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NSAIDs Flashcards

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1
Q

What are the four components of inflammation?

A

Rubor
Tumor
Calor
Dolor

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2
Q

What happens to the local vessels with inflammation?

A

Vasodilation

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3
Q

What are the molecular inflammatory mediators?

A

Bradykinin
Substance P
Histamine
5HT

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4
Q

What are the three major arachidonic acid metabolites?

A

Prostaglandins
Thromboxanes
Prostacyclins

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5
Q

What is the major inflammatory cytokine?

A

TNF-alpha

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6
Q

What are the vasoactive amines?

A

histamine

5HT

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7
Q

What is the major kinin?

A

Bradykinin

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8
Q

What is the major neuropeptide that mediates pain?

A

Substance P

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9
Q

What is the role of substance P in inflammation?

A

Released from afferent neurons to cause mast cells to release histamine

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10
Q

What are the two goals of the analgesic drugs?

A

Relieve pain

Delay/arrest disease process

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11
Q

What are the four functional characteristics of NSAIDs?

A

Analgesia
Antipyretic
Anti-inflammatory
Inhibit COX1/2

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12
Q

Why is acetaminophen not an NSAID?

A

Does not have antiinflammatory properties

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13
Q

What is the primary target of NSAIDs?

A

COX1 and COX2

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14
Q

What are the two main prostaglandins that are involved in inflammation? What does these do?

A

PGE2
PGI2

increase edema and vascular permeability

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15
Q

What is the role of COX 1? When is it active?

A

Constitutively expressed housekeeping functions (e.g. stomach mucosa protection)

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16
Q

What is the role of COX 2? When is it active?

A

Inducible enzyme that increases the production of inflammatory molecules (e.g. PGI2)

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17
Q

What is the role of COX-2 in the kidney?

A

Needed for normal functioning

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18
Q

Which COX enzyme is involved in the protection of the gastric mucosa?

A

COX 1

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19
Q

What is the enzyme that creates arachidonic acid from the lipid bilayer?

A

Phospholipase A

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20
Q

What are the two pathways in which arachidonic acid can go down? What are the end results of these pathways?

A

Converted to 5-lipoxygenase to cause LTC4, LTD4, LTE4

Converted via COX to prostaglandins/thromboxanes

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21
Q

What are the two general types of NSAIDs?

A

Nonselective (e.g. ASA)

COX-2 selective (e.g. Celecoxib)

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22
Q

Which OTC drug has caffeine in it?

A

Excedrin (ASA, caffeine, acetaminophen)

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23
Q

What is the major metabolite of ASA? HOw is this excreted?

A

salicylic acid

Conjugated with glucuronic acid, and urinated

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24
Q

What is the MOA of ASA?

A

Irreversible COX inhibitor

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25
Why is there a potential for drug interactions with ASA?
highly bound to albumin
26
What are the effects of low dose ASA?
Analgesia | Antipyretic effects
27
What are the effects of high dose ASA?
Anti-inflammatory
28
What is the COD with ASA overdose?
Renal and respiratory failure
29
What is the major difference between COX inhibition with ASA as compared to other NSAIDs?
Irreversible inhibitor
30
What is the major prostaglandin that mediates fever?
PGE2 (Feeeever)
31
How does ASA mediate its antipyretic effects? (2)
Blocks production of PGE2, causing hypothalamus to reset the temp Dilation of superficial blood vessels
32
What is the effect on bleeding time of ASA?
prolongs bleeding tim
33
What is the main adverse effects of ASA?
General GI upset and ulcerations
34
Why does ASA cause GI issues?
Prostaglandins PGE2 and PGI2 decrease gastric acid secretion, and maintain mucosal resistance/enhance repair
35
How does ASA prolong bleeding time?
Inhibits platelet aggregation
36
What are the liver problems with ASA?
Hepatitis
37
What is the effect of ASA on renal function?
Decrease afferent arteriolar dilation, causing decreased renal blood flow, tubular necrosis, and Na retention
38
What is Reye's syndrome?
Encephalopathy in kiddos d/t unknown mechanism
39
What is the CNS issue with ASA, beside Reye's syndrome?
Tinnitus
40
What is the major difference between ASA and other NSAIDs?
Duration of action, and potency
41
What is Indomethacin usually used for?
Gout and ankylosing spondylitis
42
The newer NSAIDs are more selective for which COX enzyme? Why?
COX2--reduce the GI related side effects
43
What is the major side effect of COX-2 selective inhibitors?
Incidence of Cardiovascular events increased
44
Do COX-2 inhibitors impact platelet aggregation?
Nope
45
What are the three COX-2 selective inhibitors?
Celecoxib Etoricoxib Meloxicam
46
Does acetaminophen have effects on platelet aggregation? Anti-inflammatory?
Neither
47
What is the MOA of acetaminophen?
Unknown
48
What is the major side effect of acetaminophen?
Hepatotoxic
49
What is the effect of acetaminophen with EtOH?
Acetaminophen is metabolized by p450s, so will interact
50
What is the MOA of capsaicin?
Activates vanilloid receptors, leading to the release of substance P
51
NSAIDs are highly bound to albumin. What is the problem with this?
Will increase the release of drugs that are also highly bound to albumin (warfarin, phenytoin)
52
What is the effect of NSAIDs with diuretics?
Attenuates effects of the diuretics via action on Na transporters
53
What is the major COX-2 inhibitor?
Celecoxib
54
What are the NSAIDs?
``` Indomethacin Ketorolac Oxaprozin Piroxicam Sulindac ```
55
What is the cause of gout?
Hyperuricemia, secondary to increased purine breakdown
56
What are the crystals that form in gout?
uric acid crystals
57
What is the first line treatment for gout?
Indomethacin
58
What are the NSAIDs that are used to treat gout, besides indomethacin?
IBU Naproxen Sulindac
59
Why is ASA not used for gout?
Causes renal retention of uric acid
60
When are corticosteroids indicated for gout?
For pts who cannot tolerate NSAIDs
61
What is the MOA of colchicine?
Inhibits leukocyte migration and phagocytosis
62
What are the adverse effects of colchicine?
Diarrhea
63
What is the prophylaxis treatment for gout? MOA?
Allopurinol--inhibits xanthine oxidase
64
Draw out purine degradation pathway***
***
65
What is the MOA of febuxostat?
Xanthine oxidase inhibitor
66
What is the MOA of probenecid?
Increases renal clearance of uric acid by inhibiting tubular reabsorption
67
What is the MOA of sulfinpyrazone?
Increases renal clearance of uric acid by inhibiting tubular reabsorption

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