechanisms in normal cells are also present in neoplastic cells (such as Glutathione S transferase system “detoxified” alkylating agents)

These detoxifying mechanisms can be OVER expressed

i.e. Tumor cells that over express GST –> more detoxification –> resistant to alkylating agents like Cyclophosphamide

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38
Q

How do chemo drugs fail to reach their target?

A

Transport pumps (P Glycoprotein) pumps CHEMO DRUGS out of cell –> Multidrug resistance

MDR1 phenotype- not in collies

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39
Q

Cross resistance to several entire classes of chemo drugs

A

Doxorubicin
Vincristine
Vinblastine
Taxanes

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40
Q

Which tissues are already more resistant

A

Pulmonary parenchyma, hepatocellular ?

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41
Q

How do tumors contribute to a chemo drug’s ability to kill cells by inducing apoptosis?

A

Tumors overexpress BCL-2 (Anti-apoptosis)

Tumors with mutations in Tumor suppressor gene-p53 can be resistant to apoptosis

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42
Q

4 different responses to chemo

A

Complete response, partial response, stable disease, progressive disease

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43
Q

Complete response

A

Resolution of clinically apparent disease (palpable masses, radiographic disease, leukemic cells, paraneoplastic syndromes)

At least 1 month

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44
Q

Partial response

A

Reduction of tumor dimensions by at least 50% for 1 month duration

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45
Q

Stable disease

A

No change to <50% reduction in tumor dimensions

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46
Q

Progressive Disease

A

Growth of lesion or appearance of new lesions

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47
Q

RECIST

A

Response Evaluation Criteria in Solid Tumors

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48
Q

Recist criteria based on what?

A

Based on one dimension

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49
Q

Recist criteria with the 4 responses

A

Complete response- tumor no longer detectable
Partial response - greater than 30% decrease in longest dimension
Stable Disease- less than 30% decrease, or less than 20% of tumor growth
Progressive Disease - more than 20% increase in longest dimension observed

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50
Q

Clinical trials – how does it work?

A

NIH and pharmaceutical companies– screen compounds against a panel of tumor cell lines –> efficacacious compounds tested in rodents first –> efficacy –> Phase 1 clinical trials

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51
Q

Phase 1 clinical trial

A

recruit patients with advanced tumors, with no effective treatment –> determine MAX tolerated dose –> if ANY efficacy –> phase II

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52
Q

Phase 2 clinical trial goal

A

determine which tumor type the drug is efficacious for

again, recruit patients with advanced tumors of various types –> efficacy towards a tumor TYPE –> phase 3

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53
Q

Phase 3 clinical trial goal

A

to determine if drug candidate + other drugs = improvement over “gold standard”

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54
Q

Vetmed drug screening vs FDA approved drugs

A

for vetmed, drugs just need to be “safe” – not necessarily efficacious!

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55
Q

Body Surface Area (BSA) correlates with what 3 things

A

CO, GFR, BMR

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56
Q

BSA does not correlate better with what

A

Bone marrow stem cell turnover

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57
Q

BSA– see charts with the Meters squared

A

..

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58
Q

BSA equation

A

BSA in M^2 = (km x W ^2/3) / 10^4

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59
Q

Body weight vs BSA– body weight better correlates with what

A

with myelosuppression

Dogs < 10kg (less weight) more likely to develop myelosuppression if based on BSA (vs body weight)

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60
Q

Common toxicities- BAG

A

Bone marrow
Alopecia and Anaphylaxis
GIT

also infertility (more problematic in people)

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61
Q

Bone marrow suppression- which cells are affected

A

Neutrophils first, then platelets and RBCs

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62
Q

Alopecia – dose this affect pets as much?

A

not as much since dogs and cats do not have constantly growing hair (hair follicles = rapidly dividing cells)

some breeds more affected (Poodles, English sheepdog)

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63
Q

GI toxicities

A

Anorexia, Nausea, VD

less common in veterinary patients

64
Q

Cisplatin and GI toxicities

A

Premed to prevent nausea (Cisplatin = #1 vomit inducer)

65
Q

Lomustine and GI toxicities

A

Give at bedtime to allow sleeping through nausea

66
Q

Doxorubicin and GI toxicities

A

May cause colitis

67
Q

Infertility

A

Males and females, congenital malformations can occur in offspring

68
Q

What should be discussed with owner about the Maximum tolerated dose

A

Goals- Palliation (tolerate fewer side effects) vs Cure (tolerate more side effects)

69
Q

What are some guidelines for chemotherapy

A

Not used empirically (can’t just use one drug for everything)
Agent must have efficacy for tumor
Monitor with objective criteria!!!!! (i.e. US bladder each time, rads for lung nodules)

70
Q

Chemo drug toxicity– 3 things

A

Carcinogenic
Mutagenic
Teratogenic

71
Q

Chemo drug- safety issues

A

animal waste may contain active drug

Preparation– low traffic area with safety hood, gloves, closed system/chemo pins

Do not crush pills

Incinerate trash

72
Q

Alkylating agents- 3 MOA

A

Interferes with DNA replication (several mechanisms)
i.e. through alkylating –> abnormal bases –> repair enzymes can’t recognize –> DNA is fragmented

i. e. Alkylated bases form cross bridges –> prevent DNA separation for synthesis/transcription
i. e. Alkylated Guanine pairs with Thymidine –> Mutations (instead of AT, CG)

73
Q

4 examples of Alkylating agents

A 
CCLM
Cyclophosphamide (cytoxan)
Chlorambucil
Lombustine
Melphalan
74
Q

Cyclophosphamide toxicity - BAG

A

BAG with nadir at 7-14 days

75
Q

Cyclophasmadide main toxicity concern

A

Sterile hemorrhagic cystitis

  • Metabolite (acrolein) accumulates in urine
  • irreversible
76
Q

Cyclophosphamide- prevention of toxicity

A

More water intake and frequent voiding (can use Prednisone or a diuretic)

**don’t prescribe if owner can’t take them out often

77
Q

Lombustine toxicity

A

BAG
Chronic neutropenia or thrombocytopenia (nadir 1-3 weeks)
LIVER, renal, lung toxicity long term!!

78
Q

Chlorambucil toxicity and use

A

BAG

Used instead of cyclophosphamide (if pts don’t tolerate it)

79
Q

Lymphoma protocols

A

Primary use = Cyclophosphamide

Also lombustine; chlorambucil (low grade lymphomas)

80
Q

Mast cell tumor or Histiocytic sarcoma– drugs

A

Lombustine

81
Q

Alkylating agents- DOSING

A

METRONOMIC = given at low constant dose to suppress angiogenesis

82
Q

Mitotic inhibitors- MOA

A

Bind microtubules –> interfere with cell division

83
Q

Mitotic inhibitors name 2 examples

A

Vinca Alkaloids

Taxanes

84
Q

Vinca alkaloids - 2 drugs

A

Vincristine (Oncovin)

Vinblastine

85
Q

Taxanes- name a drug

A

Paclitaxel (from pacific yew tree)

86
Q

Vinca alkaloids– toxicity (name 3)

A

BAG (Vinblastine more bone marrow suppressive than vincristine)
Vesicant (one stick protocol)
Neurotoxicity (irreversible) i.e. hum
ans feel tingly fingers

87
Q

Paclitaxel toxicity

A

BAG

Also removed from market Feb 2017!

88
Q

Mitosis Inhibitors- clincal uses of vincristine

A

Lymphoma protocols

TVT

89
Q

Vinblastine uses

A

Canine mast cell tumor, lymphoma

90
Q

Paclitaxel uses

A

Mammary tumors, ScCMA

91
Q

Mitosis inhibitors- route of admin

A

Injectables only, NO ORAL

92
Q

Antibiotics MOA

A 
Intercalation into DNA
Inhibits Topoisomerase (this enzyme unwinds DNA for transcription)

Interferes with DNA and RNA synthesis

93
Q

Antioiotics– 2 examples

A

Doxorubicin
Mitoxantrone

“red death or blue thunder:

94
Q

Antibiotics Toxicity - BAG

A

BAG with nadir at 7-10 days

95
Q

Antibotics toxicity - heart

A

cumulative cardiac toxicity (Doxorubicin) that is irreversible!!

96
Q

Antibiotics toxicity- GI

A

Colitis (hemorrhagic)

97
Q

Antibiotics toxicity– vesicant

A

DOXORUBICIN
SEVERE tissue reaction if SQ
ONE STICK PER VEIN

98
Q

Antibiotics- clinical use

A

Lymphoma protocols

Sarcomas (Doxo is best because broad spectrum)

99
Q

Antibiotics- newer analogues efficacy

A

May be less cardiotoxic, but not as efficacious as doxorubicin

100
Q

Antibiotics- bleomycin

A

Electrochemotherapy mostly

101
Q

Platinum compounds MOA

A

Intra-strand cross link DNA interfering with RNA synthesis + DNA replication

102
Q

Platinum compounds- 2 examples

A

Cisplatin

Carboplatin

103
Q

Platinum compounds- toxicity (BAG)

A

Cisplatin is EMETOGENIC so patients need pre treatment ANTI EMETICS

104
Q

Carboplatin- nadir

A

Bimodal at day 6 and 15 (less predictable)

105
Q

Platinum compounds- nephrotoxicity

A

Cisplatin! Need diuresis (pre, during, post TX)

Carboplatin = less nephrotoxin

106
Q

Platinum compounds- ears and resp

A

Ototoxicity

Respiratory:
*Cisplatin –> Fatal pulmonary edema in cats
carboplatin safer in cats

107
Q

Cisplatin is agent of choice for _____ but largely replaced by ____ due to decreased toxicity and ease of admin

A

Osteosarcoma

Carboplatin

108
Q

Other uses of cisplatin

A

Carcinomas

Intralesional in EQUINE sarcoids

109
Q

Antimetabolites MOA

A

Interfere with purine and pyrimidine synthesis and incorporation into DNA

110
Q

Antimetabolites- 4 examples

A

CAM 5FU

Cytosine arabinoside
Azathiprine
Methotrexate
5 Fluorouracil

111
Q

Methotrexate BAG

A

Nadir at 6-9 days

112
Q

What makes Methotrexate have drug interaction potential

A

Highly protein bound

113
Q

5FU toxicity

A

BAG

CENTRAL NEUROTOXICITY = FATAL IN CATS !!!

114
Q

Azathioprine toxicity

A

BAG- lower frequency in dogs

MYELOSUPPRESSION - avoid in cats

115
Q

Cytosine arabinoside - BAG

A

Nadir in 1-14 days (can drop rapidly in just a day!)

116
Q

Clinical use of Methotrexate

A

older UW madison protocol for lymphoma (not used much anymore)

117
Q

Clinical use of 5FU

A

Carcinomas!!!!

118
Q

Clinical use of Azathioprine

A

Immune mediated disease

119
Q

Clinical use of cytosine arabinoside

A

Canine non infectious encephalitis (Neuro department!!)

Acute leukemia and lymphoma in horses

120
Q

L asparaginase MOA

A

Deprives tumor of asparagine -> inhibits PR synthesis – KILLS LYMPHOCYTES QUICKLY

good in the short term

121
Q

L asparaginase toxicity

A

Allergic reactions (pretreat with Antihistamines) “asparaginase, allergies…ASPPPP and PPPPancreatitis”

Relatively BM sparing except if used with Vincristine

Pancreatitis
+- Vomiting

122
Q

Clinical use of L asparaginase

A

Lymphoma

123
Q

L asparaginase route of admin

A

Give SQ

DO NOT GIVE IV –> Anaphylaxis

124
Q

NSAIDS MOA (proposed) Name 4

A

COX2 may be overexpressed in many tumors –> block COX2

NSAIDS may enhance APOPTOSIS, decrease tumor invasiveness, block angiogensis

125
Q

Piroxicam- current usage

A

rarely used now (COX2 selective agents may be better)

Used for Transitional cell tumors and paillation of other tumor types

126
Q

Piroxicam– toxicity

A

NSAID so GI ulcers, renal

127
Q

Tyrosine Kinase Inhibitors– MOA

A

Inhibit cell signaling (proteins involved in cell replication)

128
Q

Tyrosine Kinase Inhibitors– name an agent used in vetmed

A

Toceranib phosphate (Palladia)

129
Q

Palladia usage

A

1st FDA approved drug for treating cancer in vet patients

Grade II and III mast cell tumors

130
Q

Palladia– what is important to remember

A

92% protein bound, so AVOID NSAIDS

131
Q

Besides Palladia, what is another Tyrosine Kinase inhibitor

A

Masitinib (Kinavet-CA1)
Also treats Grade 2 and 3 mast cell tumors
and protein bound

CURRENTLY OFF THE MARKET IN USA

132
Q

Tyrosine Kinase Adverse effects

A

Neutropenia
GI ulcers (AVOID NSAIDS)
Vasculitis (Thromboembolic disease)
PLN

basically with TK-I, think 3 blood things and PLN

133
Q

Canine melanoma vaccine MOA

A

DNA vaccine: HUMAN tyrosinase (human form so dogs can respond)

Tyrosinase is present on surface of melanoma cells, triggers immune response
??

134
Q

Canine Melanoma vaccine ONCEPT usage and dosing

A

USDA approved
Stage 2 or 3 melanoma in conjunction with standard tx for local disease

4 doses: 2 weeks apart + 6 month booster

135
Q

Efficacy of melanoma vaccine

A

Initially looked great, but more recent studies showed there were no differences in survival

136
Q

Melanoma vaccine– adverse effects

A

Injection site pain, Fever, Hypersensitivity (rare), localized vitilligo

137
Q

Metronomics- define

A

Lose doses, more frequently

May have anti-angiogenic effects

138
Q

Metronomics– tends to be ____ agents

A

alkylating agents, because oral

139
Q

Metronomic Lomustine study

A

discontinued due to toxicities (GI, Liver, azotemia, thrombocytopenia, neutropenia)

140
Q

Metronomic cyclophosphamide toxicity??

A

Cystitis?

141
Q

How to manage nausea/vomiting effects of chemo drugs

A

Maropitant

Odansetron, Butorphanol (specific- PRIOR to cisplatin)

142
Q

Drugs causing diarrhea

A

Doxorubicin most likely
Loperamide
Morphine
Metronidazole (esp if due to bacterial overgrowth)

143
Q

What is imporatnt about Loperamide

A

must know MDR1 status!

144
Q

How to prevent excess histamine effects from mast cell tumors

A 
Prevent GI ulceration with H2 blockers (famotidine)
Use PPIs (omeprazole)
145
Q

Managing neutropenia depends on what two things

A

Grade and Presence of fever

Can be grade 1-2, Grade 3-4, or Febrile

146
Q

Grade 1-2 neutropenia

A

Afebrile
Oral antibacterial agent
Selection based on most likely source of infection

147
Q

Grade 3-4

A

Afebrile
Oral antibacterial agent
4 quadrant coverage

148
Q

Febrile stage

A

Parenteral

4 quadrant coverage

149
Q

What can you give prior to treatment of a cytotoxic drug, that can cause prolonged neutropenia

A

rHG-CSF (h for Human recombinant– they get AB, thus not used often)

Don’t keep neutropenic patients in hospital too long!!!

150
Q

Which drugs are substrates for P-gp

A

Vincristine and vinblastine
Doxorubicin
Paclitaxel

151
Q

Which chemo drugs considered “natural products”

A

Vincristine and vinblastine

152
Q

Dogs with MDR1 mutation (even heterozygotes) more likely to develop what

A

BM suppression (neutropenia, thrombocytopenia)
GI (vincristine!)
Neuropathy

153
Q

Why do dogs with MDR1 mutation develop problems

A

P-gp mediated biliary excretion (Vincristine and vinblastine, doxorubicin, paxiltaxel)

154
Q

Who to test for MDR1 mutation

A

ALL herding breeds, mixed breeds

severe adverse affects!

155
Q

What dose reduction (%) should be made for MDR1 mutant/mutant

A

50% decrease

156
Q

What dose reduction (%) should be made for MDR1 mutant/normal

A

25%

157
Q

Case example with MDR1- rhonda

A

see case

looks like Doxorubicin, Vinorelbine, Taxol (Paclitaxel) cause severe BM suppression

Clinical Pharmacology (7 decks)

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