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Exam 1 Year 3 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

What could a dose of 300-900mg 4/6 hourly prn Aspirin be given for?

A

Analgesic

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2
Q

What are the special patient group for Aspirin?

A

-Children under 16
-Ulcers
-Bleeding disorders
-Severe cardiac failure
-Hypersensitivity to NSAID/Aspirin
-Elderly
-Asthma

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3
Q

What does Aspirin interact with?

A

-Drugs which increase risk of GI irritation / bleeding
-Steroids/NSAIDS/SSRI’s/DOACS
-Drugs with renal side effects -Bisphosphonates
-Drugs where Aspirin can increase toxicity of other drugs - methotrexate

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4
Q

How long does it take for an NSAID to have it’s full effect for pain relief?

A

1 Week

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5
Q

How long does it take for an NSAID to have its full anti-inflammatory effect?

A

3 weeks

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6
Q

What are the key side effects of NSAIDS?

A

*GI irritation
*Kidneys
*Cardiovascular

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7
Q

If NSAIDS are used, they should be used for the lowest effective dose for the shortest duration, True or False?

A

True

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8
Q

What COX selective has less GI effects but more CV effects?

A

COX-2

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9
Q

What are examples of non selective NSAIDS?

A

Ibuprofen, Indometacin, Mefamic acid, Naproxen

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10
Q

What are examples of COX-2 preference NSAIDS?

A

Diclofenac, Etorloic, Meloxicam,

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11
Q

What are examples of COX-2 selective NSAIDS?

A

Celecoxib
Etoricoxib

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12
Q

Why do Gi side effects happen from NSAIDS?

A

1) Suppression of physiological homeostatic prostanoid (COX-1) inhibition
2) Topical irritation and direct epithelia damage

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13
Q

What NSAIDS carry a high GI risk?

A

Piroxicam, Ketoprofen, Ketorolac

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14
Q

What NSAIDS carry an intermediate GI risk?

A

Indomethacin, Diclofenac, Naproxen

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15
Q

What NSAIDS carry a low GI risk?

A

Ibuprofen - dose up to 1.2g!!
COX-2 selective ‘coxibs’

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16
Q

What NSAIDS carry the lowest risk of GI irritation?

A

COX 2 selective ‘coxibs’

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17
Q

What should be co-prescribed with NSAIDS?

A

PPI

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18
Q

What NSAIDS carry the highest CV risk?

A

COX-2 inhibitors, diclofenac 150mg OD, Ibuprofen 2.4g

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19
Q

What NSAIDS have a lower thrombotic risk?

A

Naproxen 1g OD

20
Q

What are the contraindications of Diclofenac and High dose Ibuprofen and COX-2 inhibitors?

A

Ischaemic heart disease, cerebrovascular , and some stages of heart failure.

21
Q

What conditions are NSAIDS cautioned in?

A

HF, Cerebrovascular disease, heart disease, risk factor groups for CVD

22
Q

What group of drugs do NSAIDS reverse the effect of?

A

Anti-hypertensives

23
Q

Can you give anticoagulants and NSAIDS together?

A

NO as the bleeding risk is increased!
-If given, close monitoring must be done!

24
Q

What organ can NSAIDS reduce function of?

A

Kidneys

25
Q

How do you monitor for renal impairment in use of NSAIDS?

A

Bp, Electrolytes Na&K, Oedema,

26
Q

What should be monitored in someone with NSAIDS?

A

-Symptoms of Dyspepsia, Gi irritation
-HB
-Signs of Gi bleeding - haemoptysis, dark stools

27
Q

What is the prostaglandin pathway?

A

1) Cell membrane phospholipids is converted to Arachidonic acid by phospholipase A2
2) Arachidonic Acid is converted to Prostaglandin G2 (PGG2) by COX
3) Prostaglandin G2 is converted to Prostaglandin H2 (PGH2) fast!
4) PGH2 is then converted into PGE2, PGF2a, PGD2

28
Q

Where is COX 1 found?

A

In all cells

29
Q

Where is COX 2 found?

A

Released in inflammatory events

30
Q

What is within the COX2 active site?

A

*Active site Haem
*Val 523
*Arg 120
*Hydrophilic side pocket
*Hydrophobic channel

31
Q

What is within the COX1 active site?

A

*Active site Haem
*Iso 523
*Arg 100
*Hydrophobic channel

32
Q

What generally do NSAIDS contain?

A

*Acid group
*One carbon
*Flat surface
*Lipophilic area

33
Q

MOA of NSAIDS?

A

Affect COX1 and COX2, non-selective and competitive and reversible.
They compete for the arachidonic binding site, if arachidonic is increased the NSAID effect disappears!

34
Q

What are/does the acid group in NSAID’s do?

A

*Carboxylic acid, enol, hydroxamic acid or masked acid that can be metabolised
*Mimics acid of arachidonic acid and binds to Arg 120
*Allows accumulation in sites of inflammation

35
Q

What are/does the one carbon group in NSAIDS do?

A

2 or 3 carbons reduce activity, can be substituted but only by methyl

36
Q

What are/does the flat surface do within NSAIDS?

A

-Can be aromatic or heteroaromatic
-Corresponds to double bonds at 5 & 8 in arachidonic acid

37
Q

What does/are the lipophilic area within NSAID?

A

-Nancolanar with aromatic ring
-Aromatic or aliphatic
-Can be fused
-Corresponds to double bond at 11

38
Q

What groups does Ibu pro fen have?

A

Ibu - Iso-butyl
Pro - Phenyl
Fen - Propionic acid

39
Q

What are examples of Arylalkonoic acid?

A

Indomethacin, Sulindac, Diclofenac

40
Q

What are examples of N-Arylanthronlik acids?

A

‘Femamic acids’

41
Q

What are examples of Enolic acids?

A

‘Oxicams’

42
Q

What is the MOA of COX-2 selective NSAIDS?

A

COX-2 selective, competitive reversible inhibitors. Increase concentration of arachidonic acid over comes it’s activity.

43
Q

If a NSAID binds to the hydrophilic pocket what is it?

A

COX-2 selective!

44
Q

Chemically how do cox-2 selective NSAIDS work?

A

*Bulky and gets in the way, it fits the hydrophilic pocket, stops arachidonic acid.

45
Q

What occurs in a Hydrophilic pocket?

A

H bond interactions!!

Exam 1 Year 3 (40 decks)

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