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%
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 gene
b. the loss of normal function of two alleles of a gene
c. 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 fludarabine c. fludarabine can impair the metabolism of Cytarabine d. fludarabine can increase the metabolism of Cytarabine e. 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 of a. genetic variation that gives rise to differing response to drugs
b. 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 to
a. CNS prophylaxis
b. Systemically increase the level of methotrexate c. 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 intrathecally c. None of the above
21. Prognosis is
a. the prior knowledge of outcome of a disease
b. the increase in intensity of therapy c. 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 temperature c. 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 units c. 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. VP16
b. prednisone c.All of the above d. None of the above
29. The TPMT polymorphism is significant for the dosing and toxicity of: a. Dexamethasone
b. 6-thioguanine c. 6-mercaptopurine
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 remains
d. None of the above e. All of the above
31.The goal of consolidation therapy for All is
a. Bring the disease into remissionb. 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
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 __________chromosome a. Phildelphia chromosome
b. BCR1
c. 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.T
b.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
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 therapy
a.High risk treatment was Anti-metabolite based
b.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 years
b.Decreased WBC c.White race
42. this curve shows that worst survival is for D15 BM
a.0% blasts b.1-4% 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
a. one reinduction b. double reinduction
46. Toxicities Associated with CNS Irradiation are a.Second malignancy
c.Endocrinopathy
d. all of the above
47. Principles of Treatment in ALL includes a. Risk-directed therapy
b. delayed intensification of chemotherapy c. 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/m2
52. Pharmaceutical care is………
a- Individual patient oriented service b- Disease oriented service
c-Product oriented service d - Doctor oriented service
53. Clinical pharmacy service started from ………..
a- 1950 b- 1970 c- 1960 d- 1990
54. 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 interactions
57. 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. 59. Source of patient database is……
a- Patient family. b- Patient profile. c- Patient doctor. 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 use b. advice on side effects c. storage
d. diet and life style modifications e. All
f. only a,b,c g. None
62. . ………….. is the one who sees the patient and the Medications just before administration. a.Nurse b.Pharmacist c.Physician d.All e.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.All e.None
64.Only with smart communication, Pharmacist will be able to provide the following:
a.Design Pharmaceutical Care Plan
b.Achieving Successful Clinical Intervention c.Patient Counseling d.All e.Only a,b f.Only b,c g.Only a,c h.None
65.The following may influence the process of patient counseling except: a.Cost of medication
b.Pharmacist communication skills c.Patient culture
d.Availability of medical information e.All f.None
66.Considerations throughout Patient Interview: a.Rapport
b.Successful Communication c.Patient-centered language d.All
e.None
67.In order to attract patient attention and to ensure positive response to information provided through patient counseling, pharmacist should :
a.Show professionalism during interview by talking with patient about drug pharmacokinetics
b.Skip patient complaints about his drugs which may not be -according to references- of clinical importance
c.Highlight and describe prescription errors committed by the prescriber and the corrections
d.Stand very close to patient
e.Focus on medications and medical conditions f.Use medical terminology during patient interview. g.All
h.none
68.The first step of patient counseling is: a.Providing information
b.Non drug options
c.Gathering patient information d.None
69.The last step of patient counseling: a.Follow up and closure
b.Providing information c.Non drug options
d.Gathering patient information e.None
70.The following is not important information to provide through patient counseling:
a.Medication identity b.Indications
d.Potential interactions or therapeutic contraindications e.Side effects
f.All g.None
71. All of the following from the common side effects of chemotherapy except: a. Nausea
b. Vomiting c. Headache d. Mucositis
72-Neo-adjuvant chemotherapy means: a. Make a tumor smaller before surgery b. Destroy the tumor after surgery c. Use chemotherapy with radiotherapy d. None of the above
73-The goal of using chemotherapy with radiotherapy in some types of cancer is: a. Increase efficacy of the chemotherapy
b. Decrease the side effect of the chemotherapy c. Increase the cancer cell sensitivity to radiation
74-All of the following are Asparaginase side effects except : a. Hyperglycemia
b. Anaphylaxis
c. Loss of tendon reflex d. Thrombosis
75-The max dose of vincristine is : a. 2 ml
b. 2mg c. 20 mg d. 0.2 ml
76-Before Doxorubicin administration you must check: a. Random blood sugar
b. ECHO
c. Blood pressure d. Creatinine clearance 77-Doxorubicin is infused over;
a. 2 hr b. 23 hr c. 4 hr d. Iv push
78-Before Etoposide you must check: a. Random blood sugar
b. ECHO
c. Blood pressure d. Chest x-ray
79-Cisplatin is infused over : a. 24 hr
b. 6hr c. 4hr d. 2hr
80-Before Methotrexate infusion you must check : a. Chest x-ray
b. ECHO
c. Blood pressure d. Random blood sugar
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 IV
Folinic Acid 175 mg IV 82. How does Irinotecan act?
a. Topoisomerase I inhibitor b. Topoisomerase II inhibitor c. Alkylating agent
d.Antimetabolites
83. Irinotecan is converted by carboxylesterases to its more active metabolite, 7-ethyl-10 hydroxy-camptothecin, or SN-38. T F
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 phase
c. a and b
86. Fluorouracil is converted to FdUMP, leading to a.inhibition of TS
b.depletion of deoxythymidine triphosphate (dTTP) pools
c. 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 DNA b.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
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.diarrhea
b.neutropenia c. 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 syndrome
b. 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 mg
b. Loperamide c. Senna extract
95. Late events of diarrhea are managed successfully by administering a. IV or SC atropine 0.25 to 1.0 mg
b. 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 F
98. Freezing irinotecan of irinotecan should be done . T F 99. 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).
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-38 b. T20 c. 3A4 d. 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 failure b. Depression
c. Severe neutropenia d. 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 F
107. 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 agent b. 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.
b. phase-specific
112. MM ,68 Y., Non Small cell Lung Cancer taking 1st course of MIT
chemotherapy • Mitomycin 6mg/m2 • Ifosfamide 3 g/m2 • Mesna • Cisplatin 50 mg/m2 • GFR 50ml/min Main ADR of MIT is /are?
a. Myelosuppression, Nausea and vomiting b. Pulmonary toxicity
c.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 doxorubicin
c. a and b
114. Radiation recall reactions is caused by a.5FU
b. Irrinotecan c. Mitomycin d. 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 of a. MIT
b. carboplatin and paclitaxel c.FAC
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 phase
b. S phase c. M phase
124. Does combination carboplatin and docetaxel provide advantage?
a. Yes b. NO
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 restriction b. diuretics
c. a and b
126. The incidence and severity of Docetaxel-induced fluid retention increase in incidence with
a. 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 Ototoxicities
130.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. intravenously c. I.M
d.oral
132. Amifostine after reconstitution with a. G5%
b. G/NS C. 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 cell
b.altered dihydrofolate reductase enzyme -- lower affinity for methotrexate c.decreased polyglutamate formation
d. 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 phase
b. S phase c. 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
a. CXR before every dose b. measure creatinine clearance c. measure liver functions d. 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 3
c. Cyclophosphamide 1 2 3
135. 5 FU Effects on RNA occur especially with
a. bolus administration
b. Continuous Infusion
136. Fluorouracil is cell cycle phase-specific
a. G phaseb. S phase c. 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.
• 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.
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 LDH
HCG Human Chorionic
Gonadotropin A nonspecific marker for pancreatic, pituitary, and placental tumors; elevated levels may be present in pancreatic cancer.
TUMOR MARKERS CANCERS WHAT ELSE? WHEN/HOW USED USUAL SAMPLE
AFP (Alpha-feto protein)
Liver, germ cell cancer of ovaries or testes
Also elevated during pregnancy Help diagnose, monitor treatment, and determine recurrence
Blood
TUMOR MARKERS CANCERS WHAT ELSE? WHEN/HOW USED USUAL SAMPLE
microglobulin) and lymphomas including Crohn's disease and hepatitis; often used to determine cause of renal failure
CA 15-3 (Cancer antigen 15-3)
Breast cancer and others, including lung, ovarian
Also elevated in benign breast conditions; doctor can use CA 15-3 or CA 27.29 (two different assays for same marker)
Stage disease, monitor treatment, and determine recurrence
Blood
CA 19-9 (Cancer antigen 19-9)
Pancreatic, sometimes colorectal
and bile ducts
Also elevated in pancreatitis and
inflammatory bowel disease
Stage disease, monitor treatment, and determine recurrence
Blood
CA-125 (Cancer antigen 125)
Ovarian Also elevated with endometriosis, some
other benign diseases and conditions; not recommended as a general screen
Help diagnose, monitor treatment, and determine recurrence
Blood
Calcitonin Thyroid medullary carcinoma Also elevated in pernicious anemia and
thyroiditis
Help diagnose, monitor treatment, and determine recurrence
Blood
CEA (Carcino-embryonic antigen)
Colorectal, lung,
breast, thyroid, pancreatic, liver,
cervix, and bladder
Elevated in other conditions such as
hepatitis, COPD, colitis, pancreatitis, and in cigarette smokers
Monitor treatment and determine recurrence Blood Chromogranin A (CgA) Neuroendocrine tumors (carcinoid tumors, neuroblastoma)
May be most sensitive tumor marker for carcinoid tumors
To help diagnose and monitor
Blood
Estrogen receptors Breast Increased in hormone-dependent cancer Determine prognosis and
guide treatment
Tissue
hCG (Human chorionic gonadotropin)
Testicular and trophoblastic disease
Elevated in pregnancy, testicular failure Help diagnose, monitor treatment, and determine recurrence
Blood, urine
TUMOR MARKERS CANCERS WHAT ELSE? WHEN/HOW USED USUAL SAMPLE
copies in 20-30% of invasive breast cancer
guide treatment
Monoclonal immunoglobulins
Multiple myeloma and Waldenstrom’s macroglobulinemia
Overproduction of an immunoglobulin or antibody, usually detected by protein electrophoresis
Help diagnose, monitor treatment, and determine recurrence
Blood, urine
Progesterone receptors
Breast Increased in hormone-dependent cancer Determine prognosis and
guide treatment
Tissue
PSA (Prostate specific antigen), total and free
Prostate Elevated in benign prostatic hyperplasia,
prostatitis and with age
Screen for and help diagnose, monitor treatment, and determine recurrence
Blood
Thyroglobulin Thyroid Used after thyroid is removed to
evaluate treatment
Determine recurrence Blood
Other Tumor Markers Less Widely Used
BTA (Bladder tumor antigen)
Bladder Not widely available, but gaining acceptance
Help diagnose and determine recurrence
Urine
CA 72-4 (Cancer antigen 72-4)
Ovarian No evidence that it is better than
CA-125 but may be useful when combined with it; still being studied
Help diagnose Blood
Des-gamma-carboxy prothrombin (DCP)
Hepatocellular carcinoma (HCC)New test; often used along with an imaging study plus AFP and/or AFP-L3% to evaluate if someone with
To evaluate risk of developing HCC; to evaluate treatment; to
TUMOR MARKERS CANCERS WHAT ELSE? WHEN/HOW USED USUAL SAMPLE
chronic liver disease has developed HCC
monitor for recurrence
EGFR (Her-1) Solid tumors, such as of the lung (non small cell), head and neck, colon, pancreas, or breast
Not available in every laboratory Guide treatment and determine prognosis
Tissue
NSE (Neuron-specific enolase)
Neuroblastoma, small cell lung cancer
May be better than CEA for following this particular kind of lung cancer
Monitor treatment Blood
NMP22 Bladder Not widely used Help diagnose and determine recurrence
Urine
Prostate-specific membrane antigen (PSMA)
Prostate Not widely used; levels increase
normally with age
Help diagnose Blood
Prostatic acid phosphatase (PAP)
Metastatic prostate cancer, myeloma, lung cancer
Not widely used anymore; elevated in prostatitis and other conditions
Help diagnose Blood
S-100 Metastatic melanoma Not widely used Help diagnose Blood
Soluble Mesothelin-Related Peptides
(SMRP)
Mesothelioma Often used in conjunction with imaging tests
To monitor progression or recurrence
Blood
TA-90 Metastatic melanoma Not widely used, being studied Help diagnose Blood
Drugs
Consequence of interactionProcarbazine +
Sympathomimetics or
tyramine-containing food
May cause an abrupt
increase in BP, resulting in a potentially fatal hypertensive crisis (procarbazine is a weak MAOI)
Procarbazine
+
Benzodiazepines
Procarbazine is cyp450 inhibdec metab of BDZ & barbiturates & narcotics
Interleukin-2 +
Antihypertensive drugs
Cause enhanced hypotensive effects
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 themyelosuppressive 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
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
IL-2 + aminoglycosides Concurrent administration of drugs possessing nephrotoxic (e.g., aminoglycosides, indomethacin), myelotoxic (e.g., cytotoxic chemotherapy), cardiotoxic (e.g., doxorubicin) or 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 + 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+MTX
Teniposide (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
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
Nausea and vomitingAnticipatory 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.
Extravasation Stop the injection/infusion. Disconnect the 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 whether
neither is required; and what further
treatment is recommended. Follow guidance in flow chart
below accordingly.
_ Note that for Neutral drugs, neither a cold pack nor a hot pack is required. Aspirate as much
fluid as possible, and then remove the peripheral cannula. No further treatment should be
required. 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.
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. 8. Topical agents
9. Laser therapy 10. Growth factors.
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
Drugs
Important Adverse Effects
Cyclophosphamide Acute hemorrhagic cystitis.
Methotrexate
Kidney damage, pulmonary fibrosis,
hepatotoxicity & stomatitis.
Paclitaxel
Hypersensitivity & peripheral
neuropathy
Cisplatin
Nephrotoxicity, severe emesis,
neurotoxicity & ototoxicity.
Ifosfamide
Acute hemorrhagic cystitis
Asparaginase
Coagulation deficiencies, liver injury,
hypersensitivity reactions
Doxorubicin
Cardiotoxicity (cardiomyopathy)
Bleomycin
Fatal lung toxicity
Vincristine
Peripheral neurotoxicity
Interferon
Flu like syndrome, dizzness, diarrhea,
anorexia, wt loss, abdominal pain,
thyroid dysfunction and depression
Interleukin-2
Capillary leak syndrome
Flutamide
Hepatotoxicity, gynecomastia &
diarrhea
Leuprolide
Initial flare of prostate symptoms
Irinotecan
Acute cholinergic syndrome (diarrhea,
abdominal cramps, increased
secretions)
Tamoxifen
Thromboembolism & increased risk of
endometrial carcinoma
Trastuzumab
Hypotension, flushing,
bronchconstriction, skin rash &
sensitizes patients to cardiotoxicity.
143.
Pharmaceutical Care & Pharmacotherapy Workup 1. the two arms of leukemia are :
a. b.
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 2. Purinethol is a drug used in treatment of ___________________ 3. When should a patient take Purinethol?
4. Asparaginase MEDAC is ____potency of Asparaginase MERK 5. Methotrexate has a high Vd,what should we look for in the patient 6. Methotrexate is >90% plasma protein bound which lab should we
follow
7. 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 decreased a.
11. Increase in PH with alkalnization will affect Allantoin solubility T-F 12. 25% of AML patients will have _______ gene mutation
13. ATRA is used to _______________APL cells
14. Dexamethasone is used for Brain tumor patients during ChemotherapyT-F
15. 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
145. Patient Counseling
1- 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).
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: 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:
- 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.
- Cyclo & Ifosfamide: Void urine frequently (every 2 hrs), drink fluids & report any
burning sensation.
- 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.
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) Phenytoin E) C + DF) B + D
152.Itraconazole should to be stopped with the following Chemotherapy except: A) CytarabineB) VincristineC) EtoposideD) Doxorubicin
E) 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
154.
1. What is missing from this physician order?
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.
158.
What is different between 1st and 2nd ADE?
159.
160.
Why is Voriconazole used ?
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 patients
b. 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 are a.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 disease
f. the increase in intensity of therapy g. 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 acid
f. an anticancer alkylating agent g. All of the above
171. Storage of Asparaginase Medac
e. Must be in the refrigerator
f. Can be in Room temperature g. 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 units
e. 8000 international units f. 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 week e. 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 Toxicities Eliminate cranial irradiation
Limit 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 isomers
c. All of the above d. None of the above
177.TPMT is responsible for
a. Inactivation of 6MP b. Activation of 6MP c. All of the above d. None of the above
178.Heterozygocity means Loss of heterozygosity (LOH) in a cell represents
a. the loss of normal function of one allele of a gene
b. the loss of normal function of two alleles of a gene
c. 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 to
e. CNS prophylaxis
f. Systemically increase the level of methotrexate g. All of the above
h. None of the above
181.Methotrexate ,Cytosar and Hydrocortisone
d. Can be given together as intrathecal injection e. Drug drug interaction prevent co-administration f. None of the above
182.Vincristine
d. Is Fatal if given intrathecally e. Is only given intrathecally f. None of the above
1. Causes for mortality and morbidity of children n the developing world are ranked as follows : ( ) Accidents ( ) Malnutrition ( ) Malaria ( ) Respiratory Infections ( ) HIV ( ) Cancer 2. Leukemogenesis concerns a. b. c.
3. the two arms of leukemia are : a.
b.
4. which of the following is good prognosis for ALL a. MLL rearrangement b. Hyperdiploidy
5. Determinant of treatment response include a.
b. c. d.
6. The lymphoid arm produces a. b.
7. Principles of treatment of leukemia based on St. Jude total XV are a.
b. c.
8. Another name for BCR-ABL fusion gene is __________chromosome 9. The drug targeting BCR/ABL fusion gene is _________________ 10. ALL stands for _______________
11. ALL treatment phases includes
Phase Goal
13. A patient is taking Enoxeprine for coagulopathy and his due to receive his intrathecal
after tomorrow ,what instructions should the pharmacists tell the patient? 14. TPMT is the enzyme metabolizing _____________to its inactive form 15. Purinethol is a drug used in treatment of ___________________ 16. When should a patient take Purinethol?
17. Asparaginase MEDAC is ____potency of Asparaginase MERK 18. Methotrexate has a high Vd,what should we look for in the patient 19. Methotrexate is >90% plasma protein bound which lab should we follow 20. The three important P450 Cytochrome include
a. b. c.
21. In tumor lysis syndrome the following lab values are increased a.
b. c.
22. In tumor lysis syndrome the following lab values are decreased a.
23. Increase in PH with alkalnization will affect Allantoin solubility T-F 24. 25% of AML patients will have _______ gene mutation
25. ATRA is used to _______________APL cells
26. Dexamethasone is used for Brain tumor patients during Chemotherapy T-F
27. Three most common pediatric cancers include a.
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
