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PHRM 825 Therapeutics > Exam 2- Lecture 20 & 21 NSAIDS > Flashcards

Exam 2- Lecture 20 & 21 NSAIDS Flashcards

1
Q

what is the most abundant and important precursor of eicosanoids?

A

arachidonic acid

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2
Q

arachidonic acid is released from membrane phospholipids by what molecule?

A

phospholipase A2 (PLA2)

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3
Q

arachidonic acid is an omega ___ ?

A

6

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4
Q

are eicosanoids long-lived or short-lived mediators?

A

short-lived (seconds to minutes)

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5
Q

PGE2 function on blood vessels, bronchi, uterus?

A

dilation; dilation; oxytocic dilation

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6
Q

PGF2α function on blood vessels, bronchi, uterus?

A

constriction; constriction; oxytocic constriction

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7
Q

PGI2 function on blood vessels and platelets?

A

dilation; inhibits aggregation

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8
Q

TXA2 function on blood vessels and platelets

A

constriction; aggregation

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9
Q

eicosanoids bind to what receptors?

A

GPCRs

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10
Q

PGH synthase has what two enzyme activities?

A

cyclooxygenase (COX) and hydroperoxidase activities

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11
Q

of the 2 isoforms of PGH synthase, which is constitutively expressed in various tissues?

A

PGH synthase-1

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12
Q

of the 2 isoforms of PGH synthase, which is expressed upon stimulus in inflammatory and immune cells?

A

PGH synthase-2

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13
Q

which isoform of PGH-synthase has “housekeeping” functions?

A

PGH synthase-I

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14
Q

PGH synthase is inhibited by what class of drugs?

A

NSAIDs

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15
Q

alprostadil use

A

erectile dysfunction by injection or as suppository (it relaxes smooth muscles and expands blood vessels)

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16
Q

misoprostol use (3 of them)

A

cytoprotective, prevents peptic ulcer, terminates early pregnancy in combination with mifepristone (RU-486)

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17
Q

latanoprost is a derivative of

a. PGE2
b. PGF2α
c. PGI2
d. TXA2

A

b. PGF2α

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18
Q

prostacyclin (eproprostenol) use

A

treat pulmonary arterial hypertension by IV injection or inhalation

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19
Q

prostacyclin is similar to what molecule:

a. PGE2
b. PGF2α
c. PGI2
d. TXA2

A

c. PGI2

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20
Q

NSAIDs mechanism of action (2 of them, slide 16)

A

-inhibition of prostaglandin endoperoxide H synthase (PGHS or COX), which catalyzes the formation of prostaglandins
-many NSAIDs inhibit both COX-1 and COX-2 receptors

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21
Q

5 classes of NSAIDs to know

A

-salicylates
-arylacetic acids
-arylpropionic acids
-non-carboxylate NSAIDs
-COX-2 selective NSAIDs

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22
Q

aspirin is in which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

a. salicylates

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23
Q

ibuprophen is in which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

b. aryl propionic acids

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24
Q

meloxicam is in which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

d. non-carboxylate NSAIDs

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25
Q

celecoxib is in which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

e. COX-2 selective NSAIDs

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26
Q

indomethacin is in which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

c. aryl acetic acids

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27
Q

rank these NSAIDs from most to least GI side effects:

naproxen, indomethacin, sulindac, aspirin

A

aspirin ~ indomethacin > naproxen > sulindac

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28
Q

why does sulindac have few adverse GI side effects?

A

it is a prodrug

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29
Q

Reye’s syndrome is specific to which class of NSAIDs?

a. salicylates
b. aryl propionic acids
c. aryl acetic acids
d. non-carboxylate NSAIDs
e. COX-2 selective NSAIDs

A

a. salicylates

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30
Q

what is Reye’s syndrome?

A

rare, acute, life-threatening condition characterized by vomiting, delirium, and coma (20-30% mortality)

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31
Q

to reduce chance of Reye’s syndrome, what medicine should not be given to anyone under the age of 12 who has a fever?

A

aspirin

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32
Q

prevention of GI side effects (slide 21, 3 of them)

A

-misoprostol
-proton pump inhibitors
-combination products (ex. naproxen/esomeprazole)

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33
Q

esomeprazole mechanism of action

A

proton pump inhibitor

34
Q

what percent of NSAIDs are bound to serum albumin?

35
Q

NSAIDs combination with oral anticoagulants (3 outcomes, slide 22)

A

-inc plasma conc of free anticoagulant
-ability of salicylate to produce GI bleeding and inhibit the clotting mechanism aggravates the problem
-necessitates a possible decrease in the dosage of anticoagulant

36
Q

SAR in NSAIDs. They commonly contain a(n) __________ group

A

acidic (ex. carboxylic acid)

37
Q

drugs that end in “profen” are derivatives of what?

A

propionic acid

38
Q

drugs that end in “profen” are derivatives of what?

A

propionic acid

39
Q

4 salicylates drugs to know

A

-salicylic acid
-aspirin (acetylsalicylic acid)
-salsalate (Disalcid)
-diflunisal (Dolobid)

40
Q

true or false: salicylic acid inhibits COX-1 and COX-2 irreversibly

A

false

(it is reversible)

41
Q

which is the only NSAID that irreversibly inhibits COX by acetylating a serine residue in the active site?

A

aspirin (acetylsalicylic acid)

42
Q

what does asprin (acetylsalicylic acid) block?

A

TXA2 (platelet-aggregating factor)

(inc risk of bleeding but also reduces risk of myocardial infarction)

43
Q

why does aspirin irreversibly inhibit COX?

A

irreversible because the acetyl group on aspirin can modify serine residue. Salicylic acid does not have this group

44
Q

salsalate is hydrolyzed to two salicylates in which organ?

A

small intestine

45
Q

does salsalate (Disalcid) cause GI bleeding?

46
Q

Diflunisal (Dolobid) is a (more/less) potent analgesic than aspirin

47
Q

Diflunisal has (more/less) antipyretic activity than aspirin

48
Q

how much longer is the half-life for Diflunisal (Dolobid) compared to aspirin?

A

3-4 fold longer half life

49
Q

is indomethacin suitable for long-term or short-term use?

A

short-term

(one of the most potent NSAIDs, so has high incidence of side effects)

50
Q

is sulindac suitable for long-term or short-term use?

A

long-term

(long-term for chronic inflammation)

51
Q

4 arylacetic acid drugs to know

A

-indomethacin
-sulindac
-etodolac
-diclofenac

52
Q

is etodolac suitable for long-term or short-term use?

A

long-term

(used long-term for osteoarthritis)

53
Q

most widely used NSAID in the world

A

diclofenac

54
Q

diclofenac is somewhat selective for which COX?

55
Q

diclofenac inhibits what two pathways?

A

COX, lipoxygenase pathways

56
Q

3 arylpropionic acid drugs to know

A

-ibuprofen (Advil or Motrin)
-naproxen (Aleve)
-ketorolac

57
Q

ibuprofen is more potent than __________ but less potent than __________

A

aspirin, indomethacin

58
Q

which enantiomer of ibuprofen possesses greater activity in vitro?

A

S-(+)-enantiomer

59
Q

the R-(-)-enantiomer is converted to S-(+)-enantiomer (in vitro/in vivo)

60
Q

between ketorolac and etodolac, which is used for long-term?

61
Q

between ketorolac and etodolac, which is used for short-term?

62
Q

is diclofenac used for long-term or short-term?

63
Q

naproxen (aleve) is used to treat what two conditions?

A

rheumatoid arthritis, osteoarthritis

64
Q

how many rings does etodolac have and are they connected?

65
Q

how many rings does ketorolac have and are they connected?

A

3, no (2 are connected and one isn’t)

66
Q

which arylpropionic acid is a widely accepted alternative to narcotic analgesics?

67
Q

should you take NSAIDs with food?

68
Q

2 non-carboxylate drugs to know

A

-nabumetone
-meloxicam

69
Q

true or false: nabumetone is an acidic prodrug

A

false

(it is nonacidic)

70
Q

nabumetone is metabolized to what molecule, which is an effective inhibitor of COX?

A

MNA (6-methoxynaphthalene-acetic acid)

71
Q

nabumetone is a potent __________, but weak __________ activity

a. analgesic, anti-inflammatory
b. anti-inflammatory, analgesic

A

a. anti-inflammatory, analgesic

72
Q

is meloxicam long acting or short acting?

A

long acting (single daily dose)

73
Q

consequences of COX-1 inhibition (5 of them)

A

-stomach irritation and ulceration
-blockade of platelet aggregation
-inhibition of uterine motility
-inhibition of prostaglandin-mediated renal function
-hypersensitivity reactions

74
Q

what are the 3 selective COX-2 inhibitors?

A

-celecoxib (Celebrex)
-refecoxib (Vioxx)
-valdecoxib (Bextra)

75
Q

valine in the NSAID binding site of COX-2 is substituted for what AA in that of COX-1?

A

isoleucine

76
Q

side effects of selective COX-2 inhibitors (4 of them, slide 36)

A

-elevated bp and accelerated atherogenesis
-reduces PGI2, so more blood clotting
-does not affect production of TXA2 by COX-1; heightened thrombotic response on the rupture of atherosclerotic plaque
-increase cardiovascular hazard (heart attack and stroke)

77
Q

what is celecoxib used for? (2 things)

A

osteoarthritis, rheumatoid arthritis

(also has good efficacy against pain, inflammation, fever)

78
Q

true or false: celecoxib has no antiplatelet activity

A

true (bc it is not selective for COX-1)

79
Q

acetaminophen mechanism of action

A

scavenges peroxynitrite required for PGH synthase activity

80
Q

why is acetaminophen toxic to liver at high doses?

A

acetaminophen -> N-acetylimidoquinone is mediated by P450, N-acetylimidoquinone reacts with glutathione. Toxic doses overload the glutathione and cell damage occurs in the liver

PHRM 825 Therapeutics (25 decks)

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