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MODULE 7 - Skin and Bones > PHARMACOLOGY - NSAIDS > Flashcards

PHARMACOLOGY - NSAIDS Flashcards

1
Q

What are the five clinical uses of NSAIDS?

A

Management of inflammatory disorders
Management of pain
Management of endotoxaemia in large animals
Management of prothrombotic states
Management of tumours

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2
Q

What is the mechanism of action for NSAIDS?

A

NSAIDS are reversible inhibitors of the cyclooxygenase (COX) enzyme

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3
Q

Which NSAID is an irreversible inhibitor of the cyclooxygenase enzyme?

A

Aspirin

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4
Q

What are the two main isoforms of cyclooxygenase (COX)?

A

Cyclooxygenase-1 (COX-1)
Cyclooxygenase-2 (COX-2)

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5
Q

Which cyclooxygenase isoform is mainly involved in physiological function?

A

Cyclooxygenase-1 (COX-1)

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6
Q

Which cyclooxygenase isoform is up-regulated in response to inflammatory stimuli?

A

Cyclooxygenase-2 (COX-2)

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7
Q

What are the five useful effects of NSAIDS?

A

Analgesic
Anti-pyretic
Anti-inflammatory
Anti-thrombotic
Anti-endotoxic

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8
Q

How do NSAIDS act as peripheral analgesics?

A

NSAIDS inhibit prostaglandin synthesis at the site of inflammation, thus reducing the exposure of nociceptive nerve ending to inflammatory mediators

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9
Q

How do NSAIDS act as central analgesics?

A

NSAIDS inhibit prostaglandin synthesis, reducing central neural excitation, hyperalgesia and pain

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10
Q

How do NSAIDS act as anti-pyretics?

A

Inflammation stimulates the production of endogenous pyrogens which act on the anterior hypothalamius to simulate prostaglandin production which acts on the thermoregulatory centre within the preoptic area of the hypothalamus, causing pyrexia. NSAIDS inhibit prostaglandin synthesis, preventing the increased temperature associated with pyrexia

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11
Q

How do NSAIDS act as anti-inflammatory drugs?

A

NSAIDS inhibit prostaglandin synthesis at sites of inflammation, reducing the inflammatory response and number of vasodilatory prostaglandins produced - reducing oedema

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12
Q

How do NSAIDS act as anti-thrombotics?

A

NSAIDS inhibit COX-1 and thus the synthesis of thromboxane A, inhibiting platelet aggregation

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13
Q

Why are NSAIDS more effective as anti-thrombotic agents at lower doses?

A

A low dose of NSAIDs inhibits COX-1 in platelets, inhibiting the production of thromboxane A which is usually pro-thrombotic. However, high dose NSAIDS can also inhibit COX-2 in endothelial cells, inhibiting the production of PGI2 which would usually prevent platelet aggregation. This can cause the pro-thrombotic/anti-thrombotic balance to shift in favour of thrombosis

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14
Q

How does aspirin have a long term anti-thrombotic action?

A

Aspirin binds irreversibly to both COX-1 and COX-2. COX-2 is found in endothelial cells which can produce more receptors and override the effects of aspirin as these cells have a nucleus however platelets do not have a nucleus and cannot produce more COX-1 receptors, meaning when aspirin binds to COX-1 on platelets, it permanently inhibits the enzyme and thus has a long term anti-thrombotic action

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15
Q

How do NSAIDS act as anti-endotoxic drugs?

A

Endotoxins cause damage to white blood cells and the vascular endothelium causing the release of vasoactive mediators which trigger a cascade of events resulting in endotoxic shock. NSAIDS can inhibit the synthesis of vasoactive mediators and prevent endotoxic shock

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16
Q

What are the physiological roles of prostaglandins within the gastrointestinal tract?

A

Within the gastrointestinal tract, prostaglandins inhibit gastric secretion and cause vasodilation to increase blood flow to the stomach and increase mucus production to protect the gastric mucosa

17
Q

Which cyclooxygenase isoform primarily mediates prostaglandin production within the gastrointestinal tract?

A

Cyclooxygenase-1 (COX-1)

18
Q

How do NSAIDS affect the gastrointestinal tract?

A

NSAIDS inhibit cyclooxygenase-1 (COX-1) and thus reduce prostaglandin synthesis which will cause a reduction in blood flow to the gastric mucosa, mucosal ischaemia followed impairment of the protective mucosal barrier which will expose the gastric mucosa to the gastric acid causing ulceration

19
Q

Why should NSAIDS always be given with food?

A

NSAIDS should always be given with food to protect the gastrointestinal mucosa as the contact area of the tablet will receive a high localised concentration of the drug which will increase the risk of ulceration in that area

20
Q

Where in the kidneys are renal prostaglandins produced?

A

Renal medulla
Glomerulus

21
Q

What are the physiological roles of prostaglandins in the kidneys?

A

Renal prostaglandins have a vasodilatory effect and thus increase renal blood flow, improving renal function and excretion. Prostaglandins also provides compensatory vasodilation, i.e. maintains renal blood flow in the presence of vasocontrictors

22
Q

How do NSAIDS affect the kidneys?

A

NSAIDS inhibit cyclooxygenase and thus reduce prostaglandin production which will impair renal blood flow

23
Q

(T/F) Impaired renal blood flow due to NSAIDS has very little effect on healthy, well-hydrated animals

A

TRUE. However, patients suffering from trauma, haemorrhage or undergoing prolonged surgery are at a higher risk of dehydration and are more likely to undergo acute renal failure in response to NSAIDS

24
Q

How should NSAIDS be administered?

A

NSAIDS should be administered orally in combination with food

25
Q

Are NSAIDS weak acids or weak bases?

A

NSAIDS are weak acids

26
Q

Which two properties of NSAIDS allow them to selectively target inflamed tissue?

A

Weak acids
Highly plasma protein bound

27
Q

Describe how NSAIDS selectively target inflamed tissues

A

NSAIDS are weak acids and thus within an acidic environment like inflamed tissue, their equilibrium will shift and the majority of the drug will exist in its unionised form and are thus be able to cross cell membranes and carry out their functions. NSAIDS are also highly plasma protein bound (>99%) and since these plasma proteins are a major consistuent of acute inflammatory exudate, this creates a reservoir of NSAIDS within the inflamed tissue. When the uncharged, unbound NSAIDS are used up, the equilibrium shifts causing the bound NSAIDS to be released from the plasma proteins and cross the cell membranes to carry out their function

28
Q

How are NSAIDS metabolised?

A

NSAIDS are metabolised by conjugation in the liver

29
Q

How are NSAIDS excreted?

A

NSAIDS are metabolised via renal excretion

30
Q

Give an example of a non-COX inhibiting NSAID

A

Grapiprant

31
Q

What is the mechanism of action for Grapiprant?

A

Grapiprant is an EP4 prostaglandin receptor antagonist. EP4 mediates pain caused by inflammation, thus inhibition of this receptor results in pain reduction

MODULE 7 - Skin and Bones (22 decks)

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