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Pharmacology 4090 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Inflammation

A

Active response of tissues to injury (beneficial or harmful)

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2
Q

Processes involved in inflammation

A

Immune responses, coagulation cascade, regeneration and repair

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3
Q

4 changes involved in inflammation

A

Vasodilation, edema, WBCs enter tissue, pain

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4
Q

Fibrosis

A

Scarring as a result of chronic inflammation

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5
Q

Inciting causes of inflammation

A

Infection, trauma, necrosis, immune-mediated disease

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6
Q

Beneficial outcomes of inflammation

A

Eliminates agent, repairs + regenerates

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7
Q

Harmful outcomes of inflammation

A

Loss of function, systemic effects, scar formation

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8
Q

Synthesis of inflammatory mediators

A

Some synthesized in advance (histamine), some synthesized at the site (prostaglandins)

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9
Q

Redundancy of inflammatory mediators

A

Many trigger the same response

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10
Q

Major classes of pro-inflammatory mediators

A

Eicosanoids (prostaglandins, thromboxane, prostacyclin), leukotrienes

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11
Q

Non-pharmacological treatments of inflammation

A

Rest, heat/cold, weight reduction, surgery

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12
Q

Pharmacological treatments of inflammation

A

NSAIDs, glucocorticoids

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13
Q

Oldest NSAID

A

Aspirin

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14
Q

Mechanism of aspirin

A

Inhibits prostaglandin synthesis

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15
Q

Main benefits of NSAIDs

A

Anti-inflammatory, antipyretic, analgesic

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16
Q

Normal physiological roles of prostaglandins

A

Synthesized from arachidonic acid by COX enzymes

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17
Q

COX1

A

Housekeeping enzyme at lowlevels in all tissues; produces thromboxane, other prostaglandins, prostacyclins

18
Q

COX2

A

Normally present at very low levels in most tissues, very important for homeostasis in some tissues

19
Q

TXA2

A

Thromboxane, important for platelet aggregation

20
Q

PGD2, PGE2

A

Prostaglandins synthesized by both cox enzymes; maintain blood flow and are involved in gastric mucosa protection

21
Q

PGI2

A

Prostacyclin; inhibit platelet aggregation, vasodilate, and protect gastric mucosa

22
Q

Prostaglandin roles during inflammation

A

COX2 is upregulated locally, causing the 5 main symptoms of inflammation

23
Q

NSAIDs mechanism

A

Inhibit usually both COX1 and COX2

24
Q

Major benefit of NSAIDs

A

Reduces blood flow to the site of injury

25
Q

Adverse effects of NSAIDs

A

Inhibit normal protective effects of gastric mucosa (ulcers and bleeding), increased bleeding tendencies, renal medullary hypoxia and papillary necrosis

26
Q

Pk of NSAIDs

A

Weak acids, bound to protein, hepatic metabolism, variable elimination

27
Q

Adverse effects of NSAIDs

A

GI ulceration, increased bleeding, inhibition of uterine motility, decreased renal perfusion, renal necrosis in dehydrated patients

28
Q

Contraindications of NSAIDs

A

Gi ulcers, renal disease, hepatic disorder. Hypoproteinemia, dehydration, cardiac disease, hypersensitivity, concurrent use

29
Q

Clinical uses of NSAIDs

A

Relief of musculoskeletal and inflammatory pain

30
Q

Mechanism of aspirin

A

Inhibits COX1 irreversibly, causing prolonged effects

31
Q

Effective uses for aspirin

A

Musculoskeletal and cutaneous pain, not visceral

32
Q

Adverse effects of aspirin

A

Bleeding, dose-dependent gastric ulceration, renal damage

33
Q

Contraindications for aspirin

A

Bleeding disorders, prone to gi ulcers

34
Q

Ibuprofen mechanism

A

Inhibits COX1 and COX2

35
Q

Effective uses for ibuprofen

A

Arthritis and musculoskeletal pain

36
Q

Adverse effects of ibuprofen

A

Gastric ulceration, myocardial infarction risk

37
Q

Celoxicib mechanism

A

Selective for COX2

38
Q

Effective uses of celecoxib

A

Osteoarthritis (not analgesia)

39
Q

Benefits of celecoxib

A

Less likely to cause GI ulceration and bleeding

40
Q

Adverse effects of celecoxib

A

Reduced renal function, increased risk of stroke and MI, concern with chronic use

41
Q

How coxibs increase risk of stroke and MI

A

They only inhibit COX2, producing less PGI2 which prevents platelet aggregation, but doesn’t inhibit COX1 so thromboxane is not inhibit el

42
Q

Acetaminophen

A

Inhibits central PG synthesis in the CNS, so it is only an antipyretic and analgesic

Pharmacology 4090 (11 decks)

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