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pharm - OBG > 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

They inhibit the production of prostanoids by COX enzymes

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4
Q

What are the main prostanoids?

A

Prostaglandins (D2, E2 and 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

Prostanoid receptors aren’t very specific - they are named 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

DP1, DP2

EP1, EP2, EP3, EP4

FP

IP1, IP2

TP

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8
Q

What type of receptor are all the prostanoid receptors?

A

G protein coupled receptors (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 four different EP receptors and EP3 has two mechanisms of action and five pathways

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10
Q

State some unwanted actions of PGE2.

A

Increased pain perception

Thermoregulation

Acute inflammatory response

Tumorigenesis

Inhibition of apoptosis

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11
Q

How does PGE2 increase pain perception?

A

There is involvement of EP4 receptors and endocannabinoids

The mechanism is unclear

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12
Q

How does PGE2 affect body temperature?

A

PGE2 stimulates hypothalamic neurones initiating a rise in body temperature

NOTE: there is a bit of a lag between PGE2 rising and temperature rising

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13
Q

Which prostanoid receptor is responsible for signalling in acute inflammation?

A

EP3 (on mast cells)

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14
Q

Which prostanoid receptor is responsible for the effects of PGE2 on the immune system?

A

EP4

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15
Q

Which diseases are treated with NSAIDs due to its effects on the immune system?

A

Multiple Sclerosis and Rheumatoid Arthritis (Th17 involvement)

Contact Dermatitis (Th1 cells involved)

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16
Q

What is the problem with PGE2 inhibiting apoptosis?

A

Inhibition of apoptosis increases the likelihood of necrosis

NOTE: there are 3 prostanoids, 7 prostanoid receptors and 2 downstream signalling pathways involved

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17
Q

State some desirable actions of PGE2 and other prostanoids.

A

GASTROPROTECTION

Regulation of renal blood flow

Bronchodilation

Vasoregulation

18
Q

Describe the gastroprotective action of PGE2.

A

PGE2 downregulates stomach acid production

PGE2 stimulates mucus production

PGE2 stimulates bicarbonate production

19
Q

What effect do NSAIDs have on the GI tract?

A

Increased risk of GI ulceration

20
Q

What main effects does PGE2 have on the kidneys?

A

Increase renal blood flow

21
Q

What effect do NSAIDs have on the kidneys?

A

Constriction of the afferent arteriole

Reduction in renal artery flow

Reduced GFR

22
Q

Why should NSAIDs not be given to asthma patients?

A

Most prostaglandins are bronchodilators, so a reduction in prostaglandin production due to COX inhibition could exacerbate asthma

Furthermore, inhibition of COX favours the production of leukotrienes, which are bronchoconstrictors

23
Q

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

A

Increased risk of MI and stroke because chronic use of NSAIDs cause:
 Small rise in blood pressure
 Sodium retention
 Vasoconstriction
 Can reduce the effectiveness of anti-hypertensives

24
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 occasionally used so low risk of side effects

Anti-inflammatory use – often sustained use with higher doses = higher risk of side effects

25
Q

Name two non-selective COX inhibitors.

A

Ibuprofen

Indomethacin

26
Q

Name a COX-2 selective inhibitor.

A

Celecoxib

27
Q

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

A

They have a significantly increased risk of cardiovascular disease than conventional NSAIDs

28
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

29
Q

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

A

It reduces the effectiveness of anti-hypertensive drugs

It will reduce the drop in blood pressure that has been seen when the anti-hypertensives are used without ibuprofen

30
Q

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

A

Non-selective NSAIDs and COX-2 selective NSAIDs both increase cardiac work

Also, all NSAIDs produce oxygen free radicals, which can contribute to cardiovascular disease

31
Q

State some 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 is essential, administer omeprazole or another proton pump inhibitor

Minimise NSAID use in patients with other risk factors and reduce risk factors where possible e.g. alcohol consumption, anticoagulant use

32
Q

Describe the action of aspirin.

A

It irreversibly binds to cox enzymes (binds covalently)

It is selective for COX-1

33
Q

Explain how aspirin reduces platelet aggregation.

A

Aspirin irreversibly inhibits COX-1 in platelets meaning that they can’t produce thromboxane A2, which enhances platelet activation and aggregation

Furthermore, aspirin preserves the production of prostacyclin, which decreases platelet action

34
Q

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

A

A low dose will allow the endothelial cells to resynthesise COX-1, which can then continue to produce prostacyclin

A high dose would mean that the COX-1 in the endothelial cells would be inhibited as it is being produced, thus decreasing prostacyclin production as well as thromboxane production

35
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’d like to keep COX-2 inhibition low

36
Q

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

A

Gastric irritation and ulceration

Bronchospasm in sensitive asthmatics

Prolonged bleeding times

Nephrotoxicity

37
Q

Why is paracetamol NOT an NSAID?

A

It does not have anti-inflammatory action

38
Q

Explain how paracetamol overdose can cause liver failure.

A

Paracetamol is metabolised to produce a toxic metabolite (N-acetyl-p-benzochinon imine (NAPQI))

This is normally mopped up rapidly by glutathione
In overdose, the glutathione stores are depleted and the free toxic metabolite binds indiscriminately to any –SH groups

The –SH groups tend to be on key hepatic enzymes and this interference leads to cell death

39
Q

What is the antidote for paracetamol poisoning?

A

IV Acetyl cysteine

This has a lot of –SH groups

If this is given too late, the liver damage could be permanent

40
Q

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

A

No more than 2 packs per transaction

Illegal to sell more than 100 paracetamol in 1 transaction

pharm - OBG (25 decks)

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