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3921 > 1 NSAIDs > Flashcards

1 NSAIDs Flashcards

1
Q

Why do we use NSAIDs (3)

A

Vasodilation cytokines
Increased microvascular permeability
Stimulation of afferent nerves

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2
Q

What are the three phases of the immune response time course

A

Immediate - myeloid cell and clotting phase
Secondary - adaptive lymphocyte and tissue restoration phase
Resolution - of acute inflamamtion phase

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3
Q

What do COX-1 and COX-2 catalyse

A

Conversion of arachidonic acid into the intermediate metabolite PGH2

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4
Q

Where is COX-2 constitutively expressed in compared to COX-1

A

Brain and kidney

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5
Q

What prostanoids do COX-1 produce

A

Mediate homeostatic functions: gastric, small intestine, bowl mucosa
Kidney
Platelets
Vascular endothelium

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6
Q

What do COX-2 produce

A

Prostanoids that mediate inflammation, pain and fever

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7
Q

Where are COX-2 induced

A

Inflammatory sites by NK-KB mediated cytokine signalling pathways

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8
Q

What are NSAIDs first-line therapy for

A

Acute and chronic pain, particularly inflammatory pain

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9
Q

What is a non-selective COX inhibitor

A

Aspirin

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10
Q

What do NSAIDs differ mainly in (3)

A

Aspects affecting pharmacokinetics:
Route of administration - oral, topical and parenteral
Bioavailability
Cl and Half-life

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11
Q

How the effects of NSAIDs mediated

A

Anti-inflammatory (COX-2)
Analgesic (COX-2)
Anti-pyretic (COX-2)
Anti-thrombotic (COX-1)

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12
Q

Paracetamol is a weak COX-1 and COX-2 inhibitor true or false

A

True

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13
Q

What else does paracetamol also inhibit outside of COX-1 and COX-2

A

EP3

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14
Q

Where is COX-1 found

A

ER

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15
Q

What two catalytic sites do COX-1 have

A

Peroxidase active site

Cyclooxygenase active site

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16
Q

How does aspirin interact with COX-1 protein

A

Carboxylic acid group forms salt bridge with Arg 120 which is in close proximity to acetylate Ser530, blocks active site

17
Q

What is larger in COX-2

A

Hydrophobic channel can accomodate for aromatic ring structure

18
Q

What is different about COX-2 binding

A

COX-2 binding site is more accomodating and is characterised by a ‘side pocket’ which can accomodate bulky groups

19
Q

What are three amino acid changes between COX-1 and COX-2

A

1) Leu in COX-2 less bulky than Phe and allows for larger groups
2) Val is less bulky than Ile and allows for larger sulphonamide
3) Arg provides hydrogen bonding stabilisation

20
Q

What are propionic acid derivatives (3)

A

Naproxen
Ibuprofen
Ketoprofen

21
Q

What are acetic acid derivatives (4)

A

Indomethacin
Sundilac
Ketorolac
Diclofenac

22
Q

What are enolic derivatives (2)

A

Meloxicam

Piroxicam

23
Q

Which COX activity is linear

A

COX-2

24
Q

When does COX-2 inhibition occur

A

> 80%

25
Q

When is inhibition of platelet TXA2 > 95%

A

Cardioprotective

26
Q

Are coxibs cardioprotective

A

No because TXA2 inhibition < 50%

27
Q

What are some side effects of NSAIDs

A 
GI toxicity  (ulceration, bleeding COX-1 by inhibiting PGE2, in mucosa)
Renal function (COX-1 by inhibiting PGI2, PGE2 and PGD2 in renal arteriole endothelium leading to vasoconstriction, changing GFR)
Cardiovascular toxicity (COX-1 and COX-2)
Allergy and hypersensitivity reactions (IgE and T-cell mediated, mainly rash, but also asthma-like bronchochonstriction and anaphylaxis)
28
Q

How do prostaglandins protect gastric mucosa from stomach acid? (3)

A

Increasing blood flow to mucosa (PGE2 and PGI2 - vasodilators)
Increasing mucous production and bicarbonate secretion (PGE)
Decreasing gastric acid secretion (PGE2 and PGI2)

29
Q

NSAID pharmacokinetics (6)

A

Almost all are weak acids
Easily absorbed in stomach and small intestine
Highly protein bound
Most subject to Phase 1 and 2 hepatic drug metabolism
CL variable and dependent on dose
Excretion mainly urine

3921 (22 decks)

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