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Clinical pharmacology and therapeutics > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Describe the WHO analgesic ladder

A

Step 1 - non opioid analgesic +/- adjuvant analgesic

Step 2 - opioid analgesic for mild to moderate pain +/- non opioid analgesic +/- adjuvant analgesic

Step 3 - opioid analgesic for moderate to severe pain +/- non opioid analgesic +/- adjuvant analgesic

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2
Q

Name some non opioid anlagesics

A

NSAIDs

Paracetamol

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3
Q

Name an opioid analgesic for mild to moderate pain

A

Codeine phosphate

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4
Q

Name an opioid analgesic for moderate to severe pain

A

Morphine sulfate

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5
Q

Where is aspirin derived from?

A

Willow trees

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6
Q

Where is Ibuprofen derived from?

A

Propionic acid

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7
Q

Name some NSAIDs

A 
Naproxen
Diclofenac
Ibuprofen
Aspirin (salicylate) 
Indomethacin
Phenylbutazone 
Meloxicam 
Ketoprofen
Etoricoxib
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8
Q

What does the term NSAID stand for?

A

Non steroidal anti inflammatory drug

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9
Q

Describe the mechanism of action of all NSAIDs

A

Exert effects on inhibition of prostaglandin synthesis

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10
Q

What is the primary site of action of NSAIDs?

A

Cyclooxygenase enzyme - COX1 and COX2

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11
Q

What is the role of prostaglandins?

A 
Modulate components of inflammation
Control of body temperature - fever
Platelet aggregation - thromboxane A2
Pain transmission 
Support renal function
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12
Q

Describe the storage and release of prostaglandins

A

They are not stored. They are produced and released on demand

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13
Q

How long is the half life of prostaglandins?

A

minutes

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14
Q

What does COX catalyse?

A

Conversion of arachidonic acid to prostaglandins and endoperoxide

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15
Q

What does constitutively mean?

A

Produced at a steady rate regardless of physiological demand

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16
Q

Where is COX 1 expressed?

A

Most tissues

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17
Q

What is the function of COX 1?

A

Protects the gastric mucosa

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18
Q

Where is COX 2 expressed?

A

Brain and kidney, is induced in sites of inflammation

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19
Q

Which COX is present in platelets?

A

COX 1

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20
Q

What do older NSAIDs block?

A

Both COX isoforms

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21
Q

What NSAID blocks both COX isoforms

A

Ibuprofen

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22
Q

Blocking which COX isoform is undesirable and why?

A

COX 1

Stomach (PGE2,PGI2), intestine, kidney (PGE2, PGI2), platelet (thromboxane A2)

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23
Q

Which NSAID works on blocking thromboxane A2?

A

Aspirin

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24
Q

What do glucocorticoids do?

A

Block mRNA expression of COX2

25
Q

How does celecoxib act?

A

Blocks COX2 - blocks the inflammatory effect of macrophages

26
Q

Describe the metabolism of arachidonic acid

A

Arachidonic acid is metabolised by either COX1/2 to PGG2 and then PGH2 which is then converted to thromboxane A2 and prostaglandins (PGE2 and PGI2) (BY COX 1) or Prostacyclin (PGI2) and prostaglandins (inflammation, pain and fever)

27
Q

Describe the action of thromboxane A2

A

Vasoconstriction

Stimulates platelet aggregation

28
Q

Describe the action of PGI2

A

Vasodilation

Inhibits platelet aggregation

29
Q

Name some COX 2 inhibitors

A

Etoricoxib and celecoxib

30
Q

Why are COX 2 inhibitors more preferable as NSAIDs in patients with a history of GI bleeds

A

Reduced risk of serous upper GI bleed

Do not inhibit platelet aggregation

31
Q

What is the first line treatment of gout

A

NSIADs

32
Q

What drug is given to someone with out who can not tolerate NSAIDs

A

Colchicine

33
Q

How long can the anti-inflammatory effect take to show in NSAIDs

A

3 weeks

34
Q

What conditions are NSAIDs used for their anti-inflammatory properties?

A

Gout
Sero negative arthritis
Rheumatoid arthritis
SLE

35
Q

What must be prescribed in addition to NSAIDs for long term use?

A

Gastroprotective drugs

36
Q

Describe when the effect should be present for NSAIDs used as analgesics

A

Effect after first dose, full affect takes up to 1 week

37
Q

Give the indications for using NSAIDs as analgesics

A 
Osteoarthritis 
Rheumatoid arthritis 
Soft tissue rheumatism and back pain 
Minor trauma
Soft tissue injury and sports injury
Headache
Dysmenohrrhea
Oeri-/post- operatively 
Ureteric colic
38
Q

Describe the mechanism of pyrexia

A

During inflammation Interleukin 1 releases prostaglandins into the CNS

Prostaglandins elevate the hypothalamic set point for temperature control

39
Q

Describe how NSAIDs have anti pyrexic properties

A

Prevent prostaglandins synthesis so prevent hypothalamic set point of temp control from being raised

40
Q

Name an NSAID indicated in cardiovascular disease

A

Aspirin

41
Q

Describe the action of aspirin

A

Reduces platelet aggregation and therefore reduces the bloods ability to clot

42
Q

Give some indications of aspirin

A 
Unstable angina
STEMI
NSTEMI
TIA
Ischaemic stroke
Secondary prevention
43
Q

Describe the cyclo oxygenase pathway

A

Injury/infection/trauma

Attacks the cell membrane of the cell

Cell membrane contains phospholipids

Activation of phospholipase occurs

It causes formation of arachidonic acid

Arachidonic acid is further metabolised by cyclooxygenase pathway to produce prostaglandins and the lipoxygenase pathway to produce leukotrienes

44
Q

List some common side effects of NSAIDs

A

GI discomfort - nausea, diarrhoea, oesophagitis, gastritis

Renal impairment

45
Q

List some less common side effects of NSAIDs

A

Upper GI - bleeding and Peptic ulceration
Renal - fluid retention, papillary necrosis, interstitial nephritis
Increased BP and fluid retention - CCF
Hypersensitivity rashes - erythema multiforme, angioedema and bronchospasm
Headache, dizziness
Blood disorders
Cardiovascular events

46
Q

Describe how NSAIDs can sometimes cause bronchospasm

A

COX inhibition and shunting of arachiodonic acid metabolism across the lipoxygenase pathway with resultant production of asthmogenic cysteinyl leukotreines

47
Q

Describe the steroid and NSAID drug interaction

A

Increased risk of GI bleeding

48
Q

Describe the anticoagulant and NSAID drug interaction

A

Increased risk of GI bleeding

Increased anticoagulant effect

49
Q

Describe the ACE inhibitor and NSAID drug interaction

A

Increased risk of renal impairment, hyperkalaemia and antagonism of hypotensive effect

50
Q

Describe the digoxin and NSAID drug interaction

A

May increase plasma digoxin concentrations
Increase risk of heart failure
Decrease renal function

51
Q

Describe the interaction between NSAIDs and sulfonylureas

A

Enhances sulfonylureas effect

52
Q

Describe the interaction between NSAIDs and quinolone antibiotics

A

Increased risk of seizures

53
Q

Describe the interaction between NSAIDs and phenytoin

A

Increased risk of phenytoin toxicity

54
Q

Describe the interaction between NSAIDs and SSRIs and venlafaxine

A

Increased risk of bleeding

55
Q

Describe the interaction between NSAIDs and diuretics

A

Increased nephrotoxicity risk

56
Q

Which patient groups are at risk of GI bleeding with NSAIDs

A

History of GI ulceration
Age >65
Concomitant drugs - anticoagulants, SSRIS, Steroids
Multiple NSAIDs

57
Q

Which patients are at risk of cardiovascular or renal side effects of NSAIDs

A

Patients aged over 65
Established CVD
Hypertension
Renal and hepatic impairment

58
Q

What groups of patients should be cautious of using NSAIDs

A 
Pregnant
Breast feeding
Asthmatics
Hypersensitivity 
Coagulation defects

Clinical pharmacology and therapeutics (27 decks)

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