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YR2 LCRS Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are the three major uses of NSAIDs?

A

Anti-pyretic
Anti-inflammatory
Analgesic

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2
Q

What are most deaths due to NSAIDs caused by?

A

GI ulceration

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3
Q

Broadly speaking, how do NSAIDs act?

A

Inhibit production of prostanoids by COX enzymes

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4
Q

What are the main prostanoids?

A

Prostaglandins (D2, E2 + F2)
Prostacyclin (PGI2)
Thromboxane A2

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5
Q

What does COX convert arachidonic acid to?

A 
Prostaglandin H2  
Which is then converted by specific synthases to: 
Thromboxane A2
Prostacyclin (PGI2)
Prostaglandin D2, E2, F2
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6
Q

How are prostanoid receptors named?

A

Based on which prostanoid they have the highest affinity for (e.g. DP1 has the highest affinity for PGD2)

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7
Q

List all the prostanoid receptors.

A 
DP 1 + 2 
EP 1 - 4
FP
IP 1 + 2  
TP
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8
Q

What type of receptor are all the prostanoid receptors?

A

GPCRs (though not all their actions are G protein mediated)

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9
Q

Explain why the EP receptor system is complex.

A

There are 4 different EP receptors + EP2 has 2 mechanisms of action + 5 pathways

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10
Q

State 6 unwanted actions of PGE2.

A 
Increased pain perception  
Increased body temperature 
Acute inflammatory response  
Immune responses
Tumorigenesis  
Inhibition of apoptosis
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11
Q

How does PGE2 increase pain perception?

A

PGE2 activates its receptor increases cAMP, activates pKa, activates nociceptors
Inflammatory mediators recruit more PGE2 which produce more cAMP, activating more nociceptors
Through Epac pathway there is recruitment of more nociceptors

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12
Q

How does PGE2 affect body temperature?

A

PGE2 stimulates hypothalamic neurones initiating a rise in body temperature
Theres a lag between PGE2 rising + temperature rising

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13
Q

State 4 desirable actions of PGE2 and other prostanoids.

A

Gastroprotection
Renal salt + water homeostasis
Bronchodilation
Vasoregulation

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14
Q

Describe the gastroprotective action of PGE2.

A

PGE2 downregulates HCl secretion

PGE2 stimulates mucus + bicarbonate secretion

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15
Q

What effect do NSAIDs have on the GI tract?

A

Increased risk of GI ulceration

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16
Q

What main effects does PGE2 have on the kidneys?

A

Increase renal blood flow

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17
Q

What effect do NSAIDs have on the kidneys?

A

Constriction of the afferent arteriole
Reduction in renal artery flow
Reduced GFR

18
Q

Why should NSAIDs not be given to asthma patients?

A

Most prostaglandins are bronchodilators, so reduced production due to COX inhibition could exacerbate asthma
Furthermore, inhibition of COX favours production of leukotrienes, which are bronchoconstrictors

19
Q

Prostanoids are vasoregulators, so what are 4 consequences of NSAIDs on the cardiovascular system?

A

Increased risk of MI + stroke because chronic use of NSAIDs:
Increases BP
Increases Water + Na+ retention
Increases Vasoconstriction
Can reduce effectiveness of anti-hypertensives

20
Q

What is the difference in terms of risk of side effects when using NSAIDs for analgesic use compared to anti-inflammatory use?

A

Analgesic use: usually occasional use so low risk of side effects
Anti-inflammatory use: often sustained use with higher doses = higher risk of side effects

21
Q

Name two non-selective COX inhibitors.

A

Ibuprofen

Indomethacin

22
Q

Name a COX-2 selective inhibitor.

A

Celecoxib

23
Q

What is the major problem with COX-2 selective NSAIDs?

A

Increased risk of CVD than conventional NSAIDs

24
Q

Describe the relative GI and CVS risks of COX-1 selective and COX-2 selective NSAIDs when compared to non-selective NSAIDs.

A 
COX-1 selective: 
Same CVS risk as non-selective NSAIDs
Increased GI risk 
COX-2 selective: 
Decreased GI risk 
Increased CVS risk
25
Q

What effect does ibuprofen have on the action of anti-hypertensive drugs?

A

Reduces effectiveness of anti-hypertensive drugs

Reduce the drop in BP that has been seen when the anti-hypertensives are used without ibuprofen

26
Q

What are the potential reasons for increased risk of cardiovascular disease with non-selective and COX-2 selective NSAIDs?

A

Non-selective NSAIDs + COX-2 selective NSAIDs both increase cardiac work
Also, all NSAIDs produce oxygen free radicals, which can contribute to CVD

27
Q

State 5 strategies for avoiding/limiting the GI side effects of NSAIDs.

A

Use topical application
Minimise NSAID use in patients with a history of GI ulceration
Treat H. pylori if present
If NSAID essential, administer omeprazole or other PPI
Minimise NSAID use in patients with other risk factors + reduce risk factors where possible e.g. alcohol consumption, anticoagulant use

28
Q

Describe the action of aspirin.

A

Irreversibly binds to cox enzymes (binds covalently)
Selective for COX-1
Anti-inflammatory, Analgesic + Anti-pyretic actions
Reduces platelet aggregation

29
Q

Explain how aspirin reduces platelet aggregation.

A

Irreversible inhibition of COX-1 in platelets means they can’t produce thromboxane A2, which enhances platelet activation + aggregation
Furthermore, aspirin preserves the production of prostacyclin, which decreases platelet action

30
Q

Why is it important to use a low dose of aspirin?

A

A low dose will allow endothelial cells to resynthesise COX-1, which can then continue to produce prostacyclin
A high dose would mean COX-1 in endothelial cells would be inhibited as it is being produced, thus decreasing prostacyclin production as well as thromboxane production

31
Q

Why don’t you want to inhibit COX-2 too much?

A

Inhibition of prostacyclin synthesis is proportional to inhibition of COX-2
We don’t want to inhibit prostacyclin production too much so we keep COX-2 inhibition low

32
Q

What are the major side effects of therapeutic doses of aspirin?

A

Gastric irritation + ulceration
Bronchospasm in sensitive asthmatics
Prolonged bleeding times
Nephrotoxicity

33
Q

Why is paracetamol NOT an NSAID?

A

It does not have anti-inflammatory action

34
Q

Explain how paracetamol overdose can cause liver failure.

A

Paracetamol is metabolised to produce a toxic metabolite (NAPQI) which is normally mopped up rapidly by glutathione
In OD, glutathione stores are depleted + NAPQI binds indiscriminately to any –SH groups
The –SH groups tend to be on key hepatic enzymes + this interference leads to cell death

35
Q

What is the antidote for paracetamol poisoning?

A

IV Acetyl cysteine
Has a lot of –SH groups
If given too late, liver damage could be permanent

36
Q

What legislation was brought in to try and reduce paracetamol related deaths?

A

No more than 2 packs per transaction

Illegal to sell > 100 paracetamol in 1 transaction

37
Q

How else may PGE2 cause increased pain perception?

A

Involvement of EP 1 + 4 receptors

Involvement of endocannabinoids

38
Q

Name a COX-1 selective drug and 1 unwanted effect it has

A

Aspirin

Causes bad GI ulcers

39
Q

What is the action of the Coxib family?

A

Selectively reversibly inhibit COX-2

40
Q

Why do side effects tend to be worse with Aspirin than other NSAIDs?

A

Because it irreversibly inhibits COX with strong covalent bonds

41
Q

What syndrome does Aspirin increase likelihood of development of and who is this mostly seen in?

A

Reye’s syndrome
Under 20’s when a viral infection is being treated with aspirin
Permanent damage to mitochondria leads to ammonia production results in damage to astrocytes + oedema in brain

42
Q

What are the actions of paracetamol?

A

Analgesic

Anti-pyretic

YR2 LCRS Pharm (34 decks)

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