NSAIDs Flashcards

(42 cards)

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
Adverse effects of NSAIDs
Inhibit normal protective effects of gastric mucosa (ulcers and bleeding), increased bleeding tendencies, renal medullary hypoxia and papillary necrosis
26
Pk of NSAIDs
Weak acids, bound to protein, hepatic metabolism, variable elimination
27
Adverse effects of NSAIDs
GI ulceration, increased bleeding, inhibition of uterine motility, decreased renal perfusion, renal necrosis in dehydrated patients
28
Contraindications of NSAIDs
Gi ulcers, renal disease, hepatic disorder. Hypoproteinemia, dehydration, cardiac disease, hypersensitivity, concurrent use
29
Clinical uses of NSAIDs
Relief of musculoskeletal and inflammatory pain
30
Mechanism of aspirin
Inhibits COX1 irreversibly, causing prolonged effects
31
Effective uses for aspirin
Musculoskeletal and cutaneous pain, not visceral
32
Adverse effects of aspirin
Bleeding, dose-dependent gastric ulceration, renal damage
33
Contraindications for aspirin
Bleeding disorders, prone to gi ulcers
34
Ibuprofen mechanism
Inhibits COX1 and COX2
35
Effective uses for ibuprofen
Arthritis and musculoskeletal pain
36
Adverse effects of ibuprofen
Gastric ulceration, myocardial infarction risk
37
Celoxicib mechanism
Selective for COX2
38
Effective uses of celecoxib
Osteoarthritis (not analgesia)
39
Benefits of celecoxib
Less likely to cause GI ulceration and bleeding
40
Adverse effects of celecoxib
Reduced renal function, increased risk of stroke and MI, concern with chronic use
41
How coxibs increase risk of stroke and MI
They only inhibit COX2, producing less PGI2 which prevents platelet aggregation, but doesn't inhibit COX1 so thromboxane is not inhibit el
42
Acetaminophen
Inhibits central PG synthesis in the CNS, so it is only an antipyretic and analgesic