NSAIDs Flashcards

1. Describe the mechanism of action of aspirin, list its major side effects and signs associated with overdose, describe the treatment of aspirin overdose, and list the contraindications to the use of aspirin 2. Describe the major differences in duration of action, key uses and key side effects of aspirin, salicylic acid, diflunisal, indomethacin, ketorolac, ibuprofen, naproxen, meloxicam and celecoxib. 3. Describe the mechanism of action and special considerations for the use of colchicin

1
Q

major sites of COX-1 that can result in NSAID toxicity

A

platelets, blood vessels, stomach, kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

expressed during inflammation

A

Cox-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

typical NSAID theraputic uses

A

analgesic, anti-inflammatory, antipyretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

decrease the pain threshold

A

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

mediate edema response

A

PGE2/PGI2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ways NSAIDS reduce inflammation

A

inhibit PGE2/PGI2 and reduce neutrophil migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

alters body temp set point

A

PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

clinical uses of NSAIDS

A

Pain, primary dysmonorrhea, Joint inflammation, fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

GI Side effects of NSAIDS

A

distress, damage, bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

way that NSAIDS increase stomach acid

A

inhibit PGE2/PGI2 which normally inhibit the H+/K+ ATPase, and increase bicarb production in the paritel cells. This leads to more proton release and less buffering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

renal side effects of NSAIDS

A

fluid retention , decresed sodium excretion, decreased GFR, instersitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How NSAIDS can increase bleeding

A

in pts with reduced clotting factors, TXA2 may be needed more to clot - NSAIDS reduce TXA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ways NSAIDS can increase BP

A

reduces PGI2, which oppose vascular contractions. inhibition of COX-1/2 decreases Na+ and H2O excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

salicylate prototypes (3)

A

asprin, aslicylic acid, difunisal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acetic acid derivitaves (2)

A

indomethacin, ketorolac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

proprionic acid derivitives (2)

A

ibuprophen, naproxen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

enolic acid derivtive

A

meloxicam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

COX-2 selective inhibitor

A

celecoxib

19
Q

MOA of salicylates

A

binds to COX irreversably, alters ratio of PGI2/TXA2 in vasculature

20
Q

Sx of salicylate toxicity

A

theraputic doses: GI bleedin, decreased uric acid excretion, hypersenstivy reactions

mild intox (salicylism): tinnitus, vomiting, vertigo, hyperventalation due to resp alkalosis

moderate tox: increased metabolic rate, fever, metabolic acidosis

severe tox: resp depression, dehydration, come, organ failure

21
Q

theraputic dose of salicylate

A

2-4 g.day

22
Q

lethal dose of salicylate

A

160 g/day

23
Q

tx for salicylate tox

A

1) cool, rehydrate, correct acid.base imbalances
2) prevent further absorption via emesis and lavage
3) alkalinize urine
4) hemodyalsis
5) diazepam for convulsions

24
Q

Contraindications for salicylates

A

renal disease, bleeding disorders, gout, young kids, 3rd trimester preg

25
Q

advantages of naproxen

A

long t 1/2, intermediate potency

26
Q

most potent NSAID

A

indomethacin

27
Q

uses of indomethacin

A

acute gout, arthritis, closing PDA

28
Q

SE of indomethacin

A

GI distress and aplastic anemia

29
Q

IV NSAID often uses with opiate

A

ketoralac

30
Q

partially selective COX-2 inhbitor used fir RA and OA in adults

A

meloxicam

31
Q

reason most COX-2 inhibitors taken off market

A

high risk of CV events

32
Q

population that is advised not to take non-asprin NSAIDS at all

A

people with known CV disease

33
Q

triggers inflamation in gout

A

granulocytes trying to remove urate crystals in joints

34
Q

DOC for acute gout

A

colchicine

35
Q

MOA of colchicine

A

inhibits release of chemotactic and inflammatory factors

36
Q

disadvantage of colchicine

A

highly toxic - very low TI

37
Q

side efects of colchicine

A

n/v, diarrhea

38
Q

DOC for prevention of gout

A

probenecid and sulfinpyrazone, allopurinol, feboxustat

39
Q

MOA of probenecid and sulfinpyrazone

A

inhibits renal reabsorption of urate

40
Q

MOA of allopurinol

A

suicide inhibitor of xanathine oxidase - blocks urate synthesis

41
Q

SE of allopurinol

A

GI irritation and skin reactions, inhibits other enzymes in purine pathway

42
Q

febuxostat MOA

A

nonpurine inhibitor of xanthine oxidase - blocks urate synthesis

43
Q

SE of febuxostat

A

liver tox and GI irritation