Conventional Anti-inflammatory

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Last updated 11:00 PM on 9/7/26
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15 Terms

1
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Why are RA and OA considered similar?

Increases inflammatory mediators → Increases inflammatory pain

2
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What is the precursor of all eicosanoids?

Arachidonic acid

3
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What three kinds of signals are released after AA is transformed from COX?

Thromboxane A2, PGE2, PGI2,

4
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What does thromboxane A2 syntheses?

Platelet aggregation and vasoconstriction

5
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6
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How does PGE2 amplify the pain signal?

Decreases nociceptors activation threshold which increases the ability to excite

7
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What does PGI2 syntheses?

Vascular endothelium = inhibition of platelet aggregation

8
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What does PGE2 syntheses?

Mucosal protection & Inflammatory cells → nociceptor sensitization + pro-inflammatory signaling

9
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What is the difference between COX-1 and COX-2?

COX-2 promotes inflammation

COX-1 maintains homeostasis used more with gastric mucosa

10
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What kind of inhibition does ibuprofen do?

Noncovalent inhibition

11
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What kind of inhibition does aspirin do?

Irreversible covalent modification

12
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What is converted into PGE2?

PGH2

13
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Define this:

How much more potently a drug inhibits one target than another

Selectivity

14
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Define this:

Less drug required to inhibit that target by 50%

Lower IC50

15
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