Drugs for Inflammation Flashcards

1
Q

What is the general action of glucocorticoids?

A

inhibit AA release and metabolism

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2
Q

What is the action of NSAIDs?

A

COX inhibition

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3
Q

What is the effect of antagonising CysLT1 receptors?

A

block LTC4 and LTD4 actions. Prevent bronchospasm and nasal congestion

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4
Q

T/F The action of the inducible Cox-2 is not as strong as the constitutive Cox-1

A

False, Cox-2 can be 100x more potent

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5
Q

What is one reason why tumor cells often cause acute and chronic inflammation

A

tumors induce Cox-2

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6
Q

Which prostaglandin is most related to inflammation

A

PGE2

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7
Q

What prevents us from using prostaglandin as drugs?

A

too unstable and expensive

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8
Q

T/F Aspirin is indicated for patients with gout

A

False, although anti-inflammatory, aspirin can compete with the clearance of urea at the kidneys

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9
Q

Why is NSAID useful for gout?

A

It blocks the action of PGE2, hence reducing inflammation

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10
Q

How does NSAID cause analgesia?

A

by removing sensitisation from AA products

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11
Q

Why is paracetamol preferred as an antipyretic?

A

aspirin tends to cause gastric bleeding more so than paracetamol

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12
Q

How does NSAID cause gastric ulcer?

A

by inhibiting PGE2, it also inhibits the ability to repair gastric mucosa. Without the protective effect of PGE2, there may be acid reaching the gastric lumen

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13
Q

T/F NSAID is an anti-coagulative

A

True

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14
Q

T/F low dose aspirin can prevent CV disease

A

True, because it affects only platelets in the portal circulation, reducing TXA2 but not affecting vascular PGI2

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15
Q

T/F NSAIDs can sometimes cause bronchoconstriction

A

True, some individuals are hypersensitive, and can overproduce leukotrienes

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16
Q

How is aspirin different to other NSAIDs?

A

it’s irreversible

17
Q

Which drug is Reye’s syndrome associated with?

A

aspirin

18
Q

How is paracetamol different to NSAIDs?

A

it’s analgesic, antipyretic, but not anti-inflammatory

19
Q

What is the theory of COX-2 selectivity?

A

its hydrophobic pocket for AA is larger than that of COX-1, so it can reduce GIT side effect while retaining efficacy

20
Q

Why has some COX-2 agents been withdrawn?

A

they increase CV risk in the long run, because COX-2 is the main contributor of coronary artery integrity

21
Q

What are the three mechanisms of action of glucocorticoids?

A

direct transactivation
direct transrepression
tethered transrepression

22
Q

Which protein is the target of tethered transrepression?

A

NF-kB, important for the induction of cytokines