Oncology Treatment Flashcards

1
Q

Primary vs. Adjuvant vs. Neoadjuvant chemo

A
  1. Primary - used w/o surgery
  2. adjuvant - used after surgery
  3. neoadjuvant - used before surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Constitutional S/E of Chemotherapy

A
  1. weight loss
  2. fever
  3. chills
  4. anaphylactic reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hematologic S/E of Chemotherapy

A
  1. pancytopenia

2. associated infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

HEENT S/E of Chemotherapy

A
  1. headaches
  2. mucositis
  3. thrush
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Skin S/E of Chemotherapy

A
  1. rash
  2. hyperpigmentation
  3. desquamation
  4. edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cardiac S/E of Chemotherapy

A
  1. CHF

2. arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pulmonary S/E of Chemotherapy

A
  1. pneumonitis

2. pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

GI S/E of Chemotherapy

A
  1. N/V
  2. diarrhea
  3. constipation
  4. bowel obstruction
  5. mucositis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

renal S/E of Chemotherapy

A
  1. acute kidney injury

2. chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Urinary S/E of Chemotherapy

A
  1. hemorrhagic cystitis
  2. urine discoloration
  3. painful urination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

reproductive S/E of Chemotherapy

A
  1. infertility

2. premature ovarian failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Musculoskeletal S/E of Chemotherapy

A
  1. weakness
  2. motor neuropathy
  3. fractures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neurological S/E of Chemotherapy

A
  1. neuropathy
  2. confusion
  3. seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Psychiatric S/E of Chemotherapy

A
  1. depression
  2. anxiety
  3. anticipatory nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Alkalating Agents examples

A
  1. cyclophosphamide

2. bendamustine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Alkalating Agents MOA

A

interfere with DNA replication to prevent cells from reproducing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Alkalating Agents are derived from what

A

nitrogen mustards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Alkalating Agents indications

A
  1. solid (lung, breast, ovary)

2. hematologic (leukemia, lymphoma, multiple myeloma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Alkalating Agents S/E

A
  1. hemorrhagic cystitis
  2. pancytopenia
  3. secondary malignancy (leukemia MC)
  4. alopecia
  5. N/V
  6. kidney injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alkalating Agents metabolism

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Do Alkalating Agents cross the blood brain barrier

A

only bendamustine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Alkalating Agents long term effects

A
  1. secondary malignancy
  2. leukemia
  3. ovarian failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antimetabolites examples

A
  1. methotrexate
  2. fluorouracil
  3. mercaptopurine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Antimetabolites MOA

A

interferes w/ RNA/DNA replication by limiting metabolites necessary for cell division (ie. folic acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Antimetabolites indications

A
  1. solid (sarcoma, breast, ovary, GI)

2. hematologic (CNS leukemia/lymphoma IT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Antimetabolites SE

A
  1. alopecia
  2. GI stomatitis
  3. liver dysfunction
  4. renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Antimetabolites metabolism

A

kidney and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

do Antimetabolites cross the blood brain barrier?

A

yes, high dose methotrexate (used as monotherapy for CNS lymphoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Antimetabolites long term effects

A
  1. infertility
  2. cirrhosis
  3. kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Other uses for methotrexate

A
  1. psoriasis
  2. lupus
  3. RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

methotrexate in pregnancy?

A

teratogenic, causes demise of fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

methotrexate route of chemo administration

A

intrathecal (given in CSF fluid to prevent cells from spreading across blood brain barrier)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Anthracycline example

A

doxorubicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

doxorubicin MOA

A

interfere w/ DNA by stopping cell division by interfering with coiling of double helix structure

kills cancer and healthy cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

doxorubicin indications

A
  1. leukemia
  2. lymphoma
  3. solid tumors (breast, lung, stomach, thyroid, sarcoma)
    - -> very common in breast cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

doxorubicin SE

A
  1. cardiotoxicity (acute rhythm abnormalities, CHF and delayed CHF) –> constrictive cardiomyopathy!!
  2. myelosuppression
  3. nausea
  4. alopecia
  5. mucositis
  6. tissue necrosis if infiltrated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

doxorubicin metabolism

A

GI and renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

does doxorubicin cross the blood brain barrier?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

long term monitoring for doxorubicin

A

echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

special consideration for doxorubicin

A

need echo prior to every other dose of chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Bleomycin MOA

A

damages DNA (G2 phase cell cycle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Bleomycin indications

A
  1. Hodgkin’s lymphoma

2. solid tumors (head/neck, cervis, testis, bladder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what kind of cell is pathonomonic for Hodgkin’s lymphoma?

A

Reed-Sternberg cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Bleomycin SE

A
  1. pneumonitis
  2. cutaneous peeling, erythema, hyperpigmentation usually on pales/soles
  3. N/V
  4. hypersensitivity (give test dose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Bleomycin metabolism

A

through tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

does Bleomycin cross the BBB?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Bleomycin special consideration

A

PFTs prior to initiation and throughout treatment, pulmonary fibrosis may be fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Vinca Alkaloids indications

A
  1. leukemia
  2. lymphoma
  3. testicular cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Vinca Alkaloids examples

A
  1. vincristine

2. vinblastine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Vinca Alkaloids MOA

A

interferes with formation of microtubules necessary for mitosis “M phase”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

caution for Vinca Alkaloids

A

fatal if given intrathecally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Vinca Alkaloids SE

A
  1. severe neuropathy (most significant, usually stocking-glove, usually reversible but can be permanent)
  2. constipation
  3. myelosuppression
  4. alopecia
  5. N/V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Taxanes examples

A
  1. paclitaxel

2. docetaxel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Taxanes MOA

A

stop microtubules from breaking down, cell becomes overcrowded and cannot divide (M phase)

55
Q

Taxanes indications

A
  1. breast
  2. lung
  3. prostate
  4. ovarian
  5. Kaposi’s sarcoma (AIDs)
56
Q

Taxanes SE

A
  1. neurotoxicity - confusion, headache, seizure
  2. peripheral neuropathy
  3. fluid retention
  4. hypersensitivity reaction
57
Q

Taxanes metabolism

A

liver

58
Q

do Taxanes cross the BBB?

A

no

59
Q

long term effects of Taxanes

A

neuropathy

60
Q

Examples of platinum compounds

A
  1. carboplatin
  2. cisplatin
  3. oxaliplatin
61
Q

platinum compounds MOA

A

damage DNA

62
Q

platinum compounds SE

A
  1. oxaliplatin - spasm with cold exposure
  2. nephrotoxicity
  3. neurotoxicity
  4. ototoxicity
  5. peripheral neuropathy
  6. myelosuppression
63
Q

platinum compounds metabolism

A

renal - carboplatin dose adjusted every time based on renal function of the patient that day

64
Q

platinum compounds long term effects

A
  1. neuropathy
  2. hearing difficulties
  3. infertility
65
Q

Red flag for what drug if you see lung toxicity in primary care

A

bleomycin

66
Q

Red flag for what drug if you see cardiomyopathy in primary care

A

doxorubicin

67
Q

Red flag for what drug if you see secondary malignancy in primary care

A

cyclophosphamide

68
Q

Red flag for what drug if you see hemorrhagic cystitis

A

Ifosfamide/cyclophosphamide

69
Q

Red flag for what drug if you see neurotoxicity in primary care

A
  1. cisplatin
  2. taxanes
  3. vinca alkaloids
70
Q

Red flag for what drug if you see kidney failure in primary care

A
  1. cisplatin

2. high dose methotrexate

71
Q

what are molecular targeted therapies?

A

drugs that block the growth and spread of cancer by interfering with specific receptors that are on the cancer cells that are involved with growth or spread of cancer

72
Q

types of targeted molecular therapy and routes of delivery

A
  1. monoclonal antibodies - injection or infusion

2. small molecules (can pass through cell wall) - pill

73
Q

what are monoclonal antibodies? how are they made?

A

delivery system for transmitting a drug, antigen injected into animal –> animal makes antibodies –> antibodies are taken off the cells and developed into drug

74
Q

BRAF-MEK inhibitors indication

A

melanoma

75
Q

BRAF-MEK inhibitors SE

A
  1. secondary malignancy
  2. hemorrhage
  3. HTN
  4. visual changes
  5. GI
  6. fetal toxicity
76
Q

Trastuzumab (Herceptin) indications

A

HER2 positive breast cancer

77
Q

Trastuzumab (Herceptin) SE

A

CHF

78
Q

BCR-ABL kinase inhibitors indication

A

CML / ALL (CML is a translocation)

79
Q

what drug class is tamoxifen

A

selective estrogen receptor modulator

80
Q

who is tamoxifen used in?

A
  1. pre-menopausal women

2. if aromatase inhibitors are contraindicated

81
Q

tamoxifen MOA

A

inhibits growth of breast cancer cells by acting as competitive antagonist of estrogen receptor

82
Q

tamoxifen SE

A
  1. VTE
  2. NASH
  3. sexual dysfunction
  4. hot flashes
  5. vaginal discharge
  6. menstrual irregularities
  7. endometrial hyperplasia
83
Q

is tamoxifen used alone or in combo?

A

either - alone or in combo with chemo or targeted therapy

84
Q

length of tamoxifen treatmetn

A

minimum of 5 years, may be 10 years if high risk

85
Q

tamoxifen indication

A

estrogen receptor and/or progesterone receptor positive breast cancer

86
Q

who should aromatase inhibitors be used in ?

A

1, postmenopausal women

2. premenopausal high risk

87
Q

aromatase inhibitors example

A

anastrazole

88
Q

aromatase inhibitors MOA

A

suppressed plasma estrogen levels by inactivating aromatase (which converts androgens to estrogens)

89
Q

aromatase inhibitors SE

A
  1. MSK (carpal tunnel)
  2. joint pain/stiffness
  3. osteoporosis
  4. CV disease long term
  5. sexual dysfunction
90
Q

aromatase inhibitor length of treatment

A

minimum of 5 year

91
Q

length of effect of aromatase inhibitors

A

improves outcomes up to 10 years

92
Q

indications for gonadotropin-releasing hormone agonists

A

advanced prostate cancer

93
Q

gonadotropin-releasing hormone agonist examples

A
  1. Leuprolide (Lupron)

2. Gosrelin (Zoladex)

94
Q

gonadotropin-releasing hormone agonist MOA

A

potent inhibitor of gonadotropin release

95
Q

gonadotropin-releasing hormone agonists SE

A
  1. sexual dysfunction
  2. osteoporosis/fractures
  3. hot flashes
  4. loss of lean body mass
  5. fatigue, anemia
  6. gynecomastia
  7. emotional/cognitive changes / confidence issues
  8. altered personality
96
Q

gonadotropin-releasing hormone agonist treatment schedule

A

do intermittent to decrease SE

every other month or every 3 months

97
Q

benefit of gonadotropin-releasing hormone agonists

A

help with bone pain and other symptoms associated with cancer

98
Q

how does immunotherapy work?

A

Block PDL-1 or similar receptors that mask cancer cell from being recognized by T cell so patient’s own immune system can identify and destroy the cancer

99
Q

Opdivo (Nivolumab) MOA

A

PDL1 inhibitor

100
Q

Opdivo (Nivolumab) indications

A
  1. metastatic lung cancer
  2. metastatic melanoma
  3. head and neck cancer
  4. Hodgkin lymphoma
  5. colorectal cancer
  6. hepatocellular cancer
  7. renal cell cancer
  8. urothelial cell cancers
101
Q

Opdivo (Nivolumab) SE

A

most tolerate very well but if they do have SE, they are severe - immune system starts attacking healthy cells

  1. rash
  2. colitis
  3. hepatotoxicity
  4. pneumonitis
  5. endocrinopathies: hypothyroid, “hypophysitis” (starts attacking pituitary gland)
102
Q

How do you treat Opdivo (Nivolumab) SE?

A

high dose steroids

103
Q

what is Car-T Cell

A

way of modifying patient’s T cells to make them more aggressive

take WBC out of patient’s body, attach lab-made antibody bead to T cells and infuse back into patient

104
Q

Car-T Cell SEs

A
  1. anaphylactic reaction

2. immune response to WBC

105
Q

examples of integrative oncology treatments

A
  1. music, arts, expressive therapy
  2. meditation
  3. yoga, physical exercise
  4. acupuncture
  5. massage
  6. aromatherapy
  7. lifestyle nutrition
  8. pet therapy
106
Q

causes of cancer related pain

A
  1. neuropathy
  2. radiation
  3. metastases: bone, liver
  4. secondary to radiation
  5. post surgical pain
  6. nerve impingement
  7. phantom pain
  8. wounds
  9. pleural irritation
107
Q

non-narcotic options for cancer-related pain

A
  1. gabapentin - neuropathic pain
  2. effexor - neuropathic pain
  3. topical lidocaine
108
Q

why do you avoid tylenol and NSAIDs

A
  1. tylenol - can mask a fever and fever may be only sign of infection in immunocompromised patient
  2. NSAIDs - increase risk of kidney damage
109
Q

6 As of opioid therapy

A
  1. appropriate?
  2. adjuvants?
  3. analgesia? (acceptable pain level)
  4. activities of daily living? (what are the goals?)
  5. adverse drug reactions? (already have constipation, somnolence?)
  6. aberrant drug behavior?
110
Q

MC opioid used

A

oxycodone

oxycontin is long-acting version

111
Q

benefit of fentanyl patches

A

don’t have to worry about swallowing w/ nausea, mouth sores

112
Q

special consideration for fentanyl patches

A

need enough body fat or else drug may not be transmitted to blood well (needs subcutaneous fat)

113
Q

other opioid routes of administration

A

liquid, rectal suppositories, concentrate

114
Q

which laxatives do you need to be cautious about giving and why

A

saline laxatives - need to make sure good renal function before giving magnesium

115
Q

categories of chemotherapy induced N/V

A
  1. highly emetic: >90% risk of emesis
  2. moderately emetic: 30-90% risk of emesis
  3. low emetogenicity: 10-30% risk of emesis
  4. minimally emetic: <10% risk of emesis
116
Q

types of chemotherapy induced N/V

A
  1. acute N/V: w/in 24 hours
  2. delayed N/V: 24 hours to 7 days
  3. anticipatory emesis: related to anxiety
117
Q

anti-emetic agents

A
  1. NK1R: Neurokinin-1 receptor antagonists
  2. 5-HT3 antagonists
  3. glucocorticoids
  4. ativan - for anticipatory emesis
  5. zyprexa (olanzapine)
118
Q

examples of Neurokinin-1 receptor antagonists

A
  1. aprepitant

2. fosaprepitant

119
Q

Neurokinin-1 receptor antagonists indications

A

highly emetogenic chemo; acute and delayed

120
Q

Neurokinin-1 receptor antagonists MOA

A

inhibits substance P / neurokinin 1 and augments 5HT3 receptor

121
Q

how are Neurokinin-1 receptor antagonists used?

A

added to 5-HT3 and dexamethasone for highly emetogenic chemo

122
Q

Neurokinin-1 receptor antagonists SE

A
  1. hiccups
  2. fatigue
  3. interacts with inhibitors of CYP3A4
123
Q

5-HT3 antagonists examples

A
  1. ondansetron (zofran)

2. palonosetron (longer acting)

124
Q

5-HT3 antagonists indications

A

acute and delayed nausea

125
Q

5-HT3 antagonists MOA

A

block 5-HT3-receptors which in turn block serotonin, works centrally and peripherally

126
Q

what anti-emetic is most effective?

A

5-HT3 antagonists

127
Q

5-HT3 antagonists SE

A
  1. QT prolongation
  2. headache
  3. malaise
  4. constipation
128
Q

zyprexa use

A

treat anticipatory emesis (anxiety type reaction) and delayed nausea

take the night before chemo or a scan

129
Q

example of highly emetic chemo

A

doxorubicin + cyclophosphamide

130
Q

example of moderately emetogenic chemo

A

carboplatin

131
Q

treatment regimen for highly emetic chemo

A

Day 1: NK1R antagonist + 5-HT3 receptor, dexamethasone, zyprexa
Day 2-4: zyprexa nightly

132
Q

treatment regimen for moderately emetic chemo

A

Day 1: NK1R + 5HT3 + dexamethosone

133
Q

treatment regimen for low emetogenic chemo

A

dexamethasone