Anti-inflammatory drugs Flashcards

1
Q

How is hereditary angioedema (HAE) treated?

A
  1. B2​ antagonists
  2. Kallikrein antagonists
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2
Q

What is a selective bradykinin B2 receptor inhibitor?

A

Icatibant

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3
Q

What is a kallikrein inhibitor?

A

Ecallantide

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4
Q

What is the purpose of TrkA inhibition?

A

Treatment of inflammatory pain by NGF.

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5
Q

What is a TrkA antagonist?

A

Tanezumab

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6
Q

What is the mechanism of action of tanezumab?

A
  • Monoclonal antibody that binds to and inhibits TrkA
  • Prevents NGF mediated pain sensitisation
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7
Q

What is the mechanism of action of bufexamac?

A

Inhibition of LTA4 hydrolase

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8
Q

What is the therapeutic use of bufexamac?

A

Anti-inflammatory

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9
Q

What is the mechanism of action of zafirlukast?

A

CysLT1 receptor antagonist

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10
Q

What is the mechanism of action of zileuton?

A

5-lipoxygenase inhibitor

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11
Q

What is the therapeutic use of zafirlukast and zileuton?

A

Treatment of asthma

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12
Q

What is the function and mechanism of action of lexipafant?

A
  • Function: Treatment of inflammatory conditions
  • Mechanism: PAF receptor inhibitor
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13
Q

What is the function and mechanism of action of rupatadine?

A
  • Function: Treatment of fever and urticaria
  • Mechanism: Recombinant histamine H1 and PAF receptor antagonist
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14
Q

What is the mechanism of action of most NSAIDs?

A

Enters hydrophobic tunnel and forms H-bond with Arg120 to prevent entry of arachidonic acid (reversible inhibition)

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15
Q

What are COX-2 selective drugs?

A
  • Etoricoxib
  • Rofecoxib
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16
Q

What are the actions of aspirin on platelets?

A
  • Irreversibly inhibits COX 1 in both platelets and endothelial cells.
  • Prevents platelet production of TXA2 (promotes platelet aggregation and vasoconstriction).
  • Prevents endothelial cell production of PGI2 (inhibits platelet aggregation and promotes vasodilation).
  • Endothelial cells can re-synthesise COX1 but platelets can’t.
17
Q

What is the mechanism of action of eicosapentanoic acid in fish oil in decreasing heart attacks?

A
  • Eicosapentanoic acid results in production of TXA3 and PGI3.
  • TXA3 has much less potent pro-platelet aggregation effect compared to TXA2.
  • PGI3 has only slightly less potent anti-platelet aggregation effect compared to PGI2.
  • Balance tipped in favour of anti-aggregation PGI3 and thus risk of thrombo-embolism decreased.
18
Q

How can gastric side effects of NSAIDs by countered?

A
  1. Use in combination with synthetic PGE2 analogue such as misoprostol
  2. Use with proton pump inhibitor such as omeprazole
19
Q

How can paracetamol overdose be treated?

A

Acetylcysteine and methionine to increase hepatic glutathione production