Inflammation Pharm Flashcards

Dr. Welsh

1
Q

Aspirin, Ibuprofen, Naproxen, Indomethacin, and Diclofenac are all ______s

A

NSAID

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2
Q

NSAIDS inhibit the _____ enzyme, by binding to Arachidonic acid and not allowing it to be converted

A

COX-2

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3
Q

What is special about Asprin’s binding mechanism?

A

It’s Irreversible!

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4
Q

Bradykinin _____ the blood pressure and stimulates pain receptors

A

Lowers

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5
Q

The main prostanoid in inflammation is PG_____

A

E2

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6
Q

The Eicosanoid _____ Promotes thrombosis and vasoconstricts (Opposite of PGI2)

A

TXA2

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7
Q

Selective COX-2 Inhibitors increase the risk of _____, because there’s a slight excess of _____

A

Thrombosis, TXA2

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8
Q

Prostaglandin _____ promotes gastric mucus secretion and inhibits acid secretion; PROTECTION, but also INFLAMMATION everywhere else

A

E2

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9
Q

Cox____ maintains homeostasis while Cox_____ is more involved with inflammation

A

1, 2

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10
Q

A reduction in “housekeeping” prostaglandins like PGE2 protecting the stomach gets wrecked by too much _____, that’s why people with ulcers are not reccomended to take this medicine

A

Aspirin

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11
Q

_____ not an NSAID, but has anti-pyretic and analgesic properties; over-dose can happen at 2-3 times of Tx and get NAPQI

A

Acetaminophen

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12
Q

Blocking COX1 and COX2 with NSAIDs causes a buildup of Arachidonic acid and causes it to be acted on by _____ to get Leukotrienes LTC4, LTD4, LTE4 for “4llergic” reactions

A

5-Lipoxygenase

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13
Q

Prostaglandin _____ INHIBITS clots and vasodilates (opposite of TXA2)

A

I2 (Prostacyclin)

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