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PT 2 > Block 10 - L1-L2 > Flashcards

Block 10 - L1-L2 Flashcards

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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
Which chemo drug can cause pulmonary toxicity?
Bleomycin
26
Which chemo drug can cause nephrotoxicity?
Cis-DDP
27
How is the absolute neutrophil count calculated?
ANC = WBC x (% neutrophils + % bands)
28
List the pharmacologic agents available to ameliorate nausea and emesis.
1. Prochlorperazine 2. Ondansetron/Granisetron (5-HT3 receptor antagonists) 3. Lorazepam (anticipatory) 4. Aprepitant (highly emetogenic regimens) 5. Dexamethasone
29
List the pharmacologic agents available to ameliorate neutropenia.
Colony stimulating factors (filgrastim - G-CSF) Also - infection precautions, broad spectrum antibiotics if febrile neutropenia
30
What is stomatitis?
Inflammation of the mucus membranes of the oral cavity
31
What is cumulative toxicity?
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.
32
Some chemo drugs are vesicants - what does this mean?
Substance that causes tissue blistering
33
What is the general MOA and cell cycle target of alkylating agents?
MOA - bind covalently to the DNA, alkylate N-7 of guanine, causing interstrand and intrastrand crosslinks, which interfere with DNA synthesis CCNS
34
What can cause resistance to alkylating agents?
1. Enhanced DNA repair | 2. Binding to sulfur containing molecules (inactivate the drug)
35
Does cyclophosphamide require bioactivation? If so, how?
Yes - microsomal enzymes (P-450 oxidase) convert the drug to aldophosphamide; this is cleaved to acrolein and phosphoramide mustard, the active compound
36
What is the MOA of cyclophosphamide, once activated?
Phosphoramide mustard bifunctionally alkylates the N7 position of guanine, forms crosslinks
37
How is cyclophosphamide excreted?
In the urine
38
What are the AE of cyclophosphamide? What is dose-limiting?
AE - N/V, hair loss, myelosuppression, hematuria, (occasional occurrence of acute leukemia) DL - myelosuppression
39
What causes hematuria in cyclophosphamide use and how can it be mitigated?
Metabolites of the drug are toxic to the urothelium; mitigate via administration of the drug in the morning, frequent urination, and maintaining hydration
40
What are the indications of cyclophosphamide?
Breast cancer | Non-Hodgkin's lymphoma
41
How is cyclophosphamide administered?
IV or oral
42
What is a more potent isomer of cyclophosphamide?
Ifosfamide
43
What are the AE of ifosfamide? What is dose-limiting?
AE - N/V, hair loss, myelosuppression, lethargy and confusion at high doses DL - myelosuppression
44
Why is ifosfamide always coadministered with mesna? What is its MOA?
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
What are the indications of ifosfamide?
Sarcoma | testicular cancer
46
Cyclophosphamide and ifosfamide are bifunctional alkylating agents - what is a monofunctional alkylating agent?
Temozolomide
47
How does Temozolomide differ from the other alkylating agents in its activation?
Spontaneously hydrolyzed, no enyzmes needed for bioactivation
48
What are the AE of Temozolomide?
N/V, hair loss, myelosuppression
49
When Temozolamide is given over a prolonged period of time, what prophylactic treatment must be given?
Prophylaxis for PJP pneumonia
50
What are the indications for Temozolomide?
Primary malignant brain tumors (glioblastoma)
51
What are platinum coordination compounds?
Non-classical DNA alkylating agents that covalently bind to DNA Cisplatin Carboplatin Oxaliplatin
52
What is the cell-cycle specificity of the Pt coordination compounds?
CCNS
53
What is the MOA of the Pt coordination compounds?
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
What are the AE of cisplatin? What is dose limiting?
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
Why is renal damage significant in cisplatin treatment, and what can be done?
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
What are the indications of cisplatin and carboplatin?
``` Testicular cancer (curative) Bladder cancer Head and neck cancer Ovarian cancer Small cell and non-small cell lung cancer ```
57
How does carboplatin differ from cisplatin?
NOT nephrotoxic | DL - myelosuppression
58
How is carboplatin dosed and why?
Targeted AUC due to the linear relationship between clearance and GFR Dose (mg) = AUC x (GFR + 25)
59
How does oxaliplatin differ from carboplatin in regard to AE?
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
What is the indication for oxaliplatin?
Colorectal cancer
61
List the plant alkaloids.
Vincristine, Vinblastine, Vinorelbine Paclitaxel, albumin bound paclitaxel, docetaxel, cabataxel, etoposide
62
Which part(s) of the cell cycle do Vincristine, Vinblastine, Taxol target?
CCS - M
63
What is the MOA of Vincristine/Vinblastine?
Inhibition of mitotic spindle formation
64
What are the AE of vincristine? DL? Compare these to those of vinblastine.
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
When must the dose of vincristine be reduced?
Elevated bilirubin
66
What are the indications of vincristine?
Lymphoma Hodgkin's disease Lymphoblastic leukemia
67
What is vinorelbine indicated for?
Lung cancer | Breast cancer
68
What is the MOA of Paclitaxel (and other taxols)?
Prevents tubulin disassembly
69
What are the AE and DL of Paclitaxel?
AE - myelosuppression, N/V, stomatitis, peripheral sensory neuropathy, myalgias, arthralgias, hair loss DL - myelosuppression
70
What are the special features/dose modifications of Paclitaxel?
1. Pre-mediate with steroids, diphenhydramine, H2 blocker | 2. Dose reduction for hepatic dysfunction
71
What are the indications of paclitaxel?
Ovarian cancer Non-small cell lung cancer Gastoesophageal cancer Breast cancer
72
How does albumin bound paclitaxel differ from paclitaxel?
There is NO hypersensitivity reaction, less myelosuppression, and less peripheral neuropathy
73
What is the indication of docetaxel?
Prostate cancer (combined with prednisone)
74
What is the indcation of cabazitaxel?
Prostate cancer
75
What is the cell cycle specificity and MOA of etoposide?
G1/S Inhibition of topoisomerase II, causing DNA strand breakage
76
What are the AE and DL of Etoposide?
N/V, hair loss, myelosuppression, leukemia (rarely) DL - myelosuppression
77
What dose reduction is needed for etoposide?
Kidney and liver dysfunction
78
What is the indication of etoposide?
Testicular cancer Small cell lung cancer Lymphomas

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