NSAIDs Flashcards

1
Q

Give examples of NSAIDs

A

Ibuprofen

Naproxen

Diclofenac

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2
Q

What are the 3 primary effects of NSAIDs?

A

Analgesia

Anti-inflam

Antipyretic

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3
Q

What is the role of inflammation?

A

Protective = reduce risk of further damage by MO

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4
Q

What are autacoids?

A

Local molecular mediators/signalling agents with a short half life

Induce expression of COX 2

E.g. Bradykinin, histamines, cytokines, leukotrienes

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5
Q

What is the role of cyclo-oxylase (COX) enzymes?

A

Aid the synthesis of prostaglandins

COX 1/2 produce PGs D, E, F, I

E = most important in mediating inflam response

COX 1 = constitutively expressed (constant) in wide range of tissues

COX 2 = induced by injurious stimuli like inflam mediator bradykinin

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6
Q

What is the main therapeutic effect of NSAIDs?

A

COX 2 competitive inhibition = prostaglandin synthesis inhibition = inflam inhibition

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7
Q

Most ADRs caused by NSAIDs are due to what?

A

COX 1 inhibition

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8
Q

How do prostaglandins work?

A

Bind GPCRs

Binding enhances actin of other autacoids

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9
Q

Outline how prostaglandins are involved in the inflam response

A

Injury = autocoids and prostanoids released

= induced expression of COX 2

= aid synthesis of prostaglandins

= enhanced action of other autacoids (bradykinin and histamine) and potent vasodilator

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10
Q

How do prostaglandins enhance pain reception ?

A

Bind/activate GPCRs =

Increased neuronal sensitivity to bradykinin

Inhibition of K+ channels

Increased Na channels sensitivity

ALL = increased C fibre (carry pain impulses) activity

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11
Q

Explain how central nociception is sensitised

A

PGs active GPCR EP2 receptors =

Removes interneuronal inhibition = greater sensitivity to pain

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12
Q

What are the stages of pain?

A

1) sensitisation of peripheral pain fibres

2) long term pain then causes increased pain perception

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13
Q

Outline the role of each prostaglandin receptor

A

EP 1 = sensitising peripheral pain by increasing C fibre activity

EP 2 = increase vasodilation, sensitising central pain by inhib of inhibitory interneurons

EP 3 = increased heat production and decreased heat loss

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14
Q

What are the general therapeutic effects of NSAIDs?

A

Anti inflam = rheumatoid, osteoarthritis

Analgesics = mild/moderate pain

Antipyretics

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15
Q

What ADRs are associated with NSAIDs

A

COX 1 inhib = many side effects

Elderly long term use = iatrogenic morbidity/mortality

GI = pain, nausea, heartburn, gastric bleeding, ulceration (offset with PPIs)

Renal = decreased GFR

Vascular = increased risk of bleeding

Hypersensitivity = rashes, bronchial asthma

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16
Q

Outline the potential drug interactions NSAIDs can have

A

Combined with low dose opiates = extends therapeutic range for treating pain

NSAIDs in combination = increased risk of ADRs

NSAIDs together = effect each others PK/PD due to competition for plasma proteins

NSAID + low dose aspirin = interfere with cardioprotective action of aspirin

17
Q

What drugs are affected by NSAIDs and why?

A

Highly protein bound drugs = sulphonylurea, warfarin, methotrexate

Competitive displacement

18
Q

Discuss the use of paracetamol

A

No anti-inflam action

Effective analgesic and antipyretic

Weak COX 1/2 inhibitor

Primarily acts in CNS

Caution in those with compromised hepatic function (alcoholics)

NAPQI at normal dose is detoxified by conjugation with glutathione

Overdose = oral activated charcoal and start N-acetylcysteine IV

19
Q

What does of paracetamol is potentially fatal?

A

Single dose >10 g (20 tabs)