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PCOL2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are the cardinal signs of inflammation?

A

Pain, redness, heat, swelling, often loss of function.

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2
Q

What are four roles of COX-1 prostaglandins?

A

Gastric protection
Renal blood flow
Platelet aggregation
Starting parturition (labour)

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3
Q

COX-_ is constitutive, whereas COX-_ is induced.

A

COX-1: constitutive

COX-2: induced

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4
Q

Prostaglandins and thromboxanes are both…

A

eicosanoids

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5
Q

What are two important eicosanoids involved in the therapeutic effect of NSAIDs?

A

prostaglandins and thromboxanes. Mostly he talks about prostaglandins.

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6
Q

What are two examples of major COX-2 inducers?

A

IL-1, TNF-a

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7
Q

1) Scientists generally attribute the therapeutic effects of NSAIDs to ___ inhibition, and the side effects to ___ inhibitinon.
2) but now we know that’s an oversimplification. How do we know that?

A

COX-2 (therapeutic)
COX-1 (side effects)

We know that’s an oversimplification because newer COX-2 selective inhibitors aren’t anywhere near tolerated as we predicted.

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8
Q

What might explain why COX-2 selective inhibitors didn’t work as well as we thought?

A

COX-2 probably mediates some healing functions (inc. inflammation in general), and after the switch (following unselective inhibitors), damage (esp. GI) took longer to resolve.

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9
Q

What’s the flagship 1st gen NSAID?

What’s the flagship 2nd gen NSAID?

A

Aspirin

Coxib

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10
Q

What is aspirin’s mechanism of preventing platelet formation?

A

Irreversible inhibition of COX-1

->Reducing Thromboxane TXA2 synthesis.

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11
Q

To prevent platelet aggregation, aspirin prevents the synthesis of which eicosanoid by COX-1?

A

the thromboxane TXA2

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12
Q

What do PGs do that normally mediates inflammatory pain?

A

They sensitise nociceptive nerve fibres to inflammatory mediators like:
bradykinin,
seratonin,
histamine

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13
Q

What (e.g. of) inflammatory mediators are normally responsible for sensitising nociceptive nerve fibres to the basic pain message?

A

bradykinin, seratonin, histamine

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14
Q

How would NSAIDs help with oedema?

A

Preventing [PG-mediated] vasodilation

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15
Q

What about inflammation DON’T NDAIDs prevent?

A

Migration of inflammatory cells.

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16
Q

How do prostaglandins normally adjust the set-point temperature of the body, causing fever?

A

IL-1 triggers PG production in the hypothalamus, which is used in the process of pyrogenesis.

Bonus: because this is inflammatory-mediated, NSAIDs don’t affect temperature in normal conditions.

17
Q

What is aspirin’s mechanism of inhibiting COX?

A

irreversible acetylation of COX [at ser530].

18
Q

What function of COX-1 in the body is relevant to the side effect of fluid retention?

A

Increasing renal flow. NSAIDs reduce GFR.

19
Q

What do prostaglandins do in the stomach - what’s the side effect when they’re inhibited?

A

They decrease pepsin/acid and increase mucus.

COX-1 inhibition therefore has the opposite effect - leading to mucosal irritation in the tummy.

20
Q

What are three common indications for aspiring despite high GI effects?

A
  • Mild pain
  • CV: antiplatelet following MI or prophylactically for ischaemic syndromes.
  • rheumatic fever/arthritis (antipyretic & analgesic).
21
Q

Why is ibuprofen the drug of choice for inflammatory joint problems, as well as SHOULD be more generally for mild pain management?

A

Effective and well tolerated - much lower incidence of symptoms.
Recall it’s just a competitive substrate.

22
Q

What will I find piles of in C’s room?

A

Ibuprofen - dysmenorrhea.

23
Q

What’s an example of a [weakly] COX-2 selective NSAID?

A

Piroxicam.

24
Q

What’s the downside of paracetamol? (Crossover with toxicology)

A

NPBQI

25
Q

Which people suffer most from NSAID side effects?

Recall - what would those side-effects be?

A

Oldies.

26
Q

What would scare concerned aussie mums about giving their kids aspirin?
Why are they sorta right?

A

Reye’s Syndrome (following viral infections).

Kids should be given panadol, not aspirin.

27
Q

Why have a lot of Coxibs been withdrawn?

A
  • significant gastroduodenal stress
  • useless for cardiac events (no antiplatelet action)
  • slowed peptic ulcer healing
28
Q

Aspirin PK:
<600mg (low dose): __th order kinetics with a ___ hour half life.
>4g (anti-inflammatory dose): __ order kinetics with a ___ hour half life.

A

600mg: 1st; 3.5h

>4g: 0th; >15h

29
Q

The doses for prophylaxis vs. anti-inflammation are different in magnitude. The kinetics in ______ doses are zero order and the half life is drastically extended.

A

Antiinflammatory - zero order.

PCOL2 (24 decks)

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