Therapeutics Hematology/oncology Exam 2

Front 1

top 3 cancers in men

Back 1

1. prostate
2. lung and bronchus
3. colon and rectum

Front 2

top 3 cancers in women

Back 2

1. breast
2. lung and bronchus
3. colon and rectum

Front 3

top 3 death causing cancers in men

Back 3

1. lung and bronchus
2. prostate
3. colon and rectum

Front 4

tope 3 death causing cancers in women

Back 4

1. lung and bronchus
2. breast
3. colon and rectum

Front 5

which phase of cell cycle:

when the cell senses growth signals or mitogens. These start the process of cell division

Back 5

G1

Front 6

which phase of the cell cycle:

Cell crosses a restriction point at 8-10 hours into G1. This is a point of no return, the cell is committed to divide or die.

Back 6

G0

Front 7

which phase of cell cycle:

arrest here for cancer cells, leads to apoptosis

Back 7

G1/S

Front 8

which phase of cell cycle:

DNA is synthesized. Many cytotoxic anti-cancer drugs act here to disrupt DNA synthesis

Back 8

S phase

Front 9

which phase of cell cycle:

Cell arranges and checks chromosomes. There is a major checkpoint here to ascertain that DNA replication has successfully occurred. If not, a normal cell undergoes apoptosis

Back 9

G2/M phase

Front 10

which phase of cell cycle:

In mitosis chromosomes drawn apart by molecular motors, cell divides. Many cancer drugs like taxol act here freezing the process and causing apoptosis. There is a checkpoint to ensure chromosomes are correctly attached to the spindles before segregation.

Back 10

M phase

Front 11

Genetic material in cell that transform normal cell into cancer cell (over expression of this causes cancer)

Back 11

Oncogenes

Front 12

Provide negative controls of cell proliferation (aka anti-oncogene; prevents normal cell from mutating to cancer cell)

Back 12

Tumor Suppressor Genes

Front 13

Causes of cancer (9)

Back 13

1. industrial pollutants
2. UV light
3. radiation
4. tobacco smoke (primary or secondary)
5. diet (inc red meat = inc risk for colorectal cancer)
6. drugs
7. hormones
8. hereditary factors
9. virus

Front 14

Chemosensitive cancers (curative) (3)

Back 14

1. acute lymphocytic leukemia
2. testicular cancer
3. small cell lung cancer

Front 15

Chemoinsensitive cancers (palliative, non-curative) (4)

Back 15

1. renal cell
2. hepatoma
3. pancreatic
4. non-small cell lung cancer

Front 16

Ways that acquired drug resistance occur (5)

Back 16

1. Decreased activation of prodrug
2. changes in the target enzyme
3. alterations in cell's ability to repair drug-induced damage
4. increased drug inactivation
5. decreased uptake of drugs secondary to alterations in transport systems

Front 17

Enhances the export of toxins out of the cell

Back 17

P-glycoprotein (PGP)

Front 18

What gene encodes for p-glycoprotein?

Back 18

MDR1

Front 19

Characteristics in combination chemotherapy (4)

Back 19

1. each drug should be active by itself
2. avoid resistance
3. different mechanisms or sites of action
4. minimally overlapping toxicities

Front 20

General CT toxicities (all chemo drugs will have) (7)

Back 20

1. Bone marrow suppression (BMS): anemia, thrombocytopenia, neutropenia
2. GI tract: mucositis, diarrhea, N/V
3. cardiotoxicity
2. nephrotoxicity
4. pulmonary toxicity: pneumotitis, fibrosis
5. extravasation
6. carcinogenesis (actually causes cancer)

Front 21

Which cell cycle phase dependent agents are dependent on S phase? (4)

Back 21

1. methotrexate
2. 6-mercaptopurine
3. 6-thioguanine, ara-C
4. hydroxyurea

**4 works at a different place compared to the others (diff MOA, diff target, etc.)

Front 22

Which cell cycle phase dependent agents are dependent on M phase? (4)

Back 22

1. vincristine
2. vinblastine
3. paclitaxel
4. docetaxel

**1 and 2 work at different places in metaphase (diff MOA, diff target, etc.) as compared to 3 and 4

Front 23

Which cell cycle phase dependent agents are dependent on G1 phase? (1)

Back 23

L-asparaginase

Front 24

Which cell cycle phase dependent agents are dependent on G2 phase? (1)

Back 24

bleomycin

Front 25

which class of CT?

Substitutes alkyl groups for H+ atoms resulting in breaks in the DNA molecule and cross-linking of DNA strands, this interferes with DNA replication and RNA transcription

Back 25

alkylating agents

Front 26

Toxicities associated with cyclophosphamide (4)

brand: Cytoxan
class: alkylators I (oxazaphosphorines)

Back 26

1. N/V
2. BMS
3. cardiac necrosis at high doses
4. hemorrhagic cystitis at higher doses

**hepatically eliminated (80%)

Front 27

Toxicities associated with Ifosfamide (2)

brand: Ifex
class: alkylators I (oxazaphosphorines)

Back 27

1. renal (because this is renally eliminated)
2. bladder
3. hemorrhagic cystitis

Front 28

What is given with ifosfamide to help limit toxicities that would lead to hemorrhagic cystitis?

Back 28

mercaptoethane sulfonate (Mensa)

**Hemorrhagic cystitis caused by acrolein metabolite that is lessened by hydration diuresis and mercaptoethane sulfonate (mesna)

Front 29

Agents in alkylators II: Mustard derivatives (3)

Back 29

1. chlorambucil
2. busulfan
3. melphalan

Front 30

Toxicities associated with busulfan (1)

brand: myleran
class: alkylators II (mustard derivatives)

Back 30

1. veno-occlusive disease (of liver)

Front 31

Agents in alkylators III: nitrosureas (2)

Back 31

1. carmustine
2. lomustine

Front 32

clinical use of alkylators III: nitrosureas (1)

Back 32

1. brain tumors**

also used for lymphomas

Front 33

Toxicities associated with alkylators III: nitrosureas (1)

Back 33

1. pulmonary fibrosis: interstitial infiltrate leads to fibrosis (increased risk with hx of lung disease and carmustine dose >1500 mg/m2)

Front 34

Agents of alkylators IV: platinum compounds (3)

Back 34

1. cisplatin
2. carboplatin
3. oxaliplatin

Front 35

DLT associated with carboplatin (1)

Back 35

1. thrombocytopenia

Front 36

DLT associated with oxaliplatin (1)

Back 36

1. peripheral neuropathy

Front 37

Toxicities associated with cisplatin (2)

Back 37

1. severe N/V: may last for days after medication is administered
2. nephrotoxicity: prevention with prehydration (sulfur compounds bind to compound and reduce toxicity but chance of decreased efficacy)

Front 38

Which class of CT:

1. topoisomerase II inhibition
2. DNA intercalation causing single and double strand DNA breaks
3. Free radical generation by drug metabolites (cardiotoxicity dose limiting)
4. disruption of cell membranes

Back 38

antibiotics I: anthracyclines

Front 39

Lifetime dose limit on doxorubicin

Back 39

550 mg/m2

Front 40

Lifetime dose limit on daunorubicin

Back 40

400-600 mg/m2

Front 41

Agents of antibiotics I: anthracyclines (3)

Back 41

1. doxorubicin
2. daunorubicin
3. idarubicin

Front 42

Cardiac toxicity of doxorubicin and daunorubicin can be antagonized by?

Back 42

dexrazoxane (Zinecard)--unknown how this affects efficacy of doxo/daunorubicin

Front 43

Which antibiotic II agent?

inhibits DNA-dependent RNA synthesis

Back 43

dactinomycin

Front 44

which antibiotic II agent?

1. topoisomerase II inhibition, DNA intercalation, and minimal generation of free radical
2. similar to anthracyclines (anthraacenedione), but blue in color and less cardiac toxicity

Back 44

mitoxantrone

Front 45

Agents of antibiotic II (2)

Back 45

1. dactinomycin
2. mitoxantrone

Front 46

Agents of antibiotic III (1)

Back 46

1. bleomycin--inhibits DNA synthesis

Front 47

toxicity associated with bleomycin (4)

Back 47

1. pulmonary fibrosis
2. hypersensitivity (natural product)
3. cutaneous toxicity
4. Raynaud's syndrome

Front 48

Which class of CT?

Enzymatic cleavage of asparagine into aspartic acid and ammonia. Leukemia cells require asparagine for cell process.

Back 48

Antibiotics IV: L-asparaginase

Front 49

Adverse effects/toxicities associated with L-asaparaginase (2)

Back 49

1. anaphylaxis (natural product)
2. Disseminated intravascular coagulopathy (DIC)--basically a clot forming

Front 50

Which class of CT?

Inhibition of dihydrofolate reductase (responsible for intracellular activation of folates to their chemically reduced form) resulting in depletion of tetrahydrofolates and thymidine (which are needed for DNA synthesis)

Back 50

Antimetabolites I: folic acid analogs

1. methotrexate

Front 51

Reasons for high-dose MTX use (6)

Back 51

1. overcome defective transport
2. overcome increased levels of DHFR or altered binding affinity
3. prolong drug exposure
4. prevent or delay emergence of resistance
5. penetrate sanctuary sites or poorly perfused tumors
6. rescue of cancer cells + normal cells by leucovorin (antidote; dose 1mg leucovorin per 1 mg MTX)

Front 52

____ inhibits xanthine oxidase and interferes with the inactivation of 6- mercaptopurine and 6-thioguanine

Back 52

allopurinol

Front 53

Agents of antimetabolites II: purine analogs I (6-thiopurines) (2)

Back 53

1. 6-mercaptopurine
2. 6-thioguanine

Front 54

which antimetabolite II: purine analog II agent?

blocks adenosine deaminase (1)

Back 54

1. cladribine

Front 55

which antimetabolite II: purine analog II agent?

inhibits DNA primase, DNA polymerase alpha, and ribonucleotide reductase (1)

Back 55

1. fludarabine

Front 56

Agents of antimetabolites III: pyrimidine analogues (2)

Back 56

1. cytarabine (ara-C)
2. 5-FU
3. gemcitabine

Front 57

toxicities associated with cytarabine (ara-C) (2)

Back 57

1. flu-like syndrome
2. neurotoxic (HD ara-C)

Front 58

toxicities associated with 5-FU (2)

Back 58

1. hand-foot syndrome
2. neurotoxicity

**leucovorin enhances 5-FU cytotoxcity by stabilizing the complex with thymidylate synthetase

Front 59

what is the oral prodrug that forms 5-FU after metabolism?

Back 59

capecitabine

Front 60

Drugs that can cause hand-foot syndrome (5)

Back 60

1. capecitabine
2. 5-FU
3. doxorubicin
4. liposomal doxorubicin
5. interleukin 2

Front 61

Agents of antimitotics I: vinca alkaloids (3--2 in US, 1 Europe only)

Back 61

1. vincristine
2. vinblastine
3. vinorelbine

Front 62

DLT associated with vincristine and vinorelbine (1)

Back 62

1. BMS

Front 63

DLT associated with vinblastine (1)

Back 63

1. neurotoxicity

Front 64

Which class of CT medications cause death if given by intrathecal administration?

Back 64

vinca alkaloids

1. vincristine
2. vinblastine
3. vinorelbine

Front 65

Which class of CT?

Binds tubulin, which prevents polymerization of microtubules. Cells accumulate in the M phase and leads to apoptosis (cell death)

Back 65

antimitotics I: vinca alkaloids

Front 66

Which class of CT?

Stabilzes tublin bundles, prevents the destabilization of microtubules

Back 66

antimitotics II: taxanes

Front 67

toxicities associated with taxanes (paclitaxel, docetaxel) (2)

Back 67

1. peripheral neuropathy
2. hypersensitivity reactions

Front 68

How would you premedicate patients who are going to receive paclitaxel (3 agents)

Back 68

1. diphenydramine
2. corticosteroid
3. H2 antagonist

Front 69

How would you premedicate patients who are going to receive docetaxel? (1 agent but with schedule)

Back 69

1. dexamethasone: 8 mg BID x 1 day, then 4 mg BID x 2 days

Front 70

Agents of antimitotics II: taxanes (2)

Back 70

1. paclitaxel
2. docetaxel

Front 71

Agents of topoisomerase II inhibitors (2)

Back 71

1. Etoposide
2. Teniposide

Front 72

Which class of CT?

Stabilizes the topo II/DNA complex causing double stranded DNA breaks

Back 72

topoisomerase II inhibitors

1. etoposide
2. teniposide

Front 73

toxicities associated with etoposide and teniposide (2)

Back 73

1. BMS
2. 2nd malignancy (may be harder to cure; usually takes several years but dependent on frequency of administration)

Front 74

Which class of CT?

inhibition of topoisomerase I (causes single stranded DNA breaks)

Back 74

camptothecins

1. irinotecan
2. topotecan

Front 75

toxicity associated with irinotecan (1)

Back 75

1. severe diarrhea

acute: treat with atropine (0.25 mg IV)
delayed: treat with loperamide, lomotil (atropine + diphenoxylate), others

Front 76

toxicity associated with topotecan (1)

Back 76

1. BMS

Front 77

Which class of CT?

Block tumor estrogen receptors

Back 77

Steroids I: SERMs

1. tamoxifen
2. reloxifen: no established role in breast cancer, indicated for the treatment and prevention of osteoporosis in postmenopausal women, decrease risk of invasive breast cancer in postmenopausal women with osteoporosis

Front 78

Agents of steroid I: SERMs (2)

Back 78

1. tamoxifen
2. reloxifen

Front 79

Which class of CT?

Inhibit the final enzyme in the estrogen production pathway

Back 79

Steroid I: aromatase inhibitors

1. non steroidal: anastrazole
2. non-steroidal: letrozole
3. steroidal: exemestane

Front 80

agents of steroid I: aromatase inhibitors (3)

Back 80

1. anastrazole (nonsteroidal)
2. letrozole (nonsteroidal)
3. exemestane (steroidal)

Front 81

which class of CT?

Blocks all estrogen receptors, down regulate and degrade estrogen receptors

Back 81

Steroid I: estrogen antagonists

1. fulvestrant

Front 82

Which class of CT?

Block androgen binding

Back 82

steroid II: antiandrogens (antiandrogens for prostate cancer)

1. flutamide
2. bicalutamide
3. nilutamide

Front 83

Which class of CT?

Stops production of sex hormones (testosterone and estrogen)

Back 83

Steroid II: gonadotropin-releasing hormone analogs (used for hormone-sensitive prostate and breast cancer)

1. goserelin
3. leuprolide

Front 84

Agents of steroid II: gonadotropin-releasing hormone analogs (2)

Back 84

1. goserelin
2. leuprolide

Front 85

Which class of CT?

Causes lymphocyte lysis; used as part of multi-drug regimen for leukiemia and lymphoma

Back 85

Corticosteroids

1. dexamethasone
2. methylprednisolone
3. prednisone
4. hydrocortisone

Front 86

Which CT agent?

Binds with retinoic acid-1 receptor in promyelocytes in acute promyelocytic leukemia resulting in differentiation of the leukemic blast into a more mature form which undergoes cell death

use: acute promyelocytic leukemia--not curative, induces complete remission prior to BMT (bone marrow transplant)

Back 86

tretinoin (45 mg/m2/day oral)

Front 87

Which CT agent?

T-cell growth factor which promotes immunologic responses to cancer. Non-specific immune response can lead to capillary leak syndrome.

Back 87

Interleukin-2 (IL-2, aldesleukin, proleukin)

Front 88

toxicities associated with interleukin-2 (2)

Back 88

1. circulatory collapse
2. hypotension

Front 89

Which CT agent?

Enhances host immune response and direct antiproliferative effects on cancer cells

Back 89

interferons

1. interferon alfa-2a
2. interferon alfa-2b

Front 90

toxicities associated with interferon alfa-2a and interferon alfa-2b (2)

Back 90

1. flu-like symptoms
2. BMS

Front 91

Which CT agent?

Recombinant humanized murien monoclonal anti-body to B-cell surface marker CD20. Antibody recruits cytotoxic reaction to lymphoma cells mediated by complement activation

Back 91

Rituximab

Front 92

toxicity associated with rituximab (1)

Back 92

1. hypotension (especially with 1st infusion)

Front 93

Which CT agent?

Monoclonal antibody to her-2-neu, a protein overexpressed on the surface of about 1/3 of breast carcinomas. Results in complement activation and subsequent cytoxicity.

Back 93

trastuzamab (Herceptin)

Front 94

Trastuzamab (Herceptin) has synergistic cytotoxicity with what class of agents? (1)

Back 94

1. taxanes (paclitaxel, docetaxel)

Front 95

toxicities associated with trastuzamab (Herceptin) (1)

Back 95

1. cardiotoxicity in patients with prior anthracycline (doxorubicin, daunorubicin) exposure

Front 96

Which CT agent?

Monoclonal AB that binds specifically to the extracellular domain of EGFR. Binds to EGFR on both normal and tumor cells and competitively inhibits the binding of epidermal growth factor and other ligands, such as transforming growth factor. Binding of this agent to the EGFR results in inhibition of cell growth, induction of apoptosis, and inhibition of VEGF production.

use: monotherapy or in combination with other anticancer agents in the treatemnt of metastatic colorectal cancer. Also approved for use in head and neck cancer either by itself or in combination with radiation.

Back 96

Cetuximab

Front 97

Which CT agent?

Selective EGFR-tyrosine kinase inhibitor. Inhibits EGFR activity by competing with adenosine triphosphate for its binding site on the EGFR tyrosine kinase cytosolic domain, which blocks the tyrosine kinase cascade of downstream signaling, and ultimately interferes with proliferation and growth of cancer cells

use: treatment of locally advanced or metastatic non-small-cell lung cancer as a second line agent. Also approved for use in pancreatic cancer

Back 97

erlotinib

Front 98

adverse effects associated with erlotinib (2)

Back 98

1. Diarrhea
2. rash

Front 99

Which CT agent?

Humanized MoAB directed against circulating VEGF. It binds to all biologically active circulating isoforms of VEGF and prevents the activation and promotion of angiogenesis

use: in combination with 5-FU based chemotherapy, for the initial treatemtn of metastatic colorectal cancer and for first- line treatment, in combination with carboplatin and paclitaxel, for unresectable, locally advanced, recurrent or metastatic nonsquamous non-small cell lung cancer.

Back 99

Bevacizumab

Front 100

adverse effects associated with bevacizumab (4)

Back 100

1. hypertension

black box warnings:
2. GI perforation
3. wound dehiscence
4. fatal hemoptysis

Front 101

Risk factors for breast cancer (11)

Back 101

1. age >40
2. personal or family hx
3. <12 y/o at menarche
4. >55 y/o at menopause
5. >/= 30 y/o at first live birth
6. nulliparity
7. radiation
8. alcohol (>2 drinks/day)
9. HRT (hormone replacement therapy)
10. current use of oral contraceptives (>10 years)
11. high density breast tissue

Front 102

Candidates for prevention in breast cancer (5)

Back 102

1. BRCA 1, BRCA2, PTEN, or P53 mutations
2. >2 first-degree relatives with breast or ovarian cancer
3. hx of thoracic irradiation
4. hx of LCIS (lobular carcinoma in situ)
5. >35 years with a 5 year risk of 1.7% or greater

Front 103

What agent and dose is the gold standard for prevention in those at risk for development of breast cancer

Back 103

tamoxifen 20 mg QD x 5 years (premenopausal)

1. reduces breast cancer risk by 49%
2. post menopausal women >35 years use roloxifene

Front 104

S/s of localized disease breast cancer (5)

Back 104

1. ~10% of cases are asymptomatic
2. painless lump is the most common sign
3. change in size, shape, color, or feel of the breast/ areola/ nipple
4. nipple discharge, erosion, tenderness, inversion
5. stabbing or aching pain

Front 105

S/s of advanced disease breast cancer (5)

Back 105

1. bone pain
2. difficult breathing
3. abdominal enlargement
4. jaundice
5. mental status changes

Front 106

Characteristics of diagnosing breast cancer (7)

Back 106

1. hx and presentation, family hx
2. clinical breast exam
3. mammogram
4. ultrasound
5. breast biopsy
6. hormone receptor status (ER/PR)
7. her-2-neu status

Front 107

AJCC staging of breast cancer

1. lobular carcinoma in situ (LCIS)
2. ductal carcinoma in situ (DCIS)

Back 107

stage 0

Front 108

AJCC staging of breast cancer

<2 cm, confined to breast

Back 108

stage 1

Front 109

AJCC staging of breast cancer

1. less than 5 cm with or without ipsilateral LN metasteses
2. greater than 5 cm without LN involvement

Back 109

stage 2

Front 110

AJCC staging of breast cancer

1. direct extension to ipsilateral LN or chest tissue
2. greater than 5 cm with metastases to moveable ipsilateral LN
3. any size with metastases to fixed ipsilateral LN

Back 110

stage 3

Front 111

AJCC staging of breast cancer

1. distant metastases (bone, liver, lung, brain)

Back 111

stage 4

Front 112

Goals of therapy for breast cancer

1. stage 1-3 (2)
2. stage 4 (3)

Back 112

1. stage 1-3: cure, prevent reoccurrence
2. stage 4: palliation of symptoms, improve QOL, prolong survival

Front 113

1. marker identifying women at high risk for breast cancer (25%)
2. treatment options: observation following biopsy (offer tamoxifen for 5 years); bilateral prophylactic total mastectomies

Back 113

lobular carcinoma in situ (LCIS)

Front 114

1. noninvasive, precancerous lesion
2. may progress to become invasive cancer (<30% within 5-10 years)
3. treatment options: breast conservation (local excision and RT; negative margins; consider post-surgical tamoxifen x 5 years, esp if hormone receptor positive); Total mastectomy with or without reconstruction (wide spread disease or positive margins; young women with high lifetime risk of cancer)

Back 114

ductal carcinoma in situ (DCIS)

Front 115

Stage 1-3 breast cancer treatment options (4)

Back 115

1. breast conservation: lumpectomy with LN dissection with RT
2. total mastectomy with axillary LN dissection
3. simple mastectomy with SLN biopsy
4. adjuvant therapy with hormonal therapy (ER/PR positive patients) or chemotherapy (LN involvement or tumor greater than 1 cm in diameter)

Front 116

Adjuvant chemotherapy options for breast cancer stage 1-3 (3)

1. LN involvement
2. tumor greater than 1 cm in diameter

Back 116

1. AC x 4 (every 21 days)--gold standard: doxorubicin (adriamycin) and cyclophosphamide (**consider addition of doxetaxel or paclitaxel to AC regimen for LN positive patients)
2. FAC or FEC x 6 (every 21 days): Fluorouracil, doxorubicin/ epirubicin, cyclophosphamide
3. CMF x 6 (every 28 days): cyclophosphamide, methotrexate, fluorouracil

Front 117

adjuvant hormonal therapy options for breast cancer stage 1-3 (3)

1. ER/PR postive patients

Back 117

1. SERMs: tamoxifen 20 mg QD x 5 years
2. aromatase inhibitors (postmenopausal): anastrazole (1 mg QD), letrozole (2.5 mg QD), exemestane (25 mg QD)
3. LHRH agonists (premenopausal): investigational*

Front 118

metastatic breast cancer treatment options (4)

Back 118

1. endocrine therapy (ER/PR positive)
2. Chemotherapy
3. trastuzumab (her-2-neu overexpression)
4. palliative care

Front 119

treatment for ER/PR positive breast cancer

1. post-menopausal (2)
2. premenopausal (2)
3. progression or symptomatic metastases (2)

Back 119

1. postmenopausal: aromatase inhibitor; antiestrogen
2. premenopausal: antiestrogen; with or without ovarian ablation (oophorectomy, ovarian irradiation, LHRH analogs)
3. progression or symptomatic metastases: trial of new hormone therapy; chemotherapy

Front 120

Endocrine therapy for metastatic breast cancer (6)

Back 120

1. SERMs: tamoxifen 20 mg QD; toremifene 60 mg QD
2. SERDs: fulvestrant 250 mg IM q 28 days (selective estrogen receptor downregulator)
3. Aromatase inhibitor (postmenopausal)
4. LHRH analogues (premenopausal): goserelin; leuprolide; triptorelin
5. progestins: megesterol acetate 80 mg BID
6. androgens: fluoxymesterone 10 mg BID

Front 121

Chemotherapy for metastatic breast cancer

preferred single agents (5)

Back 121

1. anthracyclines (doxorubicin, daunorubicin, idarubicin)
2. taxanes (paclitaxel, docetaxel)
3. capecitabine (oral form of 5-FU)
4. vinorelbine
5. gemcitabine

Front 122

Chemotherapy for metastatic breast cancer

preferred combinations (higher response rates, but no evidence delay time to progression or improve survival) (4)

Back 122

1. AC (doxorubicin, cyclophosphamide)
2. FAC/ FEC (fluorouracil, doxorubicin/ epirubicin, cyclophosphamide)
3. CMF (cyclophosphamide, methotrexate, fluorouracil)
4. AT (doxorubicin, and taxane (paclitaxel, docetaxel))

Front 123

Risk factors associated with lung cancer (8)

Back 123

1. smoking
2. asbestos
3. radon
4. inhaled chemicals/minerals
5. air pollution
6. RT to the chest
7. personal/family history
8. beta-carotene supplements

Front 124

S/s of advanced disease lung cancer (7)

Back 124

1. bone pain with or without fracture
2. neurologic deficits
3. spinal cord compression
4. liver dysfunction
5. anorexia
6. weight loss
7. fatigue

Front 125

types of non-small cell lung cancer (3)

Back 125

1. adenocarcinoma
2. squamous cell
3. large cell

Front 126

1. 80% of lung cancers
2. slower growing
3. 50% present with metastases
4. not sensitive to chemotherapy
5. types: adenocarcinoma, squamous cell, large cell

Back 126

non-small cell carcinoma

Front 127

1. 20% of lung cancers
2. rapid proliferation
3. 60-70% of patients present with metastases
4. highly sensitive to chemotherapy/ RT

Back 127

small cell lung cancer

Front 128

staging of SCLC

1. primary tumor contained to hemithorax
2. ipsilateral hilar lymph nodes
3. supraclavicular or mediastinal lymph nodes

Back 128

limited-stage disease

Front 129

staging of SCLC

1. metastatic lesions in the contralateral lung (both lungs)
2. distant metastatic involvement
3. pleural effusion

Back 129

extensive-stage disease

Front 130

staging of NSCLC

carcinoma in situ

Back 130

stage 0

Front 131

staging of NSCLC

confined to lung

Back 131

stage 1

Front 132

staging of NSCLC

spread to local lymph nodes, diaphragm, mediastinal pleura, or parietal pericardium

Back 132

stage 2

Front 133

staging of NSCLC

involvement of mediastinal, contralateral, or supraclavicular LN

Back 133

stage 3

Front 134

staging of NSCLC

distant metastasis (bone, liver, CNS)

Back 134

stage 4

Front 135

limited stage SCLC treatment options (3)

Back 135

1. surgical resection: small isolated lesions only
2. chemotherapy with XRT (EP/EC/CP)
3. prophylactic cranial irradiation (PCI): for patients achieving complete remission; decrease risk of CNS metasteses by >50%

Front 136

chemotherapy options for SCLC (3)--limited stage disease or in combination therapy for extensive stage disease

Back 136

1. EP = etoposide + cisplatin
2. EC = etoposide + carboplatin
3. CP = irinotecan (CPT-11) + cipslatin

Front 137

combination chemotherapy options for SCLC extensive stage disease (6)

Back 137

1. EP = etoposide + cisplatin
2. EC = etoposide + carboplatin
3. CP = irinotecan (CPT-11) + cipslatin
4. CAV = cyclophosphamide + doxorubicin + vincristine
5. CAE = cyclophosphamide + doxorubicin + etoposide
6. ICE = ifosfamide + carboplatin/ cisplatin + etoposide

Front 138

treatment options for recurrent disease of SCLC relapse < 3 months (4)

Back 138

Switch to monotherapy with one of these options:
1. ifosfamide
2. paclitaxel
3. docetaxel
4. gemcitabine

Front 139

treatment options for recurrent disease of SCLC relapse 3-6 months (8)

Back 139

1. topotecan**
2. irinotecan
3. CAV (cyclophosphamide, doxorubicin, vincristine)
4. gemcitabine
5. paclitaxel
6. docetaxel
7. etoposide
8. venorelbine

Front 140

treatment options for recurrent disease of SCLC relapse >6 months (1)

Back 140

1. revert back to original regimen

Front 141

first line therapy for NSCLC chemotherapy

Back 141

cisplatin or carboplatin + one other agent (paclitaxel, docetaxel, gemcitabine, vinorelbine, vinblastine, irinotecan, etoposide

Front 142

second line therapy for NSCLC chemotherapy (3)

Back 142

1. docetaxel
2. pemetrexed
3. EGFR inhibitors (erlotinib, gefitinib)

Front 143

Which CT agent?

1. multitargeted antifolate that disrupts thymidine and purine synthesis (inhibits TS, DHFR, GARFT)
2. indication: single agent therapy in locally advanced or metastatic NSCLC following prior chemotehrapy
3. as effective as docetaxel in recurrent NSCLC (less myelosuppression, neuropathy, alopecia)
4. SE: myelosuppression, mucositis, rash, desquamation

Back 143

pemetrexed

Front 144

lifestyle type risk factors associated with colorectal cancer (6)

Back 144

1. alcohol
2. physical inactivity
3. obesity
4. diets high in fat and red meat
5. diets low in fiber, calcium, and folate
6. smoking

Front 145

s/s of early stages of colorectal cancer (6)

Back 145

1. change in bowel habits (constipation, diarrhea)
2. rectal bleeding
3. narrow stools
4. feeling of incomplete emptying
5. n/v, abdominal cramping, distention
6. fatigue

Front 146

s/s of advanced stages of colorectal cancer (7)

Back 146

1. hepatomegaly
2. jaundice
3. leg edema
4. weight loss
5. thrombophlebitis
6. fistula formation
7. pain of the lower back/leg

Front 147

staging of colorectal cancer

carcinoma in situ

Back 147

stage 0

Front 148

staging of colorectal cancer

tumor invasion of submucosa or musclaris propria

Back 148

stage 1

Front 149

staging of colorectal cancer

serosa involvement or spread to nearby tissues or organs

Back 149

stage 2

Front 150

staging of colorectal cancer

invasion of nearby LN

Back 150

stage 3

Front 151

staging of colorectal cancer

distant metastases

Back 151

stage 4

Front 152

treatment options for each stage of colorectal cancer

1. stage 1 =
2. stage 2 =
3. stage 3 =
4. stage 4 =

Back 152

1. stage 1 = surgical resection
2. stage 2 = surgical resection (colon cancer: with or without chemotherapy; rectal cancer: 5-FU/ leucovorin + RT)
3. stage 3 = surgical resection (colon: post-op chemo x 6 months; rectal: pre-op 5-FU/ RT + post op chemo)
4. stage 4 = chemotherapy (palliative resection and RT)

Front 153

1. infusional 5-FU + leucovorin + oxaliplatin
2. superior to 5-FU/leucovorin
3. increased neutropenia, peripheral neuropathy

Back 153

FOLFOX

Front 154

first line therapies for colorectal cancer with metastatic disease (4)

Back 154

1. FOLFOX +/- bevacizumab
2. FOLFIRI +/- bevacizumab: infusional 5-FU/leucovorin/irinotecan; similar survival advantage as FOLFOX; increased diarrhea
3. IFL + bevacizumab: bolus 5-FU/ leucovorin/ irinotecan; inferior to FOLFOX or FOLFIRI
4. patients unable to tolerate intensive therapy use: capecitabine, 5-FU/leucovorin +/- bevacizumab, 5-FU

Front 155

second line therapies for colorectal cancer with metastatic disease (4)

Back 155

1. FOLFOX
2. FOLFIRI
3. irinotecan and/or cetuximab
4. best supportive care

Front 156

risk factors for prostate cancer (3)

Back 156

1. age >50
2. family history
3. race: african american > caucasian = hispanics >asian

Front 157

s/s of localized prostate cancer (1)

Back 157

1. asymptomatic

Front 158

s/s of locally invasive prostate cancer (5)

Back 158

1. urinary hesitation
2. urinary dribbling
3. urinary retention
4. pain with urination/ ejaculation
5. impotence

Front 159

s/s of advanced prostate cancer (6)

Back 159

1. back pain/stiffness
2. spinal cord compression
3. lower extremity edema
4. bone fractures
5. anemia
6. weight loss

Front 160

What stage of prostate cancer?

carcinoma in situ

Back 160

stage 0

Front 161

What stage of prostate cancer?

clinically undetectable tumor

Back 161

stage 1

Front 162

What stage of prostate cancer?

tumor confined to prostate with invasion of lobes; can be felt on exam

Back 162

stage 2

Front 163

What stage of prostate cancer?

tumor extends through prostate capsule

Back 163

stage 3

Front 164

What stage of prostate cancer?

invasion of adjacent structures, LN, or metastatic disease (bones)

Back 164

stage 4

Front 165

treatment options for prostate cancer (5)

Back 165

1. expectant management
2. radiation therapy
3. radical prostatectomy
4. androgen ablation (AA)
5. antiandrogens

Front 166

With expectant management when would you perform:

1. PSA =
2. DRE =

Back 166

1. PSA = every 3-6 months
2. DRE = every 6-12 months

Front 167

With expectant management when would you intervene (3)

Back 167

1. PSA doubling time <3 years
2. increased Gleason grade
3. greater extent of prostate tumor

Front 168

Disadvantages of expectant management (7)

Back 168

1. missed opportunity for cure
2. risk of progression/ metastases
3. more complex treatment
4. nerve sparing more difficult
5. anxiety
6. frequent med exams
7. uncertain long term natural history of prostate cancer

Front 169

Treatment for stage 1-2 prostate cancer

risk of recurrence: low (gleason 6 or less) (2)

Back 169

1. life expectance <10 years: expectant management
2. LE >10 years: expectant management or XRT or radical prostatectomy

Front 170

Treatment for stage 1-2 prostate cancer

risk of recurrence: intermediate (gleason 7) (2)

Back 170

1. LE < 10 years: expectant management or XRT or radical prostatectomy
2. LE > 10 years: radical prostatectomy or XRT

Front 171

Treatment for stage 1-2 prostate cancer

risk of recurrence: high (gleason 8 or more) (1)

Back 171

1. androgen ablation + XRT or radical prostatectomy

Front 172

Treatment for stage 3 prostate cancer (1)

Back 172

1. androgen ablation +/- XRT (2-3 years)

Front 173

Treatment for stage 4 prostate cancer (2)

Back 173

1. LN involvement only: androgen ablation +/- XRT
2. distant metastasis: androgen ablation

Front 174

methods for androgen ablation (2)

Back 174

1. orchiectomy (removal of testicles)
2. LHRH agonst: Leuprolide 7.5 mg IM q 28d, Goserelin 3.6 mg SQ q 28 days, triptorelin 3.75 mg IM q 28d

Front 175

Antiandrogens for prostate cancer (3)

Back 175

1. flutamide 750 mg QD
2. biclutamide 50 mg QD
3. nilutamide 300 mg QD x 1 month then 150 mg QD

Front 176

hormone refractory prostate cancer

options for testosterone suppression (3)

Back 176

1. antiandrogens
2. ketoconazole +/- glucocorticoids
3. estrogens

Front 177

hormone refractory prostate cancer

Options for systemic chemotherapy (2)

Back 177

1. docetaxel + prednisone (first chemo to show benefit)
2. mitoxantrone + prednisone

Front 178

hormone refractory prostate cancer (5)

Back 178

1. bisphosphonates
2. radioisotopes: strontium-89, samarium-153
3. local RT
4. analgesia
5. corticosteroids

Front 179

Malignant transformation of a single abnormal progenitor cell with indefinite self-renewal (clonal disease)

Back 179

leukemia

Front 180

Clinical/ Laboratory findings of chronic myelogenous leukemia (5)

Back 180

1. malaise
2. fatigue
3. splenomegaly
4. weight loss
5. elevated WBC

Front 181

Rapid increase in blast count >100,000

Back 181

blast crisis

Front 182

1. MOA: inhibits bcr-abl, PDGF-R, and c-kit receptor tyrosine kinases
2. AE: BMS, rash, febrile neutropenia, elevated LFTs, N/V/D, edema
3. Dasatinib for refractory CML

Back 182

imatinib mesylate

Front 183

CLL: RAI staging

Lymphocytosis; lymphocytes in blood >15,000 mcL and >40% lymphocytes in the bone marrow

Back 183

stage 0

risk status = good

Front 184

CLL: RAI staging

lymphocytosis; lymphadenopathy. No hepato- or splenomegaly; number of RBC and platelets are normal

Back 184

stage 1

risk status = intermediate

Front 185

CLL: RAI staging

stage 1 with either hepatomegaly or splenomegaly or both (stage 1:lymphocytosis; lymphadenopathy. No hepato- or splenomegaly; number of RBC and platelets are normal)

Back 185

stage 2

risk status = intermediate

Front 186

CLL: RAI staging

stage 2 with HgB <11 g/dL or Hct >33%

(stage 2:stage 1 with either hepatomegaly or splenomegaly or both (stage 1:lymphocytosis; lymphadenopathy. No hepato- or splenomegaly; number of RBC and platelets are normal)

Back 186

stage 3

risk status = high

Front 187

CLL: RAI staging

stage 3 with platelets HgB less than 100,000 or Hct less than 33%

(stage 2:stage 1 with either hepatomegaly or splenomegaly or both (stage 1:lymphocytosis; lymphadenopathy. No hepato- or splenomegaly; number of RBC and platelets are normal)

Back 187

stage 4

risk status = high

Front 188

CLL: Binet staging

Fewer than 3 areas of enlarged lymphoid tissue

Back 188

Stage A

Front 189

CLL: Binet staging

More than 3 areas of enlarged lymphoid tissue

Back 189

Stage B

Front 190

CLL: Binet staging

Anemias plus thrombocytopenia (platelets <100,000/ mm3)

Back 190

Stage C

Front 191

CLL clinical presentation/ laboratory findings (7)

Back 191

1. fatigue
2. weight loss
3. abdominal discomfort
4. CBC: lymphocytosis (abnormal or smudge cells), with nuetropenia, anemia, and thrombocytopenia
5. lymphadenopathy
6. organomegaly (spleen and liver)
7. immunology defects: hypogammoglobulinemia; reversal of T4/T8 ratio

Front 192

First line treatment in chronic lymphocytic leukemia (5)

No cure! just palliative

Back 192

1. fludarabine +/- rituximab
2. cyclophosphamide + prednisone
3. chlorambucil + prednisone
4. CVP (cyclophosphamide + vincristine + prednisone)
5. fludarabine + cyclophosphamide +/- rituximab

Front 193

Second line treatment in chronic lymphocytic leukemia (2)

NO CURE JUST PALLIATIVE!!!

Back 193

1. alemtuzumab
2. pentostatin + cyclophosphamide +/- rituximab

Front 194

supportive care for chronic lymphocytic leukemia (2)

Back 194

1. antibiotics
2. blood products

Front 195

Reed Sternberg cells are characteristic of which lymphoma?

Back 195

Hodgkin's disease

Front 196

Which stage of lymphoma (Ann Arbor staging)

single LN region

Back 196

stage 1

Front 197

Which stage of lymphoma (Ann Arbor staging)

more than 1 LN region, but same side of diaphragm

Back 197

stage 2

Front 198

Which stage of lymphoma (Ann Arbor staging)

bi-diphragmatic dx

Back 198

stage 3

Front 199

Which stage of lymphoma (Ann Arbor staging)

diffuse disease

Back 199

stage 4

Front 200

Which stage of lymphoma (Ann Arbor staging)--letters

no symptoms

Back 200

A

Front 201

Which stage of lymphoma (Ann Arbor staging)--letters

fever, night sweats, wt loss (>10%)

Back 201

B

Front 202

Which stage of lymphoma (Ann Arbor staging)--letters

bulky disease

Back 202

X

Front 203

Which stage of lymphoma (Ann Arbor staging)--letters

extra lymphatic dx

Back 203

E

Front 204

Which stage of lymphoma (Ann Arbor staging)--letters

spleen involvement

Back 204

S

Front 205

systematic dx of hodgkins disease (3)

Back 205

1. unexplained fever >38C for 3 consecutive days
2. weight loss >10%
3. night sweats

Front 206

Laboratory findings for hodgkins (5)

Back 206

1. anemia
2. lymphophenia
3. thrombocytopenia
4. t-cell dysfunction
5. CXR: mediastinal mass (2/3 children; 1/3 adults)

Front 207

poor prognostic factors for hodgkins (6)

Back 207

1. advanced age
2. male sex
3. B symptoms (fever, night sweats, weight loss >10%)
4. leukocyte depleted histology
5. mediastinal mass >1/3 chest diameter
6. extranodal extension

Front 208

HD treatment

Stage 1 (low risk)

Back 208

XRT alone

Front 209

HD treatment

Stage 1 (B symptoms or bulky disease) or stage 2 (2)

Back 209

1. ABVD (doxorubicin + bleomycin + vinblastine + dacarbazine) for 4-6 then XRT
2. Stanford V (doxorubicin + vinblastine + mechlorethamine + etoposide + vincristine + bleomycin + prednisone) then XRT

Front 210

ICE =

Back 210

Ifosfamide
Cisplatin
Etoposide

Front 211

ESHAP =

Back 211

Etoposide
Methylprednisolone
Cytarabine (High dose)
Cisplatin

Front 212

Which anti-emetic agents are the least sedating? (3)

Back 212

1. butyrophenones (haloperidol)
2. corticosteroids
3. serotonin antagonists

Front 213

Which type of CINV?

within first 24 hours of chemo

Back 213

acute

Front 214

Which type of CINV?

24 hours after and lasting up to 5 days

Back 214

delayed

Front 215

Which agents are usually associated with delayed CINV? (4)

Back 215

1. cisplatin
2. carboplatin
3. cyclophosphamide
3. anthracyclines

Front 216

Which type of CINV?

conditioned response that occurs prior to a planned course following significant N/V due to previous chemo

Back 216

anticipatory

Front 217

Which type of CINV?

occurs despite preventatives

Back 217

breakthrough

Front 218

Which type of CINV?

occurs during subsequent cycles when antiemetic prophylaxis or rescue therapy has failed in earlier cycles

Back 218

refractory

Front 219

risk factors for CINV (8)

Back 219

1. emetic potential of drug
2. age <50
3. female
4. dose of medication
5. high pretreatment expectation of nausea or history of previous CINV
6. history of low alcohol consumption
7. history of motion sickness
8. history of morning sickness during pregnancy

Front 220

emetic risk for cisplatin

Back 220

high

Front 221

emetic risk for etoposide

Back 221

low

Front 222

emetic risk for bleomycin

Back 222

minimal

Front 223

High emetic risk and AC (doxorubicin and cyclophosphamide) treatment (prophylaxis) (days 1-4)

Back 223

day 1 = 5HT, dexamethasone, NK1 antagonist

day 2 & 3 = dexamethasone, NK1 antagonist

day 4 = dexamethasone (optional)

Front 224

moderate emetic risk treatment (prophylaxis) (day 1-3)

Back 224

day 1 = palonosetron, dexamethasone

day 2 & 3 = dexamethasone

**if palonesetron not available, may sub 5HT3; limited evidence supports adding NK1 antagonist; if added, any one of the 5HT3s is appropriate

Front 225

low emetic risk treatment (prophylaxis) (day 1 only)

Back 225

day 1 = dexamethasone 8 mg

Front 226

minimal emetic risk treatment (prophylaxis)

Back 226

no routine prophylaxis

Front 227

Which agents are considered lower therapeutic index anti-emetics, not first choice anti-emetics, reserved for patients intolerant to 5HT3s, NK1 antagonists, and dexamethasone, and are considered for rescue meds at home? (6)

Back 227

1. metoclopramide
2. butyrophenones (haloperidol, droperidol)
3. phenothiazines (prochlorperazine)
4. cannabinoids (dronabinol, nabilone)
5. olanzapine
6. scopolamine patch

Front 228

5HT3 receptor antagonists are the most effective class preventing ____ CINV but little effect on ____CINV

Back 228

1. acute
2. delayed

Front 229

Oral NK1 antagonist (1)

Back 229

1. aprepitant

Front 230

IV NK1 antagonist (1)

Back 230

1. fosaprepitant

Front 231

Chemo-induced diarrhea worst offenders (4)

Back 231

1. fluorouracil
2. methotrexate
3. cytarabine
4. stem cell transplant conditioning

Front 232

what to do if CID persists for more than 24 hours on loperamide

Back 232

increase loperamide to 2 mg q 2h and consider starting oral antibiotics for infectious prophylaxis

Front 233

what to do if CID persists for more than 48 hours on loperamide (2)

Back 233

1. stop loperamide and start 2nd line anti-diarrheal (octreotide, tincture of opium, paregoric, budesonide)
2. complte stool and blood work up; replace fluids and electrolytes as needed.

Front 234

high risk febrile neutropenia patients (4)

Back 234

1. prolonged (>7 days) and profound neutropenia (ANC <100 cells/mm3 post chemo)

AND/OR
2. clinically unstable
3. significant medical co-morbid conditions: hypotension, pneumonia, new onset of abdominal pain, neurologic changes
4. require hospitalization

Front 235

High risk patients of febrile neutropenia inpatient IV antibiotics that are given as empiric antibiotic monotherapy (4)

Back 235

1. piperacillin/tazobactam
2. carbapenem
3. ceftazidime
4. cefepime

Front 236

G-CSF: stimulates production, maturation, and activation of neutrophils; also activates neutrophils to increase migration and cytotoxicity (2)

Back 236

1. filgrastim
2. pegfilgrastim

Front 237

GM-CSF: stimulates proliferation, differentiation, and functional activity of neutrophils, eosinophils, monocytes, and macrophages (1)

Back 237

1. sargramostim

Front 238

ESA: boost RBC (2)

Back 238

1. epoetin alfa
2. darbepoetin

Front 239

thrombopoietic growth factor (1)

Back 239

1. oprelvekin

Front 240

keratinocyte growth factor (1)

Back 240

1. palifermin

Front 241

Agents that most generally have a hypersensitivity response to (2)

Back 241

1. asparaginase
2. paclitaxel

Front 242

class of CT drugs that have never been reported to cause HSR (1)

Back 242

1. nitrosureas (carmustine, lomustine)

Front 243

Agents that may cause (higher rates than others) alopecia (5)

Back 243

1. anthracyclines
2. ifosfamide
3. etoposide
4. vinca alkaloids
5. taxanes