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Block 5 Pharmacology > Introduction to Cancer Chemotherapy > Flashcards

Introduction to Cancer Chemotherapy Flashcards

1
Q

What is the number one cancer by INCIDENCE?

A

Non melanoma skin cancer

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2
Q

What is the number one cancer by MORTALITY

A

Respiratory System Cancer (NMSC doesnt even make top 3 high incidence low mortality)

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3
Q

What are carcinogens? 5 examples

A

Agents that induce DNA alterations and epigenetic changes in critical tumor genes, increase risk of developing cancer

  • Physical agents (radiation, non ion radiation)
  • Chemical/occupational carcinogens (benzenes)
  • Microorganisms (HPV)
  • Medical drugs (cyclophosphamide)
  • lifestyle (poor diet, cigarettes)
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4
Q

Classify the 3 UV Ray types by Wavelength, Energy, and % encountered

A

90% UV-A: 320-400nm-WL (higher WL = LOW energy)
10% UV-B: 280-320nm-WL (lower WL= HIGH energy)
0% UV-C: 200-280nm-WL (lowest WL=HIGHEST)
0% UVC because ozone layer currently blocks it

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5
Q

What types of effects do you experience from UV-A rays

A

Aging

Melanoma

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6
Q

What types of effects do you experience from UV-B rays

A

Non melanoma Skin Cancer

Melanoma

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7
Q

Name 4 types of Chemical/Occupational carcinogens and the cancers they cause

A
  • Benzenes: Leukemia
  • Radon: Lung Cancer
  • Ionizing Radiation: Leukemia, Thyroid, etc
  • Asbestos: Mesothelioma
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8
Q

What classes of microorganisms can be carcinogens

A
  • Viruses
  • Bacteria
  • Fungi
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9
Q

Name 3 viruses that are carcinogens and the cancers they cause

A
  • HPV: Cervical Cancer
  • HHV8: Kaposi Sarcoma
  • EBC: Burkitts Lymphoma, Hodgkins
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10
Q

Name a bacteria that is a carcinogen and the cancers it causes

A
  • H. Pylori: Gastric Cancer
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11
Q

Name a Fungi that is a carcinogen and the cancers it causes

A

Aflatoxin (aspergillus toxin): Liver cancer (HCC)
- Aflatoxin is a strong initiator of HCC and exposure strongly correlates to HCC incidence (mozambique exposure 5x thailand, HCC incidence is almost 20x)

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12
Q

What makes Epigenetic tumor development different

A

Promotes changes in gene expression WITHOUT alteration of DNA sequence (DNA methylation, miRNA)

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13
Q

What are Proto-Oncogenes and name 4 types

A

Genes that encode proteins which regulate cell growth

  • Growth Factors (egf)
  • Growth Factor Receptors (egfr)
  • Signal transduction Proteins (ras)
  • Transcription Factors (cjun)
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14
Q

What are Tumor suppressors 2 examples

A

Normal Genes that

  • Prevent unregulated Cell growth (Rb)
  • Monitor Cell environment for damaging events (p53)
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15
Q

What is the change in Tumor Suppressors and Proto-Oncogenes that causes issues

A
  • Tumor Suppressors: LOSS of Function

- Proto-Oncogene: GAIN of Function

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16
Q

Which type of gene follows knudsons 2 hit hypothesis

A

Tumor suppressor Gene
Both copies must be altered to eliminate activity

In inherited you only need to acquire 1 more mutation thus making the cancers more frequent

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17
Q

Name the 8 general classes of chemotherapeutic agents

A
  • DNA synthesis inhibitors
  • DNA Alkylating Drugs
  • DNA Intercalating Drugs (some are natural, not all)
  • Mitotic Inhibitors (Natural)
  • DNA Topoisomerase Inhibitors (Natural)
  • Monoclonal Antibodies (Targeted)
  • Kinase Inhibitors (Targeted)
  • Hormonal Modulators (Targeted)
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18
Q

What are 2 ways in which the DNA synthesis inhibitors class normally acts

A
  • Structural analogues of Cellular molecules [folates (methotrexate) , purines or pyrimidines (6mp) ]
  • Block enzymes involved in DNA synthesis [ribonucleotide reductase inhibitors (gemcitabine) ]
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19
Q

What is the mechanism by which DNA Alklyating agents generally act

A

Cross-link DNA strands by forming covalent bonds between the drug and bases on separate strands of DNA, damages DNA by preventing strand separation due to covalent bonds and activates repair proteins which damage the DNA trying to remove the agent

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20
Q

3 examples of DNA Alkylating agents

A
  • Nitrogen Mustards (cyclophosphamide)
  • Nitrosoureas (carmustine)
  • Platinum compounds (cisplatin)
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21
Q

Mechanism of DNA Intercalating drugs and 2 examples of them

A

Form strong (not covalent) bonds to dna parallel between base pairs and distorts DNA structure (also activates repair enzymes for more damage effect)
PREVENTS DNA AND RNA SYNTHESIS
- Anthracyclines (doxorubicin)
- Bleomycin

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22
Q

Mechanism of Mitotic inhibitors and 2 examples of them

A

Alter microtubule polymerization/depolymerization preventing MITOSIS

  • Taxanes (paclitaxel)
  • Vinca Alkaloids (vincristine)
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23
Q

Mechanism of Topoisomerase inhibitors and 2 examples of them

A

Block the religation step and cause DNA strand breakage

  • Epipodophyllotoxins (etoposide)
  • Camptothecins (Topotecan)
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24
Q

Monoclonal Antibody mechanism and common target/ use

A

Bind to proteins or ligands to inhibit their action
Protein target is often an ONCOGENE
End result is inhibition in tumor cell proliferation

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25
Q

Mechanism of Hormonal modulators

A

Hormones generally promote proliferation of hormone responsive cells so anti cancer hormonal modulators:
- inhibit hormone receptors
- inhibit hormone synthesis
- inhibit hormone release
End result is inhibition of tumor cell proliferation

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26
Q

Name the 5 cell cycle phases and what is occuring in them

A

G1: G -ap phase 1- preparation for S-phase
S: DNA S -ynthesis (replication
G2: G -ap Phase 2- Prep for M phase
M: M -itosis (chrom org and seg and cell division)
G0: Rest

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27
Q

Which drugs are considered Cell Cycle Specific

A
  • DNA Synthesis Inhibitors (methotrexate)
  • Topo 2 Inhibitors (etoposide)
  • Taxanes (pacletaxel)
  • Vinca Alkaloids (Vincristine
  • Bleomycin
28
Q

Which Drugs are considered Cell Cycle Non Specific

A
  • Alkylating Agents
  • Anthracyclines (doxorubicin)
  • Topo 1 inhibitors (irinotecan)
    ALL ARE BOTH CCS AND CCNS
29
Q

What are the scenarios for use of a CCS drug or a CCNS drug

A
  • For hematopoietic cancer cells and small solid tumors CCS DRUGS ARE BEST because these are rapidly dividing which means CCS can target them well
  • For large solid tumors the outside is rapidly dividing but the inside becomes slower dividing and resting so USE A COMBO OF CCS (for outside) and CCNS (for center)
30
Q

What are 3 types of cancer treatment modalities

A
  1. Local therapy
    • Removal of tumor mass
    • Radiation therapy (expose tumor or whole body)
  2. Systemic therapy (chemotherapy)
    • admin of chemicals to reduce burden
  3. Combined modality (combined local and systemic
    • Adjuvant
    • Neoadjuvant
31
Q

What is Adjuvant therapy and when is it used

A

Chemo is administered after removal of tumor with local therapy (Local first then systemic)

Used when risk of relapse or metastasis is high
If there is a low relapse/met risk Adjuvant is NOT APPROPRIATE

32
Q

What is Neoadjuvant therapy and when is it used

A

Chemo is administered BEFORE local therapy

Used for early therapy of micrometastatic disease and for tumor debulking to allow for more effective local therapy

33
Q

What are the 4 types of chemotherapeutic regimen types

A
  • Induction Therapy
  • Consolidation Therapy
  • Maintenance Therapy
  • Intermittent Therapy
34
Q

Define Induction Therapy and its goals/use parameters

A
  • Initial step to reduce tumor cell burden; see rapid reduction in symptoms for patient
  • High dose combination chemotherapy (multi drugs)
  • Given weeks to months
35
Q

Define Consolidation Therapy and its goals/use parameters

A
  • Given after induction to further reduce cancer cell count; Aim is to achieve complete remission
  • Given as a lower drug dose (different drugs than induction drugs)
  • Given for months
36
Q

Define Maintenance Therapy and its goals/use parameters

A
  • Aim is to sustain remission as long as possible
  • There are fewer courses of lower drug dose
  • Given for months to years
37
Q

Define Intermittent Therapy and its goals/use parameters

A
  • Time in between other therapies (ie between induction and consolidation or consolidation and maintenance)
  • No chemotherapeutic agents given, meant to allow marrow and other normal host cells to recover
38
Q

What are 4 common mechanisms of resistance to Chemo drugs

A
  • Decreased drug accumulation
  • altered drug target
  • increased drug target expression
  • decreased drug activation or inc drug inactivation
39
Q

What are mechanisms by which cancers decrease drug accumulation

A

Drug Efflux pumps (drug enters but is ejected) ATP binding cassette family of proteins (see below)

  • P-glycoprotein or MDR
  • MRP
40
Q

What is p-glycoprotein resistance

A
  • efflux pump product of MDR gene
  • ejects mainly NATURALLY occurring drugs from cell
    • Anthracyclines
    • Vinca Alkaloids
    • Taxanes
  • See multidrug resistance
41
Q

What is MRP resistance

A
  • Remoces glutathione conjugated drugs from tumor cells

- Removes similar drugs as p-gp removes EXCEPT TAXANES ARE NOT EASILY REMOVED

42
Q

What is the general mechanism of resistance by drug activation/inactivation changes and give example of each

A

Activation: some drugs must be activated to have full activity like methotrexate which needs folypolyglutamate synthase to become its more active form, by down regulating that enzyme it dec MTX act

Inactivation: Increase in expression of the enzymes which degrade the drug 5FU broken down to DHFU (inactive) by Dihydropyrimidine dehydrogenase (DPD)

43
Q

List 5 common toxicities of antineoplastic drugs

A
  • Bone marrow Suppression
  • Gastrointestinal toxicity
  • Hair follicle toxicity
  • Nausea and vomiting
  • Organ system toxicity
44
Q

What is the pathophsyiology of bone marrow supression and how is it treated

A
  • inhibition of marrow activity leads to deficiency in production of wbc, rbc, and or platelets
  • Treat: bone marrow transplant or Hematopoietic growth factor administration
45
Q

Name 3 Hematopoietic Growth factors and what they do

A

Recovery time from Marrow suppression dec by administering these:

  • Epoetin: stimulates RBC production
  • Filgrastim: Granulocyte colony stimulating factor, involved in regulation and production of neutrophils
  • Sargramostim: Granulocyte macrophage colony stimulating factor, primary effect is to stimulate myelopoiesis
46
Q

What is the pahtophysiology of GI toxicity of anticancer drugs

A

Agents induce serotonin relase from enterochromaffin cells in gut that can produce GI cramping

47
Q

What are 3 potential downstream effects of Hair follicle toxicity

A

Causes allopecia (hair loss) which can:
- Cause psych effects warranting antidepressants
- Impact compliance
- alter texture of hair when/if it grows back
generally hair loss is reversible but may be permenant

48
Q

Define CIE; how is it different from nausea

A

Chemotherapy induced emesis (also known as CINV)
Vomiting associated with or caused by drug treatments for cancer (protective mech against ingested toxins)

nausea is the sensation which often but not always PRECEDES vomiting

49
Q

What are the 4 types of CIE and their definition

A
  • Acute Emesis: within 24 hours of chemo
  • Delayed Emesis: greater than 24 hours after chemo
  • Breakthrough Emesis: Vomiting despite use of antiemeitcs
  • Anticipatory Emesis: Learned response developed as a result of previous emetic responses to chemotherapy
50
Q

How do you treat each type of CIE:

A
  • Acute: antiemetic agents
  • Delayed: antiemetic agents
  • Breakthrough: antiemetics w/different MOAs
  • Anticipatory: antiemetic + anxiolytic (lorazepam)
51
Q

What 4 chemo drugs are considered level 4 high risk for incidence of emesis

A
  • Carmustine
  • Cisplatin
  • Cyclophosphamide
  • Dacarbazine
    NOTE THIS IS NOT RANKING SEVERITY OF EMISIS JUST RISK OF OCCURANCE
52
Q

What 3 antiemetic types are most commonly used for CIE

A
  • Serotonin Receptor antagonists
  • Tachykinin Receptor antagonists
  • Corticosteroids
53
Q

What 2 antiemetic types are most commonly used for Breakthrough Emeisis

A
  • Dopamine Receptor antagonists

- Cannabinoid Receptor AGONISTS

54
Q

What are the 2 routes by which chemo drugs induce emesis

A
  1. Activate chemoreceptor trigger zone (CTZ) which induces emesis
  2. Activate enterochromaffin cells in the GI causing them to release 5HT and substance P. Which act on abdominal vagal afferents which then trigger CNS (NTS to central pattern generator) to cause emesis
55
Q

What is the most effective class of antiemetic for CIE and why

A

5HT3 Receptor Antagonists

Because they are located in the abdominal vagal afferents, NTS, and CTZ so they hit all routes

56
Q

What are the 5HT3 antagonists most effective against and what are 3 examples of the antagonist drugs

A

Greatest efficacy against high and moderate risk emetogenic agents

  • ondansetron
  • granisetron
  • palonosetron
57
Q

How do Tachykinin receptor antagonists work and where are they found

A

Bind to neurokinin 1 2 and 3 receptors located on abdominal vagal afferents, NTS, and CTZ

58
Q

What are the Tachykinin receptor antagonists most effective against and what is an example of the antagonist drugs

A

Effective against high and moderate risk emetogenic agents
- Aprepitant
Coadministered with 5HT3 antagonist and Corticosteroids

59
Q

What is the Mechanism of coritcosteriods in antiemesis, what are they effective against, and 2 examples

A
  • Unclear MOA, but possible non competitive antagonism of 5HT3 receptors
  • Effective for high, moderate, and LOW risk emetogenic agents
  • Dexamethazone and methylprednisolone
    Administered with 5HT3 antagonist and aprepitant
60
Q

What is the bonus of cannabinoid receptor agonists, and what are 2 examples of the agonists

A

Stimulates appetite - munchies
- Nabilone
- Dronabinol
Commonly used for breakthrough but not firstline for normal CIE

61
Q

Which Chemo agents cause Cardiotoxicity and what treatment/prevention can be used?

A
  • Agent: Doxorubicin and other anthracyclines

- Treat/Prevent: Dexrazoxane

62
Q

Which Chemo agents cause Hemorrhagic Cystitis and what treatment/prevention can be used?

A
  • Agent: Cyclophosphamide

- Treat/Prevent: MESNA

63
Q

Which Chemo agents cause Renal Toxicity and what treatment/prevention can be used?

A
  • Agent: Cisplatin

- Treat/Prevent: Hydration, Mannitol, and Sodium Thiosulfate

64
Q

Which Chemo agents cause Pulmonary Fibrosis and what treatment/prevention can be used?

A
  • Agent: Bleomycin, Busulfan, Carmustine, Cyclophosphamide

- Treat/Prevent: Corticosteroids and treatment cessation

65
Q

Which Chemo agents cause Peripheral Neuropathy and what treatment/prevention can be used?

A
  • Agent: Vinca alkaloids and Taxanes

- Treat/Prevent: Maintain dosage/Treatment cessation

Block 5 Pharmacology (8 decks)

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