Page 1 of 84 2012 exam 1. Clinical pharmacy activities During the prescription are : a. Clinical trials b. Formularies c. Drug information d. Counselling activity 2. Clinical pharmacy activities after the prescription are Except : a. Formularies b. Counselling activity c. Preparation of personalised formulation d. Drug use evaluation 3. The term of dose intensity (DI) is used to define a. the drug dose delivered per time unit and is expressed as mg/m2 per week b. the patient ideal body weight c. the protocol identified dosage form 4. the mechanism of resistance to methotrexate is a. decreased uptake of dihydrofolate b. increased dihydrofolate reductase (DHFR) activity c. a and b 5. Methotrexate mechanism of action is a. decreased uptake of dihydrofolate b. increased dihydrofolate reductase (DHFR) activity c. folic acid analogue which inhibits dihydrofolate reductase d. all of the above 6. Methotrexate affect 1-C atom metabolism by a. one-carbon transfer reactions requires specific coenzymes synthesized in the cell from tetrahydrofolic acid b. Methotrexate inhibit the cell from producing methylsalicylate c. None of the above 7. Methotrexate inside the cell will be converted to a. Polyglutamate form ,7 isomers b. Acetate form , 7 isomers c. All of the above d. None of the above 8. TPMT is responsible for a. Inactivation of 6MP b. Activation of 6MP c. All of the above d. None of the above 9. Significant of D15 MRD results a. Additional 3 asparaginase if MRD >1%
Transcript
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2012 exam
1. Clinical pharmacy activities During the prescription are :a. Clinical trialsb. Formulariesc. Drug informationd. Counselling activity
2. Clinical pharmacy activities after the prescription are Except :a. Formularies b. Counselling activityc. Preparation of personalised formulationd. Drug use evaluation
3. The term of dose intensity (DI) is used to define a. the drug dose delivered per time unit and is expressed as mg/m2 per week b. the patient ideal body weight c. the protocol identified dosage form
4. the mechanism of resistance to methotrexate is a. decreased uptake of dihydrofolate b. increased dihydrofolate reductase (DHFR) activity c. a and b
5. Methotrexate mechanism of action is a. decreased uptake of dihydrofolate b. increased dihydrofolate reductase (DHFR) activity c. folic acid analogue which inhibits dihydrofolate reductased. all of the above
6. Methotrexate affect 1-C atom metabolism by a. one-carbon transfer reactions requires specific coenzymes synthesized
in the cell from tetrahydrofolic acidb. Methotrexate inhibit the cell from producing methylsalicylate c. None of the above
7. Methotrexate inside the cell will be converted to a. Polyglutamate form ,7 isomers b. Acetate form , 7 isomersc. All of the above d. None of the above
8. TPMT is responsible for a. Inactivation of 6MP b. Activation of 6MPc. All of the above d. None of the above
9. Significant of D15 MRD results a. Additional 3 asparaginase if MRD >1% b. Not significant c. Need additional Adriamycin d. None of the above
10. Heterozygocity means 11. Loss of heterozygosity (LOH) in a cell represents
a. the loss of normal function of one allele of a geneb. the loss of normal function of two alleles of a genec. All of the above d. None of the above
12. Polymorphism in TPMT will cause a. Accumulation of active drug causing toxicity b. Increasing the metabolism of the active drug reducing the effectiveness c. All of the above d. None of the above
13. When using Fludara and Cytosar together a. Cytarabine can impair the metabolism of fludarabine . b. Cytarabine can increase the metabolism of fludarabinec. fludarabine can impair the metabolism of Cytarabined. fludarabine can increase the metabolism of Cytarabinee. None of the above
14. Inhibition of phosphorylation of arabinosyl-2-fluoroadenine will result in a. plasma levels of the active fludarabine triphosphate, F-ara-ATP, are
decreased. b. plasma levels of the active fludarabine triphosphate, F-ara-ATP, are increased. c. None of the above 15. F-ara-ATP can potentiate deoxycytidine kinase and will result in
a. the phosphorylation of cytarabine. As a result, plasma levels of the active cytarabine triphosphate, ara-CTP, are increased.
b. the phosphorylation of cytarabine. As a result, plasma levels of the active cytarabine triphosphate, ara-CTP, are decreased
c. None of the above 16. When using Fludara and Cytosar together
a. cytarabine be given as a relatively short-term infusion following fludarabine
b. We can not use both together c. None of the above
17. Pharmacogenetics,Pharmacogenetics is generally regarded as the study or clinical testing ofa. genetic variation that gives rise to differing response to drugsb. genetic differences in metabolic pathways which can affect individual
responses to drugs, both in terms of therapeutic effect as well as adverse effects
c. All of the above d. None of the above
18.The Intrathecal therapy is given toa. CNS prophylaxis b. Systemically increase the level of methotrexatec. All of the above d. None of the above
19. Methotrexate ,Cytosar and Hydrocortisone a. Can be given together as intrathecal injection b. Drug drug interaction prevent co-administration c. None of the above
20. Vincristine a. Is Fatal if given intrathecally b. Is only given intrathecallyc. None of the above
21. Prognosis is a. the prior knowledge of outcome of a disease b. the increase in intensity of therapyc. All of the above d. None of the above
22. In Acute lymphoblastic leukemia a child with 12 years will be a. Bad prognosis b. Good prognosis c. Not a prognostic factor d. None of the above
23. The gene function is expression of a. Proteins b. Chromosomes c. All of the above d. None of the above
24. Asparaginase is a. an enzyme that catalyzes the hydrolysis of asparagine to aspartic acid b. an anticanceralkylating agent c. All of the above d. None of the above
25. Storage of Asparaginase Medac a. Must be in the refrigerator b. Can be in Room temperaturec. All of the above d. None of the above
26. Calculating a dose of Asparaginase Medac 10000 international units in a 0.8 m2 child will be a. 4000 international units b. 8000 international unitsc. None of the above
27. It has been suggested that cytarabine be given as a relatively short-term infusion following fludarabine to a. minimize metabolic interference with the subsequent fludarabine dose b. maximize ara-CTP synthesis.c. All of the above d. None of the above
28. 2ry malignancy can occur with following medications a. VP16b. prednisone c.All of the above d. None of the above
29. The TPMT polymorphism is significant for the dosing and toxicity of: a.
30. In Induction chemotherapy for All the goal of induction therapy is to
a. Bring the disease into remission
b. To reduce the number of disease cells left in the body
c. To destroy any disease cells that remainsd. None of the above
e. All of the above
31.The goal of consolidation therapy for All is a. Bring the disease into remission
b. To reduce the number of disease cells left in the body
c. To destroy any disease cells that remainsd. None of the above
e. All of the above
32. The goal of Maintenance Therapy for ALL is a. Bring the disease into remission
b. To reduce the number of disease cells left in the body
c. To destroy any disease cells that remains d. None of the above
e. All of the above
33. which of the following is good prognosis for ALL
a. MLL rearrangement b. Hyperdiploidy
34. Another name for BCR-ABL fusion gene is __________chromosomea. Phildelphia chromosome b. BCR1c. None of the above
35. A patient is taking Enoxeprine for coagulopathy and his due to receive his intrathecal after tomorrow ,what instructions should the pharmacists tell the patient?
a.nothing b.stop Enoxeprine 24 hrs before the procedure c.continue Enoxeprine
36. Dexamethasone is used for Brain tumor patients during Chemotherapy a.Tb.F
37. The best hope for continued progress lies in the better understanding of the a.pathogenesis of ALL b.basis of resistance to chemotherapy
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c.all of the above 38. Evidence based practice (EBP) is the thorough, concise, and sensible use of the a. current best evidence in making decisions about the care of individual patients.b. intituition c. physician experience
39. Evidence base practice considers:a.the benefits and risk of other patient management strategies,b. the role of patients’ values and preferences in trading off those benefits and risks.c. a and b
40. In ALL Risk directed therapya.High risk treatment was Anti-metabolite basedb.Standard risk treatment was Intensive Multi-agent
c.Low risk treatment was Allogeneic Transplantation
41. Adverse Prognostic Factors in the 1990s for ALL were
a. Age<1, > 10 yearsb.Decreased WBCc.White race
42. this curve shows that worst survival is for D15 BM
a.0% blasts
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b.1-4% blast c.> 5% blast
43. The following figure stands for
a. Risk classification schema b. staging of leukemia c. None of the above
44. looking to this curve the following is true
a.E. Coli is less effective b.Erwinia is less effective 45. looking to the following curve what should you recommend
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a. one reinduction b. double reinduction
46. Toxicities Associated with CNS Irradiation are a.Second malignancyb.Neuropsychologic dysfunctionc.Endocrinopathy
d. all of the above 47. Principles of Treatment in ALL includes
a. Risk-directed therapyb. delayed intensification of chemotherapyc. short continuation treatment
48. The discipline of pharmacoeconomics is defined as the science of a. measuring the costs and outcomes associated with the use of pharmaceuticals in health care delivery.b. measuring the outcomes associated with the use of pharmaceuticals in health care delivery.c. measuring the costs associated with the use of pharmaceuticals in health care delivery.49. Change is like a dragon what should you do a. Fight it. b.Ignore it c. ride it.
50. In 57357 the cure rate for ALL is aimed to be a.40%b. 50%c. 80%
51. In total 15 protocol , dose of methotrexate for ALL SR is……….a- 2500 mg/m2 b- 1125 mg/m2 c- 5000 mg/m2 d-
1250 mg/m252. Pharmaceutical care is………
a- Individual patient oriented service b- Disease oriented service
c-Product oriented service d - Doctor oriented service
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53. Clinical pharmacy service started from ………..a- 1950 b- 1970 c- 1960
d- 199054. Pharmaceutical care planning is written, individualized, a systematic,
comprehensive process.a- Written & individualized b- real &
individualized c- accurate & real d- all answers are correct
55. primary function of Pharmaceutical care planning is a- Identify a patient's actual and potential drug-related problems. b- Resolve the patient's actual drug-related problems. c- Prevent the patient's potential drug-related problems.d- all answers are correct
56. All of these are related drugs problems except……a- Failure to receive drugs b- Overdose
c- Patient education d- Drug interactions57. Clinical Pharmacist can reduce to …………. of direct cost of drug related
problems.a- 20% b- 30% c- 40%
d- 50%58. All of these are steps of the care planning process except
a- Creation of a comprehensive patient database.b- Assess drug-related problems.c- Patient clinical examination. d- Establish therapeutic goals.
d- Patient history.60. For assess drug-related problems we should…...
a- Review patient profile. b- Determine additional drug therapy is needed. c- Determine if any of the drug-related problems may have been caused by
medication. d- All answers are correct.
61. Patient counseling is defined as providing medication information orally or in written form to the patients or their representatives on:a. directions of useb. advice on side effectsc. storaged. diet and life style modificationse. Allf. only a,b,cg. None
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62. . ………….. is the one who sees the patient and the Medications just before administration.
a.Nurseb.Pharmacistc.Physiciand.Alle.None
63. .One of the following is right :a.Pharmacists with poor communication skills and excellent clinical knowledge are more likely to be successful than pharmacists with excellent communication skills and good clinical knowledge.b.Pharmacists with excellent communication skills and good clinical knowledge are more likely to be successful than pharmacists with poor communication skills and excellent knowledge.c.Pharmacists with excellent communication skills and good clinical knowledge are more likely to be successful than pharmacists with excellent communication skills and excellent knowledge.d.Alle.None
64.Only with smart communication, Pharmacist will be able to provide the following:
65.The following may influence the process of patient counseling except:a.Cost of medicationb.Pharmacist communication skillsc.Patient cultured.Availability of medical informatione.All f.None
66.Considerations throughout Patient Interview:a.Rapportb.Successful Communicationc.Patient-centered languaged.Alle.None
67.In order to attract patient attention and to ensure positive response to information provided through patient counseling, pharmacist should :
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a.Show professionalism during interview by talking with patient about drug pharmacokineticsb.Skip patient complaints about his drugs which may not be -according to references- of clinical importancec.Highlight and describe prescription errors committed by the prescriber and the correctionsd.Stand very close to patiente.Focus on medications and medical conditions f.Use medical terminology during patient interview.g.Allh.none
68.The first step of patient counseling is:a.Providing informationb.Non drug optionsc.Gathering patient informationd.None
69.The last step of patient counseling:a.Follow up and closureb.Providing informationc.Non drug optionsd.Gathering patient informatione.None
70.The following is not important information to provide through patient counseling:
a.Medication identityb.Indicationsc.Onset of action. d.Potential interactions or therapeutic contraindicationse.Side effectsf.Allg.None
71. All of the following from the common side effects of chemotherapy except:a. Nauseab. Vomitingc. Headached. Mucositis
72-Neo-adjuvant chemotherapy means:a. Make a tumor smaller before surgeryb. Destroy the tumor after surgeryc. Use chemotherapy with radiotherapy d. None of the above
73-The goal of using chemotherapy with radiotherapy in some types of cancer is:
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a. Increase efficacy of the chemotherapy b. Decrease the side effect of the chemotherapyc. Increase the cancer cell sensitivity to radiation
74-All of the following are Asparaginase side effects except :a. Hyperglycemiab. Anaphylaxis c. Loss of tendon reflexd. Thrombosis
75-The max dose of vincristine is :a. 2 mlb. 2mg c. 20 mg d. 0.2 ml
76-Before Doxorubicin administration you must check:a. Random blood sugar b. ECHOc. Blood pressured. Creatinine clearance
77-Doxorubicin is infused over;a. 2 hrb. 23 hr c. 4 hrd. Iv push
78-Before Etoposide you must check:a. Random blood sugar b. ECHOc. Blood pressured. Chest x-ray
79-Cisplatin is infused over :a. 24 hrb. 6hrc. 4hrd. 2hr
80-Before Methotrexate infusion you must check :a. Chest x-rayb. ECHOc. Blood pressured. Random blood sugar
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81. MR DK ,71 year, male, metastatic Carcinoma of the colon was admitted for the 4th
cycle of second-line chemotherapy.Medications: Atropine 250 ug, sc Irinotecan 350 mg IV 5FU 800 mg IVFolinic Acid 175 mg IV
82. How does Irinotecan act?a. Topoisomerase I inhibitor b. Topoisomerase II inhibitorc. Alkylating agentd.Antimetabolites
83. Irinotecan is converted by carboxylesterases to its more active metabolite, 7-ethyl-10 hydroxy-camptothecin, or SN-38. T F 84.according this curve
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a.In the comparative trial vs 5-FU, CAMPTOSAR increased median survival b.In the comparative trial vs 5-FU, CAMPTOSAR decreased median survival
85. The clinical activity of both 5-FU/leucovorin and irinotecan in patients with metastatic colorectal is clinically attractive. There is reason to believe, however, that this therapeutic combination may result in antagonism. a. 5-FU may inhibit the DNA synthesis required for the cytotoxicity of SN-38. b. SN-38 may cause cells to accumulate in the G2 rather than in the S phasec. a and b
86. Fluorouracil is converted to FdUMP, leading to a.inhibition of TSb.depletion of deoxythymidine triphosphate (dTTP) poolsc. inhibition of DNA synthesis, resulting in G1/S cell-cycle arrest.d. all of the above
87.The active metabolite of irinotecan, SN-38,a. stabilizes the covalent complex between topoisomerase I and nuclear DNAb.lead to DNA double-strand breaks c. lead to accumulation of cells in the G2 phase of the cell cycle.d. all of the above
89. Mullany et al observed a sequence-dependent interaction of SN-38 and 5-FU plus leucovorin T F
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90. Mullany et al observed a sequence-dependent interaction of SN-38 and 5-FU plus leucovorin so a. Irrinotecan should be administered first b. 5-FU should be administered first
91. The doselimiting toxicities of irinotecan is/are a.diarrheab.neutropeniac. a and b
92. Two distinct types of diarrhea associated with irinotecan have been identified – a.an early onset b. lateonset diarrhea.c. a and b
93. early onset types of diarrhea associated with irinotecan are called a. nervous syndromeb. cholinergic syndrome c. Gilberts syndrome
94. Acute events of diarrhea are managed successfully by administering a. IV or SC atropine 0.25 to 1.0 mgb. Loperamide c. Senna extract
95. Late events of diarrhea are managed successfully by administering a. IV or SC atropine 0.25 to 1.0 mgb. Loperamide c. Senna extract
96. Avoid grapefruit, pomegranate, starfruit, Seville oranges, their juices or products during irinotecan treatment T F
97. The concurrent administration of irinotecan with irradiation is not recommended T F98. Freezing irinotecan of irinotecan should be done . T F99. irinotecan should be labeled Protect from light T F 100. How do genetic polymorphisms to UGT1A1*28 increase the risk for life-threatening neutropenia when receiving irinotecan?
• Patients at greatest risk for toxicity are those over the age of 65, those having previously received pelvic/abdominal irradiation, patients with low performance status, and patients heterozygous (TA6/TA7) or homozygous (TA7/TA7) for UGT1A1*28 allele.
101. What does heterozygous and homozygous mean? Since all humans have 2 copies of a gene coding sequence (or allele), a person
is heterozygous if they carry 1 copy of the normal gene and 1 copy of the mutant gene and are homozygous if they have two identical copies of the mutant gene (or gene variation).
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102. what role does UGT1A1*28 polymorphism play in causing irinotecan-induced myelosuppression?
patients with UGT1A1*28 make less UGT1A1 than normal patients and thus cannot efficiently metabolize the potent irinotecan metabolite, SN-38.
103. Which of the following is the main metabolite of irinotecan?a. SN-38b. T20c. 3A4d. SN-21 104 . What side effect is a patient at greatest risk of developing if they are homozygous for UGT1A1*28 and receiving irinotecan?a. Congestive heart failureb. Depressionc. Severe neutropeniad. Arthritis
105. GW is a 61-year-old man who presents to your clinic with a chief complaint of abdominal discomfort and cramping for the past 3 weeks not relieved with over-the-counter medications. While obtaining your medical history, he states that he also has seen small amounts of blood in his stool on and off for 4 months. He has a past medical history positive for hypertension and obesity. He states that he has smoked 1 pack of cigarettes per day for the past 40 years and drinks 4 to 6 beers every couple of days.
• What risk factors does GW have for colon cancer?• Does he have clinical symptoms suggestive of colon cancer?• What additional tests need to be ordered to diagnosis colon cancer?
106. 5-Flurouracil-based chemotherapy is the standard regimen used in adjuvant treatment of colon cancer T F107. Adjuvant therapy consisting of 5-fluorouracil-based chemotherapy in combination with radiation therapy should be offered to patients with stage II or III cancer of the rectum. T F
108. How does Mitomycin acts?a. bifunctional and trifunctional alkylating agentb. antimetabolites c. spindle poison 109. Mitomycin is cell cycle a.phase-nonspecific.b. phase-specific
110. 5FU is cell cycle a.phase-nonspecific.b. phase-specific
111. Irrinotecan is cell cycle a.phase-nonspecific.
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b. phase-specific
112. MM ,68 Y., Non Small cell Lung Cancer taking 1st course of MIT chemotherapy
Main ADR of MIT is /are? a. Myelosuppression, Nausea and vomitingb. Pulmonary toxicityc.hemolytic-uremic syndrome
113. The incidence of cardiotoxicity may be increased a. in patients receiving mitomycin in combination with doxorubicin b. in patients who have had prior exposure to doxorubicinc. a and b
114. Radiation recall reactions is caused by a.5FUb. Irrinotecanc. Mitomycind. a and c
115.Myelosuppression has not been noted with intravesical administration of Mitomycin . T F
116. MM, 30 y, 3rd course of 3 days BEP chemotherapy Bleomycin, Etoposide, Cisplatin is treatment for a. Testicular cancer b. Breast Cancer c. Lung Cancer d.Endometrial cancer
117. MM,30 y,3rd course of 3 days BEP chemotherapy Pigmentation on his back and marked acne Swelling and tenderness of finger tips What could be the cause of the patient skin condition?a. Bleomycin, b. Etoposide, c. Cisplatin
118. Bleomycin is a.phase-nonspecific.b. phase-specific
119. RH ,54 y, female ,stage III ovarian cancer should take a cycle ofa. MITb. carboplatin and paclitaxelc.FAC
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120. RH ,54 y, female ,stage III ovarian cancer should take ,2nd cycle of carboplatin and paclitaxel 175 mg/m2 .Nausea in the first few days post chemotherapy Pain in the back of her legs (last week) 1.68 cm Ht, wt62 kg and GFR 73 ml/minWhat caused Leg pain? a.carboplatin b. paclitaxel
121. How does carboplatin act ?Highly reactive platinum complexes are formed intracellularly. These complexes inhibit DNA synthesis through covalent binding of DNA molecules to form intrastrand and interstrand DNA crosslinks.
122. Carboplatin is considered to be a.phase-nonspecific.b. phase-specific
123. PA 60 y, male,Stage IIB Lung Cancer Surgical resection and receive carboplatin and docetaxel What type of chemotherapy is he receiving?a. neo-adjuvant b. adjuvant
124. Docetaxel is considered to be Cell cycle specific a. G phaseb. S phasec. M phase
124. Does combination carboplatin and docetaxel provide advantage?
a. Yes b. NO
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125. Docetaxel-induced fluid retention is generally reversible but may be severe with ascites, and pleural or pericardial effusions. Peripheral edema can be treated with standard measures a.sodium restrictionb. diureticsc. a and b 126. The incidence and severity of Docetaxel-induced fluid retention increase in incidence witha. age b. risk factors c. cumulative doses of 400 mg/m2 or greater
127. Docetaxel-induced fluid retention Premedication with oral corticosteroids has been reported to delay the onset and decrease the severity of fluid retention, and all patients should receive premedication. Patients with existing effusions should be monitored closely from the first dose to detect possible exacerbations of effusions.
128. AM ,45 y ,male , testicular cancer ,Cisplatin plus amofostine , ondansetron and diazepam prior to each session.
• Total protein 3.4 g/dl• Albumin 2 g/dl• Plt 100 000 /mm3hb 9.8 g/dl• WBC 2.9 X 10 9
How does cisplatin work? Cisplatin is an inorganic complex formed by an atom of platinum surrounded
by chlorine and ammonia atoms in the cis position of a horizontal plane. Intracellularly, water displaces the chloride to form highly reactive charged platinum complexes. These complexes inhibit DNA through covalent binding leading to intrastrand, interstrand, and protein cross-linking of DNA, leading to apoptosis.
129.What are major Cisplatin ADRs? The major dose limiting toxicity of cisplatin is cumulative nephrotoxicity
Nephrotoxicity Hypomagnesemia (magnesium wasting) severe nausea and
vomiting Neurotoxicity Ototoxicities130.What is the rationale for combining cisplatin and amifostine?
• Amifostine is a cytoprotective adjuvant used in cancer chemotherapy involving DNA-binding chemotherapeutic agents. Also commonly known as WR-1065 in its active form. It is marketed by MedImmune under the trade name Ethyol.
• Amifostine is used therapeutically to reduce the incidence of neutropenia-related fever and infection induced by DNA-binding chemotherapeutic agents including alkylating agents (e.g.cyclophosphamide) and platinum-containing agents (e.g. cisplatin). It is also used to decrease the cumulative nephrotoxicity associated with platinum-containing agents. Amifostine is also indicated to reduce the incidence of xerostomia in patients undergoing radiotherapy for head and neck cancer.
• Amifostine is an organic thiophosphate prodrug which is hydrolysed in vivo by alkaline phosphatase to the active cytoprotective thiol metabolite. The selective protection of non-malignant tissues is believed to be due to higher alkaline phosphatase activity, higher pH, and vascular permeation of normal tissues.
131. Amifostine can only be administered___________________________, a. s.c.b. intravenouslyc. I.Md.oral 132. Amifostine after reconstitution with a. G5%b. G/NSC. NS
133. Amifostine Infusions lasting less than 15 minutes decrease the risk of adverse effects. T F 134. With Amifostine Infusions the patient should be well-hydrated before administration. T F 135. Discuss rational for using the following medication in this case ;AM ,45 y ,male , testicular cancer ,Cisplatin plus amofostine , ondansetron and diazepam prior to each session. • Total protein 3.4 g/dl , Albumin 2 g/dl , Plt 100 000 /mm3hb 9.8 g/dl• WBC 2.9 X 10 9
a. Ondansetron Antiemetic regimen (I will add dexa and avil ) b.Diazepam Antiemetic for delayed and breakthrough
136. Tumor resistance to methotrexate:a.decreased drug transport into the cellb.altered dihydrofolate reductase enzyme -- lower affinity for methotrexatec.decreased polyglutamate formationd. quantitative increase in dihydrofolate reductase enzyme concentration in the cell e. all of the above
137. Methotrexate is considered to be Cell cycle specific a. G phaseb. S phasec. M phase
138. The most common adverse effects of Methotrexate are(3) stomatitis, myelosuppression gastrointestinal effects
139. Renal toxicity form Methotrexate may be related to precipitation of methotrexate in the renal tubules and collecting ducts. 140.Urinary methotrexate levels in excess of 1 mmol/L exceed the solubility of methotrexate at pH 5.0 and promote drug precipitation. 141.The risk of renal failure due to high-dose methotrexate (>1 g/m2) can be minimized by
diuresis, alkalinization of the urine (adjust urinary pH with IV sodium bicarbonate to maintain >7.0).
142. Clearance of methotrexate is delayed in the presence of fluid in the third space (e.g., pleural effusions, ascites), and toxicity may be enhanced. It is recommended a. CXR before every doseb. measure creatinine clearance c. measure liver functionsd. Increase hydration
143.1. a.damages DNA by intercalation, metal ion chelation,
b.generats of free radicals. c.inhibit DNA topoisomerase II which is critical to DNA function. d. Cytotoxic activity is cell cycle phase non-specific.
2. b.causes prevention of cell division primarily by cross-linking DNA and RNA strands.c. It is considered to be cell cycle phase-nonspecific.
3. The active form inhibits DNA synthesis by inhibiting thymidylate synthetase and the normal production of thymidine.
a. 5-FU 1 2 3 b. Doxorubicin 1 2 3c. Cyclophosphamide 1 2 3 135. 5 FU Effects on RNA occur especially with a. bolus administrationb. Continuous Infusion
136. Fluorouracil is cell cycle phase-specific a. G phaseb. S phasec. M phase
137. Principles of combination chemotherapy • (1) It provides maximum cell kill within the range of toxicity tolerated by the
host for each drug; • (2) it offers a broader range of coverage of resistant cell lines in a
heterogeneous tumor population; • (3) it prevents or slows the development of new drug-resistant cell lines.
138. Safety in administration of Herceptin • Mix in 250 mL bag NS. Do not use D5W. Do not shake.
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• Infuse loading dose IV over 90 minutes; subsequent infusions may be given over 30 minutes if the initial loading dose is well-tolerated.
• DO NOT ADMINISTER AS AN IV PUSH OR BOLUS. • Should not be mixed or diluted with other drugs. • Herceptin infusions should not be administered or mixed with Dextrose
solutions. • Diluent supplied - Bacteriostatic Water for Injection (BWFI)- contains benzyl
alcohol 1.1%; if patient is hypersensitive to benzyl alcohol, may reconstitute with Sterile Water for Injection, but must be used immediately and discard unused portion. =
• Solution reconstituted with the supplied BWFI is stable up to 28 days refrigerated.
• Do not freeze the reconstituted solution
139.Abbreviation Tumor marker Significance
CEA Carcinoembryonic Antigen malignancies arising in entodermal (embryonic) or gastrointestinal tissue. Persistent elevated levels indicate residual or recurrent metastatic carcinoma.
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CA-125 Cancer Antigen-125 monitoring for ovarian cancer by measuring an antigen to epithelial neoplasms circulating in blood serum
AFP Alpha-fetoprotein Serum levels elevated in Hepatocellular cancer. also found in certain ovarian and teratocarcinoma or embryonal carcinoma of the testis.
PSA Prostate Specific Antigen may be elevated in benign prostatic hypertrophy; greatest elevation occurs in stage C and D prostate cancer. After radical prostatectomy or radiation therapy, rising levels of PSA indicate residual disease or recurrence. Note: test results may be affected by recent prostatic massage or palpation
ERA Estrogen Receptor Assay A laboratory test of breast cancer tissue to determine the responsiveness of the tumor to endocrine therapy or to removal of the ovaries. Tumors which are negative for estrogen receptors rarely respond to hormone manipulation
PRA Progesterone Receptor Assay determine the responsiveness of breast cancer to endocrine therapy or to removal of the ovaries. Progesterone receptor assay increases the reliability of estrogen receptor assay results.a positive progesterone receptor assay indicates greater likelihood that the patient will respond to hormone therapy
LDH Lactic Dehydrogenase All tumors produce LDHHCG Human Chorionic
GonadotropinA nonspecific marker for pancreatic, pituitary, and placental tumors; elevated levels may be present in pancreatic cancer.
TUMOR MARKERS CANCERS WHAT ELSE? WHEN/HOW USEDUSUAL SAMPLE
AFP (Alpha-feto
protein)
Liver, germ cell cancer of
ovaries or testes
Also elevated during pregnancy Help diagnose, monitor
Interleukin-2 + Doxorubicin Increase risk of cardiotoxicity
Interleukin-2 + Aminoglycosides Increase risk of nephrotoxicity
Interleukin-2 + Asparaginase Increase risk of hepatotoxicity
Paclitaxel + Cisplatin - Platinum Derivatives may enhance
the myelosuppressive effect of
paclitaxel.
Mercaptopurine + Allopurinol -Allopurinol may decrease the
metabolism of Mercaptopurine
( Allopurinol inhibits xanthine oxidase,
the enzyme responsible for metabolism
of mercaptopurine
Asparaginase + Methotrexate Asparaginase may diminish or abolish
methotrexate's effect on malignant
cells.
Carmustine+Cimetidine: May decrease the metabolism of Carmustine
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Cisplatin+furosemide : May enhance the nephrotoxic effect of CISplatin. Loop Diuretics may enhance the ototoxic effect of CISplatin. Risk C: Monitor therapy
Cisplatin+Aminoglycosides: CISplatin may enhance the nephrotoxic effect of Aminoglycosides. Risk C: Monitor therapy
Methotrexate+Penicillins: May decrease the excretion of Methotrexate. Risk C: Monitor therapy
Methotrexate+Bile Acid Sequestrants(cholestyramine): May decrease the absorption of Methotrexate. Risk C: Monitor therapy
Methotrexate+ (salicylate)Nonsteroidal Anti-Inflammatory Agents: May decrease the excretion of Methotrexate. Risk D: Consider therapy modification
Methotrexate+Probenecid: May increase the serum concentration of Methotrexate. Management: Avoid concomitant use of probenecid and methotrexate if possible. If used together, consider lower methotrexate doses and monitor for evidence of methotrexate toxicity. Risk D: Consider therapy modification
Methotrexate+alcohol: the increased risk of liver damage is significant for people who are drinking alcohol while taking methotrexate
Estramustine+Calcium Salts: May decrease the absorption of Estramustine. Exceptions: Calcium Chloride. Risk D: Consider therapy modification
Tamoxifen+Vitamin K Antagonists (eg, warfarin): Tamoxifen may increase the serum concentration of Vitamin K Antagonists. Risk X: Avoid combination
Vincristine+Cardiac Glycosides(digoxin): Antineoplastic Agents may decrease the absorption of Cardiac Glycosides. This may only affect digoxin tablets. Exceptions: Digitoxin. Risk C: Monitor therapy
Procarbazine+ Sympathomimetic agents, tricyclic anti-depressants, tyramine-rich foods, ginseng, levodopa, MOA and COMT inhibitors (see Procarbazine in patient information Headache, flushed face, palpitations, rise in blood pressure mechanism: Procarbazine is a weak MAO inhibitor
Procarbazine+ Drugs which should not be used with MAOI Increased toxicity of these agents
Procarbazine+ CNS depressants Potentiation of CNS depression
IL-2 + Hypotensive Agents: May enhance the adverse/toxic effect of other Hypotensive Agents. Risk C: Monitor therapy
Interleukin-2 (IL-2) + doxorubicin have synergistic antitumor activity
with Proleukin may increase toxicity in these organ systems. The safety and efficacy of Proleukin in combination with any antineoplastic agents have not been established.IL-2 + methotrexate hepatotoxic (e.g., methotrexate, asparaginase) effects with Proleukin may increase toxicity in these organ systems. The safety and efficacy of Proleukin in combination with any antineoplastic agents have not been established.IL-2 + L-asparaginasehepatotoxic (e.g., methotrexate, asparaginase) effects with Proleukin may increase toxicity in these organ systems. The safety and efficacy of Proleukin in combination with any antineoplastic agents have not been established.IL-2 + glucocorticoids Glucocorticoids suppress the cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and IFN-γ, the most important of which is IL-2. Smaller cytokine production reduces the T cell proliferation.IL-2 + narcotic analgesics Proleukin may affect central nervous function. Therefore, interactions could occur following concomitant administration of psychotropic drugs (e.g., narcotics, analgesics, antiemetics, sedatives, tranquilizers).
IL-2+ Benzodiazepines Proleukin may affect central nervous function. Therefore, interactions could occur following concomitant administration of psychotropic drugs (e.g., narcotics, analgesics, antiemetics, sedatives, tranquilizers).
Paclitaxil+cisplatin: Taxane Derivatives: Platinum Derivatives may enhance the myelosuppressive effect of Taxane Derivatives. Administer Taxane derivative before Platinum derivative when given as sequential infusions to limit toxicity. Risk D: Consider therapy modification
Altretamine+cimetidine: Cimetidine Potentially increased half-life and toxicity of altretamine1 21
6-MP+ allopurinol: Allopurinol: May decrease the metabolism of Mercaptopurine. Risk D: Consider therapy modification
Asparaginase+ MTX Prevention of Methotrexate Cytotoxicity by Asparaginase Inhibition of Methotrexate Polyglutamate Formation
Teniposdie+MTXTeniposide (VM-26) can increase intracellular methotrexate (MTX) and its polyglutamate derivatives in vitro and thus has the potential to improve the therapeutic index of regimens containing MTX
Etoposide+Warfarin:Vitamin K Antagonists (eg, warfarin): Antineoplastic Agents may enhance the anticoagulant effect of Vitamin K Antagonists. Antineoplastic Agents may diminish the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Etoposide may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
141. Supportive treatment in cancer patients
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Nausea and vomiting
Anticipatory emesis Behavioral therapy involving systematic desensitization can be helpful in managing anticipatory emesis. Also, benzodiazepines appear to be useful. However, the best approach to anticipatory emesis is prevention, which underscores the need to provide the most effective and appropriate antiemetic regimens with the initial course of emesis producing chemotherapy.
Neutropenia Three approches*delay or reduce the drugs *administer prophylactic antibiotics * give haematopoietic growth factors or myeloid growth factors in a prophylactic strategy.
Febrile neutropenia
Extravasation Stop the injection/infusion. Disconnect the
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intravenous tubing._ Withdraw as much of the drug as possible, via existing cannula or central venous access device(CVAD)._ Mark area of skin with indelible pen. Take a photograph of the area as soon as possible.(Cameras are often available from Accident & Emergency departments)_ If appropriate, remove the peripheral cannula (do not remove the CVAD)._ Open extravasation kit (see Appendix B for list of contents)._ Refer to Appendix C to establish: whether a hot pack or cold pack should be used, or whetherneither is required; and what further treatment is recommended. Follow guidance in flow chartbelow accordingly._ Note that for Neutral drugs, neither a cold pack nor a hot pack is required. Aspirate as muchfluid as possible, and then remove the peripheral cannula. No further treatment should berequired. Manage the situation symptomatically. Document the incident in the patient’s notes._ Inform patient’s Consultant oncologist / haematologist (or SpR if Consultant not available)
Mucositis 1. Improvement of oral care 2. Mucosal sparing radiation therapy technique 3. Mucositis pain control :The use of aspirin
mucilage and xylocaine viscous gurgle and oral rinse are being used in practice in mucositis related pain.
4. Infection control. the use of topical antibiotic lozenge containing polymyxin-B, tobramycin and amphotericin-B reduced oral mucositis due to radiotherapy (20, 21). Chlorhexidine mouthwash too shown to reduce oral mucositis
5. Anti-inflammatory agents: Benzydamine, a non-steroidal anti-inflammatory agent that inhibit TNF-a, shown to be effective to control oral mucositis and pain due to radiotherapy (29).
6. Reactive Oxygen Species (ROS) inhibitors.
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ROS production is the first step of initiation of mucositis following radiotherapy and chemotherapy. Hence inhibition of the ROS could be a promising option of mucositis prevention. Amifostine; a thiol compound and a potent ROS scavenger found effective to prevent DNA damage following radiotherapy.
7. Salivary function modifiers: Some of the chemotherapeutic agents secreated through saliva leading to mucositis. Etoposide and 5-fluorouracil are known to secreate through saliva. Propanthelin, an anti-cholinergic agent has been shown to reduce oral mucositis among patients receiving etoposide chemotherapy.
Tumor lysis syndrome Empirical guidelines recommend the use of topical dimethylsulfoxide (DMSO) and cooling after extravasation of anthracyclines or mitomycin, locally injected hyaluronidase after extravasation of vinca alkaloids, and locally injected sodium thiosulfate (sodium hyposulfite) after extravasation of chlormethine (mechlorethamine; mustine). Plastic surgery may be necessary when conservative treatment fails to prevent ulceration. The possibility of late local reactions must also be considered in the management of patients receiving chemotherapy.
Nephrotoxicity recommended dose modifications in patients with renal insufficiency
2. which of the following is good prognosis for ALL
a. MLL rearrangement b. Hyperdiploidy
3. The lymphoid arm produces
a. b.
4. Principles of treatment of leukemia based on St. Jude total XV are
a.
b.
c.
5. Another name for BCR-ABL fusion gene is __________chromosome
6. The drug targeting BCR/ABL fusion gene is _________________
7. ALL stands for _______________
8. ALL treatment phases includes
Phase /Goal
9. Intrathecal chemotherapy is used for _______________________
10. A patient is taking Enoxeprine for coagulopathy and his due to receive his intrathecal
after tomorrow ,what instructions should the pharmacists tell the patient?
Lymphoid /Myeloid
b. Hyperdiploidy
B and T cells
a. To avoid over- or under-treatment, immunologic and molecular assays are used to measure the level of minimal residual leukemia after remission induction to increase the precision of risk-directed therapy.
b. Pharmacodynamic and pharmacogenetic principles will be applied to optimize therapy.
c. Cranial irradiation and epipodophyllotoxins are omitted in all but a very few high-risk cases to prevent the development of therapy-related brain tumor and acute myeloid leukemia.
Philadelphia
Imatinib
Acute lymphocytic leukemia
Induction/remission
Consolidation /
Continuation/
CNS prophylaxis
Should stop enoxeprine 24 hrs before procedure
144.1. TPMT is the enzyme metabolizing _____________to its inactive form
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2. Purinethol is a drug used in treatment of ___________________3. When should a patient take Purinethol?4. Asparaginase MEDAC is ____potency of Asparaginase MERK5. Methotrexate has a high Vd,what should we look for in the patient6. Methotrexate is >90% plasma protein bound which lab should we
follow7. The three important P450 Cytochrome include
a.b.
8. c.9. In tumor lysis syndrome the following lab values are increased
a.b.c.
10. In tumor lysis syndrome the following lab values are decreaseda.
11. Increase in PH with alkalnization will affect Allantoin solubility T-F12. 25% of AML patients will have _______ gene mutation13. ATRA is used to _______________APL cells14. Dexamethasone is used for Brain tumor patients during
ChemotherapyT-F15. Three most common pediatric cancers include
a.b.c.
16. CD20 is targeted by _____________________17. PCP prophylaxis is done by ___________________18. If the patient has deficient G6PD we can give Sutrim T-F
*Capsule form:- Doses ≤ 300 mg: given once daily in the middle of lunch, with apple, orange or lemonade
juice (acidic beverage) (q 24 hours at the same time each day).- Doses > 300 mg: divide every 12 hours in the middle of food, with apple, orange or
lemonade juice (acidic beverage) (the patient will be old enough to be convinced to eat well with each dose).
*Syrup form: - Preferably divide every 12 hours on empty stomach (1 hr before or 2 hrs after food).
2- Itraconazole most possible interactions at the day care unit: *The following applies only on the capsule form (not the syrup form):- Antacids, Calcium carbonate & Potassium bicarbonate (sachets): separate them at least 6
hrs before Itraconazole capsules and at least 2 hours after Itraconazole.- Proton pump inhibitors (as Pantoprazole or Esomeprazole): DO NOT GIVE PPIs with
Itraconazole capsules, switch to minimal dose of Ranitidine (2 mg/kg once daily at bedtime).
*The following applies on all forms of Itraconazole (capsule & syrup form):- Multivitamins, minerals & Iron: separate them at least 6 hrs before Itraconazole & at least
3 hours after Itraconazole.*Chemotherapy & Itraconzole:- Patients on Total XV protocol:
Itraconazole will be stopped for 3 days: 48 hrs before & 48 hrs after doses of: Vincristine, Doxorubicin & Cyclophosphamide.i.e.: If the patient is due to a week that contains any of the above at 10/8 for example, he will skip Itraconazole at 9/8, 10/8 & 11/8 and continue on 12/8 as usual.Itraconazole will be given safely with weeks of methotrexate/6mp or asparaginase/6mp only.GIVE THE PARENTS A COPY OF THE ROAD MAP: mark the weeks at which Itraconazole will be held, educate the parents when to hold and when to resume Itraconazole, revise with them at each visit. Tell them this is TO DECREASE CHEMOTHERAPY SIDE EFFECTS.
- Patients on other protocols: Itraconazole should be held with all chemotherapy EXCEPT: 6-mp, 6-thioguanine, Asparaginase, Cytarabine, Carboplatin, Cisplatin, Flurouracil & weekly low-dose Methotrexate (IM or PO). Consult the DIC for further information.Itraconazole will be held at least 48 hrs before the chemotherapy course (or longer) and at 24-48 hrs after, (according to half lives of the last-day chemotherapy).EDUCATE THE PARENTS TO HOLD ITRACONAZOLE 2 DAYS BEFORE EACH COURSE.
3- Voriconazole administration & Interactions: - Given 1 hour before or 2 hours after meals.- Interactions with chemotherapy : the same as Itraconazole but separate it just 12-24 hrs
before and 24-36 hours after chemotherapy.
4- Enoxaparin (Clexane®) precautions in the day care unit:
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- Do NOT administer into upper arms (just to avoid administering it intramuscularly). Administer by deep subcutaneous injection between the left and right anterolateral and left and right posterior abdominal.
- Hold Enoxaparin for INTRATHECALS: Give last dose 24-48 hours prior to procedure. Restart 24 hours after the procedure. YOU MAY GIVE THE PARENTS A COPY OF THE ROAD MAP: mark the weeks at which Enoxaparin will be held. Or YOU MAY JUST HIGHLIGHT THAT IF THE PATIENT WILL BE FASTING FOR AN ITH, that’s when Enoxaparin should be held.
5- Miscellaneous precautions for the patients: - Separate Ciprofloxacin oral from antacids, calcium salts, Iron salts (like in
multivitamins) at least 6 hrs before Ciprofloxacin and at least 2 hours after Ciprofloxacin.- Ciprofloxacin : 1 hr at least before meals. Avoid direct sunlight, & drink plenty of fluids.- Separate Ursodiol (Ursofalk, Ursogall) from aluminum containing antacids at least 6 hrs
before Ursodiol and at least 2 hours after Ursodiol.- Separate Dexamethasone oral from antacids, calcium carbonate at least 2 hrs before and
after.- Sutrim® : shake well & refrigerate for 2 weeks (if suspension), drink plenty of fluids.- Sutrim® : Separate the three days of prophylaxis from IM or oral Methotrexate by 48 hrs,
Ex: If the patient is taking methotrexate at Thursday, tell him to take Sutrim at Sunday, Monday & Tuesday.
- Carboplatin is always BEFORE Etoposide & Cyclophosphamide is always BEFORE Doxorubicin.
6- General regulations in the day care unit: 1- If a course has begun at a date other than when it was written, please write clearly in
file when was day 1, to prevent errors afterwards.2- Check the delivered continuing I.V. medications with the charge nurse 1 hour before
your shift ends, if there are patients that did not come for their medications, get their phone numbers from CERNER & call them right away to get them coming.
3- Same thing for oral medications, call the parents who left their medications at the same day or right at the next day.
4- Always be careful with the NEW ONES (like week 1 continuation Total XV, induction of TXV, day 22, week 1 of any protocol) these are at high risk of forgetting, missing & errors. They should be educated slowly & carefully.
5- Also be careful with 1st times (1st time 6-mp together with dexa at week 72 continuation SR, 1st time delivering IM methotrexate for the NEXT week, NOT TODAY).
6- When a pharmacist in the outpatient clinic writes before his signature: “Patient is on …………… drugs”. You should revise with the parents, the names of these medications, are they taking them regularly or not, when will they have follow ups & are the amount of these medications with them sufficient till the next follow up or not.
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147.
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148. Concomitant administration of Itraconazole will increase the toxicity of the following except:A) DoxorubicinB) VincristineC) CyclosporineD) Cytarabine
149.The following medications cannot be safely coadministrated with HDMTX except:A) PhenytoinB) TazocinC) AmphotericinB D) Ceftazidime 150.G.N a case of B.T maintained on Valproic acid and Carbamazepine as anticonvulsants now she is stable and no convulsions since 3 months but the trough total Carbamazepine level is 1 mcg / ml. It was recommended by a pharmacist to increase the dose 3 folds at least to obtain a level 3mcg / ml.After the dose increase by 7 days the patient admitted with CV, hepatic and GIT complications. A new level was obtained and it was 6 mcg / ml.IN your opinion: The pharmacist was right or wrong in her recommendation and why?
151. Increase in Cyclosporine trough level is expected when coadministrated with the following except:A) VoriconazoleB) ItraconazoleC) RifampicinD) PhenytoinE) C + DF) B + D
152.Itraconazole should to be stopped with the following Chemotherapy except:A) CytarabineB) VincristineC) EtoposideD) DoxorubicinE) A + DF) B + D
153. It is recommended to change the Vancomycin dose according to peak levels not trough from the efficacy point of view T F
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154.
1. What is missing from this physician order?
2. In which treatment phase is the patient now?
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155.
What is the importance of D15 for the treatment decision?
156.
Why methylprednisolone is replacing Predsol forte?
What is the difference e between Predsol and Predsol forte?
Why is Zyloric prescribed ?
157.
What is the drug this patient should take for the diagnosis written ?
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158.
What is different between 1st and 2nd ADE?
159.
1. Why is Vancomycin added?Why is the Infusion over 11/2?
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160.
Why is Voriconazole used ?
What is the difference between daunorubicin and doxorubicin?
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161. Evidence based practice (EBP) is a. the thorough, concise, and sensible use of the current best evidence in making decisions about the care of individual patientsb. intuition based c. unsystematic clinical experience,and pathophysiologic rationale as sufficient grounds for clinical decision-making,
162.Evidence-based medicine puts less emphasis on:a.intuition, b.unsystematic clinical experience,and pathophysiologic rationale as sufficient grounds for clinical decision-making, c a and b
163.Evidence base practice considers: a. The benefits and risk of other patient management strategies,b. the role of patients’ values and preferences in trading off those benefits and risks.c. a and b
164.The new view to managing the overload of information a.How do I keep up with new developments in medicine? b.What developments in medicine do I need to keep up with?c. all of the above d. none of the above
165.The steps to Evidence Based Practice area.What is the question?b.How do I find the evidence?c.Are the methods valid?d.What are the results?e.All of the above
166.Chemotherapy in ALL include a.Cisplatin b.Taxol c.Vincristine d.Dexamethasone e. c and d
167.Prognosis is e. the prior knowledge of outcome of a diseasef. the increase in intensity of therapyg. All of the above h. None of the above
168.In Acute lymphoblastic leukemia a child with 12 years will be e. Bad prognosis f. Good prognosis g. Not a prognostic factor h. None of the above
169. The gene function is expression of e. Proteins f. Chromosomes g. All of the above h. None of the above
170.Asparaginase is e. an enzyme that catalyzes the hydrolysis of asparagine to aspartic acidf. an anticancer alkylating agent g. All of the above h. None of the above
171. Storage of Asparaginase Medac e. Must be in the refrigerator f. Can be in Room temperatureg. All of the above h. None of the above
172.Calculating a dose of Asparaginase Medac 10000 international units in a 0.8 m2 child will be
d. 4000 international unitse. 8000 international unitsf. None of the above
173.The term of dose intensity (DI) is used to define d. the drug dose delivered per time unit and is expressed as mg/m2 per weeke. the patient ideal body weight f. the protocol identified dosage form
174.The mechanism of resistance to methotrexate is d. decreased uptake of dihydrofolate e. increased dihydrofolate reductase (DHFR) activity f. a and b
175.Total XV: Strategies to Decrease ToxicitiesEliminate cranial irradiationLimit the cumulative dose of Limit the cumulative dose of cyclophosphamide
176.Methotrexate inside the cell will be converted to a. Polyglutamate form ,7 isomers b. Acetate form , 7 isomersc. All of the above d. None of the above
177.TPMT is responsible for a. Inactivation of 6MPb. Activation of 6MPc. All of the above d. None of the above
178.Heterozygocity means Loss of heterozygosity (LOH) in a cell representsa. the loss of normal function of one allele of a geneb. the loss of normal function of two alleles of a genec. All of the above d. None of the above
179.Polymorphism in TPMT will cause a. Accumulation of active drug causing toxicity b. Increasing the metabolism of the active drug reducing the effectiveness c. All of the above d. None of the above
180.The Intrathecal therapy is given toe. CNS prophylaxis f. Systemically increase the level of methotrexateg. All of the above h. None of the above
181.Methotrexate ,Cytosar and Hydrocortisone d. Can be given together as intrathecal injectione. Drug drug interaction prevent co-administration f. None of the above
182.Vincristine d. Is Fatal if given intrathecallye. Is only given intrathecallyf. None of the above
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183. Pharmaceutical Care & Pharmacotherapy Workup1. Causes for mortality and morbidity of children n the developing world are ranked asfollows :( ) Accidents( ) Malnutrition( ) Malaria( ) Respiratory Infections( ) HIV( ) Cancer2. Leukemogenesis concernsa.b.c.3. the two arms of leukemia are :a.b.4. which of the following is good prognosis for ALLa. MLL rearrangement b. Hyperdiploidy5. Determinant of treatment response includea.b.c.d.6. The lymphoid arm producesa. b.7. Principles of treatment of leukemia based on St. Jude total XV area.b.c.8. Another name for BCR-ABL fusion gene is __________chromosome9. The drug targeting BCR/ABL fusion gene is _________________10. ALL stands for _______________11. ALL treatment phases includesPhase Goal
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12. Intrathecal chemotherapy is used for _______________________13. A patient is taking Enoxeprine for coagulopathy and his due to receive his intrathecalafter tomorrow ,what instructions should the pharmacists tell the patient?14. TPMT is the enzyme metabolizing _____________to its inactive form15. Purinethol is a drug used in treatment of ___________________16. When should a patient take Purinethol?17. Asparaginase MEDAC is ____potency of Asparaginase MERK18. Methotrexate has a high Vd,what should we look for in the patient19. Methotrexate is >90% plasma protein bound which lab should we follow20. The three important P450 Cytochrome includea.b.c.21. In tumor lysis syndrome the following lab values are increaseda.b.c.22. In tumor lysis syndrome the following lab values are decreaseda.23. Increase in PH with alkalnization will affect Allantoin solubility T-F24. 25% of AML patients will have _______ gene mutation25. ATRA is used to _______________APL cells26. Dexamethasone is used for Brain tumor patients during ChemotherapyT-F27. Three most common pediatric cancers includea.b.c.28. CD20 is targeted by _____________________29. PCP prophylaxis is done by ___________________30. If the patient has deficient G6PD we can give Sutrim T-F
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7- Itraconazole administration: *Capsule form:- Doses ≤ 300 mg: given once daily in the middle of lunch, with apple, orange or lemonade
juice (acidic beverage) (q 24 hours at the same time each day).- Doses > 300 mg: divide every 12 hours in the middle of food, with apple, orange or
lemonade juice (acidic beverage) (the patient will be old enough to be convinced to eat well with each dose).
*Syrup form: - Preferably divide every 12 hours on empty stomach (1 hr before or 2 hrs after food).
8- Itraconazole most possible interactions at the day care unit: *The following applies only on the capsule form (not the syrup form):- Antacids, Calcium carbonate & Potassium bicarbonate (sachets): separate them at least 6
hrs before Itraconazole capsules and at least 2 hours after Itraconazole.- Proton pump inhibitors (as Pantoprazole or Esomeprazole): DO NOT GIVE PPIs with
Itraconazole capsules, switch to minimal dose of Ranitidine (2 mg/kg once daily at bedtime).
*The following applies on all forms of Itraconazole (capsule & syrup form):- Multivitamins, minerals & Iron: separate them at least 6 hrs before Itraconazole & at least
3 hours after Itraconazole.*Chemotherapy & Itraconzole:- Patients on Total XV protocol:
Itraconazole will be stopped for 3 days: 48 hrs before & 48 hrs after doses of: Vincristine, Doxorubicin & Cyclophosphamide.i.e.: If the patient is due to a week that contains any of the above at 10/8 for example, he will skip Itraconazole at 9/8, 10/8 & 11/8 and continue on 12/8 as usual.Itraconazole will be given safely with weeks of methotrexate/6mp or asparaginase/6mp only.GIVE THE PARENTS A COPY OF THE ROAD MAP: mark the weeks at which Itraconazole will be held, educate the parents when to hold and when to resume Itraconazole, revise with them at each visit. Tell them this is TO DECREASE CHEMOTHERAPY SIDE EFFECTS.
- Patients on other protocols: Itraconazole should be held with all chemotherapy EXCEPT: 6-mp, 6-thioguanine, Asparaginase, Cytarabine, Carboplatin, Cisplatin, Flurouracil & weekly low-dose Methotrexate (IM or PO). Consult the DIC for further information.Itraconazole will be held at least 48 hrs before the chemotherapy course (or longer) and at 24-48 hrs after, (according to half lives of the last-day chemotherapy).EDUCATE THE PARENTS TO HOLD ITRACONAZOLE 2 DAYS BEFORE EACH COURSE.
9- Voriconazole administration & Interactions: - Given 1 hour before or 2 hours after meals.- Interactions with chemotherapy : the same as Itraconazole but separate it just 12-24 hrs
before and 24-36 hours after chemotherapy.
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10- Enoxaparin (Clexane®) precautions in the day care unit: - Do NOT administer into upper arms (just to avoid administering it intramuscularly).
Administer by deep subcutaneous injection between the left and right anterolateral and left and right posterior abdominal.
- Hold Enoxaparin for INTRATHECALS: Give last dose 24-48 hours prior to procedure. Restart 24 hours after the procedure. YOU MAY GIVE THE PARENTS A COPY OF THE ROAD MAP: mark the weeks at which Enoxaparin will be held. Or YOU MAY JUST HIGHLIGHT THAT IF THE PATIENT WILL BE FASTING FOR AN ITH, that’s when Enoxaparin should be held.
11- Miscellaneous precautions for the patients: - Separate Ciprofloxacin oral from antacids, calcium salts, Iron salts (like in
multivitamins) at least 6 hrs before Ciprofloxacin and at least 2 hours after Ciprofloxacin.- Ciprofloxacin : 1 hr at least before meals. Avoid direct sunlight, & drink plenty of fluids.- Separate Ursodiol (Ursofalk, Ursogall) from aluminum containing antacids at least 6 hrs
before Ursodiol and at least 2 hours after Ursodiol.- Separate Dexamethasone oral from antacids, calcium carbonate at least 2 hrs before and
after.- Sutrim® : shake well & refrigerate for 2 weeks (if suspension), drink plenty of fluids.- Sutrim® : Separate the three days of prophylaxis from IM or oral Methotrexate by 48 hrs,
Ex: If the patient is taking methotrexate at Thursday, tell him to take Sutrim at Sunday, Monday & Tuesday.
- Carboplatin is always BEFORE Etoposide & Cyclophosphamide is always BEFORE Doxorubicin.
12- General regulations in the day care unit: 7- If a course has begun at a date other than when it was written, please write clearly in
file when was day 1, to prevent errors afterwards.8- Check the delivered continuing I.V. medications with the charge nurse 1 hour before
your shift ends, if there are patients that did not come for their medications, get their phone numbers from CERNER & call them right away to get them coming.
9- Same thing for oral medications, call the parents who left their medications at the same day or right at the next day.
10- Always be careful with the NEW ONES (like week 1 continuation Total XV, induction of TXV, day 22, week 1 of any protocol) these are at high risk of forgetting, missing & errors. They should be educated slowly & carefully.
11- Also be careful with 1st times (1st time 6-mp together with dexa at week 72 continuation SR, 1st time delivering IM methotrexate for the NEXT week, NOT TODAY).
12- When a pharmacist in the outpatient clinic writes before his signature: “Patient is on …………… drugs”. You should revise with the parents, the names of these medications, are they taking them regularly or not, when will they have follow ups & are the amount of these medications with them sufficient till the next follow up or not.
Page 52 of 62
1 رقم امتحان ساعة : نصف االمتحان مدة
ذكر مع التالية العبارات ( ) أمام ( ) أو عالمة ضع : األول السؤالالسبب:
( ) معدي مرض . السرطان1( ) جيني مرض . السرطان2( ) وراثي مرض سرطاني مرض . كل3( ) ثانوي سرطان يسبب . الفبسيد4( ) جيدا الزجاجة رج يتم المحلول زجاجة في الفبسيد جرعة نضع . عندما5( ) فجأة االورازون تناول إيقاف الصحيح . من6( ) بسرعة وريد الفبسيد إعطاء من ضرر . ال7( ) الخارج إلى الداخل من بالكحول الكانوال إدخال مكان تطهير . يتم8( ) الداخل إلى الخارج من التنظيف بطريقة الدم من األرض تطهير . يتم9
( ) كبير بحجم ورم وجود حالة في الزيلوريك إعطاء . يتم10( ) الثالجة في الفبسيد وضع . يتم11( ) آخر سيتوسار أي عن يختلف ال الظهر حقنة . سيتوسار12( ) شفاؤه من أمل ال ، قاتل مرض . السرطان13( ) زجاج علي االريديا توضع أن . يجب14
: اختيارك سبب ذكر مع الصحيحة اإلجابة اختار : الثاني السؤال: أي جيني مرض السرطان.1 مرض . كل3 الجينات في خلل سببه مرض . السرطان2 معدي مرض . السرطان1
وراثي مرض سرطانيالسرطان مرض عالج.2 1،2،3 .4 كيماوي.3 إشعاع.2 جراحة.1للعالج: نستخدم فنحن إزالته يستطاع الورم كان إذا.3 .كيماوي3 .إشعاع2 .جراحة1 فنحن معين موقع في محدد لكنه و إزالته يستطاع ال الورم كان .إذا4
للعالج: نستخدم كيماوي. 3إشعاع.2جراحة.1ب: الدم سرطان نعالج.4 كيماوي. 3إشعاع. 2جراحة.1علي: الفبسيد تحضير يتم.5 ج/م.3%5 ج.2 ملح.1: تحليل عمل يتم البالتينول إعطاء قبل.61.s-creatinine 2.ALT 3.AST : االورازون بأخذ المريض ننصح.7 االكل قبل.1 خالية معدة علي.2 االكل بعد.3 علي تحتوي التي المريض محاليل زجاجة علي كتابتها المهمة البيانات.8
11 . Sarcomas تعني الغضاريف و العظم سرطان.1الليمفاوية الغدد و الدم سرطان.2 الجلد و األعضاء تبطن التي الخاليا سرطان .34. 1،2،3
12 .Carcinomas الغضاريف و العظم .سرطان1الليمفاوية الغدد و الدم .سرطان2 الجلد و األعضاء تبطن التي الخاليا .سرطان3 4 .1،2،3
13 .Lymphomas and Leukemias الغضاريف و العظم .سرطان1الليمفاوية الغدد و الدم .سرطان2 الجلد و األعضاء تبطن التي الخاليا .سرطان3 4 .1،2،3
: التالية العبارات اكمل : الثالث السؤال السرطان عالج في نستخدم.11.2.3.4. السيسبالتين مع نستخدمها التي األدوية هي ما.21.2.3.4.5.6. الشعر سقوط لتقليل االدرياميسين مع نستخدمها.3 و الفبسيد امبول من مل نسحب فنحن ، مجم150 فبسيد جرعة لدينا كان إذا .4
%0.9 ملح مل علي نضعه فنحن ، ساعة مدي علي تعليقها الطبيب طلب و ج/م مل250 زجاجة عندنا كان إذا.5
ن/ق تكون بحيث نضبطها مجم15 كانت إذا و ملح مل علي مجم25 كانت إذا االدرياميسين وضع يتم.6
. ملح مل علي توضع: االورازون مع المريض إعطاء يتم.71.2.
إلى السرطان مرض يقسم.81.2.
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3. إذا التالية األدوية من جرعته تبلغ كم سم165 طوله و كجم70 المريض وزن كان إذا.9
البروتوكول: كان2مجم/م50 ادرياميسين
2/م مجم100 فبسيد2مجم/م400 مزنا
2/م مجم1200 هولوكسان
Exam
When the goal of chemotherapy is control or palliation, the purpose of treatment is to:
a. totally eliminate the tumor b. manage symptoms caused by tumor c. improve quality of life d. reduce tumor size
DNA synthesis occurs in which phase of the cell cycle? a. G1b. Sc. G2d. M
Prophase, metaphase, anaphase and telophase occur in which phase of the cell cycle?
a. G1b. Sc. G2d. M
long term use of single agent chemotherapy has been found to: a. achieve long term remission b. cause lethal toxicities c. induce allergies in patients d. result in drug resistant
Principles followed when combining chemotherapeutic agents include:a. The agents should have the same mechanism of action b. The agents should have minimal overlapping toxicityc. The agents should be antagonistic d. Each agent should be effective alone against the tumour
Adjuvant chemotherapy is the use of chemotherapy:
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a. Prior to surgery b. To eliminate micro-metastasis c. In conjunction with radiation therapy d. To eliminate pain cause by the tumour
Chemotherapy effectiveness is influenced by: a. Drug selection b. drug scheduling c. Patient age d. Patient age
Place an (S) if the drug classification is cell cycle specific and (N) if the classification is cell cycle nonspecific:
Match between column A and B Column A Column B Drug classification Mechanism of action
1. 1.alkylators a. unknown mechanism of action 2. antimetabolites b. causes abnormal linking of DNA base pair 3. antitumor antibiotics c. alters cellular environment4. plant alkaloids d. substitutes for natural metabolites 5. hormones e. binds or reacts with DNA
6. miscellaneous agents f. binds to microtubular proteins duringAn example of combination chemotherapy is FAC answer the following:
1. drugs used in this Protocol 2. the drug classification(s) utilized in this protocol 3. the portion of the cell cycle affected by the drugs utilized by this protocol4. use of this protocol 5. doses for each drug6. administration of drugs and order of administration 7. differences between 5-FU iv-shot and infusion 8. explain the significant of Vd9. Dose limiting toxicity 10. supportive care
Complete 1. neoadjuvant treatment is _______________________________________2. The three goals of chemotherapy are 1. 2. 3.3. A cure occurs when malignant cells are _____________________.4. The administration of two or more chemotherapy agents is known as___________.
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5. One mechanism by which tumor cells become resistant to chemotherapy drugs is through the cell surface protein called ______________________, which acts as a pump and remove the drug from inside the cell before the cell is destroyed. 6. Radiation recall reaction is _____________________________________________ and is caused by _______________________________________________________7. A syndrome is _______________________________________________________8. Auto oxidation occur with ____________________9. Dose limiting toxicity of chemotherapy is _________________________________10. Mesna is used for ___________________________________________________11. Leucovorin is used before 5Fu to____________________________________ and after MTx as _______________________________. 12. VCR side effects include 1. _____________2._____________ 3._______13. Adverse prognostic factors in node –ve Breast patients are
14. CMF: Bonadonna Protocol Cyclophosphamide: ______ mg/m2, po daily x 14 days Methotrexate: -__________mg/m2, iv, days 1 & 8 5-Fluorouracil: ___________ mg/m2, iv, days 1 & 8
15.Treatment schedule: q___________weeks .For adjuvant therapy, a total of __________cycles is prescribed ,Hematological parameters: ANC_________; platelets__________ .Standard antiemetics, e.g.: metoclopramide ______mg po, Gravol 50 mg po .Consider supporting with G-CSF in face of prolonged _____________ .Encourage fluid intake of at least _____/day to minimize both ____________ toxicity as well as impact of ________________________ on bladder
16.In CMF Variants (1) Consider ________ antagonists for antiemetic prophylaxis
17.AC: Adriamycin: _______ mg/m2, iv Cyclophosphamide _______ mg/m2, iv
18.Treatment schedule: q_______weeks .Total of ______ cycles, for adjuvant therapy Haematological parameters: ANC ____________; platelets:____________ Consider nadir CBC at day ___________Antiemetic prophylaxis: ___________ antagonists +________________
19.CEF: Adjuvant Therapy in Node +ve Breast Carcinoma
20.Cyclophosphamide _______mg/m2, po x 14 days Epirubicin ______________ mg/m2, iv, days 1 & 8 5-Fluorouracil ___________ mg/m2, iv, days 1 & 8
21.Treatment schedule: q_______weeks, for total of _________cycles . G-CSF support, as indicated, to avoid ______________________
22.IV FAC/FEC 5-Fluorouracil _________mg/m2, iv Adriamycin/Epirubicin _______mg/m2, iv Cyclophosphamide __________mg/m2, iv
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23.Second and Third-Line Chemotherapy in Advanced Breast Carcinoma is _________________ 100 mg/m2, iv over 1 hour
24. Taxotere Mandatory premedication with __________ 8 mg bid x 5 days, starting 24 hours prior to taxotere. Chemotherapy cannot be given without this.
25.Navelbine Navelbine ________ mg/m2, iv, days 1, 8 & 15
26.Capecitabine Capecitabine ___________mg/m2/day, divided into 2 doses x 14 days, po
27.DLT is _____________ which may be severe .Caution regarding possible development of __________________syndrome. Treatment with pyridoxine 50 mg tid, po.
Q by patients :
1. How is chemotherapy is given? The drugs can be delivered to our circulatory system by many different routes:
2. How will I know if the chemotherapy is working? There are several ways to tell if a tumor is responding to treatment.
3.Corticosteroids : Cortisol (hydrocortisone) and cortisone: these are__________ occurring corticosteroids. Other corticosteroids are synthetic: Examples include fludrocortisone ,____________ ,prednisolone ,fluocortolone ,_______________ and betamethasone.
4.Femara New Weapon In The Battle Femara (_________________)Femara, is an______________________ inhibitor. ____________fuels the growth of about half of all breast cancers, especially those in older women. Tamoxifen, the top hormonal treatment for estrogen-fueled tumors. Commonly reported adverse events for Femara vs. Tamoxifen were _______________. Femara may cause fetal harm when administered to___________women. Tamoxifen has been linked to increases in women’s risk of _________________ cancer or blood clots.
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Extravasation:
1. Doxorubicin, daunorubicin, epirubicin and mitomycin bind to DNA, recycle locally and may cause a progressive _________________ over several weeks, requiring excision and skin grafting. In order to avoid problems of this kind, great care must be taken to assure that these agents are given into an __________ vein with a good free flow of blood. Drug may leak from sites of previous recent punctures or from veins which are occluded from any cause such as tight clothing, obstructing masses or clotting. Therefore, the insertion site should not be _______________ to a recent venipuncture or in an arm with compromised circulation. It is preferable to select, if possible, a ________vein which is not adjacent to a joint or structures which may be particularly troublesome should a tissue slough occur (such as the wrist or hand).
2. Doxorubicin and epirubicin are particularly likely to cause a ____________________ (a histamine release phenomenon) which will subside but may take thirty minutes or more after the injection is stopped. _____________ injected into the IV line may hasten clearing of the reaction, and requires a physician’s order. The injection may then be cautiously resumed.Thrombosis or sclerosis of veins may occur due to the local effect of chemotherapeutic agents on the endothelium. These can be managed conservatively with ___________ compresses to the area plus an a_________for pain, if required.
3. Extravasation Tray contain
4. Procedure for the extravasation of a VESICANT wii be :
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5. Several mechanisms by which certain agents can cause tissue necrosis by extravasation:
12345
6. Medications that may cause extravasation-
123456
7. Preventative Measures-how to prevent extravasation ?
1
2
3
4
5
6
7
8
9
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10
1. Apoptosis is ____________________________ 2.Why should a cell commit suicide? 1.
2.
2.Blood is a liquid tissue. Suspended in the watery plasma are seven types of cells and cell fragments:1
2
3
4
5
6
7
3.five kinds of white blood cells ( WBC s) or leukocytes 1
5. Two kinds of leukocytes without granules in their cytoplasm1
2
6. If one takes a sample of blood, treats it with an agent to prevent clotting, and spins it in a centrifuge, the red cells _______________while the white cells ___________ forming the _________________.The fraction occupied by the red cells is called the ____________. Normally it is approximately 45%. Values much lower than this are a sign of anemia.
7. Functions of the blood is 1
2
8. All the various types of blood cells are produced in the ______________(some 1011
of them each day in an adult human!). arise from a single type of cell called a _____________________.
9. A eukaryotic cell cannot divide into two, the two into four, etc. unless two processes alternate:
1
2
10. the cell cycle consists of:
G1 =
S =
G2 =
M =
15. The p53 protein senses DNA damage and can halt progression of the cell cycle in both G1 and G2. Both copies of the p53 gene must be mutated for this to fail so mutations in p53 are recessive, and p53 qualifies as a ____________________ gene. The p53 protein is also a key player in ____________, forcing "bad" cells to commit suicide.
