review for the test. the test 57 questions/need to answer 55 27 my section 9.30-11.30p? – 1-2...
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Review for the Test
The Test
• 57 Questions/Need to Answer 55• 27 My Section• 9.30-11.30p?
– 1-2 minutes/question
COX-2 Physiological Role
• Renin-angiotensin system• blood pressure and fluid balance
• Ovulation and labor• Wound healing
• Vascular endothelium• Vascular remodeling
Modified PGs (mostly)
• Block w-oxidation– Methyls at 15 and/or 16– Phenyl in 17-20 range
• Increase Lipophilicity– Add methyls, phenyls and esters
ADME: Metabolism
E=Esterase, O=Oxidation, R=Reduction, b=b-Oxidation, w=w-Oxidation, D=dealkylation, G=glucuronidation
E
E
R13
14
O
15
E
R13
1415
O
b
D
G
b
Talfuprost
E
R
13
14
b
b
w
Prevents Beta-oxidaton
Overview
• Prostaglandins (PGs) and Thromboxanes (TXs)• NSAIDs• Gout
PGs and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
What Prostaglandin is this?
A. PGE1B. PGE2C. PGF2alphaD. PGG2E. PGH2F. PGI2G. TXA2
:10
What Prostaglandin is this?
A. PGE1B. PGE2C. PGF2alphaD. PGG2E. PGH2F. PGI2G. TXA2
:10
What Prostaglandin is this?
A. PGE1B. PGE2C. PGF2alphaD. PGG2E. PGH2F. PGI2G. TXA2
:10
PG and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
Select the one that is not true
A. PGE2 relaxes vascular smooth muscle
B. TXA2 increases renal blood flow
C. PGI2 protects the gastric mucosa
D. PGF2alpha contracts uterine smooth muscles
E. PGF2alpha causes bronchoconstriction
:10
PG and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
Prostaglandin signaling within the cell is?
A. EndocrineB. AutocrineC. ParacrineD. Intracrine
:10
What are not involved in Prostaglandin and Thromboxane signaling
A. Plasma membrane bound GPCRs
B. Nuclear membrane bound GPCRs
C. Nuclear ReceptorsD. OATP transporter
:10
Prostaglandin E2 (PGE2) binds to what type of receptor
A. DP1B. EP1C. FPD. IPE. TP
:10
PG and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
What ways are PG and TX transported
A. Active EffluxB. Active InfluxC. Passive DiffusionD. All the above
:10
PG and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
The substrate of COX 2 is?
A. Arachidonic AcidB. PGE1C. PGE2D. PGF2alphaE. PGG2F. PGH2G. PGI2H. TXA2
:10
The product of COX 2 is?
A. Arachidonic AcidB. PGE1C. PGE2D. PGF2alphaE. PGG2F. PGH2G. PGI2H. TXA2
:10
What is not a mechanism of metabolism for PG?
A. alpha-oxidation B. beta-oxidationC. omega-oxidationD. reductionE. alcohol
dehydrogenation
:10
How is TXB2 produced
A. reductionB. oxidationC. hydrolysis D. conjugation
:10
Which Cytochrome P450 (CYP) is involved in w-oxidation?
A. CYP1A1B. CYP2C9C. CYP3A4D. CYP4A
:10
PG and TXs
• Structures• Functions• Signaling• Transport• Synthesis and Degradation• PG as drugs
NSAIDs will interfere with PG drugs because they can
A. Inhibit PG synthetasesB. Induce COX 2 expressionC. Reduce COX 2 expressionD. Inhibit COX 1E. Inhibit COX 2F. D and E
diclofenac:10
What prostaglandin is Aprostadil?
A. PGE1
B. PGE2
C. TXA2
D. Prostacyclin onlyE. PGI2 only
F. Prostacyclin and PGI2
Aprostadil:10
What is not a use of Aprostadil
A. Erectile dysfunctionB. Congenital hear
defectC. HypertensionD. Induce laborE. A and BF. C and D
:10
Aprostadil binding to a GPCR causes all but the following
A. Increase intracellular Ca2+
B. Decrease intracellular Ca2+
C. Activate adenylate cyclase
D. Increase cAMP
:10
What are not formulations of Alprostadil?
A. IV injectionB. Penile injectionC. OralD. Urethral
Suppository
:10
What are ADR of Alprostadil?
A. Pain/RashB. Light HeadedC. Bleeding and
BruisingD. Flu SymptomsE. All the above
:10
Talfluprost
The compounds on the previous pageare modified versions of what prostaglandin?
A. PGE1
B. PGE2
C. TXA2
D. PGF2a
E. PGI2
F. 15-methyl PGF2a
:10
Overview
• Prostaglandins (PGs) and Thromboxanes (TXs)• NSAIDs• Gout
NSAIDs
• COX 1, COX 2 and COX3• COX 1/COX 2 IC50 ratios• COX 1 and COX 2 inhibitor side effects• Cancer• Structural Classes of NSAIDs
NSAIDs will inhibit [blank] in a patient
A. COX 1B. COX 2C. COX 3D. COX 1 and COX 2E. COX 1, COX 2 and
COX 3
:10
COX 3 should be considered with NSAID therapeutic regiments.
A. TrueB. False
:10
COX 1 has a larger active site than COX 2.
A. TrueB. False
:10
NSAIDs
• COX 1, COX 2 and COX3• COX 1/COX 2 IC50 ratios• COX 1 and COX 2 inhibitor side effects• Cancer• Structural Classes of NSAIDs
A new COX inhibitor has a COX-1/COX-2 IC50 ratio of 0.1. What COX enzyme is it selective for?
A. COX-1B. COX-2C. Non-specificD. COX-3
:10
NSAIDs
• COX 1, COX 2 and COX3• COX 1/COX 2 IC50 ratios• COX 1 and COX 2 inhibitor side effects• Cancer• Structural Classes of NSAIDs
Inhibition of PG leads to all but the following in the GI tract
A. Increase HCO3B. Increase in H+C. Increase in mucusD. Decrease in mucusE. A and BF. B and CG. A and C
:10
What are not COX 1 side effects
A. GI bleedingB. HypotensionC. Clotting disordersD. BronchodilationE. A and BF. B and CG. B and D
:10
PG inhibition leads to bronchoconstriction through
A. PGE2B. PGE1C. PGG2D. Leukotrienes (LT)E. TXA2
:10
What type of adverse side effects do you anticipate by interfering with renin-angiotensin system through COX-2
inhibition?
A. HypertensionB. Hypertension and
Renal FailureC. Renal FailureD. Brain DamageE. None of the above
:10
NSAIDs
• COX 1, COX 2 and COX3• COX 1/COX 2 IC50 ratios• COX 1 and COX 2 inhibitor side effects• Cancer• Structural Classes of NSAIDs
What are non COX 2 functions for NSAIDs in Cancer cells?
A. Block NF-kappaB signaling
B. Activate Peroxisome proliferator receptor
C. Increase ApoptosisD. Activate NF-kappaB
signalingE. A, B and CF. All the above
:10
Which drug is non-selective for COX 1 and COX 2
A. Low dose AspirinB. High dose AspirinC. IbuprofenD. CelecoxibE. All the aboveF. B and C
:10
What is not a structural class of NSAIDs?
A. SalicylatesB. ProfensC. FenacsD. OxicamsE. Statins
:10
Salicylates inhibit by the following mechanisms
A. CompetitiveB. IrreversibleC. Non-competitiveD. UncompetitiveE. A and BF. B and CG. All the above
:10
How does low dose Aspirin prevent stroke and heart attack?
A. reduce PGE2
B. reduce PGI2
C. reduce TXA2
D. B and CE. A, B and C
:10
Oxicams are acidic by which mechanism
A. ReductionB. OxidationC. HydrolysisD. Keto-enol
tautomerism
:10
What coxib is available in U.S. markets?
A. LumiracoxibB. EtoricoxibC. RofecoxibD. CelecoxibE. ValdecoxibF. None of the above
:10
Overview
• Prostaglandins (PGs) and Thromboxanes (TXs)• NSAIDs• Gout
What is not a strategy for treating gout?
A. Decrease inflammation
B. Increase Uric Acid Reabsorption
C. Inhibit Uric Acid synthesis
D. None of the above
:10
The molecule below is?
A. Uric AcidB. AllopurinolC. XanthineD. HypoxanthineE. Allopurinol
:10
Colchicine is metabolized by
A. CYP1A2B. CYP2C9C. CYP3A4D. UGTsE. B and DF. C and D
:10
Why is it bad to take allopurinol or febuxostat with XO ligands?
A. Increase blood plasma XO ligand concentration and toxicity
B. Decrease blood plasma XO ligand concentration and increased XO ligand toxicity
C. No effect on blood plasma XO ligand concentration or toxicity
D. None of the above
:10
Good Luck on the Test: Questions