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Clinical Pharmacology > 14) NSAIDs > Flashcards

14) NSAIDs Flashcards

1
Q

What are the primary therapeutics effects of NSAIDs?

A

Analgesia, anti-inflammatory, antipyretic

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2
Q

Give some examples of autocoids:

A

Bradykinins, histamine, cytokines and leuckotrienes

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3
Q

What are the features of eicosanoids?

A

Localised release

Short half life

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4
Q

What are eicosanoids derived from?

A

Arachidonic acid

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5
Q

Give some examples of eicosanoids:

A

Prostaglandins
Prostacyclins
Thromboxanes

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6
Q

How are prostaglandins synthesised?

A

Cyclo-oxygenase enzymes

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7
Q

What prostaglandin is most important in mediating the inflammatory response and what is its effect?

A

PGe

Vasodilation, hyperalgesia, fever, immunomodulation

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8
Q

Describe the features of COX1 (including production):

A

Constitutively expressed in a wide range of tissues

Short half life

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9
Q

Where is COX1 commonly found?

A

Gastric mucosa, myocardium, renal parenchyma

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10
Q

Describe the features of COX 2 (including production):

A

Induced by inflammatory mediators

Constitutively expressed in brain and kidney

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11
Q

How do the structures of COX1 and 2 allow for selective inhibition?

A

COX1 has a ‘tight’ tunnel for arachidonic acid, whereas COX2 is ‘baggy’

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12
Q

Describe the binding of prostaglandins and their effects at the receptor:

A

Bind with GPCRs - synthesis of autocoids, potent vasodilators and peripheral nociception

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13
Q

Where does PGE2 bind in the periphery?

A

C fibres by EP1 receptor

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14
Q

What is the effect of PGE2 binding in C fibres?

A

Increased C fibre activity by increased sensitivity to bradykinin

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15
Q

What is allodynia?

A

Triggering of pain from stimuli that don’t usually provoke pain

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16
Q

What is hyperalgesia?

A

Increased pain from a stimulus that usually provokes pain

17
Q

Where does PGE2 bind centrally, and what’s its effect?

A

EP2 receptors - increase sensitivity and discharge rate of secondary interneurones

18
Q

How do prostaglandins cause pyrexia?

A

IL-1 release by macrophages causing production of PGE2 in hypothalamus that acts on EP3 to cause increased heat production

19
Q

Describe the pharmacokinetics of NSAIDs:

A

First order elimination
Half lives can vary
Heavily plasma protein bound

20
Q

When are NSAIDs indicated?

A

MSK disorders for mild-moderate pain

21
Q

When are renal adverse effects from NSAIDs common?

A

Heart failure
Renal disease
Hepatic cirrhosis
Hypovolemia

22
Q

What are some common GI adverse effects of NSAIDs?

A

Stomach pain, nausea, heartburn, gastric bleeding, ulceration

23
Q

Why do NSAIDs cause GI side effects?

A

Gastric prostglandins stimulate mucus production

24
Q

What are some common renal adverse effects of NSAIDs?

A

Sodium, potassium, chloride and water retention - hypertension

25
Q

Why do NSAIDs cause renal side effects?

A

Decrease renal perfusion, usually maintained by prostaglandins

26
Q

What are some other adverse effects of NSAIDs (not renal/GI)?

A

Increased bleeding time
Skin rashes - Stevens Johnson syndorme
Bronchial asthma
Reye’s syndrome

27
Q

What drugs can NSAIDs displace?

A

Sulphonylureas
Warfarin
Methotrexate

28
Q

What is the mechanism of action of aspirin?

A

Irreversibly inhibits COX enzymes by acetylation

29
Q

Describe the pharmacokinetics of aspirin:

A

Half life is short

High doses - zero order elimination

30
Q

What are some added beneficial effects of aspirin?

A

Reduces platelet aggregation

May reduce risk of GI and breast cancers

31
Q

What are the effects of paracetamol?

A

Mild/moderate analgesia and antipyrexial

32
Q

What are the potential mechanisms of action of paracetamol?

A

Weak COX1+2 inhibitor

Metabolite can bind with arachidonic acid

33
Q

When is paracetamol contraindicated?

A

Compromised hepatic function

Chronic alcoholics

34
Q

How is paracetamol usually metabolised?

A

Phase II conjugation by glucoronide and sulphate

Some phase I oxidation into NAPQI

35
Q

Describe the metabolism of paracetamol in overdose:

A

Phase II saturated so build up of NAPQI which can’t be removed due to glutathione depletion

36
Q

What are the effects of paracetamol overdose?

A

Necrotic hepatocyte death

Renal failure

37
Q

What is the treatment plan for someone with paracetamol overdose?

A

If within 4 hrs: activated charcoal orally
0-36 hrs - N-acteylcysteine IV
Methionine oral if NAC can’t be given promptly

Clinical Pharmacology (24 decks)

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