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Pharm > NSAIDS, RA, and gout > Flashcards

NSAIDS, RA, and gout Flashcards

1
Q

effect of inflammation?

A

can be beneficial or deleterious

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2
Q

classic inflammatory sx

A

redness (rubor), swelling (tumor), heat (calor), pain (dolor)

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3
Q

what are some of the molecular inflammatory mediators?

A

bradykinins, substance P, histamine, prostaglandin, thromboxanes, prostacyclin, TNF-alpha

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4
Q

what is the fxns of DMARDS?

A

delay or arrest of diease process

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5
Q

fxnal characteristics of NSAIDS

A
  1. analgesia
  2. antipyretic
  3. anti-inflammatory
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6
Q

is acetaminophen an nsaid?

A

NOOOO, but it does have analgesic and antipyretic properties

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7
Q

downstream effects o PGE2 and PGI2?

A

incr edema, incr vascular permeability

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8
Q

which COX is constitutively expressed, protective, is a housekeeping isozyme?

A

COX1

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9
Q

which COX is inducible, production of inflammatory molec, expressed in vascular endothelium?

A

COX-2

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10
Q

which COX promotes synthesis of PG in stomach mucosa that protect stomach lining from gastric acid?

A

COX-1

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11
Q

which NSAIDS are non-selective (both COX1 & 2)

A

ASA, ibuprofen, indomethacin

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12
Q

which NSAIDS are COX-2 selective?

A

celecoxib

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13
Q

is acetylation & inhibition of COX by ASA reversible or irreversible?

A

irreversible

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14
Q

how does ASA irritate the GI?

A

inhibit protective PG–>PGe, PGI normally decr gastric acid secretion, maintain mucosal resistance/enhance repair

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15
Q

how does ASA potentially decr kidney fxn?

A
  1. inhibition of PG–>decr renal blood flow (tubular necrosis)
  2. PG inhibition may allow fro enhanced Na/Water reabsorption
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16
Q

what is the major difference b/w ASA and other non-specific NSAIDS?

A
  1. duration of action

2. potency

17
Q

do COX-2 selective inhibitors impact platelet aggregation?

A

no (this is mediated by COX1)

18
Q

effects of COX-2 selective inhibitors?

A

analgesic, antipyretic, anti-inflammatory

19
Q

major issue assc’d with COX-2 inhibitors?

A

CV thrombotic events

20
Q

what is the bad SE effect associated with acetaminophen?

A

acute liver toxicity

p450 metab–>beware of interactions w/ ethanol, INH

21
Q

therapeutic goals with gout tx?

A
  1. terminate acute gout attacks
  2. provide control of pain and inflammation
  3. prevent future attacks
22
Q

what is the 1st line tx for gout?

A

indomethacin (NSAID)

23
Q

which NSAIDS can be used for tx of gout?

A

indomethacin, ibuprofen, naproxen, sulindac

24
Q

can you use ASA to tx gout?

A

NO, it causes renal retention of uric acid at low dose

25
Q

when to use corticosteroids as tx for gout?

A

when patients can’t tolerate NSAIDS

26
Q

what are the 3 stages of RA?

A
  1. initiation phase (nonspecific inflammation)
  2. amplification phase (T cell activation)
  3. chronic inflammation (tissue injury)
27
Q

which drugs for RA reduce inflammation, improve sx, slow bone damage, but have a slow onset of action?

A

DMARDS

28
Q

what is the 1st line DMARD tx for RA?

A

methotrexate

29
Q

what was the First agent for RA indicated for both sympt improvement and retardation of structural joint damage?

A

leflunomide

30
Q

Anti-TNFa agent; cytokine receptor fusion protein

A

Etanercept

31
Q

Anti-TNFa agent; chimeric monoclonal ab

A

Infliximab

32
Q

IL-1 inhib (IL-1 cytokine receptor decoy)

A

Anakinra

33
Q

which RA drug is an Antimetaboite & antifolate agent

A

methotrexate

34
Q

which RA drug inhibs ribonucleotide synthesis?

A

leflunomide

35
Q

how does ASA exert anti-pyretic effects?

A

blocks production of PG in CNS to reset temperature control at hypothaalmus–>dilation of superfifical blood vessels–>drop in temp

36
Q

does acetaminophen have anti-inflammatory properties?

A

nope, just used as pain relief and fever reducer

37
Q

hepatotoxicity with acetaminophen needs to be monitored with?

A

high doses, alcohol abuse, CYP450 inducers, elderly

38
Q

capaisin can be used for what?

A

RA, osteoartiritis, neuralgia

Pharm (20 decks)

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