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PT 2 > Block 10 - L1-L2 > Flashcards

Block 10 - L1-L2 Flashcards

1
Q

What are the 3 general goals of chemotherapy?

A
  1. Eradicate a cancer (overt or covert)
  2. Prevent the death of the patient
  3. Prolong the life of the patient
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2
Q

What is transformation?

A

Change to the malignant phenotype

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3
Q

Cancer is an accumulation of ___, and is a multi-step process.

A

Genetic alterations

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4
Q

What are the phases of the cell cycle?

A

G0 - non-dividing
G1 - synthesis of components needed for DNA synthesis
S - DNA synthesis
G2 - synthesis of components needed for mitosis
M - mitosis

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5
Q

Define the subclinical or latent phase of the growth of a cancer.

A

The time from the inception of a cancer (transformation of a single cell) to the time that the tumor becomes clinically detectable (at least one billion cells)

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6
Q

List the properties that
can develop during the subclinical or latent period that determine the biology of the cancer and the outcome with treatment.

A

Tumor cell heterogeneity:

  1. Growth fraction (dividing cells/total cell number)
  2. Metastatic potential and metastatic process
  3. Resistance/sensitivity to chemotherapy
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7
Q

True or false - cancer cannot be detected during the latent phase.

A

True

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8
Q

What is defined as the primary site of the cancer?

A

The organ in which the cancer begins

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9
Q

What are the 4 steps of the metastatic process?

A
  1. Clonal evolution
  2. Intravasation
  3. Extravasation
  4. Growth in the distant metastatic site
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10
Q

What indicates the extent of disease at the time of diagnosis and determines prognosis and treatment?

A

Stage of cancer

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11
Q

What is the usual staging system?

A

TNM classification

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12
Q

What are the three basic stages of cancer?

A
  1. Local (to the organ of origin)
  2. Local-regional (localized to the organ of origin with spread to the regional draining lymph nodes)
  3. Metastatic (disseminated)
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13
Q

What is the Skipper Hypothesis?

A

The ability of chemotherapy to cure is inversely proportional to the tumor burden

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14
Q

What accounts for the failure of chemotherapy to completely eradicate a malignant process?

A

Resistance to chemotherapy

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15
Q

List the available types of treatment for cancer?

A
  1. Surgery
  2. Radiation therapy
  3. Chemotherapy (drugs)
  4. Other localized therapies such as embolization, radiofrequency ablation, and regional organ perfusion
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16
Q

What is the Goldi-Coldman hypothesis?

A

The probability that a cancer would contain drug-resistant clones depends on the mutation rate and the size of the tumor

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17
Q

What is chemotherapy?

A

Drugs given to patients with a malignant process that are designed and selected to kill mammalian cells

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18
Q

What is the difference between cytotoxicity and toxicity?

A

Cytotoxicity - MOA of killing cells

Toxicity - adverse effects

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19
Q

List the categories of response to chemotherapy.

A
  1. Complete remission
  2. Partial remission (>50% reduction)
  3. Stable disease
  4. Progression of disease
  5. Cure - 100% of cells were chemosensitive
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20
Q

Define the three phases of drug development and state the goals of each of the phases.

A
  1. Preclinical testing (drug structure, MOA, etc.)
  2. Phase I clinical trials (determine dose, dose-limiting toxicity)
  3. Phase II clinical trials (determine activity)
  4. Phase III clinical trials (determine efficacy)
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21
Q

List the constitutional toxicities of chemotherapy.

A
  1. N/V
  2. Loss of appetite
  3. Fatigue
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22
Q

List the toxicities of chemotherapy due to the effect of chemotherapy on the normal dividing cells.

A
  1. Transient myelosuppression
  2. Temporary hair loss
  3. Mucositis or sore mouth, or diarrhea
  4. Sterility
  5. Secondary neoplasms
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23
Q

Define myelosuppression.

A

Depression of blood cell counts

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24
Q

Which chemo drug can cause cardiac toxicity?

A

Anthracyclines

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25
Q

Which chemo drug can cause pulmonary toxicity?

A

Bleomycin

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26
Q

Which chemo drug can cause nephrotoxicity?

A

Cis-DDP

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27
Q

How is the absolute neutrophil count calculated?

A

ANC = WBC x (% neutrophils + % bands)

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28
Q

List the pharmacologic agents available to ameliorate nausea and emesis.

A
  1. Prochlorperazine
  2. Ondansetron/Granisetron (5-HT3 receptor antagonists)
  3. Lorazepam (anticipatory)
  4. Aprepitant (highly emetogenic regimens)
  5. Dexamethasone
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29
Q

List the pharmacologic agents available to ameliorate neutropenia.

A

Colony stimulating factors (filgrastim - G-CSF)

Also - infection precautions, broad spectrum antibiotics if febrile neutropenia

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30
Q

What is stomatitis?

A

Inflammation of the mucus membranes of the oral cavity

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31
Q

What is cumulative toxicity?

A

A small amount of irreversible damage is done to an organ with each administration of a drug. With repeated administrations, the damage accumulates and a clinical problem with the function of the organ occurs.

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32
Q

Some chemo drugs are vesicants - what does this mean?

A

Substance that causes tissue blistering

33
Q

What is the general MOA and cell cycle target of alkylating agents?

A

MOA - bind covalently to the DNA, alkylate N-7 of guanine, causing interstrand and intrastrand crosslinks, which interfere with DNA synthesis

CCNS

34
Q

What can cause resistance to alkylating agents?

A
  1. Enhanced DNA repair

2. Binding to sulfur containing molecules (inactivate the drug)

35
Q

Does cyclophosphamide require bioactivation? If so, how?

A

Yes - microsomal enzymes (P-450 oxidase) convert the drug to aldophosphamide; this is cleaved to acrolein and phosphoramide mustard, the active compound

36
Q

What is the MOA of cyclophosphamide, once activated?

A

Phosphoramide mustard bifunctionally alkylates the N7 position of guanine, forms crosslinks

37
Q

How is cyclophosphamide excreted?

A

In the urine

38
Q

What are the AE of cyclophosphamide? What is dose-limiting?

A

AE - N/V, hair loss, myelosuppression, hematuria, (occasional occurrence of acute leukemia)

DL - myelosuppression

39
Q

What causes hematuria in cyclophosphamide use and how can it be mitigated?

A

Metabolites of the drug are toxic to the urothelium; mitigate via administration of the drug in the morning, frequent urination, and maintaining hydration

40
Q

What are the indications of cyclophosphamide?

A

Breast cancer

Non-Hodgkin’s lymphoma

41
Q

How is cyclophosphamide administered?

A

IV or oral

42
Q

What is a more potent isomer of cyclophosphamide?

A

Ifosfamide

43
Q

What are the AE of ifosfamide? What is dose-limiting?

A

AE - N/V, hair loss, myelosuppression, lethargy and confusion at high doses

DL - myelosuppression

44
Q

Why is ifosfamide always coadministered with mesna? What is its MOA?

A

Prevent hematuria

Mesna is a dimer in the blood and cell, and is not active; it becomes a monomer in urine and binds metabolites of ifosfamide to prevent toxic effect on urothelium

45
Q

What are the indications of ifosfamide?

A

Sarcoma

testicular cancer

46
Q

Cyclophosphamide and ifosfamide are bifunctional alkylating agents - what is a monofunctional alkylating agent?

A

Temozolomide

47
Q

How does Temozolomide differ from the other alkylating agents in its activation?

A

Spontaneously hydrolyzed, no enyzmes needed for bioactivation

48
Q

What are the AE of Temozolomide?

A

N/V, hair loss, myelosuppression

49
Q

When Temozolamide is given over a prolonged period of time, what prophylactic treatment must be given?

A

Prophylaxis for PJP pneumonia

50
Q

What are the indications for Temozolomide?

A

Primary malignant brain tumors (glioblastoma)

51
Q

What are platinum coordination compounds?

A

Non-classical DNA alkylating agents that covalently bind to DNA

Cisplatin
Carboplatin
Oxaliplatin

52
Q

What is the cell-cycle specificity of the Pt coordination compounds?

A

CCNS

53
Q

What is the MOA of the Pt coordination compounds?

A

The pro-drug undergoes a series of aquations in which the Chloride leaves, ultimatley forming the di-aquo form, which binds covalently to DNA to produce cytotoxic interstrand and intrastrand crosslinks

Di-chloro form is favored in blood

Di-aquo is favored in the cell (becomes charged and cannot leave the cell easily)

54
Q

What are the AE of cisplatin? What is dose limiting?

A

AE - Intense N/V, myelosuppression, renal toxicity, hypomagnesemia, peripheral neuropathy, 8th CN damage leading to high frequency hearing loss, allergic reactions

DL - renal toxicity

55
Q

Why is renal damage significant in cisplatin treatment, and what can be done?

A

Both nephrotoxic and renally cleared

Give with saline/mannitol diuresis (may lead to contraindication in patients with pre-existing cardiac and pulmonary problems)

Dose reductions for patients with renal insufficiency

56
Q

What are the indications of cisplatin and carboplatin?

A 
Testicular cancer (curative)
Bladder cancer
Head and neck cancer
Ovarian cancer
Small cell and non-small cell lung cancer
57
Q

How does carboplatin differ from cisplatin?

A

NOT nephrotoxic

DL - myelosuppression

58
Q

How is carboplatin dosed and why?

A

Targeted AUC due to the linear relationship between clearance and GFR

Dose (mg) = AUC x (GFR + 25)

59
Q

How does oxaliplatin differ from carboplatin in regard to AE?

A

NOT nephrotoxic

DL - neurotoxicity

(AE - N/V, myelosuppression, neurotoxicity, including acute neuropathy (cold-induced paresthesias, laryngeal dysesthesia) and chronic neuropathy (cumulative stocking glove paresthesia))

60
Q

What is the indication for oxaliplatin?

A

Colorectal cancer

61
Q

List the plant alkaloids.

A

Vincristine, Vinblastine, Vinorelbine

Paclitaxel, albumin bound paclitaxel, docetaxel, cabataxel, etoposide

62
Q

Which part(s) of the cell cycle do Vincristine, Vinblastine, Taxol target?

A

CCS - M

63
Q

What is the MOA of Vincristine/Vinblastine?

A

Inhibition of mitotic spindle formation

64
Q

What are the AE of vincristine? DL? Compare these to those of vinblastine.

A

AE - sensory and autonomic neuropathies, hyponatremia due to ADH stimulation (NO myelosuppresion, hair loss, N/V)

DL - neuropathy

Vinblastine is much less neurotoxic, DL is myelosuppression

65
Q

When must the dose of vincristine be reduced?

A

Elevated bilirubin

66
Q

What are the indications of vincristine?

A

Lymphoma
Hodgkin’s disease
Lymphoblastic leukemia

67
Q

What is vinorelbine indicated for?

A

Lung cancer

Breast cancer

68
Q

What is the MOA of Paclitaxel (and other taxols)?

A

Prevents tubulin disassembly

69
Q

What are the AE and DL of Paclitaxel?

A

AE - myelosuppression, N/V, stomatitis, peripheral sensory neuropathy, myalgias, arthralgias, hair loss

DL - myelosuppression

70
Q

What are the special features/dose modifications of Paclitaxel?

A
  1. Pre-mediate with steroids, diphenhydramine, H2 blocker

2. Dose reduction for hepatic dysfunction

71
Q

What are the indications of paclitaxel?

A

Ovarian cancer
Non-small cell lung cancer
Gastoesophageal cancer
Breast cancer

72
Q

How does albumin bound paclitaxel differ from paclitaxel?

A

There is NO hypersensitivity reaction, less myelosuppression, and less peripheral neuropathy

73
Q

What is the indication of docetaxel?

A

Prostate cancer (combined with prednisone)

74
Q

What is the indcation of cabazitaxel?

A

Prostate cancer

75
Q

What is the cell cycle specificity and MOA of etoposide?

A

G1/S

Inhibition of topoisomerase II, causing DNA strand breakage

76
Q

What are the AE and DL of Etoposide?

A

N/V, hair loss, myelosuppression, leukemia (rarely)

DL - myelosuppression

77
Q

What dose reduction is needed for etoposide?

A

Kidney and liver dysfunction

78
Q

What is the indication of etoposide?

A

Testicular cancer
Small cell lung cancer
Lymphomas

PT 2 (15 decks)

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