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Pharmacology > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are the types of cyclooxygenase (COX) inhibitors and their reversibility?

A

Non-selective COX inhibitors, which may be reversible or irreversible

COX-2 selective which are reversible

CNS-selective COX inhibitors which are reversible

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2
Q

What is the pain pathway?

A

Primary afferent neuron –> dorsal root ganglion –> dorsal horn of spinal cord –> ascends to the brain via the lateral spinothalamic tract

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3
Q

What step of the pain pathway to NSAIDs and opioids work on?

A

NSAIDs: primary afferent neurone

Opioids: CNS

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4
Q

How do steroids reduce inflammation?

A

By mimicking endogenous cortisone

which suppresses phospholipase A2

reducing inflammation

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5
Q

What mechanisms do NSAIDs block and what symptoms do they cause?

A

Decreases vasodilation which usually contributes to heating, redness and swelling

Blocks increase in vascular permeability –> reduces swelling

Reduces pain associated with inflammation

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6
Q

Why do NSAIDs have an analgesic ceiling?

A

Because they block prostaglandins, which sensitize nociceptive fibers to stimulation by inflammatory mediators

Therefore NSAIDs reduce sensitivity of the fibers but don’t block them directly. Other inflammatory mediators can still cause effects `

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7
Q

What is an irreversible, non-selective COX inhibitor that blocks prostaglandin synthesis?

A

Aspirin

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8
Q

What are the effects of action of aspirin?

A

Anti-inflammatory, analgesic, anti-pyretic and anti-platelet

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9
Q

What is the mechanism of action for the anti-inflammatory effects of aspirin?

A

Decreased vasodilation and decreased vascular permeability

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10
Q

What is the mechanism of action for the analgesic effects of aspirin?

A

By decreased sensitization of nociceptive fibers to inflammatory mediators (by decreasing prostaglandin levels)

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11
Q

What is the mechanism of action for the antipyretic effect of aspirin

A

Acts on the hypothalamus to reset the body temperature (but does not alter the normal body temp!)

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12
Q

What is the mechanism of action for the antiplatelet action of aspirin?

A

It inhibits both thromboxane A2 (which causes platelet aggregation) and prostaglandin I2 (which inhibits platelet aggregation)

However inhibition of thromboxane A2 > that of prostaglandin I2

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13
Q

What is another typical NSAID but with a long half-life of 12-24 hours? What is it used for?

A

Naproxen

More effective in women

Used for dysmenorrhea

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14
Q

What is a typical NSAID which is steroid-like and strongly anti-inflammatory?
What are its side effects?

A

Indomethacin

has CNS effects: confusion, depression, psychosis

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15
Q

What is a typical NSAID with a short half life of <2h? What is its GI risk?

A

Diclofenac

Lower risk of GI effects due to short half life

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16
Q

What are the GIT side effects of NSAIDs and their mechanisms?

A

nausea, vomiting, dyspepsia, ulcers and increased risk of bleeding

prostaglandins usually decrease stomach acid production, increase bicarb and mucus production and increase mucosal blood flow

but nsaids decrease prostaglandin production

17
Q

One of the most common vasculitides of childhood that aspirin is prescribed for is:

A

Kawasaki syndrome

17
Q

What are the non-RAAS renal effects of NSAIDs and their mechanisms?

A

Edema and hypotension

Prostaglandin E2 usually inhibits reabsorption of Na and water. Decrease in PG E2 leads to increased reabsorption and edema/hypotension

17
Q

What are the pseudo-allergy side effects of NSAIDs and their mechanisms?

A

Rashes, itching, nasal congestion, anaphylaxis

Inhibition of COX leads to shunting of arachidonic acid down the 5-LOX and 15-LOX pathway, leading to the production of leukotriene and lipoxins respectively, which are inflammatory mediators

17
Q

What are the RAAS renal effects of NSAIDs and their mechanisms?

A

Prostaglandin I2 usually stimulates RAAS

Decreased PG I2 –> decreased renin and aldosterone

This can’t be offset by increased Na and water reabsorption as the effect of lower PGE2 –> less Na reaching the DCT where aldosterone acts

17
Q

What are the asthmatic side effects of NSAIDs and their mechanisms?

A

Bronchospasms in those who are already susceptible

5-LOX present > 15-LOX present

leukotrienes > lipoxins

leukotrienes are linked to asthma

18
Q

What are the haematopoietic effects of NSAIDs and their mechanisms?

A

Bruising and bleeding

Due to anti-platelet effects

18
Q

What are the symptoms of kawasaki syndrome?

A

Higher fever for at least 5 days

Bilateral bulbar conjunctivitis

Erythema of palms/soles

Oedema of the hands and feet

Polymorphous rash

cervical lymphadenopathy

18
Q

Why should aspirin not be prescribed to children with viral infections?

A

It can result in Reye’s syndrome, which can result in:

Encephalitis, liver swelling, vomiting, confusion, delirium, convulsions or loss of consciousness

19
Q

What are examples of selective COX-2 inhibitors?

A

Celecoxib or other coxibs

20
Q

What is the effect of selective cox-2 inhibitors?

A

Selective inhibition of COX 2, reduction of GIT side effects

Mainly anti-inflammatory and analgesic, less anti-pyretic

21
Q

What are the renal effects of selective COX-2 inhibitors?

A

Nephrotoxicity due to the expression of COX 2 in the kidney

22
Q

What are the effects of selective COX 2 inhibitors on ovulation?

A

Delayed follicular rupture

23
Q

Can NSAIDs be taken during pregnancy?

A

Not during the third trimester, it may cause a premature closing of the ductus arteriosus

24
Q

What is the effect of selective COX-2 inhibitors on wound healing?

A

Impairment of wound healing

May also exacerbate ulcers

25
Q

What are the haematopoietic effects of selective COX-2 inhibitors?

A

Thrombosis

COX 2 usually produces Prostaglandin I2 which inhibits platelet aggregation, but not thromboxane 2 which promotes platelet aggregation and clotting.

When COX-2 is inhibited, the balance between PG I2 and TXA2 is disrupted.

TXA2 now > PG I2 and platelet aggregation is favoured –> thrombosis

26
Q

What is a CNS-selective COX inhibitor?

A

Paracetamol

27
Q

What is the proposed MOA of paracetamol?

A

The metabolite AM404 may modulate pain transmission by inhibiting cannabinoid reuptake, or inhibiting transient receptor potential vanilloid 1 or COX

28
Q

What are the effects of paracetamol?

A

Good analgesic and potent anti-pyretic, but weak anti-inflammatory effects.

Safe in children

Has few side effects, spares GI and has few drug-drug interactions

29
Q

What are possible side effects of paracetamol?

A

hepatotoxicity in high doses, can be exacerbated by chronic alcoholism

Allergic skin reactions may sometimes occur

Nausea/vomiting may sometimes occur

30
Q
A

Pharmacology (6 decks)

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