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PPE > 7.1 NSAIDs > Flashcards

7.1 NSAIDs Flashcards

1
Q

What are the 3 main actions of NSAIDs?

A

Antipyrexic
Anti-inflammatory
Analgesia

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2
Q

What are autocoids?

A

Autocoids are biological factors which are released in response to inflammation.
They have a short half life and act as local hormones

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3
Q

What are some examples of autocoids?

A 
Cytokines
Histomine
Serotonin
Bradykinin
NO

Neuropeptides
Leukotrines
Eicosanoids

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4
Q

What are eicosanoids?

A

20C phospholipid signalling molecules

e.g. prostaglandins

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5
Q

How are eicosanoids made?

A

They come from the cell membrane, the arachidonic acid

The synthesis is catalysed by COX enzymes

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6
Q

What are the types of prostaglandin?

Which is the main one? Why?

A

In order of being made - G, H, D E F I
They require specific enzymes to produce each one

E, most important in monitoring the inflammatory response

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7
Q

What does Prostaglandin E do?

A

Vasodilate
Hyperalgesia
Fever
Immunomodulation

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8
Q

What are the types of COX Enzyme?

WHat is their distribution

A

COX1 - always expressed in all tissues, short half life, constant production needed
COX2 - released from noxious stimuli e.g. tissue damage

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9
Q

What are the types of COX Enzyme?
What is their distribution?
What is the difference in stucture?

A

COX1 - always expressed in all tissues, short half life, constant production needed
COX2 - released from noxious stimuli e.g. tissue damage
COX 1 is tight, 2 is loose
Only small drugs e.g. Aspirin can effect COX 1

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10
Q

What is the function of COX1

A

It is cytoprotective e.g. in gastric mucosa

It increases tissue perfusion

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11
Q

What is the function of COX2

A

Stimulates inflammation by converting prostaglandins e.g Pg E
It is mainly in the brain and kidneys

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12
Q

Which COX enzyme do NSAIDs give most effects through?

A

COX 2

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13
Q

What are the receptors that prostaglandins act on?
What GPCR is it?
Their action?

A

EP1 - Gq (increase nociception)
EP2 - Gs (vasodilate)
EP3 - Gi (pyrexia)

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14
Q

What is EP1?

A

Prostaglandin Receptor
Increases C fibre activity and activate silent C fibres (lowers threshold)

Inhibits K+ channel, Increases Na+ sensitivity and bradykinin sensitivity, Increases Ca2+ for more NTs

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15
Q

How does central sensititsation occur?

A

The increase in peripheral nociception leads to an increase in cytokines in the dorsal horn.
This increases COX-2 and PgE synthesis
PgE acts on EP2 to increase cAMP/PKA to increase pain perception
Inhibits glycine inhibition

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16
Q

What is EP3?

A

IL2 –> PGE2

PGE2 acts on the Gi receptor, to increase heat production

17
Q

How do NSAIDs work?

A

They selectively inhibit COX enzymes

Most effect comes from inhibiting COX 2

18
Q

What are some properties of NSAIDs?

A

Highly protein bound
GI Effects (reduce PG in stomach –> ulcers/reflux)
Increase bleeding risk
Typically oral preparations

19
Q

What is Celecoxib?

A

A selective COX2 inhibitor

Tried to overcome the COX 1 side effects, but increases CVS risk

20
Q

What is Asprin?

A

A COX inhibitor

Cardioprotective

21
Q

Why is Asprin special?

A

It is the only one to irreversibly bind to COX

22
Q

Properties of Asprin?
Half Life
Order

A

Short Half Life
Wide Spread
1st order at low doses, high=zero order

23
Q

What is Paracetamol?

A

NOT an NSAID

It is a NOAD (non-opiod analgesic drug)

24
Q

What does Paracetamol do?

A

NO anti-inflammatory action

Prevents pain

25
Q

Why use paracetamol?

A

Has fewer ADRs

26
Q

Why have you got to be careful with paracetamol?

A

Low TI
Overdose! –> toxic to hepatocytes
NAPQI toxic metabolite from phase 1 conjugation

27
Q

How do you treat paracetamol overdose?

A

<4hrs - activated charcoal to prevent uptake

0-36hrs - N-acetylcystine or methionine orally

28
Q

What are some ADRs of NSAIDS?

A 
GI 
Renal (when compromised)
Increase bleeding risk
Hypersensitivity (Asthma, rashes)
Reyers Syndrome
29
Q

Examples of NSAIDS?

A

Aspirin
Ibuprofen
Celocoxib

PPE (25 decks)

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