Anticancer Drugs MCQS. 74

01. Mechanism of action of Methotrexate?

A. Dihydrofolate reductase inhibitor

B. Inhibition of purine ring 

C. Inhibit dTMP biosynthesis 

D. A & B

E. All of the above 

Answer: E. All of the above 

Methotrexate: Small amount of MTX undergo hydroxylation at the 7th position to form 7-hydroxymethotrexate which is less water soluble than MTX and lead to crystalluria. That's why patients should be well hydrated to avoid renal toxicity.

02. Mechanism of action of 5-Fluorouracil?

A. Dihydrofolate reductase inhibitor 

B. Inhibit dTMP synthesis 

C. Terminate DNA chain elongation 

D. Scission of DNA by oxidation

E. Disrupts DNA function 

Answer: B. Inhibit dTMP synthesis 

Needed for DNA synthesis 

High level of dihydropyrimidine dehydrogenase DPD can increase the rate of 5FU catabolism leading to decrease in bioavailability. 

Low levels of DPD causes severe toxicity like diarrhoea, pancytopenia, mucositis.

Same like Flucytosine antimetabolite antifungal drug.

03. Mechanism of action of Cytarabine?

A. Dihydrofolate reductase inhibitor 

B. Inhibit dTMP synthesis 

C. Terminate DNA chain elongation 

D. Scission of DNA by oxidation

E. Disrupts DNA function 

Answer: C. Terminate DNA chain elongation 

04. Mechanism of action of Bleomycin?

A. A. Dihydrofolate reductase inhibitor 

B. Inhibit dTMP synthesis 

C. Terminate DNA chain elongation 

D. Scission of DNA by oxidation

E. Disrupts DNA function 

Answer: D. Scission of DNA by oxidation

 

05. Mechanism of action of Dactinomycin?

A. A. Dihydrofolate reductase inhibitor 

B. Inhibit dTMP synthesis 

C. Terminate DNA chain elongation 

D. Scission of DNA by oxidation

E. Disrupts DNA function 

Answer: E. Disrupts DNA function 

06. Mechanism of action of Leucovorin?

A. A. Dihydrofolate reductase inhibitor 

B. Inhibit dTMP synthesis 

C. Terminate DNA chain elongation 

D. Scission of DNA by oxidation

E. Reverse inhibition of dihydrofolate reductase 

Answer: E. Reverse inhibition of dihydrofolate reductase 

07. Which of the following statements about Methotrexate is wrong?

A. Anti folate agent

B. Specific for S phase 

C. Inhibit thymidylate synthase

D. Low dose for psoriasis 

E. Pemetrexed antidote to methotrexate 

Answer: E. Pemetrexed antidote to methotrexate 

Pemetrexed and Pralatrexate are also anti metabolites that inhibit DHFR. 

Pemetrexed is used for non small cell lung 

Pralatrexate is used in relapsed or refractory T-cell lymphoma 

08. Methotrexate in combination is affective against following?

A. Acute lymphocytic leukaemia 

B. Burkitt Lymphoma

C. Breast cancer 

D. Bladder cancer 

E. Head and neck carcinoma 

F. All of the above 

Answer: F. All of the above 

09. Methotrexate doesn't easily penetrate the blood brain barrier, following route used to destroy neoplastic cells in sanctuary of CNS?

A. Intravenous 

B. Intrathecally 

C. Intramuscular 

D. Sublingual 

E. Subcutaneous 

Answer: B. Intrathecally 

10. Pralatrexate and Pemetrexed should be given with following to reduce hematologic and GI toxicity?

A. Cladribine 

B. Cisplatin

C. Folic acid 

D. Cytarabine 

E. Azacitidine

Answer: C. Folic acid 

11. Following drug is administered IV rather than orally because intestinal bacteria split off the sugar to yield the very toxic metabolite, fluoroadenine?

A. 5-Fluorouracil

B. Fludarabine 

C. Azacitidine

D. 6-Mercaptopurine

Answer: B. Fludarabine 

12. Which of the following statements about 5-Fluorouracil is wrong?

A. Pyrimidine Analog 

B. Stable fluorine atom at position 5 or uracil ring

C. Fluorine interrupt conversion of deoxyuridylic acid to thymidylic acid

D. Used in slow growing solid tumor

E. Not effective for superficial basal cell carcinoma 

Answer: E. Not effective for superficial basal cell carcinoma 

Fluorine interrupt conversion of deoxyuridylic acid to thymidylic acid, this leads to lack the cell of thymidine which is an essential precursor for DNA synthesis.

13. Thymidine less death of rapidly dividing cells caused by?

A. Gemcitabine

B. Azacitidine 

C. Capecitabine 

D. 5-Fluorouracil

E. Cytarabine 

Answer: D. 5-Fluorouracil

5-FC enter the cell and converted to the deoxynucleotide(5-fluoro-deoxyuridine mono phosphate 5-FdUMP. Which competes with deoxyuridine mono phosphate for thymidylate synthase thus inhibiting it's action.

14. Inhibition of thymidylate synthase by 5-Fluorouracil causes reduced folate coenzyme, to prevent this folate reduction we use?

A. Methotrexate 

B. Leucovorin 

C. Capecitabine 

D. Azacitidine 

E. Gemcitabine 

Answer: B. Leucovorin 

15. Body surface area (BSA) is used in calculating chemotherapy doses because?

(A) BSA is anindicator of tumor cell mass.

(B) BSA correlates with cardiac output.

(C) BSA correlates with gastrointestinal transit

time.

(D) the National Cancer Institute requires that BSA

be used.

(E) the U.S. Food and Drug Administration (FDA) requires that BSA be used.

Answer: (B) BSA correlates with cardiac output.

16. The rationale for combination chemotherapy includes all of the following except

(A) biochemical enhancement of effect.

(B) rescue of normal cells.

(C) overcoming or preventing resistance.

(D) biochemical nullification of effect.

(E) cytotoxic to both resting and dividing cells.

Answer: D) biochemical nullification of effect.

17. All of the following chemotherapy agents can be administered intrathecally except

(A) methotrexate. 

(B) cytarabine.

(C) hydrocortisone. 

(D) thiotepa.

(E) vincristine.

Answer: E) vincristine.

18. Hypersensitivity reactions have been commonly associated with all of the following agents except

(A) asparaginase.

(B) busulfan.

(C) carboplatin.

(D) etoposide.

(E) paclitaxel.

Answer: B. Busulfan

19. Which of these supportive agents may have a greater risk than benefit in patients with cancer when the goal is cure due to the potential increased risk of tumor progression?

(A) Antiemetics

(B) Colony-stimulating factors

(C) Corticosteroids

(D) Erythropoietin-stimulating agents

(E) Oprelvekin (IL-11)

Answer: D) Erythropoietin-stimulating agents

20. How do antimetabolites exert their cytotoxic effect?

(A) Inhibiting DNA synthesis by sliding between DNA base pairs

(B) Inhibiting RNA synthesis by sliding between RNA base pairs

(C) Actingasfalsemetabolitesinthemicrotubules

(D) Acting as false substitutions in the production of

nucleic acids

(E) Promoting microtubule assembly and

stabilization

Answer: D) Acting as false substitutions in the production of

nucleic acids

21. All of the following chemotherapy agents work through affecting microtubule function except

(A) docetaxel.

(B) vinblastine. 

(C) mitoxantrone. 

(D) vincristine. 

(E) vinorelbine.

Answer: A) docetaxel.

22. When does the neutrophil nadir associated with chemotherapy agents generally occur?

(A) During administration of the chemotherapy

(B) 1 to 2 days after therapy

(C) 10 to14 days after therapy

(D) 1 month after therapy

(E) When the platelet count begins to rise

Answer: C) 10 to14 days after therapy

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Anticancer Drugs MCQS. 73

01. Chemotherapy therapy with Methotrexate, following drug is used to reverse the inhibition of dihydrofolate reductase?

A. Allopurinol 

B. 5-fluorouracil

C. Ifosfamide 

D. Mesna 

E. Leucovorin 

Answer: E. Leucovorin 

Leucovorin is used to reverse the inhibition of dihydrofolate reductase enzyme that is needed to convert folic acid to its active tetrahydrofolic acid (FH4). 

02. Which of the following drugs is antidote of Methotrexate?

A. Allopurinol 

B. Vincomycin

C. Warfarin 

D. Naloxone 

E. Leucovorin 

Answer: E. Leucovorin 

Two more antidotes, thymidine and glucarpidase

03. Dihydrofolate reductase enzyme that convert folic acid to active tetrahydrofolic acid (FH4) in inhibited by?

A. Methotrexate 

B. Etoposide 

C. Cisplatin

D. Fludarabine

E. 6-mercapopurine

Answer: A. Methotrexate 

Also Pemetrexed and Pralatrexate.

04. Dihydrofolate reductase enzyme that convert folic acid to active tetrahydrofolic acid (FH4) in inhibited by?

A.  Pemetrexed

B. Etoposide 

C. Cisplatin

D. Fludarabine

E. 6-mercapopurine

Answer: A. Methotrexate 

Also methotrexate and Pralatrexate.

05. Chemotherapy given before the surgical procedure in an attempt to shrink the cancer is called?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: B. Neoadjuvant

06. A patient is about to undergo the three cycle of chemotherapy prior to surgery for bladder. Which best describes chemotherapy in this setting?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: B. Neoadjuvant

07. Chemotherapy given in lower doses to assist in prolonging a remission is known as?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: D. Maintenance 

08. Chemotherapy is indicated when neoplasm are disseminated and are not able to surgery. This therapy is called?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: C. Palliative 

In advance stages of cancer, controlling the cancer is low and the goal is palliative ( alleviation of symptoms and avoidance of life threatening toxiy. Survival is extended with this therapy but the patient eventually dies of the disease. 

09.  In advance stages of cancer, controlling the cancer is low and the goal is alleviation of symptoms and avoidance of life threatening toxicity?therapy called?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: C. Palliative therapy 

10. Chemotherapy used as supplemental treatment to attack micrometastases following surgery and radiation treatment is called?

A. Adjuvant

B. Neoadjuvant

C. Palliative 

D. Maintenance 

Answer: A. Adjuvant 

11. Which of the following cells are more sensitive to chemotherapy?

A. Rapidly dividing cells 

B. Slowly proliferating cells 

C. Nondividing Cells 

D. Normal cells 

Answer: Rapidly dividing cells 

Less sensitive to slowly proliferating cells while non dividing cells (G0 phase) servive the toxic effects of many chemotherapy drugs.

12. Leukaemic or other tumor cells find sanctuary in tissue such as CNS where some chemotherapeutic drugs can't enter. Which of the following route is suitable to eliminate these cells?

A. Oral 

B. Intrathecal

C. Sublingual  

D. Intramuscular 

Answer: B. Intrathecal

Some drugs are unable to penetrate certain areas of solid tumours.

13. Which of the following is the advantage of combination chemotherapy?

A. Max cell killing within tolerated toxicity 

B. Delay the development of resistant cell lines 

C. Prevent the development of resistant cell lines 

D. Effective against broader range of cell lines 

E. All of these 

Answer: E. All of these 

14. Inhibit the de novo synthesis of purine ring and inhibit nucleotide interconversions?

A. 6-Mercaptopurine

B. 6- Thioguanine

C. Methotrexate 

D. A & B

E. All of the above 

Answer: D. A & B

Both drugs are purine antimetabolites and 6MP is a thiol analog of hypoxanthine. First purine analog to treat neoplastic disease in acute lymphoblastic leukaemia also in Crohn's disease.

15. Azathioprine is an immunosuppressant exert its cytotoxic effects after conversion to following drug?

A. 6-Mercaptopurine

B. 5-Fluorouracil

C. Fludarabine

D. Capecitabine

E. Cytarabine 

Answer: A. 6-Mercaptopurine

Because Azathioprine is an analog of 6-MP and is benificial in treating Crohn disease.

16. 6-Mercaptopurine along with its following analog is benificial in treating Crohn's disease?

A. Methotrexate 

B. 6-Thioguanine

C. 5-Fuorouracil

D. Azathioprine 

E. Capecitabine

Answer: D. Azathioprine 

It's an immunosuppressant drug. 

17. Dose of 6-Mercaptopurine is reduced by 50%_70% when used with following drug to prevent toxicity?

A. Methotrexate 

B. 6-Thioguanine

C. 5-Fuorouracil

D. Azathioprine 

E. Capecitabine

Answer: D. Azathioprine 

It's an immunosuppressant drug. 

18. Inhibition of dihydrofolate reductase leads to an inhibition of purine ring and dTMP biosynthesis?

A. 6-Mercaptopurine

B. 6- Thioguanine

C. Methotrexate 

D. A & B

E. All of the above 

Answer: C. Methotrexate 

dTMP( deoxythymidine monophosphate

19. Which of the following statements about Antimetabolites is wrong?

A. Structurally related to cell compounds 

B. Interfare with purine & pyrimidine

C. Inhibit synthesis of Purine and pyrimidine

D. Max cytotoxic effect in S phase

E. Cell cycle nonspecific 

Answer: E. Cell cycle nonspecific 

20. Which of the following statements is incorrect about Folic Acid?

A. Obtained from dietary sources 

B. Produced by intestinal flora 

C. Transfer one carbon unit in metabolic reaction 

D. Essential for cell replication 

E. Methotrexate is an agonist of Folic acid 

Answer: E. Methotrexate is an agonist to folic acid 

Methotrexate (MTX) is an antagonist to folic acid and is structurally related to folic acid 

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Anticancer Drugs MCQS. 72

01. Which of the following anticancer drugs causes Ototoxicity?

A. Cisplatin

B. Ifosfamide

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: A. Cisplatin

02. Which of the following anticancer drugs causes Chemical Conjunctivitis?

A. Cisplatin

B. Ifosfamide

C. Cytarabine  

D. Oxaliplatin 

E. Doxorubicin 

Answer: C. Cytarabine 

03. Which of the following anticancer drugs causes Cardiotoxicity mainly?

A. Cisplatin

B. Ifosfamide

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: E. Doxorubicin 

04. Which of the following anticancer drugs causes Diarrhoea?

A. Cisplatin

B. Ifosfamide

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: C. Irinotecan 

05. Which of the following anticancer drugs causes Peripheral neuropathy?

A. Oxaliplatin

B. Vincristine 

C. Taxanes 

D. A & B 

E. All of the above 

Answer: E. All of the above 

06. Which of the following anticancer drugs causes Hemorrhagic cystitis?

A. Cisplatin

B. Ifosfamide

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: B. Ifosfamide

07. Which of the following anticancer drugs causes Hemorrhagic cystitis?

A. Cisplatin

B. Cyclophosphamide 

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: B. Cyclophosphamide 

08. Which of the following anticancer drugs causes Pulmonary toxicity?

A. Cisplatin

B. Bleomycin

C. Irinotecan 

D. Oxaliplatin 

E. Doxorubicin 

Answer: B. Bleomycin and Busulfan

09. Patients should receive antiviral prophylaxis for herpes zoster while undergoing treatment with which agent for multiple myeloma?

A. Bortezomib 

B. Cisplatin

C. Ipilimumab

D. Dabrafenib

Answer: A. Bortezomib 

10. Which of the following drugs causes herpes zoster reactivation in patients receiving treatment for multiple myeloma?

A. Bortezomib 

B. Cisplatin

C. Ipilimumab

D. Dabrafenib

Answer: A. Bortezomib 

Patients should receive antiviral prophylaxis while on Bortezomib therapy. Also Ixazomib has similar case

11. A drug causes severe birth defects when used in morning sickness?

A. Thalidomide 

B. Lenalidomide

C. Pomalidomide

D. A & B

E. All of the above 

Answer: E. All of the above 

12. Following should be administered prior to an infusion of the monoclonal antibody rituximab?

A. Allopurinol and acetaminophen 

B. Folic acid and H2 receptor antagonist 

C. Antihistamine and acetaminophen 

D. Hepatitis B & Vitamin B12

Answer: C. Antihistamine and acetaminophen 

13. On the first cycle, patient experience an infusion reaction (hypotension, bronchospasm, angioedema) after receiving following?

A. Cetuximab

B. Rituximab

C. Bortezomib 

D. Iplimumab

Answer: B. Rituximab

That's why antihistamine and acetaminophen and corticosteroids pretreatment is required to reduce these effects.

Slower infusion rate also reduce infusion reaction. 

Along with these symptoms fever and chills also occurs especially in patients with high circulating levels of neoplastic cells because of rapid activation of complement which results in release of tumor necrosis factor-alpha and interleukin.

14. Pretreatment with Antihistamine and acetaminophen reduce the infusion reaction prior to administration of following monoclonal antibody?

A. Rituximab 

B. Bortezomib 

C. Cetuximab

D. A & B

E. All of the above 

Answer: A. Rituximab  

15. Appearance of facial rash with Cetuximab is associated with a?

A. Negative response to therapy 

B. Positive response to therapy 

C. Drug allergy 

D. Infusion reaction 

Answer: B. Positive response to therapy 

Cetuximab is a monoclonal antibody that inhibit epidermal growth factor receptor (EGFR). Patients receiving this therapy develop an acneiform like rash on the face, chest, upper back and arms. This rash appearance has correlated with an increased response of therapy.

16. Appearance of facial rash is correlated with increased and positive response to therapy of following drug?

A. Bortezomib 

B. Cetuximab 

C. Sunitinib

D. Thalidomide 

E. Etoposide 

Answer: B. Cetuximab (inhibit EGFR)

17. Infusion related reactions such as hypotension, bronchospasm, and angioedema are common with following anticancer therapy?

A. Tyrosine kinase inhibitors 

B. Immunotherapy 

C. Monoclonal antibody therapy 

D. Steroids therapy 

E. Antibiotics therapy 

Answer: C. Monoclonal antibody therapy 

18. A 64 year old man is scheduled to undergo chemotherapy for rhabdomyosarcoma, and the regimen includes ifosfamide. Which is most appropriate to include in chemotherapy orders for this patient?

A. IV hydration, mesna and frequent urinalysis 

B. Leucovorin and frequent urinalysis 

C. Allopurinol and frequent urinalysis 

D. IV hydration, prophylactic antibiotics and frequent urinalysis 

Answer: A. IV hydration, mesna and frequent urinalysis 

19. A unique toxicity of ifosfamide is following?

A. Haemorrhagic cystitis 

B. Diarrhoea 

C. Cardio toxicity 

D. Ototoxicity

Answer: A. Haemorrhagic cystitis 

20. Bladder toxicity (Haemorrhagic cystitis) is caused by the toxic metabolites of following drug?

A. Cisplatin

B. Cytarabine 

C. Ifosfamide 

D. Bleomycin 

E. Irinotecan 

Answer: C. Ifosfamide 

To neutralise these toxic metabolites, adequate hydration as well as IV injection of mesna (sodium 2-mercaptoethane sulfonate) can minimise Bladder toxicity. Also frequent urinalysis to monitor for red blood cells should be ordered. 

21. IV adequate hydration, IV injection of mesna (sodium 2-mercaptoethane sulfonate) and frequent urinalysis can minimise Bladder toxicity in chemotherapy of following drug?

A. Methotrexate 

B. 5-FU

C. Ifosfamide 

D. Vincristine 

E. Dacarbazine

Answer: C. Ifosfamide 

Ifosfamide causes bladder toxicity (Haemorrhagic cystitis).

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Anticancer Drugs MCQS. 71

01. A drug that inhibit the topoisomerase enzyme I reducing the supercoiling of DNA?

A. Irinotecan

B. Oxaliplatin 

C. Flutamide 

D. Tamoxifen 

E. Leuprolide 

Answer: A. Irinotecan (S phase specific)

Along with Topotecan, Etoposide, these drugs inhibit the topoisomerase enzymes I that is essential for replication of DNA in human cells.

02. Which of the following drugs inhibit topoisomerase I essential for replication of DNA in human cells?

A. Camptothecin derivative 

B. Abiraterone

C. Proteasome inhibitors 

D. Micro tubules inhibitors 

E. Alkylating agent 

Answer: A. Camptothecin derivative (Irinotecan, Topotecan)

Topotecan  is used in metastatic ovarian cancer and in the treatment of small lung cancer. While Irinotecan is used with 5-FU and Leucovorin for the treatment of colorectal carcinoma.

03. Which of the following drugs inhibit topoisomerase I essential for replication of DNA in human cells?

A. Irinotecan  

B. Abiraterone

C. Proteasome inhibitors 

D. Vincristine  

E. Carboplatin  

Answer: A. Irinotecan, Topotecan

Topotecan  is used in metastatic ovarian cancer and in the treatment of small lung cancer. While Irinotecan is used with 5-FU and Leucovorin for the treatment of colorectal carcinoma.

04. SN-38 the active metabolite of following drug and is approximately 1000 times as potent as an inhibitor of topoisomerase I?

A. Irinotecan 

B. Thalidomide 

C. Etoposide 

D. Topotecan 

E. Vinorelbine 

Answer: A. Irinotecan 

05. Acute and delayed life threatening diarrhoea is the adverse effect of following drug?

A. Irinotecan 

B. Thalidomide 

C. Etoposide 

D. Topotecan 

E. Vinorelbine 

Answer: A. Irinotecan 

That's why Irinotecan requires treatment with atropine during the infusion or high doses of loperamide in the days following the infusion.

06. Irinotecan drug treatment requires atropine during the infusion because of following symptom?

A. Hypertension 

B. Diarrhoea 

C. Dry cough 

D. Myelosuppression 

E. Neutropenia 

Answer: B. Diarrhoea 

07. Irinotecan drug treatment requires Loperamide during the infusion because of following symptom?

A. Hypertension 

B. Diarrhoea 

C. Dry cough 

D. Myelosuppression 

E. Neutropenia 

Answer: B. Diarrhoea 

08. Etoposide is a semisynthetic derivative of the plant alkaloid, podophyllotoxin has major target on cell?

A. Topoisomerase I

B. Topoisomerase II

C. Micro tubules 

D. Estrogen receptor

E. Replication of DNA

Answer: B. Topoisomerase II

09. Which of the following drugs block topoisomerase II in the late S to G2 phase of the cell cycle?

A. Topotecan 

B. Irinotecan 

C. Etoposide 

D. Thalidomide 

E. Vinorelbine 

Answer: C. Etoposide 

Persistent of the transient, Cleaveable form of the complex thus renders it susceptible to irreversible double strand breaks.

10. A drug that block the check points molecules such as programmed death (PD-1) receptor to attack the tumor and causes destruction?

A. Abiraterone

B. Thalidomide 

C. Nivolumab

D. Topotecan 

E. Etoposide 

Answer: C. Nivolumab

11. A drug that block the check points molecules such as programmed death (PD-1) receptor to attack the tumor and causes destruction?

A. Abiraterone

B. Thalidomide 

C. Pembrolizumab

D. Topotecan 

E. Etoposide 

Answer: C. Pembrolizumab  

These drugs block the immune check point molecules such as Programmed death (PD-1) receptor to help the immune system in check. After blocking these checkpoints immune system is better able to attack the tumor and cause destruction.

This causes severe and fatal immune mediated adverse events due to turning off the immune checkpoints and also it allows attack of the tumor. 

12. Mechanism  of action of Abiraterone acetate used in treatment of metastatic castration resistance prostate cancer?

A. Inhibit CYP17 enzyme 

B. Immune checkpoint inhibitor

C. Topoisomerase II inhibitor

D. Inhibit release of FSH and LH

E. Aromatase Inhibitor

Answer: A. Inhibit CYP17 enzyme ( An enzyme required for androgen synthesis). This block results in reduced testosterone production. 

13. Mechanism  of action of Anastrozole and Letrozole?

A. Inhibit CYP17 enzyme 

B. Immune checkpoint inhibitor

C. Topoisomerase II inhibitor

D. Inhibit release of FSH and LH

E. Aromatase Inhibitor

Answer: E. Aromatase inhibitor (Aromatase inhibitor decrease the production of Estrogen. Aromatase reaction is responsible for synthesis of Estrogen from androstenedione.

14. Mechanism  of action of Pembrolizumab and Nivolumab?

A. Inhibit CYP17 enzyme 

B. Immune checkpoint inhibitor

C. Topoisomerase II inhibitor

D. Inhibit release of FSH and LH

E. Aromatase Inhibitor

Answer:  B. Immune checkpoint inhibitor 

15. Mechanism  of action of Etoposide?

A. Inhibit CYP17 enzyme 

B. Immune checkpoint inhibitor

C. Topoisomerase II inhibitor

D. Inhibit release of FSH and LH

E. Aromatase Inhibitor

Answer:  C. Topoisomerase II inhibitor 

16. Mechanism  of action of Leuprolide, Goserelin, and Triptorelin?

A. Inhibit CYP17 enzyme 

B. Immune checkpoint inhibitor

C. Topoisomerase II inhibitor

D. Inhibit release of FSH and LH

E. Aromatase Inhibitor

Answer:  D. Inhibit release of FSH and LH 

17. Coadministration of following drug with Abiraterone acetate need to help lessen the effect of mineralocorticoid excess results from CYP17 inhibition?

A. Thalidomide 

B. Prednisone 

C. Etoposide 

D. Irinotecan 

E. Vinorelbine 

Answer: Prednisone 

18. A drugs work by inhibiting proteasome preventing the degradation of proapoptotic factors leading to promotion in programmed cell death (apoptosis)?

A. Bortezomib

B. Ixazomib

C. Carfilzomib

D. A & B

E. All of the above 

Answer: E. All of the above 

19. A drugs work by inhibiting proteasome preventing the degradation of proapoptotic factors leading to promotion in programmed cell death (apoptosis)?

A. Tamoxifen 

B. Ixazomib

C. Etoposide

D. A & B

E. All of the above 

Answer: B. Ixazomib

Along with Bortezomib and Carfilzomib

20. Mechanism of action of  Bortezomib, Ixazomib and Carfilzomib?

A. Proteasome inhibitor 

B. Estrogen release inhibitor 

C. Inhibit EGFR tyrosine kinase 

D. Inhibit mutated BRAF kinase 

E. Inhibit bruton tyrosine kinase 

Answer: A. Proteasome inhibitor 

  

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Steps Of Pharmacist Registration in the USA?

How to Become a registered pharmacist in the USA?

The USA has become a dream country for people of all the countries in the world. A lot of health professionals including physicians, Pharmacists, Nurses, and other paramedical staff always take an interest to work in the USA as the first country to migrate. Meanwhile, the USA is also inviting health professionals from all over the world to make their lifestyles better. Health professionals especially pharmacists from different countries are coming to the USA for a better future. Because pharmacists in the USA are the highest paid professionals. On average, Pharmacists are earning around  $100 K in a year. They are living a luxurious life in the USA as compared to other countries. Many Pakistani, Indians, Arabs are going to the USA for their dream life. Here you will learn how to apply for the registration process and the steps required to get a registration certificate in the USA for practice.

Different steps are required for registration as a PHARMACIST IN the USA. The first step is to after completion of your degree from a recognized University or college in your country start collecting the required documents for applying procedure. After completion of the required documents, start searching for organizations that'll evaluate your documents to start the application process. The evaluation organization for the USA is ECE (Educational credential evaluation). they'll evaluate your sealed transcript and earned credit hours to match with USA pharmacy degree requirements. If they would find any deficiency in your documents they'll send you an email of the required document or any additional information they required. After completion of your transcript and other documents evaluation, ECE sends a report directly to NABP (National association of boards of pharmacy) and one report to your given address. 

Note: Before or after receiving their evaluation report, Make an account with NABP by visiting their website and signing up for your NABP i.d. After signing in to your account they'll direct you to the FPGEC corner where you would be able to check your status of documents arrival, deficiency in any required document, and any additional information or document.

when you are sending documents to ECE for evaluation, don't wait for ECE report completion. Quickly send your required documents to NABP for FPGEC so they can also able to start the evaluation of your documents. You don't have a need to send your ECE report to NABP, ECE will send your report directly to NABP. After receiving your documents, NABP will update your login account that your documents received. It'll take 6 to 8 weeks for a complete evaluation. Depending on your documents, if there is a deficiency of any documents they'll update the deficiency status on your NABP account then you have to send again deficient document to them and the evaluation process will start again from starting and this will cost you more money and also a waste of time also they'll take another 6 to 8 weeks. So make sure before sending documents to ECE and NABP that all the documents are fully attested and sealed by the notary public. So that you can save your money and time. After completion of the evaluation process, NABP would change your status on the login account to 'Accepted' then you can buy the FPGEC exam in the coming schedule which is in October only.

Note: NABP is conducting an FPGEC exam once a year in the month of OCTOBER each year.

NABP WEBSITE: NABP

 

Applying the procedure For PHARMACIST registration in the USA in detail

 Foreign Pharmacy Graduate Examination Committee(FPGEC)

For the FPGEC registration procedure, you have to apply for the documents evaluation procedure by ECE. They will evaluate all the required documents and will send the final report directly to NABP(NATIONAL ASSOCIATION OF BOARDS OF PHARMACY).

The following documents are required for FPGEC process completion:

1. ECE Report/Documentation
2. Passing TOEFL iBT Score Report
3. FPGEC Attestation and application form
4. Licensing and/or Registration Documentation
5. Certified Copy of ID (photo identification & passport identification)

1. ECE Report/Documentation

First of all, you have to submit an application and documentation to Educational Credential Evaluators

(ECE) in the USA to verify your degree credentials. You need to submit the following documents to ECE for evaluation:

• ECE Application. To access the ECE application  visit their website  https://www.ece.org/
• Official Transcripts. Pharmacy school transcripts in a sealed envelope
• Official Proof of Degree in pharmacy. Indicating the title of the degree and the date of issuance from your school of graduation. (credential or degree earned) 

How to make an account for ECE REPORT

step by step instructions:

First step;

2nd Step;

3rd step:

4th Step:

 5th step:

6th Step:

After submitting all the documents required ECE application create an ECE evaluation report that is sent directly to FPGEC.  

2.  Passing TOEFL iBT Score Report submission

Now there are two policies:

If you have applied after January 1, 2020, then you will complete the TOEFL iBT requirement for FPGEE application acceptance. By conducting your TOEFL exam before applying for FPGEE.If you have submitted your documents before January 1, 2020, you can attempt the TOEFL exam even after taking the FPGEE exam.

3. FPGEC Attestation and application form

The documents  required for the FPGEC Certification application and the procedure is the following:

 The FPGEC they have received documents they quickly process all applications and materials. The FPGEC evaluates each document and material and all supporting documentation for accuracy and to make sure that documents are not fake.  The FPGEC will send you an email to inform you about your application status. If there is any deficiency in your documents they will update the status in your e-profile.. they will provide you the opportunity to correct any deficiency in documents identified by the FPGEC. Make sure you have submitted all the required documents to FPGEC on time so that so could purchase the exam timely.

To  start the FPGEC Certification process, you have to apply online e-Profile and submit hard copies of the following documents to FPGEC for evaluation and acceptance:

1.  Your licensing/registration documentation (Pharmacy category/license given by your country)
2.  A certified copy of FPGEC Attestation (FPGEC form from their website)
3.  A notarized copy of the photo identification. 
4. A notarized copy of your passport identification
5. Submission of a passing TOEFL iBT scores reports directly to the FPGEC by using your ETS account.

Note:

.If you have applied after January 1, 2020, then you will complete the TOEFL iBT requirement for FPGEE application acceptance. By conducting your TOEFL exam before applying for FPGEE.If you have submitted your documents before January 1, 2020, you can attempt the TOEFL exam even after taking the FPGEE exam.

After submission of all of your documents to FPGEC, they will update your status in your e-profile and then you can purchase a scheduled exam.

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Aspirin VS Acetaminophen Mechanism Of Action

Acetaminophen

Acetaminophen is also known as paracetamol. Acetaminophen don't increase clotting time of blood and does not have effect on platelet function. It's a antipyretic and analgesic drug recommended especially in those patients who are already suffering from gastric disease. A drug for mild to moderate pain and to reduce fever. This drug is recommended especially for osteoarthritis patients as an first line therapy group of the knee and hip. I has minimal anti inflammatory activity and can't be used to reduce swelling or stiffness during rheumatoid arthritis.

Antipyretic Activity of Acetaminophen 
Acetaminophen and Aspirin decrease the increased temperature of the body by interfering with the release and synthesis of PGE2 that causes an increase in the body temperature. Acetaminophen and Aspirin lowers the body temperature of patients by resetting the Thermostat towards a normal state by the release of heat in the form of sweat and peripheral vasodilation.

Analgesic Activity of Acetaminophen 
When inflammation occurs, Prostaglandin E2 causes the sensitization of Nerve ending in the action of histamine, bradykinin, and other chemical mediators that are released locally as a result of the inflammation. Acetaminophen and Aspirin decreases the synthesis of Prostaglandin E2, thus results repress the pain sensation. 

Dosage of Acetaminophen 
Acetaminophen is available in 325mg and 500mg. A prolonged dosage form caplet of 650 mg is also available.

Dose for Adults 
1. 500mg to 1000mg dose is recommended three times in a day. 
2. Maximum 4000mg dose per day for pain. It should be given not more than 10 days for pain and not more than 3 days for fever.
3. For Osteoarthritis patients 4000mg four times can be given.

Dose for children (6 years or above)
1. 325mg is recommended every 4 to 6 hours as needed.
2. Maximum dose is 1600mg per day for not longer than 5 days for pain and 3 days for fever and 2 days for sore throat.

Note:
1. Acetaminophen is recommended for Gastrointestinal Disturbance sensitive patients.
2. The patients having bleeding problems 
3. The patients hypersensitive to Salicylates 

Adverse effects of Acetaminophen are following:
At normal Doses 
When we talk about adverse effects of acetaminophen at normal therapeutic doses it's virtually free of any significant adverse effect. But infrequently 
I. Skin rash 
II. Allergic reaction may occur 
III. Altered leukocytes count (minor and transient)

At High Doses 
When high doses of Acetaminophen are used it causes following:
I. Depletion of glutathione in the liver 
II. Hepatic necrosis 
III. Renal tubular necrosis 
IV. Hypoglycaemic coma

Note : High doses of acetaminophen required periodic monitoring of liver enzymes test.

Precautions 
Chronic administration of Acetaminophen is contraindicated in Liver diseases, Viral hepatitis, and active alcoholism. Chronic 5 g or acetaminophen used for one month or more to on daily basis it leads to liver damage. Acute administration of 10g or more is hepatotoxic.

How does Acetaminophen causes toxicity when overdosed?
Acetaminophen form inactive glucuronidated or sulfated metabolites by conjugation in the liver. On the other side, Acetaminophen also hydroxylated to form N-acetylbenzoiminoquinone. This hydroxylated form is a very dangerous metabolite of Acetaminophen that reacts with sulfhydryl groups of glutathione during normal doses and circumstances. 
When high doses of acetaminophen are used then the glutathione available in the liver depleted and N-acetylbenzoiminoquinone reacts with sulfhydryl group of hepatic proteins by forming covalent bonds. This leads to hepatic necrosis.

How does N-acetylcysteine work as an antidote?
NAC also contains sulfhydryl groups to which toxic metabolites start reacting. When NAC is administered these metabolites like N-acetylbenzoiminoquinone start reacting with with sulfhydryl groups of NAC instead of reacting with sulfhydryl groups of hepatic proteins. This drug should be administered within the 10 hours of the Acetaminophen overdose.


Why acetaminophen has weak anti inflammatory activity?
Acetaminophen has very less and weak anti inflammatory activity because acetaminophen has less effect on cyclooxygenase in peripheral tissues.

Why Acetaminophen is preferred over Aspirin?
Aspirin causes damage to stomach lining thus causing GI bleeding and this adverse effect is universal when patient treated with Salicylates. That's why Acetaminophen is preferred drug in those patients who already are suffering from stomach disease and gastric complaints.

ASPIRIN

 Aspirin 

Introduction 
Aspirin is a weak organic acid. Aspirin is the only one among  NSAIDs that effects irreversibly results in the inactivation of the cyclooxygenase enzyme. Aspirin is also called Acetylsalicylic acid. When a tablet of Aspirin is taken, aspirin is converted to salicylates by the esterase enzyme because of rapid deacetylation inside the body. These salicylates work as have anti-inflammatory, antipyretic, and analgesic effects.

Function of Salicylates 

Blockage of prostaglandin synthesis at thermoregulatory centers.
Inhibition of prostaglandins at peripheral target sites.
Prevents pain sensitization receptors to both chemical stimuli and mechanical stimuli.
Salicylates (Aspirin) depress pain stimuli at subcortical sites ( thalamus and hypothalamus).
Important Note:
Salicylate at low doses exhibit analgesic activity but at higher doses, it shows the anti-inflammatory activity as well.
Aspirin 
Mechanism of Action 
Aspirin is a weak organic acid and inhibits cyclooxygenase irreversibly. Salicylate that has analgesic, antipyretic and anti-inflammatory properties is produced in the body by rapid deacetylation by esterases.  These salicylates block the synthesis of prostaglandins leading to the prevention of pain receptors sensitization, block prostaglandin synthesis at thermoregulatory centers in the hypothalamus and at peripheral target sites.
Aspirin has the following three major therapeutic activities:

Antipyrexia
Analgesic 
Anti-inflammatory 

1. Antipyretic Action 
Aspirin decrease the increased temperature of the body by interfering with the release and synthesis of PGE2 that causes an increase in the body temperature. Aspirin lowers the body temperature of patients by resetting the Thermostat towards a normal state by the release of heat in the form of sweat and peripheral vasodilation.

Note: Body temperature is controlled by the hypothalamus whenever a pyrogen such as a cytokine is released from white cells because of any infection inside the body, this causes an increase in the synthesis of PGE2. Thus fever occurs when the anterior hypothalamic thermoregulatory center set point is increased.
2. Analgesic 
When inflammation occurs, Prostaglandin E2 causes the sensitization of Nerve ending in the action of histamine, bradykinin, and other chemical mediators that are released locally as a result of the inflammation. Aspirin decreases the synthesis of Prostaglandin E2, thus results repress the pain sensation. 
3. Anti-inflammatory 
Aspirin inhibits the activity of cyclooxygenase leading to a decrease in the level and synthesis of prostaglandins. As the prostaglandins synthesis diminishes, Aspirin inhibits the inflammatory response of prostaglandins.

Difference between Low dose aspirin and high dose Aspirin
Low Dose Aspirin (60-80 mg daily)
Effects of Aspirin on Platelets
The low dose of Aspirin irreversibly inhibits thromboxane production in platelets. This occurs by acetylation of cyclooxygenase. Due to the inhibition of thromboxane, platelet aggregation is reduced. Because thromboxane increases the aggregation of platelet along with other factors. This lack of thromboxane in the platelet remains till the lifetime of the platelet (3-7 days) because the platelet doesn't have nuclei so they can not synthesize new thromboxane.
Low dose Aspirin also inhibits endothelial cells cyclooxygenase resulting in a reduction of prostacyclin also called PGI2 formation. Prostacyclin decreases platelet aggregation naturally. On the other hand, endothelial cells have nuclei so they are able to produce new cyclooxygenase. So PGI2 effect of antiplatelet remains available naturally.

High dose Aspirin (more than 325mg, 650mg to 4 gram/day)
we already have studied the function of Salicylates that Salicylates show analgesic and anti-inflammatory activity. It totally depends on the number of doses. At low doses, aspirin shows an analgesic effect but by increasing doses, it shows the anti-inflammatory activity as well. That's why a higher dose of aspirin is used in Rheumatoid arthritis and osteoarthritis with an initial dose of 3 grams/day.

Effects of Aspirin on Cardiovascular system 
Aspirin is used as platelet aggregation inhibitor along with other pharmacological effects. 
1. When Aspirin is used as a low dose it causes reduction of stroke and Also reduce the risk of recurring transient ischemic attacks (TIAs) or death especially in those people who already had suffered single or multiple episodes of stroke or TIA.
2. Low dose of Aspirin is used to reduce deaths in those patients having an acute myocardial infarction.
3. Low doses of Aspirin reduce myocardial infarction and also reduce the death in patients with previous unstable angina pectoris.
4. Reduce risk of recurrent neofatal myocardial infarction.
5. Reduce cardiovascular risk in revascularization procedures.
Effects of Aspirin on GIT
When aspirin is taken for it's pharmacological actions, some of the prostanoids (PGE2 and PGF2à) that stimulates synthesis of mucus that protects stomach and small intestine are not formed in the presence of Aspirin. Because of this gastric acid secretion is increased resulting in diminished mucus protection. This leads to epigastric distress, iron deficiency, hemorrhage and ulceration. 

Note: PGI2 also called prostacyclin inhibits secretion of gastric acid, Whereas PGE2 and PGF2à stimulates protective mucus synthesis. 

Effects of Aspirin on Kidney 
As Aspirin is a cyclooxygenase inhibitor, So cyclooxygenase inhibitors stop the synthesis of PGE2 and PGI2 prostaglandins that are needed to maintain the renal blood flow in the presence of circulating vasoconstrictors. Thus decrease in the synthesis of these prostaglandins results in retention of water and sodium leading to edema and hyperkalemia.
Other effects of Aspirin 
Aspirin increases alveolar ventilation at therapeutic doses. 
Adverse effects of Aspirin
a. Urticaria
b. Bronchoconstriction
c. Peptic ulcer disease 
d. Metabolic acidosis



In high doses, Aspirin lacks anti-platelet activity by which of the following phenomena
a. Stimulates thromboxanes
b. Stimulates prostacyclins
c. Inhibits prostacyclins
d. Stimulates leukotrienes
e. Inhibits leukotrienes


Answer: c. Inhibit prostacyclins

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