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3028PHM Human Pharm II > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Discuss the three major actions of NSAIDs

A

Anti-inflammatory –> dec PGE2 and prostacycline reduced vasodil

Antipyretic effects –> inhibition of PG production in the hypothalamus

Analgesics effect –> dec PG production –> dec sensitivity nociceptor nerve endings to inflammatory mediators

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2
Q

What are the classes of NSAIDs?

A

Acetic acids = diclofenac, indomethacin, ketorolac, sulindac

Fenamates = mefanamic acid

Propionic acids = ibuprophen, ketoprofen, naproxen, tiaprofenic acid

Oxicams = meloxicam, piroxicam

Salicylates = aspirin

Coxibs = celecoxib, parecoxib

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3
Q

Discuss aspirin generally

A

Weak acid-protonated in acidic stomach env, hydrolysed to salicylate

Modifies both COX-1 and COX-2

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4
Q

What makes aspirin different from other NSAIDs?

A

Causes irreversible inhibition of COX activity due to acetylation of serine 530 (COX1) and 516 (COX2)

Inhibits platelet cyclooxygenase for 8 to 11 days

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5
Q

Highlight the drugs that aspirin interacts with

A

Warfarin = inc risk of bleeding
Probenecid

Diuretics and ACE inhibitors = triple whammy

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6
Q

Outline Reyes Syndrome

A

Rare syndrome that occurs in <18 y/o who have taken aspirin

Typically occurs when the person is recovering from viral illness with aspirin use

abnormal accumulation of fat in liver and inc pressure in brain (encephalopathy)

20-40% mortality

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7
Q

What is the MOA and indication of ibuprofen?

A

Competitive inhibitor of COX1/2

Better tolerated than aspirin, fewer GIT ADRs

Indication = analgesic, antipyretic, anti-inflam, used in formulations w/ codeine, paracetamol

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8
Q

What drugs interact with ibuprofen?

A

Warfarin
Probenecid
diuretics, ACE inhibitors = triple whammy

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9
Q

What is the MOA and indication of Indomethacin?

A

Slow, time-dependent inhibitor of COX1 and COX2 (conformational)

Less well tolerated than aspirin and ibuprofen –> high incidence of GIT reactions

Indication = not normally for analgesic or anti-pyretic, antiinflammatory agent

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10
Q

Which drugs interact with indometacin?

A

Warfarin
Diuretics, ACEi
probenecid

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11
Q

What is the MOA and indication of paracetamol?

A

Effective analgesic, anti-pyretic traced to inhibition of PGs in the CNS

Weak anti-inflammatory agents (weak COX inhibitor in the presence of high concentrations of peroxides)

Well tolerated, hepatotoxicity in overdose (10-15g)

Indication = analgesics/anti-pyretic, useful analgesic where aspirin C/I

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12
Q

What are the ADRs of NSAIDs?

A

Inhibition of gastric COX-1 responsible for production of PGs that inhibit acid secretion and protect mucosa

Cardiac side affects

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13
Q

How do PG protect the GIT?

A

1) vasodilation –> blood flow
2) inc bicarbonate section
3) inhibit gastric acids

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14
Q

Which NSAIDs carry the greatest risk of GIT complications compared to ibuprofen?

A

Azapopazone (the most)

indometacin > naproxen > diclofenac > aspirin

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15
Q

What factors inc the risk of GI injury associated with NSAID use?

A

Age >65 yrs (esp >70)
Hx peptic ulcers
Use of two or more NSAIDs at the same time
Concomitant therapy w/ antiplatelet agents, anticoagulants, corticosteroids
Severe illness
H. pylori infection

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16
Q

What are some renal ADRs of NSAIDs?

A

renal insufficiency due to dec afferent blood flow caused by PGE2 and PGI2 inhibition

17
Q

What are some blood ADRs of NSAIDs?

A

Disturbances in platelet function, inc bleeding time due to TXA2 effects

18
Q

What are some skin ADRs of NSAIDs?

A

Mild erythemous, urticarial, photosensitivity

Stevens-Johnson syndrome (ibuprofen in young children)

19
Q

What are some C/I for NSAID use?

A

active peptic ulcers, NSAID allergies
Sulfonamide allergy (celecoxib)
COX-2 antagonists may inc thrombotic events
Inc bronchospasms

20
Q

Explain the MOA behind NSAID induced bronchospasm

A

Inhibition of COX1/2 > inc arachidonic acid > inc lipoxygenases > Inc H(P)ETE, leukotrienes, lipoxins

21
Q

How does NSAID induced inc of leukotrienes cause bronchospasms?

A

LTB4 = initiate inflam response (chemotactic)

Cysteinyl leukotrienes (LTC, D, E) = initiated inflam response
- Constrict bronchial smooth muscle, vasoconstriction

22
Q

Explain the mechanism of the triple whammy

A

NSAIDs –> reduce the afferent blood flow to the kidney dec GFR

ACEi –> dilate efferent blood, dec GFR further (asking more blood to leave kidney)

Diuretics –> reduce blood flow to the glomerulus due to inc fluid loss which dec blood vol

Dec renal function –> drying out of kidney

23
Q

What is used to reverse NSAID toxicity?

A

NO-NSAIDS (nitric oxide release NSAIDs)

NO-aspirin, NO-diclofenac, NO-Ketoprofen, MO-flurbiprofen

24
Q

How does COX-2 selectivity work?

A

COX-2 selective NSAIDs are too large to fit in to the COX-1 binding site and this can’t bind

25
Q

What are the indications for COX-2 selective NSAIDs?

A

Osteoarthritis
Rheumatoid Arthritis
Acute pain in adults

26
Q

What are some ADRs of selective COX-2 inhibitors?

A

GIT disturbance—> slower healing if ulcers

Nervous system disorders —> dizziness

Psychiatric disorders —> somnolence, insomnia

Inc BP

Resp —> bronchitis, coughing, pharyngitis, rhinitis, sinusitis, URTI

27
Q

Explain the mechanism behind NSAID induced cardiac toxicity

A

COX-2 selective NSAID > block COX2 > blocks PGI2 ability to counter COX1 platelet aggregation

Reduced PGI results in inc TXA2 mediated platelet aggregation and cardiac adverse events

28
Q

Which NSAIDs carry the greatest risk of vascular events?

A

Coxibs > Diclofenac

29
Q

Which NSAIDs carry the greatest risk of coronary events?

A

Coxibs > diclofenac

30
Q

Which NSAIDs carry the least risk of vascular events?

A

High dose naproxen > ibuprofen

31
Q

Which NSAIDs carry the lowest risk of coronary events?

A

High-dose > ibuprofen

3028PHM Human Pharm II (17 decks)

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