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Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

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
Q

Why is there a potential for drug interactions with ASA?

A

highly bound to albumin

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26
Q

What are the effects of low dose ASA?

A

Analgesia

Antipyretic effects

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27
Q

What are the effects of high dose ASA?

A

Anti-inflammatory

28
Q

What is the COD with ASA overdose?

A

Renal and respiratory failure

29
Q

What is the major difference between COX inhibition with ASA as compared to other NSAIDs?

A

Irreversible inhibitor

30
Q

What is the major prostaglandin that mediates fever?

A

PGE2 (Feeeever)

31
Q

How does ASA mediate its antipyretic effects? (2)

A

Blocks production of PGE2, causing hypothalamus to reset the temp

Dilation of superficial blood vessels

32
Q

What is the effect on bleeding time of ASA?

A

prolongs bleeding tim

33
Q

What is the main adverse effects of ASA?

A

General GI upset and ulcerations

34
Q

Why does ASA cause GI issues?

A

Prostaglandins PGE2 and PGI2 decrease gastric acid secretion, and maintain mucosal resistance/enhance repair

35
Q

How does ASA prolong bleeding time?

A

Inhibits platelet aggregation

36
Q

What are the liver problems with ASA?

A

Hepatitis

37
Q

What is the effect of ASA on renal function?

A

Decrease afferent arteriolar dilation, causing decreased renal blood flow, tubular necrosis, and Na retention

38
Q

What is Reye’s syndrome?

A

Encephalopathy in kiddos d/t unknown mechanism

39
Q

What is the CNS issue with ASA, beside Reye’s syndrome?

A

Tinnitus

40
Q

What is the major difference between ASA and other NSAIDs?

A

Duration of action, and potency

41
Q

What is Indomethacin usually used for?

A

Gout and ankylosing spondylitis

42
Q

The newer NSAIDs are more selective for which COX enzyme? Why?

A

COX2–reduce the GI related side effects

43
Q

What is the major side effect of COX-2 selective inhibitors?

A

Incidence of Cardiovascular events increased

44
Q

Do COX-2 inhibitors impact platelet aggregation?

A

Nope

45
Q

What are the three COX-2 selective inhibitors?

A

Celecoxib
Etoricoxib
Meloxicam

46
Q

Does acetaminophen have effects on platelet aggregation? Anti-inflammatory?

A

Neither

47
Q

What is the MOA of acetaminophen?

A

Unknown

48
Q

What is the major side effect of acetaminophen?

A

Hepatotoxic

49
Q

What is the effect of acetaminophen with EtOH?

A

Acetaminophen is metabolized by p450s, so will interact

50
Q

What is the MOA of capsaicin?

A

Activates vanilloid receptors, leading to the release of substance P

51
Q

NSAIDs are highly bound to albumin. What is the problem with this?

A

Will increase the release of drugs that are also highly bound to albumin (warfarin, phenytoin)

52
Q

What is the effect of NSAIDs with diuretics?

A

Attenuates effects of the diuretics via action on Na transporters

53
Q

What is the major COX-2 inhibitor?

A

Celecoxib

54
Q

What are the NSAIDs?

A 
Indomethacin
Ketorolac
Oxaprozin
Piroxicam
Sulindac
55
Q

What is the cause of gout?

A

Hyperuricemia, secondary to increased purine breakdown

56
Q

What are the crystals that form in gout?

A

uric acid crystals

57
Q

What is the first line treatment for gout?

A

Indomethacin

58
Q

What are the NSAIDs that are used to treat gout, besides indomethacin?

A

IBU
Naproxen
Sulindac

59
Q

Why is ASA not used for gout?

A

Causes renal retention of uric acid

60
Q

When are corticosteroids indicated for gout?

A

For pts who cannot tolerate NSAIDs

61
Q

What is the MOA of colchicine?

A

Inhibits leukocyte migration and phagocytosis

62
Q

What are the adverse effects of colchicine?

A

Diarrhea

63
Q

What is the prophylaxis treatment for gout? MOA?

A

Allopurinol–inhibits xanthine oxidase

64
Q

Draw out purine degradation pathway***

A
65
Q

What is the MOA of febuxostat?

A

Xanthine oxidase inhibitor

66
Q

What is the MOA of probenecid?

A

Increases renal clearance of uric acid by inhibiting tubular reabsorption

67
Q

What is the MOA of sulfinpyrazone?

A

Increases renal clearance of uric acid by inhibiting tubular reabsorption

Pharm (73 decks)

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