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2011-08-02 17:22:52

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  1. What is Paraneoplastic syndrome?
    • A distant effect of malignancy mediated by factord secreted by, or tirggered by, the malignancy
    • May develop before or during the malignancy
    • May parallel the course of the disease
  2. What are the symptoms of Hypercalcemia?
    What are objective findings?
    • Symptoms
    • Fatigue
    • Anorexia, abdominal pain, constipation
    • Polyuria, polydipsia
    • Mental status changes
    • Sudden death

    • Objective findings
    • Renal dysfunction
    • Shortened QT interval, PR prolongation, bradycardia
    • Hyporeflexia
  3. For a patient with malignancy, the finding of hypercalcemia indicates what life expectancy?
    < 6 months
  4. What is the use of steroids in the treatment of hypercalcemia?
    • Used primarily in multiple myeloma, where the tumor is responsive
    • Also useful in lymphoma and occasionally in breast cancer
    • Blocks production of the "activating factors"
    • May also increase calcium excretion in the urine
  5. How does Mithramycin work in Hypercalcemia?
    • Inhbits bone reabsorption by reducing the number and activity of osteoclasts
    • A vweicant, and must be given IV
    • Ca level should decrease within the first 48 hours
    • May require retreatment in 72-96 hours
    • Side effects include thrombocytopenia, liver toxicity, and coagulopathy
  6. What is Calcitonin's effect on hypercalcemia?
    • Inhibits bone reabsortion by binding to osteoclasts
    • Works very quickly, within hours, to decrease calcium with peak action at 48 hours
    • May develop tachyphylaxis, so cannot use it more than once or twice
    • More effective with the addition of steroids
  7. Bisphosphonates
    How do they work in hypercalcemia?
    Give two examples and their use?
    What is the primarily toxicity of bisphosphonates?
    • Mainstay of therapy for hypercalcemia
    • Concentrated in areas of high bony turnover
    • Take up by the osteoclasts and inhibit their action
    • May have effects on the osteoblasts also
    • Pamidronate has proven efficacy in all types of hypercalcemia with decreased skeletal events in both breast cancer and multiple myeloma
    • Zoledronic acid also approved for malignant hypercalcemia
    • Toxicity is primarily renal insufficiency
  8. SIADH
    What cancer primarily cause this?
    What medication is known to cause this?
    • Primarily caused by small cell lung ca
    • Associated with medications such as cyclophosphamide (Cytoxan or Neosar)
    • Arised secondary to production of ectopic ADH, which acts in the kidneys to cause retention of free water
    • Results in hyponatremia in the setting of less-than-maximally dilute urine and a normal volume status
    • May be severe with symptoms of mental status changes, nausea, anorexia, and weakness
    • When extreme, may result in coma, seizures, and death
  9. Treatment options for SIADH?
    • Fluid restriction -- works best i mild cases with restricition to 500 ml to 1 L per day
    • IV saline plus lasix
    • Conivaptan for acute treatment
    • Demeclocycline for chronic treatment
    • Treat the underlying malignancy
  10. Cushing Syndrome
    What malignancies do these freaquently occur?
    Common presentation?
    How is diagnosis made?
    What are the treatment options?
    • Occurs frequently in small cell carcinoma, carcinoid tumors, and inassociation with MEN 1 syndrome
    • Ectopic ACTH production
    • Initiates excessive production of glucocorticoids and mineralocorticoids by the adrenal glands
    • Presentation is commonly seen with hypokalemic alkalosis
    • Also see weakness, hypertension, and hyperglycemia
    • If develops slowly, will see the syndrome with a buffalo hump, moon facies, hyperpigmentation, and hirsutism

    • Diagnosis is made by finding:
    • Elevated ACTH levels
    • Elevated cortisol levels that typically do not suppress with dexamethasone

    • Treatment options include:
    • Treatment of the primary tumor
    • Inhibitors of steroid synthesis, such as ketoconazole or an aminoglutethimide
  11. Dermatomyositis
    What is this associated with?
    • Commonly associated with visceral adenocarcinomas such as stomach, breast, lung, and ovary
    • Should consider malignancy in the older pt with dermatomyositis
    • Polymyositis associated with skin changes
    • -Proximal painless muscle weakness
    • -Violaceous rash on eposed parts, especially the eyelids
    • -Dysphagia is common
    • -May develop weakness of he respiratory muscles
  12. Diagnosis of Dermatomyositis?
    • Diagnosis is made by finding:
    • -Elevated CPK, aldolase, LDH, and ESR
    • -Abnormal EMG
    • -Muscle biopsy with necrosis of muscle fibers and an inflammatory reaction

    • Treatments include:
    • -Steroids
    • -treatment of the underlying malignancy
  13. What is Hypertrophic Osteoarthropathy?
    • "Clubbing"
    • Commonly associated with lung cancers, although may be seen with CF, chronic pulmonary infections, or IBD
    • May range from clubbing to severe periostitis and arthritis
    • Cause is unknown

    • Treatment:
    • -Salicylates/NSAIDs
    • -Steroids
    • -Effective tumor therapy
  14. Eaton-Lambert Syndrome
    What is it primarily associated with?
    Initial symptom?
    How diagnosed?
    • Occurs primarily in small cell lung cacer
    • Variant of myasthenia gravis
    • Initial symptom: weakness of the proximal muscles
    • Autoimmune in nature, secondary to autoantibodies that resut in impaired release of acetylcholine
    • Diagnosis: is made by finding an abnormal EMG with improvement in strength upon repetitive stimulation
    • EMG is usually unaffected by addition of edrophonium chloride

    • Treatment includes:
    • -Treatment of malignancy
    • -Guanidine
    • -Plasma exchange
    • -IVIG
    • -Immunosuppression - Imuran, steroids, cytoxan
  15. Spinal cord compression
    Describe the common areas involved
    Thoracic > Lumbosacral > Cervical
  16. What is the gold standard for diagnosis of SC compression?
    • MRI
    • Need tissue diagnosis to decide best treatment
  17. What are the treatment options fo SC compression?
    • Radiation therapy is themainstay of therapy
    • Steroids are usually given concomitantly to reduce edema
    • Laminectomy is used for patient who need a tissue diagnosis or are unable to have radiation therapy
    • Chemotherapy is usally combined with radiation for those sensitive tumors
  18. What is the treatment for Brain mets?
    • Immediate large doses of steroids (usually IV dexamethasone)
    • If the lesion is single, resection or stereotactic treatment may be tried
    • For multiple lesions, and after any resection, whole brain radiation therapy should be given
  19. Malignant pleural effusion
    How is this diagnosed?
    • Diagnosis is by pleural fluid cytology -- exudative
    • May require multiple samples and large volume for diagnosis
    • Occasionally may need pleural biopsy or thoracoscopy for diagnosis
  20. What is the treatment for malignant pleural effusions?
    • Therapy directed to the primary tumor
    • Symptomatic management with thoracentesis
    • If recurrent, then pleurodesis with Talc, Doxycycline, or Bleomycin
  21. What cancer is the most common cause of death in both male and female?
  22. Clinical breast exam (CBE)
    • ACS recommends CBE yearly after 40
    • USPSTF concludes that evidence is insufficient to recommend for or agains routine CBE
  23. Mammogram
    What age to start?
    • ACS recommends MMG done yearl after age 40 (supported by AMA and ACR)
    • USPSTF recommends screening with or without CBE every 1-2 years after age 40
    • Controversy surrounds age to stop MMG. Should be done after 70 in healthy women
    • Some data support idea that is is not cost-effective after age 79
  24. What is the recommendation for mammogram?
    • Start from age 40 yearly all the way to age 70 and probably all the way through as long as the pt is healthy
    • Breast self exam should be done yearly after 40
  25. Breast cancer risk
    What is the most significant risk factor?
    • Age is the most significant risk factor.
    • Risk rises to 1 in 8 by age of 85
    • Involvement of 1st degree relatives with early or bilateraly breast cancer increaseas the risk substantially
    • Genes -- BRCA1 and BRCA2
    • Benign breast disease increases your risk of subsequent breast cancer
    • -Atypical ductal hyperplasia
    • -DCIS
    • -LCIS
    • Previous breast cancer also increases the risk of a second breast cancer
  26. Describe the cancer risk of the BRCA1 gene
    • Found in Chromosome 17
    • Autosomal dominant
    • Lifetime risk if developing breast cancer is 50-85%
    • Also increases the lifetime risk of developing ovarian cancer to 33%
    • Associated with an increase in the risk of breast and prostate cancer in men
  27. Cancer risk of BRCA2?
    • Chromosome 13
    • Autosomal dominant
    • Similar risk for breast cancer as BRCA1 (50-85%)
    • Somewhat smaler risk for ovarian cancer (10-20%)
    • Associated with increased incidence of breast cancer in men
  28. Presentation of Breast Cancer
    • painless breast mass detected by the patient
    • Occasionally may present as eczema
    • May complain of a nipple discharge
    • May develop nipple retraction or dimpling of the skin
  29. Workup of breast mass?
    • Solid vs. cystic
    • -Can determine using US
    • -If cystic, aspirate; if bloody fluid or recurs, then should biopsy
    • -If solid, FNA or core biopsy

    • Palpable mass without abnormality on mammogram
    • -- biopsy
  30. If malignant breast cancer is diagnosed during the workup of a breast mass, what is the next step?
    • -Should send tissue for hormone receptors -- specifically estrogen and progesterone
    • -Should send tissue for HER2/neu assay

    Prior to further intervention, will need to survey for distant metastasis
  31. Prognosis in Breast Cancer
    1. Describe the prognosis in terms of tumor size and axillary nodes
    2. What is the most important prognostic factor?
    3. What does having ER/PR receptor negative status mean?
    4. How about HER2/neu status?
    • Tumor size
    • - Greater than 2 cm denotes a worse prognosis

    • Number of involved axillary nodes
    • -most important prognostic factor
    • -prognosis worsens with each positive node
    • -can use sentinel node dissection to assay

    • Other prognostic factors:
    • -Hormone receptor status -- if ER/PR receptor-negative, then expect a higher incidence of recurrence
    • -HER2/neu status -- overexpressionof HER2/neu denotes a more aggressive tumor
  32. Breast Cancer surgery -- describe the surgical options and associated interventions
    • 1. Modified radical mastectomy
    • 2. Breast-conserving surgery
    • -Lumpectomy with axillary node dissection
    • -Should always be paired with local radiation therapy to decrease the local recurrence rate
    • -give equivalent results to mastectomy
  33. Basic rules for therapy for Breast Cancer
    1. When is treatment not indicated?
    2. When is further treatment indicated?
    3. What about patient with positive hormone receptors?
    4. How about if HER2/neu positive?
    • Tumor < 1 cm with negative nodes -- no treatment is indicated
    • Any-sized tumor with positive nodes -- needs further treatment with either adujuvant chemo OR hormonal therapy OR both
    • All patients with positive hormone receptors should receive hormonal therapy for 5 years
    • If HER2/neu positive, add tastuzumab
  34. Breast cancer treatment in Premenopausal women with the following:
    1. <1 cm tumor, node-negative, ER/PR+/-
    2. Any size tumor, node-positive, ER/PR+
    3. Any size tumor, node positive, ER/PR-
    4. If HER2/Neu+ and node-positive?
    • < 1 cm tumor, node-negative, ER/PR+/- ==> no further treatment
    • Any size tumor, node-positive, ER/PR+ ==> chemo followed by hormone therapy (tamoxifen)
    • Any size tumor, node positive, ER/PR- ==> chemo
    • Trastuzumab if HER2/Neu+ and node-positive
  35. Breast cancer treatment in Postmenopausal woment with the following:
    1. < 1 cm tumor, node-negative, ER/PR+/
    2. Any tumor size, node-positive, ER/PR+
    3. Any tumor size, node-positive, ER/PR-
    4. if HER2/neu+ and node positive
    • < 1 cm tumor, node-negative, ER/PR+/- ==> no further treatment
    • Any tumor size, node-positive, ER/PR+ ==> hormone therapy (aromatase inhibitors) +/- chemo
    • Any tumor size, node-positive, ER/PR- ==> chemo
    • Trastuzumab if HER2/neu+ and node positive
  36. Breast cancer
    Treatment if with metastatic disease?
    If hormone receptor-negative or has visceral mets?
    If with bone disease?
    • With metastatic disease: if hormone receptor-positve, may use hormonal therapy alone unless there is evidence for visceral mets
    • If hormone receptor-negative or has visceral mets, then use combination chemo
    • Bisphosphonate therapy for bony disease
  37. What is Ductal Carcinoma in Situ?
    How common?
    What do you see on the mammogram?
    What is its risk?
    • Benighn
    • Mote common than lobular
    • See microcalcifications on mammogram
    • High-grade has higher risk of evolving into invasive disease
    • Treatment is mastectomy vs. breast conservation surgery +/- XRT followed by tamoxifen
  38. What is Lobular CIS?
    What do you worry about with this diagnosis?
    • Nonpalpable with no reliable mammographic changes
    • Marker for cancer development in either breast
    • Frequently is multifocal and bilateral
    • Treament varies from observation only to tamoxifen to bilateral mastectomy
  39. Prevention of Breast Cancer?
    • The use of tamoxifen therapy has been demostrated to reduce the risk of developing breast cancer in patients with increased risk
    • Should be used in those women felt to be at high fisk for breast cancer development such as those with:
    • -Previous cancer
    • -Strong family history
    • -BRCA1 or -2- positive
    • Aromatse inhibitors also now proven for prevention
  40. What are the risks to prolonged tamoxifen use?
    • Increased risk of endometrial cancer
    • Risk of thrombosis
    • DVT/PE
    • Cataract formation
  41. What are the risks of Aromatase inhibitor use?
    • osteoporosis -- need to screen for this and prevent
    • arthralgias
    • no thrombosis or malignancy risk
  42. Cervical cancer
    What is the peak age?
    • The third most common female genital tract cancer after uterine and ovarian
    • Mortality has dropped significantly with the introduction of effective screening
    • Peak age is 20-30 with a later peak in the 60s
    • Usually slow, progressive disease
  43. Risk factor of Cervical cancer?
    What is it associated with?
    What is the primary risk factor?
    • a sexually transmitted disease
    • Associated with:
    • -Early age at first intercourse
    • -Multiple sexual partners
    • -Low socioeconomic status
    • HIV
    • Primary risk factor is HPV, especially types 16, 18
    • Testing for HPV not a good screening tool, because up to 30% of women with normal pap smears have infection
  44. What is the recommendation for the HPV vaccine?
    • Recombinant vaccine
    • Recommended for ages 9-26
    • Best if given before sexually active
    • Ages 11-12
    • Covers POV types 6, 11, 16, and 18
    • -6 and 11 estimated to cause 90% of genital warts
    • -16 and 18 cause 70% of cervical cancer
  45. Describe Cervical Cancer screening recommendations:
    • Pap smear screenig for all women over the age of 21 or within 3 years of becoming sexually active
    • Annually until age 30
    • After age 30, if 3 negatives obtained, ay screen every 2-3 years unless risk factors present
    • After age 30, may combine pap and HPV DNA test and, if both negative, repeat every 3 years
    • May stop at physician's discretion or at 70 with 3 normals and none abnormal in last 10 years
  46. What do you do with an abnormal Pap smear?
    • Requires biopsy to further define the diagnosis
    • ASCUS diagnosis -- repeat in 3-6 months and if still abnormal, need colposcopy. If glandular, go directly to colposcopy

    • Typically, LGSIL and HGSIL will require further evaluation with colposcopy and biopsy
    • --LGSIL occasionally (15%) progresses to invasive cancer
    • --HGSIL is more likely to be higher-grade dysplasia with increased risk of malignancy
  47. What is the treatment for the ff Cervical cancer result?
    CIN I
    CIN II
    • CIN I -- observation vs. cryotherapy
    • CIN II and III -- ablation or excision
    • After definitive therapy, mus follow with frequent pap smears (3-4 mos, the every 6 months)
  48. How is Cervical Cancer staged?
    • Staging is by the FIGO guidelines
    • Spreads primarily by direct extension
    • Not TNM staging
    • Clinically staged with
    • -Physical exam CXR
    • -IVP if CT scan not done
    • -CT scan/MRI
  49. Treatment options for Cervical Cancer?
    • Influenced by tumor size, nodal involvement, and depth of tumor invasion
    • Early-stage disease may be treated with surgical resection only
    • More advanced local disease is treated with radical surgery or radiotherapy
    • Bulky disease or disease that has invaded the paratetria or nodes is treated with combination chemoradiotherapy

    • Close f/u is necessary, because most recurrences occur within the first 2 years
    • Pelvie recurrence may be treated with exenteration (exenteration = everything is take out of the pelvic)
  50. Ovarian cancer
    When does it peak?
    • 5th cause of cancer death
    • Peak in 8th decade
    • Rare before 40
  51. What are the risk factors for ovarian cancer?
    • Incessant ovulation
    • --nulliparity
    • --low parity
    • --infertility
    • --obesity
    • Family history
    • -- most significant risk factor
    • --Breast-ovarian syndrome with BRCA1 and BRCA2
    • --Lynch II syndrome
  52. What are the protective factors for Ovarian cancer?
    • Oral contraceptive use
    • Breastfeeding
    • Early menopause
    • Multiple pregnancies (10% decrease in risk with each)
  53. What are the possible screening tests for Ovarian Ca?
    Who should be screened?
    There is no good screening test

    • CA-125
    • -not a sensitive tool, but elevated in at least 80% of pts with ovarian ca.
    • -May be elevated in multiple tumor types and non-malignant states.

    Recommended screening at this time is restricted to those with an increased risk (such as known BRCA1 or 2) and combines pelvic exam, transvaginal U/S, CA-125.
  54. What is an Ovarian Tumor of low malignant potential?
    • Typically in younger patients
    • Have malignant features but are not invasive
    • Diagnosed at early stage
    • Long-term survival ov > 90%
    • Managed primarily with surgery
  55. When Ovarian Ca is diagnosed, what does staging consist of?
    • CA-125 level
    • CXR
    • Abdominal CT scan
    • Abdominal US
    • +/- UGI series and barium enema
    • Staging is primarily accomplished via surgical exploration -- this should include debulking, lymph node sampling
  56. What are the treatment options for Ovarian Ca?
    • Primary surgical resection
    • --the amount of remaining disease has a direct correlation to long-term survival
    • Chemotherapy
    • --Combination of paclitaxel and cisplatin are standard of care
    • Radiation therapy -- not often used
  57. What is the treatment for Early-stage disease ovarian cancer?
    How about late-stage disease?
    • Stage I with no residual tumor is treated with surgical resection only
    • Chemo is added if poorly differentiated tumor

    Later stage disease with or withour residual disease after laparotomy primarily treated with chemo
  58. Ovarian cancer, Germ cell type:
    What is it?
    • Fewer than 5%
    • usually large tumors
    • May secrete aFP or BHCG
    • Presents with early-stage disease
    • Treated with surgery, followed by chemo with agents such as BEP (bleomycin, etoposide, and cisplatin)
  59. Testicular Cancer
    What age is it most common?
    What population is affected most?
    If patient is over 50, what should you worry about?
    • Uncommon tumor but most common in men age 15-35
    • Incidence is slowly rising,with seminoma increasing in the HIV population
    • Occurs mos often in Caucasian men
    • In men over 50, consider a testicular mass to be a lymphoma until proven otherwise
  60. What do you need to do for a 50-year old pt who present with testicular mass?
    Start workup for lymphoma. This is lymphoma until proven otherwise
  61. What are the risk factors for testicular cancer?
    • Cryptorchidism
    • Prior testicular cancer
    • Family history of testicular cancer
    • Testicualr feminization syndromes
    • Klinefilter syndrome with mediastinal germ cell
  62. Presentation of testicular cancer?
    • 90% present in the testicles, 10% are extragonadal
    • Presentation is most commonly described as a painless mass
    • May have pain or swelling suggestive of orchitis
    • Back pain ay occur with spine metastasis
    • Cough, SOB, and dyspnea with pulmonary metastasis
  63. Workup of a testicular mass?
    • Often an inital trial of antibiotics is given if epididymitis or orchitis is suspected
    • Testicular US is indicated for a painless mass or painful one that does not resolve ater antibiotics
    • US can distingiush between a solid mass and inflammatory changes
    • Markers includeing BHCG, AFP, and LDH
    • If a mass identified, then an inguinal orchiectomy is indicated for diagnosis
    • Remember: the blood supply and lympatics all originate in the abdomen
    • A transcrotal approach is contraindicated, because it may introduce tumor cells to different drainage pathways
  64. Cell types of Testicular cancers?
    • Most testicular cancers are Germ Cell Tumors
    • --seminoma vs. nonseminoma
    • -----nonseminoma --> embryonal yolk sac vs. teratoma/choriocarcinoma
  65. What are Seminoma-type testicular cancer?
    When do they usually present?
    What is never produced in seminoma type?
    • usually present in the 4th decade
    • absence of any other cell type
    • If any other elements are present, it is classified as a nonseminoma
    • May have some cell of trophoblastic origin and produce BHCG
    • They never produce AFP
    • Usually localized
    • Rarely metastasize
    • Very radiosensitive
  66. What are Nonseminoma-type Testicular cancer?
    When do they usually present?
    • Typically present in the 3rd decade
    • May be composed of any one of the four histological cell types-- or more than one (mixed germ cell tumors)
    • Higher likelihood of metastatic disease at presentation
    • 1/3 confined to the testis; 1/3 metastatic
  67. What are the tumor markers for Testicular cancer?
    What are their half-lives?
    When do you check them?
    • Tumor markers include:
    • AFP -- half-life of 5-7 days
    • HCG -- has half-life of 24-38 hours
    • LDH

    These markers should be checked pre- and post-surgery, and are valuable to predict response to therapy and relapse
  68. How do you stage Testicular cancer?
    • Staging follows the TNM system or the system devised by the IGCCCG
    • Staging requireds:
    • -Surgical removal of the tumor
    • Evaluation of the tumor markers
    • CT scan of the abdomen
  69. Define the TNM stages of Testicular cancer from Stage I to III
    • Stage I ---> confined to the scrotum
    • Stage II ---> retroperitoneal disease
    • Stage IV --> distant mets
  70. What are the treatment options for Testicular Cancer?
    • Orchiectomy
    • Radiation therapy
    • Combination chemo
    • --most common is BEP (bleomycin, etoposide, and cisplatin)
    • --also use EP
    • High-dose chemo with BMT support
    • Any remaining mass after completion of chemo should be resected
    • --in nonseminomas, find: Necrosis/fibrosis, viable tumor, teratoma
    • If you find viable tumor, should proceed with 2 additional cycles of chemo
  71. What are the late sequela of therapy of testicular cancer?
    • Infertility
    • Second primary germ cell tumor
    • Secondary AML
    • Secondary GI malignancies
  72. Extragonadal Germ Cell Tumor
    What is the prognosis of a primary mediastinal tumor?
    Mediastinal disease is associated with what chromosomal abnormality and malignancy?
    • Nonseminoma of the retroperitoneum is similar to those of testicular origin
    • Primary mediastinal has a poor prognosis
    • Mediastinal disease is associated with i(12p)
    • Mediastinal disease is associated with AML(M7) and with MDS or ET
  73. Prostate Cancer
    What is the risk factor?
    Is cigarette smoking a risk?
    • A disease of aging men, cancer of the prostate increases after the age of 50
    • More than 70% of men over the age of 80 will have malignant cells in their prostate
    • 8:1 incidence to death ratio

    • Risk factors:
    • Age
    • Family history of prostate ca
    • Increased intake of animal fat
    • African-Americans are more affected
    • Prostatic hypertrophy is not associated with an increase risk of developing invasive cancer
    • Cigarette smoking is not linked
    • Previous vasectomy is controversial
  74. PSA
    How good is it as a screening test?
    • Relatively specific to prostate tissue
    • Normal levels increase with age
    • May be elevated in other settings
    • --Prostatitis
    • --Prostate hypertrophy
    • --After prostate biopsy
    • Not a very sensitive or specific marker
    • Elevated in 65% of patients with prostate cancer
    • Combination with DRE increases the utility of the marker
    • May be more sensitive with use of the age-specific PSA or the percentage of free PSA
  75. What is the recommendation for Prostate Cancer screening?
    Screening recommendation from the ACS: Offer a PSA and DRE annually after the age of 50 to men with a life expectancy of at least 10 years. Also offer to younger men at increased risk of developing prostate cancer
  76. What PSA level is considered abnormal?
    levels over 4 ng/ml
  77. In evaluating for prostate cancer, what is the next step if the screening DRE and PSA are abnormal?
    • The diagnostic procedure of choice is a TRUS (transrectal ultrasound) - guided biopsy of the prostate gland
    • Typically, 6 biopsies are done encompassing the peripheral zones of the gland
    • Remember that BPH usually involves the transition zone, while cancer involves the periphery
    • Pathology is almost always adenocarcinoma
    • Gleason's histological grade is the most important prognostic feature for prostate cancer
    • Gives a grade to both the predominant and secondary growth pattern, and adds the scores
    • Total will be 2-10, with higher grade correlated with higher incidence of spread and mortality
    • 7 or > Gleason's score is high risk disease
  78. What is the treatment for Prostate cancer with bone mets?
    What are used for hormonal manipulation?
    What happens if there is progression?
    • Treatment at tis stage is designed to palliate symptoms and preserve quality of life.
    • Frontline therapy is generally hormonal manipulation
    • Remember that the prostate is androgen-dependent, and most cancers maintain some degree of sensitivity to androgens
    • Hormonal manipulation may be accomplished by using:
    • --anti-androgens
    • --LHRH agonists
    • --Orchiectomy
    • Progression treated with withdrawal or second-line hormonal therapy
    • All are palliative
  79. Who are at risk for Head and Neck cancer?
    • ETOH and Tobacco abusers
    • Woodworkers and textile workers
    • Previous head and neck cancer
    • A viral association is also noted
    • --EBV
    • --HPV 16 and 18
  80. Treatment of Head and Neck cancer
    • Early stage disease is treated either with surgical resection or radiation therapy
    • More advanced disease is treated with combination therapy, with surgery followed by radiation therapy
    • Neoadjuvant chemoradiotherapy may be of benefit for preservation of function, particularly in laryngeal cancer
  81. Carcinoid
    What is the clinical syndrome?
    Effects on the heart?
    • Clinical syndrome
    • Flushing
    • Abdominal cramping
    • Diarrhea
    • Palpitations
    • Wheezing

    • Effects on the heart
    • Valvular heart disease may occur
    • Associated findings include:
    • --Endocardial fibrosis
    • --Often affects the pulmonary and tricuspid valves
  82. How is carcinoid diagnosed?
    How do you treat it once metastasis has occurred?
    What is the most effective treatment?
    diagnosis requires measurement of 24-hour urinary secretion of 5-HIAA (a breakdown product of serotonin)

    • With metastatic spread to the liver or the lung, carcinoid syndrome is seen
    • Curative treatment is not available at ths stage
    • Must treat the symptoms with antidiarrheal meds, Methylsergide, cyproheptadine
    • Most effectively treated with somatostatin analogue --ocreotide (can give as a monthly injection)
    • Use of chemo is limited
  83. How do you stage for Lung Cancer?
    • CT scans, including chest and abdomen
    • Bone scan
    • PET scan
    • +/- mediastinoscopy
  84. Prognostic factors in Lung Cancer:
    • Stage (TNM)
    • Performance status
    • Absence of weight loss
    • Female (they do better)

    Age and cell type not an important factor
  85. Treatment of Lung Cancer?
    • Resection of disease if possible, consider adjuvant treatment
    • If unresectable (higher stage), consider chemo + radiation
    • Metastatic disease -- chemotherapy
  86. What type lung cancer are usually central?
    small cell and squamous
  87. What type lung cancer are usually peripheral?
    Adenocarcinoma and large cell
  88. What lung cancer is not associated with cigarette smoking?
  89. What lung cancer is the "scar carcinoma?"
    Large cell
  90. What lung cancer is associated with hypercalcemia?
    Squamous cell
  91. What syndromes are associated with small cell?
    • SIADH
    • Cushing syndrome
    • Eaton-Lambert syndrome
  92. What musculoskeletal manifestation is associated with all lung cancers?
    Hypertrophic pulmonary osteoarthropathy
  93. Renal Cell Cancer
    Who is commonly affected?
    • Unusual cancer
    • Affects men more often
    • Linked to smoking
    • More common in patients with acquired renal cystic disease
    • Common in pts with von Hippel-Lindau disease
  94. What is the classic triad of Renal Cell Carcinoma?
    • Flank pain
    • Hematuria
    • Abdominal mass
  95. Paraneoplastic syndromes asociated with RCC?
    • Erythrocytosis
    • HTN
    • Hypercalcemia
    • Amyloidosis
  96. Diagnosis of RCC?
    • Diagnosis is usually by an imaging technique
    • --CT scan
    • --MRI
    • --US
    • Pathology is typically clear cell carcinoma
  97. Therapy for RCC?
    • Therapy is successful only if the tumor is confined to the kidney and is capable of being resected
    • Radical nephrectomy vs. partial nephrectomy
    • Solitary metastases may be resected
    • May resect venous involvement
    • For metastatic disease, treatment is disappointing
    • Chemo is not very effective
    • Immunotherapy has the most success, with a-Interferon and Interleukin-2 used
    • New targeted drugs --VEGF and PDGF tyrosine kinase inhibitors
  98. What is the ACS (American Cancer Society) Screening recommendation for colon cancer?
    • Men and women, age 50+ fecal occult blood test (FOBT) annual -or-
    • Flexible sigmoidoscopy every 5 years -or-
    • Annual FOBT and flex sig every 5 years -or-
    • Double contrast BE every 5 years -or-
    • Colonoscopy every 5 years
  99. What is the only screening test shown to decrease mortality?
  100. Treatment for Melanoma?
    Metastatic disease is poorly responsive to chemo and may respond best to immune modulation with a-interferon or IL-2
  101. What are effective antiemetic intervention for N/V caused by chemo?
    • Serotonin antagonists (zofran)
    • Antihistamines
    • Phenothiazine
    • Steroids
    • Antianxiety agents such as benzodiazepines
  102. Tumor Lysis Syndrome
    • Another side effect of chemo
    • Occurs whtn tumor breakdown occurs rapidly
    • Release of intracellular contents results in the development of :
    • --Hyperuricemia
    • --Hyperkalemia
    • --Hyperphosphatemia
    • --Hypocalcemia
  103. Neutropenic Fever
    • an oncologic emergency
    • The most common cause of chemo-related death
    • Fever may result from infection but may also be a manifestation of
    • --the tumor itself
    • --Medication reactions
    • --blood products
    • But always assume the cause of fever is infection
  104. Cyclophosphamide
    What is it?
    Side effect, and what causes it?
    How do you prevent this side-effect?
    What is less likely with use of this drug?
    What can it cause in high doses?
    • Unique alkylating agent, because it must be activated in the liver
    • Breakdown product is acrolein
    • Acrolein causes hemorrhagic cystitis
    • Prevent with hydration or mesna
    • Marrow toxicity and leukemia less likely
    • SIADH can occur in high doses
  105. Cisplatin
    What are its uses?
    How is it cleared, and what is the primary toxicity
    What electrolyte should you watch out for?
    Other side effects?
    • Many uses -- testicular, ovarian, lung
    • Cleared by the kidneys; thus, primary toxicity is renal damage
    • May experience magnesium-wasting
    • Prevent with hydration
    • Also causes peripheral neuropathy and ototoxicity
  106. Carboplatin
    What does it cause?
    What is its advantage over Cisplatin?
    Interchangeability with cisplatin?
    • Causes more myelosuppression (especially thrombocytopenia)
    • Cause less renal toxicity
    • Not always interchangeable with cisplatin
    • --inferior results in testicular cancer
    • --probably equivalent in ovarian cancer
  107. Antimetabolites
    What are they?
    • Drugs that are similar to metabolites in the DNA and RNA synthesis pathways
    • Usually compete for a critical enzyme or substitute into the backbone of DNA or RNA, causing disruption
    • Maximally effective in cycling cells
    • Not associated with profound or prolonged myelosuppression
    • Not associated with risk of secondary leukemia
    • Examples of commonly used drugs include:
    • --5-FU
    • --Methotrexate
    • --Cytarabine
  108. 5-Fluoruriacil
    What is its mechanism of action?
    What is it toxic to?
    What are the side effects?
    How do you enhance the efficacy?
    • Resembles the pyrimidines, uracil, and thymidine
    • Incorporates into RNA and disrupts the transcription
    • Toxic to the GI epithelium, resulting in significant mucositis and diarrhea
    • Enhanced efficacy by the addition of leucovorin
  109. Methotrexate
    What is it?
    Mechanism of action?
    What is the "antidote?"
    What is its effect in effusions
    What are the side effects?
    What are its uses?
    • A folic acid analog
    • Blocks the enzyme dihydrofolate reductase
    • Blocks DNA synthesis due to the lack of thymidine
    • Leucovorin is the "antidote" providing the necessary reduced folate to overcome MTX
    • Works best in cells actively cycling
    • Must be careful in patients with effusions, because the drug will accumulate in the effusion and slowly leak our, causing prolonged exposure and increased toxicity
    • Side effects generally include mucositis and diarrhea
    • Used in many tumors such as ALL, head and neck tumors, and breast cancer
    • Can penetrate into CNS if used in high doses
  110. Cytarabine
    What does it do?
    What part of cell cycle is it most active?
    What is its effect on the CNS?
    What are its uses?
    • Inhibits the binding of dexycytidine to the DNA polymerase; thus, effectively blocking the production of DNA
    • Most active in S phase cells
    • In high doses, enters the CNS and may cause cerebellar toxicity
    • Used in AML and lymphoma treatment
  111. Topoisomerase I Inhibitors
    • Parent compound is camptothecin
    • Unique action, with damage occurring by the interruption of the normal nick and repair mechanism performed by the topoisomerase I enzyme
    • Cell cycle-specific drug for S phase (like cytarabine)
  112. Topotecan
    What is the dose-limiting toxicity?
    Side effects?
    • Topoisomerase I inhibitor
    • Dose-limiting toxicity is neutropenia
    • May see nausea, fever, and skin rash
    • Used for the treatment of ovarian cancer and lung cancer
  113. What are the antibiotics used in cancer therapy?
    • Anthracyclines
    • Actinomycin D
    • Bleomycin
    • Mitomycin C
  114. Anthracyclines
    Give two examples
    Mechanism of action?
    What part of the cell cycle are they active?
    What precaution to take?
    • Daunorubicin and doxorubicin
    • Intercalates DNA and disrupts replication
    • May generate DNA breaks by the creation of free radicals
    • Active thought the cell cycle
    • Must reduce dosage for hepatic toxicity
  115. What is the toxicity profile of Anthracyclines?
    When does toxicity occur?
    What is the physiologic manifestation?
    What can be used to reduce the toxicity?
    • Toxicity profile is unique
    • Cardiac toxicity occurs with increasing cumulative dosage of the drugs
    • Chronic congestive heart failure that is difficult to treat
    • Monitor by serial EF assessments and by endomyocardial biopsy
    • Reduced by dexrazoxane, which inhibits free readical formation
  116. Bleomycin
    What is its toxicity profile?
    Most common side effect?
    Skin reactions?
    What is the most significant side effect and when do you see this?
    • Can be given IV, IM, or intracavitary
    • Toxicity profile is unusual
    • --Fever is common, and occasionally anaphylaxis may be seen
    • --Skin reactions include erythema and hyperpigmentation
    • --Pulmonary fibrosis is seen with increasing doses or in those having had chest radiation
  117. Alkaloids
    Give examples
    • Plant derivatives:
    • Vincristine
    • Vinblastine
    • Etoposide
    • Taxanes
  118. Vincristine
    Mechanism of action?
    What cell phase is it most active?
    Primary toxicity?
    Used for?
    • From the periwinkle plant
    • Binds to tubulin to interrupt the microtubule formation
    • Metaphase-specific
    • Primary toxicity is neurotoxicity
    • Used in ALL, lymphomas
  119. Vinblastine
    Mechanism of action?
    Side effect?
    • Almost exactly the same drug as Vincristine
    • Mechanism is identical
    • Side effect profile is different
    • --Primarily myelotoxicity
    • --Little neuropathy
  120. Taxanes
    Mechanism of action?
    Give two examples
    • Bind to microtubules, preventing their breakdown into tubulin dimers
    • Primarily disrupts mistosis
    • Paclitaxel and docetaxel
  121. Paclitaxel
    Side-effect profile?
    How do you prevent side-effects?
    • Associated with hypersensitivity reactions, which can be prevented by premedication with steroids and histamine blockers
    • Causes bradyarrhytmias
    • Causes neuropathy, mucositis, and almost universal alopecia that is total body
  122. Monoclonal Antibodies
    Mechanism of action?
    • Take advantage of tuor-specific properties such as cell surface markers or protein products of the tumor
    • Has benefit of little toxicity to normal tissues, unless they express the marker
    • May see infusion-related toxicity
  123. Trastuzumab
    What is it used for?
    When is it most effective?
    What group of medications do you absolutely have to avoid when on this med?
    • Monoclonal antibody
    • Anti-HER2
    • Effective in breast cancer that over-expressed HER2
    • Binds to a transmembrane receptor in the family of EGFR to block the cascade that drives cell growth had division
    • Most effective when combined with chemo, but cardiotoxic when combined with anthracyclines
  124. Rituximab
    What is it used for?
    • Monoclonal antibody
    • Anti-CD20
    • Effective in CD20-positive lymphomas (B cell)
    • Has been modified by the addition of radioactive isotopes to add tumor toxicity
    • See infusion-related hypotension, pain syndromes, and hypersensitivities, usually seen in the initial infusion and none in subsequent infusions
  125. What marker is used to identify pluripotent stem cells?
  126. What is the mortality rate for an autologous bone marrow transplant?
  127. What is Venoocclusive disease of the liver?
    • Usually damage to hepatic venues from the prep chemo before the allogeneic bone marrow transplant
    • Will see increased bili, weight gain, tender RUQ
    • Difficult to treat
    • Can be fatal
  128. What is GVHD (Graft vs. Host Disease)?
    Acute presentation?
    Chronic presentation?
    • a unique toxicity to allogeneic transplant
    • Higher risk with unrelated donor source
    • May be fatal
    • Acute looks like fever, skin rash, GI tract involvement
    • Chronic looks like scleroderma
  129. How do you manage a pt with limited-stage, small cell lung cancer?
    • Prophylactic cranial irradiation reduces central nervous system relapse and improves survival in patients with limited-stage, small cell lung cancer.
    • The brain is a frequent site of first relapse in patients after complete therapeutic response. Prophylactic cranial irradiation should therefore be considered for patients with SCLC who have a response to initial chemotherapy.
  130. What do you do with a pt who is being treated for hypogonadism with testosterone, now 6 months later with continuing increase in his PSA level?
    Men with hypogonadism often have a low prostate-specific antigen level that doubles with therapy and then stabilizes by 6 months after therapy initiation; a greater increase should prompt discontinuation of therapy and evaluation for prostate cancer.
  131. How do you manage a pt with a family history of colonic polyps?
    • Patients with a family history of colon cancer or adenoma should undergo a screening protocol at age 40 years or 10 years younger than the earliest diagnosis in the affected relative and with a shortened surveillance interval compared with those at average risk of colorectal cancer.
    • The recommended surveillance modality and interval is colonoscopy every 3 to 5 years.
  132. How do you diagnose a nonseminoma prostate cancer?
    An elevated serum α-fetoprotein level is indicative of a nonseminoma; seminomas are associated with a normal α-fetoprotein level.
  133. Explain the effect on the heart of doxorubicin therapy
    Anthracycline therapy with agents such as doxorubicin can cause progressive cardiomyopathy, which can occur acutely during treatment, within weeks to months following treatment, or years after treatment.
  134. Explain the cardiac effects of radiation therapy in breast cancer treatment.
    Radiation therapy can cause cardiac side effects; the most common manifestations are pericardial disease, coronary artery disease, cardiomyopathy, valvular dysfunction, and conduction abnormalities. Most cases of radiation-induced cardiac disease occur late in the course of the patient’s disease, often 10 years or more following treatment, and occur more frequently with left-sided breast cancers than right, particularly if the internal mammary lymph nodes were not included in the radiation field.
  135. How do you manage recurrent ovarian cancer?
    • Platinum-based chemotherapy is the treatment of choice for patients with recurrence of platinum-sensitive ovarian cancer and who relapse more than 6 months after completion of initial therapy.
    • Patients who were treated for ovarian cancer with a platinum-based regimen and who maintain a platinum-free interval (the time from the completion of primary platinum-based treatment to the time of recurrence) of more than 6 months are considered to have platinum-sensitive disease.
  136. How do you diagnose spinal cord compression due to bone mets?
    MRI of the spine
  137. How do you treat metastatic renal cell carcinoma?
    Sunitinib and sorafenib are small-molecule tyrosine kinase inhibitors that improve progression-free survival in patients with metastatic renal cell carcinoma.