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

Exam 2- Lecture 20 & 21 NSAIDS Flashcards

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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
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
e. COX-2 selective NSAIDs
26
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
c. aryl acetic acids
27
rank these NSAIDs from most to least GI side effects: naproxen, indomethacin, sulindac, aspirin
aspirin ~ indomethacin > naproxen > sulindac
28
why does sulindac have few adverse GI side effects?
it is a prodrug
29
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. salicylates
30
what is Reye's syndrome?
rare, acute, life-threatening condition characterized by vomiting, delirium, and coma (20-30% mortality)
31
to reduce chance of Reye's syndrome, what medicine should not be given to anyone under the age of 12 who has a fever?
aspirin
32
prevention of GI side effects (slide 21, 3 of them)
-misoprostol -proton pump inhibitors -combination products (ex. naproxen/esomeprazole)
33
esomeprazole mechanism of action
proton pump inhibitor
34
what percent of NSAIDs are bound to serum albumin?
90-99%
35
NSAIDs combination with oral anticoagulants (3 outcomes, slide 22)
-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
SAR in NSAIDs. They commonly contain a(n) __________ group
acidic (ex. carboxylic acid)
37
drugs that end in "profen" are derivatives of what?
propionic acid
38
drugs that end in "profen" are derivatives of what?
propionic acid
39
4 salicylates drugs to know
-salicylic acid -aspirin (acetylsalicylic acid) -salsalate (Disalcid) -diflunisal (Dolobid)
40
true or false: salicylic acid inhibits COX-1 and COX-2 irreversibly
false (it is reversible)
41
which is the only NSAID that irreversibly inhibits COX by acetylating a serine residue in the active site?
aspirin (acetylsalicylic acid)
42
what does asprin (acetylsalicylic acid) block?
TXA2 (platelet-aggregating factor) (inc risk of bleeding but also reduces risk of myocardial infarction)
43
why does aspirin irreversibly inhibit COX?
irreversible because the acetyl group on aspirin can modify serine residue. Salicylic acid does not have this group
44
salsalate is hydrolyzed to two salicylates in which organ?
small intestine
45
does salsalate (Disalcid) cause GI bleeding?
no
46
Diflunisal (Dolobid) is a (more/less) potent analgesic than aspirin
more
47
Diflunisal has (more/less) antipyretic activity than aspirin
less
48
how much longer is the half-life for Diflunisal (Dolobid) compared to aspirin?
3-4 fold longer half life
49
is indomethacin suitable for long-term or short-term use?
short-term (one of the most potent NSAIDs, so has high incidence of side effects)
50
is sulindac suitable for long-term or short-term use?
long-term (long-term for chronic inflammation)
51
4 arylacetic acid drugs to know
-indomethacin -sulindac -etodolac -diclofenac
52
is etodolac suitable for long-term or short-term use?
long-term (used long-term for osteoarthritis)
53
most widely used NSAID in the world
diclofenac
54
diclofenac is somewhat selective for which COX?
COX-2
55
diclofenac inhibits what two pathways?
COX, lipoxygenase pathways
56
3 arylpropionic acid drugs to know
-ibuprofen (Advil or Motrin) -naproxen (Aleve) -ketorolac
57
ibuprofen is more potent than __________ but less potent than __________
aspirin, indomethacin
58
which enantiomer of ibuprofen possesses greater activity in vitro?
S-(+)-enantiomer
59
the R-(-)-enantiomer is converted to S-(+)-enantiomer (in vitro/in vivo)
in vivo
60
between ketorolac and etodolac, which is used for long-term?
etodolac
61
between ketorolac and etodolac, which is used for short-term?
ketorolac
62
is diclofenac used for long-term or short-term?
long-term
63
naproxen (aleve) is used to treat what two conditions?
rheumatoid arthritis, osteoarthritis
64
how many rings does etodolac have and are they connected?
3, yes
65
how many rings does ketorolac have and are they connected?
3, no (2 are connected and one isn't)
66
which arylpropionic acid is a widely accepted alternative to narcotic analgesics?
ketorolac
67
should you take NSAIDs with food?
yes
68
2 non-carboxylate drugs to know
-nabumetone -meloxicam
69
true or false: nabumetone is an acidic prodrug
false (it is nonacidic)
70
nabumetone is metabolized to what molecule, which is an effective inhibitor of COX?
MNA (6-methoxynaphthalene-acetic acid)
71
nabumetone is a potent __________, but weak __________ activity a. analgesic, anti-inflammatory b. anti-inflammatory, analgesic
a. anti-inflammatory, analgesic
72
is meloxicam long acting or short acting?
long acting (single daily dose)
73
consequences of COX-1 inhibition (5 of them)
-stomach irritation and ulceration -blockade of platelet aggregation -inhibition of uterine motility -inhibition of prostaglandin-mediated renal function -hypersensitivity reactions
74
what are the 3 selective COX-2 inhibitors?
-celecoxib (Celebrex) -refecoxib (Vioxx) -valdecoxib (Bextra)
75
valine in the NSAID binding site of COX-2 is substituted for what AA in that of COX-1?
isoleucine
76
side effects of selective COX-2 inhibitors (4 of them, slide 36)
-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
what is celecoxib used for? (2 things)
osteoarthritis, rheumatoid arthritis (also has good efficacy against pain, inflammation, fever)
78
true or false: celecoxib has no antiplatelet activity
true (bc it is not selective for COX-1)
79
acetaminophen mechanism of action
scavenges peroxynitrite required for PGH synthase activity
80
why is acetaminophen toxic to liver at high doses?
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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