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93 Cards in this Set

  • Front
  • Back
The following agent was approved by the FDA for familial adenomatous polyps (FAP):
a.Acetaminophen
b.Methotrexate
c.Celecoxib (celebrex)
d.Anakinra (kineret
e.Etanercept (enbrel)



(2006 exam 3)
c.Celecoxib (celebrex)
Methotrexate is a weak acid that depends on renal secretion for its elimination. Which of the following drugs is MOST likely to increase the serum concentrations of methotrexate?
a.Allopurinol
b.Colchicine
c.Acetaminophen
d.Hydroxychloroquine
e.Probenecid


(2006 exam 3 q10)
e.Probenecid
The following is true of etanercept (Enbrel):
a.mechanism is TNF-alpha receptor blockade
b.is effective when administered orally, by inhalation, or by subcutaneous injection
c.is a major advance since it can be administered orally once a week
d.is a disease-modifying drug that takes 6 months to become effective
e.halts the progression of joint damage


(2006 exam 3)
e.halts the progression of joint damage
A major drug target for several biologic response modifiers is:
a.IL-10
b.PGE2
c.LTC4 & LTD4
d.E-selectin
e.TNF-alpha



(2006 exam 3)
e.TNF-alpha
The following is true of infliximab (Remicade) use in patients with rheumatoid arthritis:
a.its mechanism of action is known to bind and thus neutralize TNF-alpha
b.it needs to be administered with methotrexate
c.it delays disease progression
d.it increases susceptibility of patients to opportunistic infections
e.all of the above



(2006 exam 3)
e.all of the above
Abatacept (Orencia) differs from other biologic response modifiers used in rheumatoid arthritis because:
a.it is a receptor antagonist to IL-1
b.it requires DAILY injections subcutaneously
c.it is the first agent that is a selective co-stimulator modulator
d.it inhibits T-cell function
e.c and d



(2006 exam 3)
e.c and d
The DMARD that is a first-choice drug for use in patients with newly-diagnosed rheumatoid arthritis is:
a.Hydroxychloroquine (Plaquenil)
b.Auranofin (Ridaura)
c.Leflunomide (Arava)
d.Methotrexate
e.Penicillamine



(2006 exam 3)
d.Methotrexate
The following drug is a new anti-CD-20 monoclonal antibody approved for use in rheumatoid arthritis:
a.Rituximab (Rituxan)
b.Abatacept (Orencia)
c.Adalimumab (Humira)
d.Infliximab (Remicade)
e.a and c



(2006 exam 3)
a.Rituximab (Rituxan)
The following drug is a xanthine oxidase inhibitor and is effective in maintenance therapy to prevent gouty attacks:
a.Indomethacin (Indocin)
b.Colchicine
c.Probenecid (Benemid)
d.Allopurinol (Zyloprim)
e.Sulfinpyrazone (Anturane)



(2006 exam 3)
d.Allopurinol (Zyloprim)
The following combination requires the reduction in the dose of the second drug listed:
a.Probenecid - azathioprine
b.Probenecid - aspirin
c.Allopurinol – methotrexate
d.Allopurinol – azathioprine
e.Allopurinol – acetaminophen



(2006 exam 3)
d.Allopurinol – azathioprine
Uricosuric drugs exhibit the following property:
a.inhibit the reabsorption of uric acid at therapeutic doses
b.inhibit the secretion of uric acid at therapeutic doses
c.are extremely effective in overexcretors of uric acid
d.a and b
e.all of the above



(2006 exam 3)
d.a and b
Which one of the following pairs of a drug effect and mechanism of action is accurate?

I. Etanercept antirheumatic action: inhibits dihydroorotate dehydrogenase, the enzyme in lymphocytes that is required for pyrimidine synthesis
II. Hydroxychloroquine antirheumatic action: a cytotoxic drug that kills rapidly dividing lymphocytes
III. Indomethacin closure of patent ductus arteriosus: blocks prostaglandin E production in the ductus arteriosis of the newborn
a.I only
b.III only
c.I and II
d.II and III
e.I, II, and III


(2004 exam 3)
b.III only
The following drug is available only in a parenteral preparation that has a mechanism of anti-inflammatory action of antagonism of tumor necrosis factor (TNF):
a.penicillamine
b.sulfasalazine
c.leflunomide
d.etanercept
e.methotrexate


(2004 exam 3)
d.etanercept
The following is true of infliximab (Remicade) use in patients with rheumatoid arthritis:
a.its mechanism of action is known to be through an antagonism of IL-1 and IL-6 receptors
b.it is a slow-acting DMARD requiring 6-9 months for effects to be seen
c.although it does not delay disease progression, it decreases all symptoms more than any other therapy
d.it increases susceptibility of patients to opportunistic infections
e.all of the above


(2004 exam 3)
d.it increases susceptibility of patients to opportunistic infections
42. The following is true for methotrexate:
a.it is a competitive blocker of TNF receptors
b.its use with other DMARDs or immunologic agents decreases its effectiveness
c.benefits can be seen as early as 2-3 weeks after therapy is started
d.all of the above
e.none of the above


(2004 exam 3)
c.benefits can be seen as early as 2-3 weeks after therapy is started
The following is true of etanercept (Enbrel):
a. is a chimeric human/mouse anti-TNFalpha monoclonal antibody
b. should be avoided in patients with active infections
c. is a major advance since it can be administered orally once a week
d. is a disease-modifying drug that takes 6-9 months to become effective
e. all of the above


(2005 exam 3)
b. should be avoided in patients with active infections
Anakinra differs from other biological response modifiers used in RA because:
a. it is a receptor antagonist to IL-1
b. it requires daily injections subcutaneously
c. it has an extremely wide margin of safety with no adverse reactions or side effects
d. it was approved in 1988 and thus we have a great deal of experience with it
e. a and b


(2005 exam 3)
e. a and b
The following is true for methotrexate use in RA:
a. its mechanism is known to be via inhibition of dihydroorotate
b. its effectiveness is greatest when used as single therapy, not combination therapy
c. benefits can be seen as early as 2-3 weeks after therapy is started
d. its adverse effects are the same as when it is used in cancer since the dose and schedules are the same
e. all of the above


(2005 exam 3)
c. benefits can be seen as early as 2-3 weeks after therapy is started
Allopurinol exerts its effect in gout by:
a. increasing renal excretion of uric acid in the proximal tubule
b. blocking conversion of hypoxanthine to xanthine and xanthine to uric acid
c. breakdown of uric acid deposits in the articular joints
d. decreasing uptake of purines from the small intestine
e. a, b and c


(2005 exam 3)
b. blocking conversion of hypoxanthine to xanthine and xanthine to uric acid
Drug not effective in gouty attacks, but very effective in maintenance therapy is:
a. indomethacin (Indocin)
b. colchicine
c. probenecid (Benemid)
d. allopurinol (Zyloprim)
e. sulfinpyrazone (Anturane)


(2005 exam 3)
d. allopurinol (Zyloprim)
The following combination requires the reduction in the dose of the second drug listed:
a. probenecid - azathioprine
b. probenecid - aspirin
c. allopurinol - 6 mercaptopurine
d. allopurinol - methotrexate
e. chondroitin - glucosamine


(2005 exam 3)
c. allopurinol - 6 mercaptopurine
The combination of a corticosteroid and etanercept (Enbrel) results in:
a. an increase in corticosteroid toxicity
b. a beneficial dose reduction in corticosteroid
c. a decrease in efficacy by etanercept
d. an increase in efficacy caused by the corticosteroid
e. none of the above


(2005 exam 3)
b. a beneficial dose reduction in corticosteroid
The following agent can be used in the treatment of acute gouty arthritis as well as RA:
a. allopurinol
b. probenecid
c. colchicine
d. indomethacin
e. etanercept (Enbrel)


(2005 exam 3)
d. indomethacin
Uricosuric drugs exhibit the following property:
a. inhibit the reabsorption of uric acid at therapeutic doses
b. inhibit the secretion of uric acid at high doses
c. are extremely effective in overexcretors of uric acid
d. a and b
e. all of the above


(2005 exam 3)
a. inhibit the reabsorption of uric acid at therapeutic doses
The following statement is TRUE for allopurinol:
a. it is effective in acute attacks of gout and as maintenance therapy in gouty arthritis
b. it acts by inhibition of xanthine oxidase, thus decreasing synthesis of uric acid
c. it can interact with 6-mercaptopurine to increase 6-MP's blood concentration and increase 6-MP's toxicity
d. b and c
e. all of the above


(2003 exam 4 q1)
d. b and c
The following is TRUE for colchicine:
a. effective in acute gouty attacks and in prophylactic therapy
b. decreases urate synthesis
c. increases urate excretion
d. increases tubulin polymerization leading to enhanced leukocyte migration out of inflamed regions
e. all of the above


(2003 exam 4 q2)
a. effective in acute gouty attacks and in prophylactic therapy
Probenecid and sulfinpyrazone are both able to:
a. be extremely effective, mainly in overexcretors of uric acid by the kidneys
d. decrease the renal reabsorption of uric acid
c. inhibit the synthesis of PGs in the kidney
d. be effective in acute gouty arthritis
e. all of the above


(2003 exam 4 q3)
b. decrease the renal reabsorption of uric acid
A gouty attack can be exacerbated by:
a. high doses of aspirin
b. high doses of acetaminophen
c. low doses of aspirin
d. low doses of acetaminophen
e. low doses of indomethacin



(2003 exam 4 q4)
c. low doses of aspirin
Calcineurin:
a. has 2 subunits CnA and CnB: CnA has a catalytic domain and CnB has Ca2+ binding domains
b. has 2 subunits CnA and CnB. CnA has Ca2+ binding domains and CnB has catalytic domain
c. Has 2 subregions: the N-terminal CnA region that binds calmodulin and the C-terminal region CnB region contains the catalytic domain.
d. is a Ca2+ dependent kinase that requires calmodulin binding for its activation
e. is a Ca2+ dependent kinase consisting of heteromeric chains CnA and CnB. CnA contains RGE kinase domain while CnB contains the calmodulin binding domain.



(2003 exam 4 q27)
a. has 2 subunits CnA and CnB: CnA has a catalytic domain and CnB has Ca2+ binding domains
Rapamycin-FKB12 inhibits mTOR by:
a. inhibiting amino acid binding to mTOR
b. inhibiting PA binding to FRB domain of mTOR
c. inhibiting PI3-kinase activity
d. activating phospholipase D
e. activating phospholipase C



(2003 exam 4 q28)
b. inhibiting PA binding to FRB domain of mTOR
6-mercaptopurine inhibits DNA synthesis by:
a. converting to 6-thio-GTP
b. inhibiting IMP dehydrogenase and PRPP amidotransferase
c. inhibiting DNA polymerase
d. inhibiting RNA polymerase
e. none of the above



(2003 exam 4 q31)
b. inhibiting IMP dehydrogenase and PRPP amidotransferase
Mycophenolic acid inhibits DNA synthesis by:
a. inhibiting PRPP amidotransferase
b. converting to 6-thio-GTP
c. inhibiting IMPDHase and GMP synthase
d. inhibiting inosinate dehydrogenase
e. inhibiting DNA polymerase



(2003 exam 4 q32)
c. inhibiting IMPDHase and GMP synthase
Which of the following drugs needs to have its dose reduced by more than 50% if coadministered with 6-mercaptopurine?
a. colchicine
b. allopurinol
c. probenecid
d. aspirin
e. hydroxychloroquine


(2004 exam 4 q2)
b. allopurinol (DOUBLE-CHECK; isn't it the dose of 6-MP that needs to be reduced?)
Uricosuric drugs exhibit the following property:
a. are extremely effective, mainly in overexcretors of uric acid by the kidneys
b. inhibit the reabsorption of uric acid at therapeutic doses
c. inhibit the secretion of uric acid at high doses
d. a and b
e. all of the above


(2004 exam 4 q3)
b. inhibit the reabsorption of uric acid at therapeutic doses
Xanthine oxidase can be inhibited by:
a. allopurinol
b. oxypurinol
c. low doses of aspirin
d. a and b
e. all of the above


(2004 exam 4 q4)
d. a and b
The following agent can be used in the treatment of acute gouty arthritis as well as RA:
a. allopurinol
b. colchicine
c. probenecid
d. indomethacin
e. all of the above


(2004 exam 4 q5)
d. indomethacin
Azathioprin and mycophenolate mofetil are purine synthesis inhibitors. Inasmuch as purine biosynthesis inhibitors are effective immunosuppressors, pyrimidine biosynthesis inhibitors can be effective as well. Pyrimidine biosynthesis inhibitors inhibit:
a. deoxycytidine and deoxythimidine synthesis
b. deoxyadenosine and deoxyguanocine synthesis
c. PRPP synthesis
d. Synthesis of DNA polymerase I
e. ATP hydrolysis to ADP


(2004 exam 4 q42)
a. deoxycytidine and deoxythimidine synthesis (DOUBLE-CHECK)
Which of the following is NOT a direct mechanism of azathioprine action?
a. inhibition of gene transcription
b. inhibits inositol monophosphate dehydrogenase
c. inhibits phosphoribosyl pyrophosphate amidotransferase
d. DNA synthesis
e. RNA synthesis


(2004 exam 4 q43)
b. inhibits inositol monophosphate dehydrogenase (DOUBLE-CHECK)
Calcineurin:
a. is a phosphatase responsible for dephosphorylation of CD3 phosphotyrosine
b. is a kinase responsible for phosphorylation of NF-AT
c. is a kinase responsible for the phosphorylation of protein phosphatase I
d. is a phosphatase responsible for the dephosphorylation of cytosolic NF-AT
e. is a kinase responsible for the phosphorylation of cytosolic NF-AT


(2004 exam 4 q45)
d. is a phosphatase responsible for the dephosphorylation of cytosolic NF-AT (DOUBLE-CHECK)
Phosphatidic acid binding to the FRB domain of mTOR is important for:
a. rapamycin binding
b. PLD activation
c. signaling leading to the activation of downstream S6K1
d. dephosphorylation of NF-AT
e. signaling leading to the activation of PKC


(2004 exam 4 q46)
a. rapamycin binding (DOUBLE-CHECK)
The following does not decrease the progression of RA:
a. methotrexate
b. penicillamine
c. hydroxychloroquine
d. celecoxib
e. aurothioglucose
d. celecoxib
A major problem in the use of anti-TNFalpha drugs is:
a. pancytopenia
b. osteoporosis
c. hyperglycemia and diabetes-like symptoms
d. tuberculosis
e. gastric ulcers
d. tuberculosis
The following is true of infliximab (Remicade):
a. inhibits IL-1 as its mechanism of action
b. takes 4-5 months before a beneficial effect is observed
c. has a short half-life, so needs to be injected daily
d. should not be given with methotrexate
e. is a chimeric human/mouse monoclonal antibody
e. is a chimeric human/mouse monoclonal antibody
The following is a recombinant version of the soluble human TNFalpha receptor:
a. leflunomide (Arava)
b. etanercept (Enbrel)
c. adalimumab (Humira)
d. anakinra (Kineret)
e. infliximab (Remicade)
b. etanercept (Enbrel)
The onset of action of most DMARDs is in the range of:
a.48-72 hrs
b.1-2 weeks
c.1-2 months
d.4-6 months
e.1 year


(2006 quiz 9)
d.4-6 months
A major adverse reaction seen with biologic response modifiers is:
a.Blurred vision
b.Impaired renal function
c.Hemorrhagic ulcers
d.Upper respiratory tract infections
e.Severe headache


(2006 quiz 9)
d.Upper respiratory tract infections
A major target for several biologic response modifiers is:
a.IL-10
b.PGE2
c.LTC4 & LTD4
d.E-selectin
e.TNFα


(2006 quiz 9)
e.TNFα
T/F: Drugs like methotrexate and infliximab relieve arthritis symptoms AND slow the progression of the disease


(2006 quiz 9)
true
The following is true of infliximab (Remicade) use in patients with rheumatoid arthritis:
a.its mechanism of action is known to bind and thus neutralize TNF
b.it needs to be administered with methotrexate
c.it delays disease progression
d.it increases susceptibility of patients to opportunistic infections
e.all of the above


(2003 exam 3)
e.all of the above
Abatacept (Orencia) differs from other biologic response modifiers used in rheumatoid arthritis because:
a.it is a receptor antagonist to IL-1
b.it requires DAILY injections subcutaneously
c.it is the first agent that is a selective co-stimulator modulator
d.it inhibits T-cell function
e.c and d
e.c and d
The DMARD that is a first-choice drug for use in patients with newly-diagnosed rheumatoid arthritis is:
a.Hydroxychloroquine (Plaquenil)
b.Auranofin (Ridaura)
c.Leflunomide (Arava)
d.Methotrexate
e.Penicillamine
d.Methotrexate
The following drug is a new anti-CD-20 monoclonal antibody approved for use in rheumatoid arthritis:
a.Rituximab (Rituxan)
b.Abatacept (Orencia)
c.Adalimumab (Humira)
d.Infliximab (Remicade)
e.a and c
a.Rituximab (Rituxan)
The following drug is available only in a parenteral preparation that has a mechanism of anti-inflammatory action of antagonism of tumor necrosis factor (TNF):
a.penicillamine
b.sulfasalazine
c.leflunomide
d.etanercept
e.methotrexate
d.etanercept
The following is true of infliximab (Remicade) use in patients with rheumatoid arthritis:
a.its mechanism of action is known to be through an antagonism of IL-1 and IL-6 receptors
b.it is a slow-acting DMARD requiring 6-9 months for effects to be seen
c.although it does not delay disease progression, it decreases all symptoms more than any other therapy
d.it increases susceptibility of patients to opportunistic infections
e.all of the above
d.it increases susceptibility of patients to opportunistic infections
The following is true of methotrexate use in patients with rheumatoid arthritis:
a. the dose is lower than that needed for its use in cancer patients
b. its mechanism of action is known to be through an antagonism of IL-1 and IL-6
receptors
c. it is a slow-acting compound requiring 6-9 months for effects to be seen
d. although it does not delay disease progression, it decreases all symptoms more than any other therapy
e. all of the above


(2003 exam 3 q9)
a. the dose is lower than that needed for its use in cancer patients
The following is true of infliximab (Remicade):
a. it is a monoclonal antibody that inhibits tumor necrosis factor (TNF)
b. it halts the progression of rheumatoid arthritis
c. it can enable opportunistic infections to develop and lead to fatalities
d. it needs to be administered intravenously
e. all of the above


(2003 exam 3 q10)
e. all of the above
Infliximab (Remicade) and Etanercept (Enbrel) should be avoided or used very
cautiously in which patients?
a. patients who do not respond to NSAIDs
b. patients who are receiving methotrexate
c. patients who have active infections, including sepsis
d. patients who do not respond to DMARDs
e. patients who are receiving warfarin


(2003 exam 3 q11)
c. patients who have active infections, including sepsis
Which of the following is a correct pairing?
a. leflunomide (Arava): a competitive blocker of TNF receptors
b. acetaminophen: can exacerbate bleeding when used with warfarin and other anticoagulants
c. gold salts: can only be injected
d. DMARDs (disease modifying antirheumatic drugs): more effective when combined with NSAIDs or biological agents for arthritis
e. none of the above


(2003 exam 3 q12)
d. DMARDs (disease modifying antirheumatic drugs): more effective when combined with NSAIDs or biological agents for arthritis
Enhanced excretion of uric acid is caused by which of the following drugs?
a. gold salts
b. allopurinol
c. probenecid
d. indomethacin
e. methotrexate


(2002 exam 3)
c. probenecid
The following drug can interact with antineoplastic agents like 6-mercaptopurine with severe consequences:
a. colchicine
b. allopurinol
c. sulfinpyrazone
d. gold salts
e. all of the above


(2002 exam 3)
b. allopurinol
Which statement regarding infliximab (Remicade) is true?
a. it has several negative drug interactions, including administration with methotrexate
b. it binds to TNF and prevents TNF from binding to cell surface receptors
c. it indirectly alters the activity of IL-1 by blocking purine synthesis
d. its onset of action is 4-6 months
e. c and d


(2002 exam 3)
b. it binds to TNF and prevents TNF from binding to cell surface receptors
Etanercept (Enbrel) reduces signs and symptoms of active RA by:
a. neutralizing TNF activity with its monoclonal antibody structure
b. acting as a competitive blocker of TNF receptors and thus inhibiting TNF from binding to target cell surface receptors
c. preventing the soluble human TNF receptor from binding to TNF molecules
d. allowing cytokines such as IL-1 and TNF to bind to each other
e. promoting dihydroorotate dehydrogenase, which is an enzyme required for pyrimidine synthesis


(2002 exam 3)
b. acting as a competitive blocker of TNF receptors and thus inhibiting TNF from binding to target cell surface receptors
Leflunomide (Arava) acts as an immunomodulator in patients with RA by:
a. blocking both COX and lipoxygenase enzymes
b. inhibiting dihydroorotate dehydrogenase and thus pyrimidine synthesis
c. binding to and neutralizing the activity of TNF
d. decreasing the adhesive character of PMNs and macrophages
e. inhibiting tubulin polymerization


(2002 exam 3)
b. inhibiting dihydroorotate dehydrogenase and thus pyrimidine synthesis
Azathioprine is:
a. adenosine analog
b. cytosine analog
c. PRPF analog
d. IMP analog
e. pyrimidine analog


(2002 quiz14 q1)
d. IMP analog
mTOR is:
a. PPIase
b. Tyrosine kinase
c. Protein phosphatase
d. carboxylase
e. Ser/thr kinase


(2002 quiz14 q2)
e. Ser/thr kinase
Cyclosporin A blocks:
a. calcineurin
b. calmodulin
c. Co Binding
d. PPIase
e. none of the above


(2002 quiz14 q3)
d. PPIase
FKB12 binds:
a. mTOR, calcineurin, CsA
b. FK506, Rapamycin
c. PPase 2A, p56-Lek, calcineurin
d. PPIase, FK506, FKB 56
e. PPIase, calcineurin, rapamycin


(2002 quiz14 q4)
b. FK506, Rapamycin
Calcineurin is:
a. protein kinase
b. protein tyrosine kinase
c. Ser/Thr kinase
d. protein phosphatase
e. lipid kinase


(2002 quiz14 q5)
d. protein phosphatase
Cyclophosphamide is:
a. purine biosynthesis inhibitor
b. pyrimidine biosynthesis inhibitor
c. kinase inhibitor
d. IMP analog
e. DNA cross-linker


(2002 quiz14 q6)
e. DNA cross-linker
Inactive glucocorticoid receptor associates with:
a. HSP90 and immunophilin
b. Calcineurin and calmodulin
c. mTOR and IL-2 receptor
d. FK506 and Hsp 40
e. p56-Lek and calcineurin


(2002 quiz14 q7)
a. HSP90 and immunophilin
All of the following are DMARDs except:
a. leflunomide
b. methotrexate
c. gold products
d. celecoxib
e. penicillamine


(2001 exam 3 q47)
d. celecoxib
Which of the following concerning gold salts is correct?
a. they provide immediate relief of arthritic pain
b. they primarily act by inhibiting PG synthesis
c. They frequently cause dermatologic side effects
d. they are drugs of first choice in treating arthritis
e. They must all be given intramuscularly


(2001 exam 3 q51)
c. they frequently cause dermatologic side effects
The following is true for colchicine:
a. effectively reduces pain associated with acute gouty attacks
b. decreases urate synthesis
c. increases urate excretion
d. increases tubulin polymerization leading to enhanced leukocyte migration out of inflamed regions
e. a and b


(2001 exam 3 q52)
a. effectively reduces pain associated with acute gouty attacks
The following is true for allopurinol:
a. it is not effective in acute attacks of gout, but is beneficial as maintenance therapy in gouty arthritis
b. its metabolite inhibits the synthesis of uric acid
c. it can interact with antineoplastic agents like 6-mercaptopurine with severe consequences
d. a and b
e. all of the above


(2001 exam 3 q53)
e. all of the above
The following are true for etanercept (Enbrel) except:
a. it is a competitive blocker of TNF receptors
b. it is a biological response modifier in rheumatoid arthritis
c. it must be administered by injection
d. 5-6 months are required before beneficial clinical effects are observed


(2001 exam 3 q56)
d. 5-6 months are required before beneficial clinical effects are observed
Leflunomide (Arava) acts as an immunomodulator in patients with rheumatoid arthritis by:
a. blocking both COX and lipoxygenase enzymes
b. inhibiting dihydroorotate dehydrogenase and thus pyrimidine synthesis
c. binding to and neutralizing the activity of TNF
d. decreasing the adhesive character of PMNs and macrophages
e. inhibiting tubulin polymerization


(2001 exam 3 q57)
b. inhibiting dihydroorotate dehydrogenase and thus pyrimidine synthesis
Which of the following drugs could be used to decrease the production of uric acid?
a. colchicine
b. allopurinol
c. probenecid
d. aspirin
e. hydroxychloroquine


(2004 exam 4 q1)
b. allopurinol
Which of the following is not a side effect of rapamycin (sirolimus)?
a. thrombocytopenia and leukopenia
b. hyperlipidemia
c. post transplant diabetes mellitus
d. diarrhea
e. delayed wound healing


(2004 exam 4 q48)
b. hyperlipidemia
Which of the following is not a side effect of CyPA and FK506?
a. hypoglycemia
b. acute nephrotoxicity
c. hypertension
d. gingival hyperplasia
e. post transplant diabetes mellitus


(2004 exam 4 q47)
c. hypertension (DOUBLE-CHECK)
Rapamycin-FKB12 inhibits mTOR by:
a. inhibiting amino acid binding to mTOR
b. inhibiting PA binding to FRB domain of mTOR
c. inhibiting PI3-kinase activity
D. activating phospholipase D
e. activating phospholipase C


(2004 quiz 12 q6)
b. inhibiting PA binding to FRB domain of mTOR
The role of the Zn finger of the glucocorticoid receptor is:
a. to bind glucocorticoid
b. to chelate Zn2+
c. to enhance nuclear translocation
d. to bind DNA
e. to suppress HSP90 binding


(2004 quiz 12 q7)
d. to bind DNA
6-mercaptopurine inhibits DNA synthesis by:
a. converting to 6-thio-GTP
b. inhibiting IMP dehydrogenase and PRPP amidotransferase
c. inhibiting DNA polymerase
d. inhibiting RNA polymerase
e. none of the above


(2004 quiz 12 q8)
b. inhibiting IMP dehydrogenase and PRPP amidotransferase
Mycophenolic acid inhibits DNA synthesis by:
a. inhibiting PRPP amidotransferase
b. converting to 6-thio-GTP
c. inhibiting IMPDHase and GMP synthase
d. inhibiting inosinate dehydrogenase
e. inhibiting DNA polymerase


(2004 quiz 12 q9)
c. inhibiting IMPDHase and GMP synthase
Compared to FK506 and cyclosporin A, the mechanism of action of glucocorticoids as immunosuppressors is different in that:
a. it inhibits calcineurin
b. it affects gene transcription
c. it stimulates NF-AT action
d. it stimulates NFkB action
e. it inhibits NFkB action


(2002 exam 4 q1)
b. it affects gene transcription (DOUBLE-CHECK)
Compared to FK506 and cyclosporin A, rapamycin is used for wider clinical indications including cancer. This is because:
a. rapamycin blocks key metabolic enzymes such as G6PDH
b. Rapamycin blocks cancer cell-specific antigen expression
c. rapamycin activates caspase 3, an essential enzyme in apoptosis pathway
d. rapamycin blocks growth factor signaling
e. rapamycin activates NK cells and ADCC-mediated killing


(2002 exam 4 q2)
d. rapamycin blocks growth factor signaling (DOUBLE-CHECK)
Phosphatidic acid important for the activation of mTOR is generated by:
a. PI3-K
b. PKC
c. Src kinase
d. PLC
e. PLD


(2002 exam 4 q3)
a. PI3-K (DOUBLE-CHECK)
Azathioprin and mycophenolate mofetil are purine synthesis inhibitors. Inasmuch as purine biosynthesis inhibitors are effective immunosuppressors, pyrimidine biosynthesis inhibitors can be effective as well. Pyrimidine biosynthesis inhibitors inhibit:
a. deoxycytidine and deoxythimidine synthesis
b. deoxyadenosine and deoxyguanocine synthesis
c. PRPP synthesis
d. synthesis of DNA polymerase I
e. ATP hydrolysis to ADP


(2002 exam 4 q4)
a. deoxycytidine and deoxythimidine synthesis (DOUBLE-CHECK)
Which of the following motifs of the glucocorticoid receptor targets GR to GRE?
a. Tau 1
b. Tau 2
c. Zinc finger
d. GC binding domain
e. Sticky finger


(2002 exam 4 q5)
d. GC binding domain (DOUBLE-CHECK)
Which of the following is not a mechanism of glucocorticoid-mediated immunosuppression?
a. upregulation of p56
b. upregulation of IkB
c. downregulation of IL-1
d. downregulation of PLA2
e. inhibition of AP-1, NFkB and NF-AT


(2002 exam 4 q6)
a. upregulation of p56 (DOUBLE-CHECK)
Which of the following is not the role of calcineurin?
a. regulation of calcium influx by dephosphorylation of calcium channel
b. dephosphorylation of IkB
c. Dephosphorylation of NF-AT
d. Dephosphorylation of inhibitor protein allowing activation of protein phosphatase I
e. none of the above


(2002 exam 4 q7)
b. dephosphorylation of IkB (DOUBLE-CHECK)
Which of the following statements is correct?
a. Rapamycin binds to FKB 52 and inhibits mTOR activation by binding to HEAT motif
b. mTOR activation is essential for the dephosphorylation of 4E-BP1
c. alkylating agent, cyclophosphamide, acts on liver P450 enzymes and blocks its conversion into inactive product, aldophosphamide
d. glucocorticoid receptor forms a complex with HSP-90 when activated by glucocorticoid hormone. This complex formation is needed for the receptor to translocate to the nucleus
e. rapamycin-FKB12 complex binds to FRB domain of mTOR and displaces/blocks PA from binding to that domain


(2002 exam 4 q8)
e. rapamycin-FKB12 complex binds to FRB domain of mTOR and displaces/blocks PA from binding to that domain (DOUBLE-CHECK)
For developing general immunosuppressants, which one of the following cell types should the drug be targeted against?
a. hematopoietic stem cells
b. B cells
c. Tc cells
d. Th cells
e. macrophages


(2003 quiz 13 q11)
d. Th cells
mTOR is a:
a. lipid kinase
b. phosphatase
c. serine esterase
d. phospholipase
e. protein kinase


(2003 quiz 13 q14)
e. protein kinase