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Pharmacology III > Oncology > Flashcards

Oncology Flashcards

1
Q

What types of cancers cause the most deaths yearly?

A

Lung, stomach, liver, colon, and breast cancer cause the most deaths each year

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2
Q

What are the highest risk factors associated with developing cancer?

A

Tobacco use is the most important risk factor (22% of global cancer deaths and 71% of lung cancer deaths)
High body mass index
Low fruit and vegetable intake- due to antioxidants
Lack of physical activity
Alcohol use

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3
Q

What are the characteristics that cancer shares?

A

Uncontrolled proliferation
Local invasiveness
Tendency to metastasis
Changes in some aspect of original cell morphology

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4
Q

What is cancer cure defined as?

A

The disappearance of any evidence of tumor for 5 years and a high actuarial probability of a normal life span

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5
Q

What are the three principle methods that attempt to cure or palliate cancer?

A

Surgery
Radiotherapy
Chemotherapy

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6
Q

What does chemotherapy drugs do?

A

Inhibit rate of growth
Kill cancerous cells
Have minimal effects on non-neoplastic host cells

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7
Q

What do anticancer agents target?

A

Malignant cells in preference to non-malignant cells-through the molecular differences between them

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8
Q

What are the chemotherapeutic techniques?

A

Cytotoxic therapy
Endocrine therapy
Immunotherapy

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9
Q

Cytotoxic therapy- MOA

A

-Affect DNA synthesis
-Classified according to their site of action on the process of DNA synthesis within the cancer cell.
-Most active against cycling/proliferating cells
Normal – hair, skin, stomach lining, blood cells
Malignant- goal is to target these.
-Phase specific killing–drugs that are effective at killing cycling cells during specific parts of the cell cycle.
-Cycle specific–cytotoxic throughout the cell cycle

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10
Q

Cytotoxic drugs have a low selectivity for what non-cancer cells that undergo rapid division?

A

GI
Bone Marrow
Reproductive
Immune systems

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11
Q

Why can selectivity occur w/some cancers for cytotoxic drugs?

A
  • Malignant tumors have a higher proportion of cells undergoing proliferation than in normal proliferating tissues.
  • Normal cells recover from chemotherapeutic inhibition faster than some cancer cells.
  • Synchronized cell cycling may leave discrete period of vulnerability to cytotoxic drugs
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12
Q

How do cytotoxic drugs work?

A

Cytotoxic drugs kill a constant fraction, not a constant number of cells; lays down the foundation for chemotherapeutic dosing schedules.

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13
Q

Cytotoxic drugs- resistance

A

Genetic resistance
Inherited to the cancer cell line- drugs don’t work on it at all
Acquired during the course of chemotherapy as a result of selection by the agent.
If you don’t give enough or stick to the right therapy then the patient can develop immunity.

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14
Q

Cytotoxic drugs- MOA of resistance

A

Abnormal transport
Decreased cellular retention- cell doesn’t retain the drug that you are giving
Increased cellular inactivation (binding/metabolism)- binds or metabolizes the drug away
Altered target protein
Enhanced repair of DNA- respond more like normal cells to recover faster.
Altered processing

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15
Q

When where can resistance for cancer chemotherapy occur if cancer is in pharmacologic sanctuaries?

A

Blood-brain barrier- cancers in here are hardter to treat because of the bateir and you need the meds to get past the BBB so end up doing surgery.
Large solid tumor w/low blood supply and diffusion

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16
Q

What are the cytotoxic agents?

A
  • Alkylating agents
  • Antimetabolites
  • Cytotoxic antibiotics
  • Mitotic (Microtubule) inhibitors
  • Miscellaneous agents
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17
Q

Where are alkylating agents capable of introducting alkyl groups into?

A

Capable of introducing alkyl groups into nucleophilic sites on other molecules through the formation of covalent bonds.

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18
Q

What are the nucleophilic targets of alkylating agents?

A

Nucleophilic Targets—present in macromolecules and low molecular weight compounds w/in cells:
Sulfhydryl Hydroxyl
Amino Carboxyl
Phosphate Imidazole

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19
Q

What are the macromolecular sites of alkylation damamage of alkylating agents?

A

DNA
RNA
Various enzymes
DNA synthesis inhibition requires lower drug concentrations than inhibition of RNA and protein synthesis.

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20
Q

Nitrogen mustards- Mechlorethamine (Mustargen)- pharmacokinetics

A

Plasma half-life after IV injection ~ 10 minutes (really fast)
Little or no intact drug excreted in urine (body destroys really quickly)

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21
Q

Nitrogen mustards- Mechlorethamine (Mustargen)- Indications

A

Major—Hodgkin’s disease

Treated w/MOPP (meclorethamine, (Oncovin) vincristine, procarbazine, prednisone)
Less reactive nitrogen mustards now preferred for treatment of non-Hodgkins lymphomas, leukemias and various solid tumors.

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22
Q

Nitrogen mustards- Mechlorethamine (Mustargen)- dose-limiting toxicities

A

MYELOSUPPRESSION
Maximal leukopenia and thrombocytopenia occurs w/in 10-14 days post administration—recovery complete 21-28 days.
Lymphopenia and immunosuppression may lead to activation of latent herpes zoster.

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23
Q

Nitrogen mustards- Mechlorethamine (Mustargen)- ADRs

A

Will affect rapidly proliferating normal tissues and cause: Alopecia, Diarrhea, Oral ulceration.

N/V/ 1-2 hours after inj can last up to 24 hours

Causes blistering—avoid extravasations and spillage

Reproductive toxicities
Amenorrhea
Inhibitor of oogenesis and spermatogenesis
½ premenopausal women and almost all men treated for 6 mo. w/MOPP become sterile.

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24
Q

Cyclophosphamide (Cytoxin)- MOA

A

Alkylating Agents
Must be activated by P450 enzyme system
Cytotoxic metabolites include (products that are seen when cyclophosphamide is metabolized but if you give a P450 inhibitor then you wont get these)
Phosphoramide mustard
acrolein

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25
Q

What is the most versatile and useful nitrogen mustart?

A

Cyclophosphamide (Cytoxin)

Broadest spectrum of antitumor activity of all alkylating agents.

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26
Q

Cyclophosphamide (Cytoxin)- Indications

A

Lymphomas
CVP-cyclophosphamide, vincristine and prednisone
Substitute cyclophosphamide for mechlorethamine in MOPP becomes COPP

Curative in Burkitt’s lymphoma

Orally used for less aggressive tumors such as:
Nodular lymphomas and myelomas

Breast cancer
CMF-add MTX and 5-fluorouracil

Cancer of testes and cervix

Alterantive to azathiaprine in organ transplants to prevent rejection

Also SLE (nephrotic syndrome), RA

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27
Q

Cyclophosphamide (Cytoxin)- Dose-limiting toxicity

A
  • Bone marrow suppression—affects WBC > platelets
  • Occurs maximal 10-14 days post administration
  • Recovery occurs 21-28 days
  • Impairs function of both humoral and cellular (B & T cells) immune systems
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28
Q

Cyclophosphamide (Cytoxin)- ADRs

A
  • -Increased risk of infection–Alopecia, Cystitis, Dysuria (Decreased urinary frequency, Rarely fibrosis and permanently decreased bladder capacity.)
  • -Large IV doses: Impairment of renal fxn, Hyponatremia, Increased urine osmolarity, Subendocardial necrosis, Arrhythmias, CHF, Interstitial pulmonary fibrosis
  • -Chronic treatment–Infertility, Amenorrhea, Mutagenesis, carcinogenesis
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29
Q

Ifosfamide- MOA

A 
Alkylating agents
Analogue of cyclophosphamide
Requires metabolic activation to form 4-hydroxy-ifosfamide
Kinetics similar to cyclophosphamide
Activity against broad-spectrum tumors
Germ cell cancer of the testes-more active than cyclo
Lymphomas
Sarcomas
Ca of lung, breast, and ovary
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30
Q

Ifosfamide- ADRs

A

Less mylosuppressive than cyclophosphamide
More toxic to the bladder
Alopecia
N/V
Infertility
Secondary tumors like acute leukemia
Neurologic symptoms – Confusion, Somnolence, Hallucinations

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31
Q

What drug can be co-administered w/ ifosfamide to help avoid hemorrhagic cystitis?

A

Mesna (Mesnex)

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32
Q

What are the antimetabolites?

A

Folic acid antagonist (Methotrexate)
Antipyrimidines (Fluorouracil and Cytarabine)
Antipurines (Mercaptopurine)

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33
Q

Antimetabolites (Folic acid antagonist (Methotrexate), Antipyrimidines (Fluorouracil and Cytarabine), Antipurines (Mercaptopurine))- MOA

A

Analogues of normal metabolites acting through competition, replacing the natural metabolite, subverting the cellular processes.

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34
Q

Methotrexate- MOA

A

Antimetabolite
Competitively antagonizes dihydrofolate reductase preventing regeneration of intermediates (tetrahydrofolate) essential for the synthesis of purine and thymidylate thus inhibiting the synthesis of DNA.

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35
Q

What must you administer daily with methotrexate?

A

1 mg folic acid

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36
Q

Methotrexate- ROA

A

Orally, IV, IM, IT intrathecal (into the spine)

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37
Q

Methotrexate- Indications

A 
Acute lymphoblastic leukemia
Non-Hodgkin’s lymphoma
Burkitt’s lymphoma
Rheumatoid arthritis
Psoriasis
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38
Q

Methotrexate- Monitoring

A

Chest X-ray q 6 months- infiltrates
LFTs q 6 months-long term use may lead to fibrosis
CBC

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39
Q

Methotrexate- Contraindications and cautions

A 
Pregnancy  (abortifacient) or breast feeding
Liver disease
Impaired renal function
Immunodeficiency syndrome
Pre-existing blood dyscrasias
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40
Q

Methotrexate- ADRs

A 
PULMONARY FIBROSIS
HEPATIC FIBROSIS, ACUTE TOXICITY, CIRRHOSIS
Leukopenia, thrombocytopenia
Neurotoxicity--Malaise, Fatigue, Dizziness, HA, Drowsiness, Seizures
N/V/D
Alopecia
Urticaria
Pruritus
hyperpigmentation
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41
Q

Fluorouracil (5-FU)- MOA

A

Antometabolite
Converted into a pyrimidine nucleotide, fluorodeoxyuridine monophosphate, inhibiting thymidylate synthetase impairing DNA synthesis.

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42
Q

Fluorouracil (5-FU)- ROA

A

IV usually, but can be administered orally or topically

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43
Q

Fluorouracil (5-FU)- Indications

A

Solid tumors
Malignant skin conditions
Palliative management of colon, rectal, ovarian or breast ca (not curing)
Superficial basal cell carcinoma

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44
Q

Fluorouracil (5-FU)- Contraindications

A

Bone marrow suppression

Impaired renal function

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45
Q

Fluorouracil (5-FU)- ADRs

A 
Confusion, disorientation, euphoria
Myocardial ischemia
Nystagmus
N/V/D
Leukopenia, thrombocytopenia, agranulocytosis
Alopecia, dermatitis
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46
Q

Cytarabine- MOA

A

Antimetabolite

converted intracellularly to a triphosphate form that inhibits DNA polymerase.

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47
Q

6-Mercaptopurine- MOA

A

Antimetabolite

MOA: converted into a purine nucleotide that impairs DNA synthesis.

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48
Q

What are the cytotoxic antibiotics?

A

Dactinomycin (actinomycin D)
Bleomycin (Blenoxane)
Doxorubicin (Adriamycin)
Daunorubicin (Cerubidine)

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49
Q

Cytotoxic antibiotics- Dactinomycin (actinomycin D), Bleomycin (Blenoxane), Doxorubicin (Adriamycin), Daunorubicin (Cerubidine))- MOA

A

Anthracycline antibiotics (doxorubicin/daunorubicin)-3 major activities depending on the type of cell; work best in the S and G2 phase.
Intercalation in DNA; binding cell membranes; generation of O2 radicals
Dactinomycin prevents transcription by interfering w/RNA polymerase
Bleomycin acts to fragment DNA chains.

50
Q

Cytotoxic antibiotics- Dactinomycin (actinomycin D), Bleomycin (Blenoxane), Doxorubicin (Adriamycin), Daunorubicin (Cerubidine))- ROA

A

IV

Doxorubicin can be given intravesically for bladder cancer

51
Q

Cytotoxic antibiotics- Dactinomycin (actinomycin D), Bleomycin (Blenoxane), Doxorubicin (Adriamycin), Daunorubicin (Cerubidine))- Indications

A

Dactinomycin is primarily used in pediatric cancers
Doxorubicin is used for acute leukemias, lymphomas and various solid tumors.
Bleomycin is used for lymphomas and some solid tumors.

52
Q

Cytotoxic antibiotics- Dactinomycin (actinomycin D), Bleomycin (Blenoxane), Doxorubicin (Adriamycin), Daunorubicin (Cerubidine))- ADRs

A

Generalized cytotoxicity
DOXORUBICIN PRODUCES DOSE-DEPENDENT CARDIOTOXICITY AS A RESULT OF IRREVERSIBLE FREE RADICAL DAMAGE TO THE MYOCARDIUM
BLEOMYCIN MAY CAUSE PULMONARY FIBROSIS

53
Q

What are the mitotic inhibitors- plant derived products?

A

Etoposide

Vinca alkaloids
Vincristine
Vinblastine
Vinorelbine

54
Q

Mitotic inhibitors- Etoposide, Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)- MOA

A

Act by binding tubulin and inhibiting the polymerization of microtubules which is necessary to form the mitotic spindle.
This prevents mitosis and arrests dividing cells at metaphase.

55
Q

Mitotic inhibitors- Etoposide, Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)- ROA

A

The vinca alkaloids are administered intravenously

Etoposide orally or IV

56
Q

Mitotic inhibitors- Etoposide, Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)- Indications

A

Mitotic inhibitors are used for:
Acute leukemia
Lymphomas
Some solid tumors

57
Q

Mitotic inhibitors- Etoposide, Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)- ADRs

A

Phlebitis or cellulitis if drug extravasates
N/V/D, alopecia
Vincristine produces little or no bone marrow suppression
Does cause:
NEUROLOGICAL EFFECTS
CAUSING PERIPHERAL NEUROPATHY
LEADING TO PARASTHESIAS
LOSS OF REFLEXES AND WEAKNESSES
Recovery from these side effects does occur but slowly.

58
Q

Mitotic inhibitors- Etoposide, Vinca Alkaloids (Vincristine, Vinblastine, Vinorelbine)- Contraindications

A

Never give vinca alkaloids intrathecally, is usually fatal.

59
Q

Taxanes- Paclitaxel (Taxol)- MOA and Indication

A

Mitotic inhibitors
Promotes polymerization and stabilization of microtubulesdysfunctionalcell death
Tx ovarian and breast cancer
Premedicate with benadryl and dexamethasone to prevent hypersensitivty rxn (dyspnea, urticaria, hypotension)

60
Q

Taxanes- Paclitaxel (Taxol)- Dose-limiting toxicity

A

Dose-limiting toxicity= neutropenia; treat with filgastim (granulocyte colony-stimulating factor)
V/D uncommon; alopecia; peripheral neuropathy are side effects that you can see.

61
Q

Procarbazine- MOA and ROA

A

Methylhydrazine derivative w/monoamine oxidase inhibitor actions and cytotoxicity.
It inhibits DNA and RNA synthesis by a mechanism that is unclear.
ROA- Oral

62
Q

Procarbazine- Indications

A

Hodgkin’s disease- part of MOPP

63
Q

Procarbazine- ADRs

A
  • Disulfiram-type reaction with ETOH

- N/V/D, neurotoxic (hallucinations to paresthesias), bone marrow depression (increased risk of infection)

64
Q

L-Asparaginase (Elspar)- MOA

A

Enzyme

  • Catalyzes the hydrolysis of l-asparagine to aspartic acid and ammonia.
  • L-glutamine also undergoes hydrolysis by this enzyme.
  • Depletion of exogenous asparagine and glutamine inhibits protein synthesis in cells lacking asparagine synthetase
65
Q

L-Asparaginase (Elspar)- Indications

A
  • Acute lymphoblastic leukemia-complete remission in 50-60% of patients
  • Lack of cross-resistance and bone marrow toxicity make the enzyme useful in combo tx.
  • Also used in some types of lymphoma
66
Q

L-Asparaginase (Elspar)- ADRs

A
  • Foreign protein– Hypersensitivity rxn, Urticaria, Anaphylaxis
  • GI–Nausea, Anorexia,Wt. Loss
  • Hepatotoxicity
  • CNS– Drowsiness/ Confusion, Impaired mentation/ Coma
  • Hyperglycemia w/inhibition of insulin synthesis
  • L-Asparaginase lacks bone marrow, GI and hair follicle toxicity.
67
Q

What is a benefit of L-Asparaginase (Elspar)?

A

It does not cause allopecia

68
Q

Cisplatin (Platinol)- MOA

A

Inorganic complex w/a broad range of antitumor activity
MOA:
Binds to DNA at nucleophilic sites, such as the N7 and O6 of guanine, producing alterations in DNA structure and inhibition of DNA synthesis.
Adjacent guanine residues on the same DNA strand are preferentially cross-linked. Very similar to alkylating agents.
Also binds to proteins.
Is not phase specific in the cell cycle.

69
Q

Cisplatin (Platinol)- pharmicokinetics

A

> 90% protein bound
Does not cross BBB (cannot be used in brain tumors)
Renally excreted (need dose adjustments for renal failure patients)

70
Q

Cisplatin (Platinol)- indications

A

W/bleomycin and vinblastine or etoposide produces cures in most pts. w/metastic testicular cancer or germ cell cancer of the ovary.
Some activity against carcinomas of the head and neck, bladder, cervix, prostate and lung.

71
Q

Cisplatin (Platinol)- ADRs

A
  • RENAL TOXICITY
  • Severe N/V possibly needing hospitalization
  • Mild bone marrow toxicity– Leukopenia, Thrombocytopenia, Anemia is common and may require transfusions of RBCs
  • Hearing loss in high frequencies in 10-30%
  • Peripheral neuropathies, paresthesias, leg weakness
  • Excessive urinary excretion of Magnesium.
72
Q

Carboplatin (Paraplatin)- MOA

A

Analogue of cisplatin

73
Q

Carboplatin (Paraplatin)- Kinetics

A

Plasma half life 3-5 hours (shorter than cisplatin)
No significant protein binding
Renally excreted

74
Q

Carboplatin (Paraplatin)- Indications

A

Ovarian carcinomas
Small cell lung cancers
Germ cell cancers of the testis
Most cancers resistant to cisplatin are cross-resistant to carboplatin.

75
Q

What is the advantage of using carboplatin over cisplatin?

A

reduced toxicity of the kidneys, peripheral nerves and hearing.
Less N/V
BUT More myelosuppressive

76
Q

Carboplatin (Paraplatin)- ADRs

A

Anemia
Abnormal liver fxn
Occ. Allergic rxns

77
Q

What is the major dose limiting toxicity of many chemotherapeutic drugs including alkylating agents, anthracyclines, and antimetabolites?

A

Myelosuppression
Limits many chemo regimens to dosing intervals of every 2-3 weeks or longer
Particularly affected are short lived WBCs and platelets (get leukopenia and thrombocytopenia)

78
Q

Suppression of the ANC below what increases the risk of infection?

A

<500 is really bad

79
Q

What might decreased myelosuppression?

A

May be decreased by employing a colony stimulating factor following chemotherapy
CSFs appear to act as intracellular signals to activate certain target cells

80
Q

What are the CSFs that stimulate neutraphils?

A

GM-CSF sargramostim (Leukine and Prokine)
G-CSF filgrastim (Neupogen)
PEG filgrastim (Neulasta)

81
Q

What are the CSFs that stimulate RBC?

A

Erythropoietin (EPO) and darbepoetin (Aranesp)

Use when Hgb is less than 10 and stop therapy when 12.

82
Q

CSFs- ADRs

A
  • All can cause bone pain

- GM-CSF may also cause rashes, fever and occasionally dyspnea and/or pulmonary edema

83
Q

What is febrile neutropenia?

A

Fever (> 38.3◦C) in conjunction with an ANC < 1000

84
Q

How can febrile neutropenia be prevented?

A

-Sterile technique when accessing central lines
-CSFs
Indicated when patient is receiving a chemotherapy regimen with a significant (> 40%) risk of febrile neutropenia

85
Q

What is the antibiotic treatment of febrile neutropenia?

A 
Management:
Hospitilization
Broad-spectrum abx
Cefepime 
Piperacillin + tazobactam
Imipenem or meropenem
Aminoglycoside + antipseudomonal penicillin (e.g. piperacillin)
Monotherapy no employed for severe infections
86
Q

What is the CSF treatment of febrile neutropenia?

A

Prophylaxis: continuation until ANC recovery for patients receiving a chemo regimen with high potential of causing FN
(If not instituted in a prophylactic manner) Begin at onset of FN

87
Q

What is the antifungal therapy of febrile neutropenia?

A
  • An fungicidal agent is usually initiated in patients with FN who are still febrile and neutropenic after 4-7 days of broad spec abx, or who develop sepsis unresponsive to broad spec abx
  • Most invasive fungal infections are due to candidiasis or aspergillosis
  • Amphotericin B (conventional or Liposomal- liposomal is how its prepared, its harder to dose due to preperation) (DOC)
88
Q

What is an extravasation injury?

A

Escape of chemotherapy agents into subcutaneous tissue, resulting in tissue injury

89
Q

What are the two types of extravasation injury?

A

Those that do not bind to tissue nucleic acids
Cause immediate tissue damage but are quickly metabolized or inactivated (similar to a burn)- need to be stopped
Vincristine, Vinblastine, mechlorethamine, and carmustine

Those that bind tissue nucleic acids
Cause immediate tissue injury and lodge in the tissues, binding to DNA and creating a more prolonged course
Results in most destructive damage, necrosis or skin and tissues
Anthracyclines (daunorubicin, doxorubicin), dactinomycin, mitomycin C
These are all chemotherapy abx.

90
Q

What is the prevention for extravasation injuries?

A
  • Indwelling central venous catheters are the best preventative measure
  • Flexible catheters are suggested
  • Best to admin through free flowing IV
  • Assure catheter is in vein just prior to admin- with xray
  • Stop infusion upon any complaint of burning, stinging, or if local swelling occurs
  • Intermittent ice packs and raise extremity
91
Q

What are the antidotes for extravasation injuries?

A

Controversial- but are still used
DMSO- dimethyl sulfoxide
Hyaluronidase: vinca alkaloid extravastion
Surgery- usually involves cutting off tissue.
Consult plastic surgery

92
Q

What is mucositis?

A

Mucosal injury from chemotherapy (Mucositisis the painfulinflammationandulcerationof themucous membraneslining thedigestive tract, usually as an adverse effect ofchemotherapyandradiotherapytreatment for cancer.)

93
Q

What is involved with mucositis?

A
  • Chemo or radiation interferes with mitosis
  • Usually lasts 3-5 days, seen 5-7 days after chemo or radiation
  • Most commonly associated with high dose methotrexate, 5-FU and anthracyclines
  • Virtually all patients who receive radiation to the head and neck
94
Q

What is the grading system for mucositis?

A

Grade 0- no mucositis
Grade 1- painless ulcers, erythema, or mild soreness
Grade 2- painful erythema, edema, or ulcers but can eat
Grade 3- the patient has painful erythema, edema, or ulcers and cannot eat
Grade 4- the patient requires parenteral or enteral support

95
Q

What mucousa is the most often affected in mucositis?

A

Mucosa most often affected is non-keratinized

Labial, buccal, soft palate, floor of mouth, ventral surface of tongue

96
Q

How do you prevent mucositis?

A

Correct any oral disease (poor hygiene, periodontal disease etc.)
CSFs following myelosuppressive chemotherapy may decrease severity and duration of mucositis
(Not initiated to treat mucositis but may help)

97
Q

Amifostine

A

Prevention of mucositis
Prodrug converted to an active sulfhydryl compound, that protects normal cells by scavenging free radicals and binding to active metabolites
Decreases frequency nephrotoxicity, ototoxicity, and myelosuppression from cisplatin
ADR: hypotension, N/V, may decrease effect of chemo or radiation

98
Q

Palifermin

A

Prevention of mucositis

Synthetic keratinocyte growth factor (single course therapy ~ $9,900)

99
Q

What are the places that tumors inhibit that drive hormone dependent tumors and should be removed surgically?

A

Glands
Adrenals
Pituitary

100
Q

What are the hormone derivatives?

A 
Prednisone
Tamoxifen (Nolvadex)
Flutamide (Eulexin)
Buserelin (Suprefact)
Leuprolide (Lupron)
Estrogens
101
Q

Prednisone- Indications

A

Adrenalcorticol steroids
Indications in cancer use
Inhibit the growth of cancers of the lymphoid tissues and blood
Treat some of the complications associated with cancer

102
Q

Tamoxifen (Nolvadex)- MOA

A

Estrogen Antagonist (hormone derivative)

  • Normally estrogens bind to cytoplasmic protein receptors forming hormone-receptor complex which induces the synthesis of ribosomal RNA and messenger RNA.
  • Binds to estrogen receptors and competes w/endogenous estrogens.
  • The drug-receptor complex has little or not estrogen agonist activity.
  • Tamoxifen directly inhibits growth of human breast cancer cell that contain estrogen receptors.
103
Q

Tamoxifen (Nolvadex)- Indications

A

Synthetic antiestrogen used in the treatment of breast cancer.

104
Q

Tamoxifen (Nolvadex)- kinetics

A
  • Slowly absorbed-maximum serum levels achieved 4-7 hours after oral admin.
  • Drug concentrate where estrogen receptors are located such as: Ovaries, Uterus, Vaginal epithelium, Breast
  • Drug is metabolized through hydoxylation (not a lot of drug indications) and glucuronidation of the aromatic rings.
  • Excretion in the feces.
105
Q

Tamoxifen (Nolvadex)- ADRs

A
  • Hot flashes
  • Vaginal dryness or discharge
  • Nausea
  • Exacerbation of bone pain and hypercalcemia may occur.
106
Q

What percent of women with ER-Positive will have a remission with tamoxifen?

A

60% of women w/ER-positive will have a remission as opposed to 10% w/ER-negative tumors.

107
Q

Flutamide (Eulexin)- MOA

A

Hormone derivative

  • Nonsteroidal antiandrogen that competes w/testosterone for binding to androgen receptors.
  • Flutamide prevents the stimulation of tumor growth that may occur as a result of the transient increase in testosterone secretion after the initiation of leuprolide therapy.
108
Q

Flutamide (Eulexin)- indications

A

Used to treat cancer of the prostate in conjunction w/pharmacologic castration produced by the gonadotropen-releasing hormone (GnRH) agonist Leuprolide

Drug is well absorbed orally

109
Q

Flutamide (Eulexin)- ADRs

A
  • Hot flashes- usually males don’t experience this but they can do to the anti-testosterone effects
  • Loss of libido
  • Impotence
  • N/D
110
Q

Buserelin (Suprefact) and Leuprolide (Lupron)- MOA

A

Hormone derivative

  • Peptide analogues of the hypothalmic hormone, Luteinizing hormone-releasing hormone (LH-RH).
  • Chronic exposure of the pituitary to theses agents abolishes gonadotropin release and results in markedly decreased estrogen and testosterone production by the gonads.
111
Q

Buserelin (Suprefact) and Leuprolide (Lupron)- indication and ADRs

A

Indication
Palliative hormonal therapy of prostate cancer
ADRs
Hot flashes

112
Q

Buserelin (Suprefact) and Leuprolide (Lupron)- Therapeutic note

A

Leuprolide is a potent LH-RH agonist for the first several days to a few weeks after initiation of therapy. It initially stimulates testosterone production. Therefore it should be used in combination w/flutamide.

113
Q

Estrogens

A

Hormone derivative

  • Diethylstilbestrol (a form of estrogen- used to be used for menopause)
  • Has an antiandrogenic effect used to suppress androgen-dependent prostatic cancers.
114
Q

What are the approaches for immunomodulating agents?

A
  • Tumor specific monoclonal antibodies to target drugs specifically to cancerous cells .
  • Vaccines to provide non-specific immunostimulation.
  • Vaccines prepared using tumor cells from similar cancers to raise an adaptive immune response against the cancer.
  • Drugs for immunostimulation
  • Cytokines to regulate the immune response to target cancer. Cytokines include interferon alpha, interleukin-2, and tumor necrosis factor.
  • Use of recombinant colony stimulating factors to reduce the level and duration of neutropenia
  • Recombinant human granulocyte colony-stimulating factor promoting the development of hematopietic stem cells in the marrow. Raises WBC but has not been shown to increase overall survival.
115
Q

What is the function of interferons?

A

Immunomodulating agent

Can reduce the rate of some cancerous tumors and leukemias

116
Q

What is the function of interleukins?

A

Immunomodulating agent

Activate lymphocytes to destroy cancer cells

117
Q

Interferon Alfa 2b (Intron A)- MOA

A

Recombinant DNA derived from the interferon alfa-2b gene of human WBCs
MOA: binding to plasma membrane receptor but unclear.
Plasma half-life 2-3 hours after parenteral administration

118
Q

Interferon Alfa 2b (Intron A)- Indications

A

RARE FORM OF CHRONIC LEUKEMIA (PRIME INDICATION)
HAIRY CELL LEUKEMIA- REMISSIONS IN 60-80% OF PATIENTS (PRIME INDICATION)
Remissions lasting a few months in 10-20% of patients being treated for:
Lymphomas
Multiple myeloma
Melanoma
Renal cell carcinoma
Ovarian carcinoma

119
Q

Interferon Alfa 2b (Intron A)- ADRs

A

FEVER
FLULIKE SYNDROME–Muscle aches, Fatigue, HA, Anorexia, N/D

Other effects
Leukopenia
Diarrhea
Dizziness

120
Q

Interleukins- Aldesleukin (IL-2, Proleukin) and Human recombinant interleukin-2 protein- MOA

A

enhancement of T-lymphocyte cytotoxicity,
induction of natural killer cell activity
induction of interferon gamma production.

121
Q

Interleukins- Aldesleukin (IL-2, Proleukin) and Human recombinant interleukin-2 protein- ADRs

A
  • FATALITY RATE OF 5%
  • SEVERE HPOTN IN 85% OF PATIENTS WHICH -MAY LEAD TO MIs, PULMONARY EDEMA, AND STROKES (HPOTN is thought to be due to a capillary leak syndrome.)
  • N/V/D
  • Stomatitis
  • Anorexia
  • Altered mental status
  • Fevers and fatigue.
  • Avoid in patients w/cardiac, pulmonary, renal, hepatic or CNS condition.
122
Q

What antiemetics are commonly used in cancer patients?

A

Ondansetron and dexamethasone

Pharmacology III (19 decks)

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