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Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Acetyl Salicylic Acid [Aspirin]

A

Salicyclic Acid Derivatives
(don’t know chemical groups)

salicylate ester of acetic acid

irreversibly acetylates/inactivates COX in platelets, megakaryocytes

(4-7 days, life of platelet)

anti-inflammatory, antithrombotic effects (inactivates platelets)

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2
Q

Mesalamine (5-amino salicylic acid) [Apriso®]

A

Salicyclic Acid Derivative

  • reversible inhib COX-1 and COX-2
    toxicity: GI, CNS, nasophary., hypersn

used for UC

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3
Q

Diflunisal

A

Salicyclic Acid Derivative

reversible inhib. of COX

analgesic, anti-inflammatory

little antipyretic activity

long 1/2 life (8-12 hrs), inc. pt compliance

less GI SEs, don’t use in pts with anti-ASA sn.

tox: GI (mild), ha, renal, hypersn

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4
Q

Indomethacin [IndocinR]

A

Acetic Acid Derivative

rev. inhib COX 1 and 2
tox: GI, bleeding, CV, CNS
use: RA (NOT JRA), OA, tocolytic agent

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5
Q

Etodolac

A

Acetic Acid Derivative

more COX-2 selectivity

tox: GI, less sev.
use: FA, OA, postop analgesic

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6
Q

Diclofenac

A

Acetic Acid Derivative

rev. inhib COX 1 and 2
tox: GI, CNS
use: RA, OA, anagesia/dysmenorrhea

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7
Q

Tolmetin

A

Acetic Acid Derivative

rev. inhib COX 1 and 2
tox: GI, CNS, anaphylaxis!
use: RA, JRA*, OA

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8
Q

Ketorolac

A

Acetic Acid Derivative

rev. inhib COX 1 and 2
tox: GI, CNS
use: mod sev, acute pain, NOT for RA/OA

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9
Q

Ibuprofen [MotrinR, AdvilR]

A

Propionic Acid Derivative

rev. inhib COX 1 and 2
tox: GI (less than ASA, indometh.), ocular disturbs, hypersn rash, avoid during preg/breast feeding
uses: RA, OA, analgesia, dysmenorrhea, fever

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10
Q

Naproxen [AnaproxR, NaprosynR, AleveR]

A

Propionic Acid Derivative

rev. inhib COX 1 and 2
tox: GI

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11
Q

Ketoprofen

A

Propionic Acid Derivative

rev. inhib COX 1 and 2
tox: GI, CNS
use: RHA, OA, analgesia, dysmenorrhea

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12
Q

Oxaprozin [DayproR]

A

Propionic Acid Derivative

rev. inhib COX 1 and 2
(1x/day)

tox: GI
use: RA, OA

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13
Q

Piroxicam (FeldeneR)

A

Enolic Acid Derivative: Oxicam

rev. inhib COX 1 and 2
tox: GI
use: RA, OA

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14
Q

Meloxicam (MobicR)

A

Enolic Acid Derivative: Oxicam

rev. inhib COX 2 > 1
tox: GI
use: OA

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15
Q

Nabumetone

A

Non acidic compound (Alkanones)

rev. inhib COX 2 > 1
activated by liver

tox: GI, CNS
use: RA, OA

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16
Q

Acetaminophen [TylenolR]

A

Para aminophenol derivative

weak inhibition COX-1,2,3

antipyretic by acting on hypothalamic heat-regulating center

tox: *hepatotoxicity, *nephrotoxicity, hypersn
uses: antipyretic, analgesic, OA

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17
Q

platelets only have..

A

COX-1 (not COX-2)

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18
Q

Celecoxib (CelebrexR)

A

COX-2 INHIBITOR

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19
Q

Acetyl Salicylic Acid [Aspirin] GI absorption mechs

A

more non-ionized ASA in stomach (where it’s acidic)–>can be absorbed by gastric mucosa cell

in mucosa cell: it’s ionized–>stuck there

ionized in sm. int. BUT larger surf. area so absorbed

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20
Q

Acetyl Salicylic Acid [Aspirin] pharmkin

A

widely distributed through tissues, binds plasma proteins

can diffuse through placenta and BBB–>CNS effects

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21
Q

Acetyl Salicylic Acid [Aspirin] metab/elim

A

urinary pH changes from 5 to 8 in kidneys (alkalinization with sodium bicarbonate)

*ASA in ionized state, does not diffuse back, excreted), the renal clearance of free ionized salicylate increases from 2-3% of the amount excreted to about 80%

(The opposite happens in acidic urine)

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22
Q

Acetyl Salicylic Acid [Aspirin] GI SEs

A

dyspepsia, heartburn, epigastric distress, nausea

less frequently vomiting, anorexia, abdominal pain
inc. with high doses/pre-existing ulcer

occult bleeding, gastric mucosal damage, iron def. anemia (case)
reactivate latent gastric and duodenal ulcers

*most freq. with ASA than other salicylates

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23
Q 
case: iron def. anemia
enteric-coated reg. strength ASA
1 mg warfarin
INR 1.15
tablet in ulcer of gastric antrum
tx w. endolcac and ASA -DON't DO: synergy
A

tx w. lasoprazole (PPI)

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24
Q

Misoprostol (Cytotec®)

A

prostaglandin E1 analogue

can protect stomach by lowering gastric acid production, anti ulcer with ASA tx

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25
Q

ASA otic effects

A

tinnitus and hearing loss- *reversible

200-300 μg/mL for anti-inflammatory effects, appearance of tinnitus
indicates adequate plasma concentrations have been reached

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26
Q

ASA hepatic effects

A

reversible, particularly with previous hepatic impairment and high dose salicylates
-must monitor

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27
Q

ASA renal effects

A

renal medullary ischemia as a result of inhibition of renal prostaglandin synthesis

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28
Q

ASA CV effects

A

noncardiogenic pulmonary edema, HTN

CI: CHF pts (esp. w. Na)

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29
Q

ASA hematologic effects

A

(high doses) decrease hematocrit and plasma
iron concentrations

reduce RBC life span
inc. risk of bleeding

CI in patients with bleeding disorders

*discontinue ASA 5-7 days before sx

30
Q

ASA hypersensitivity rxns

ASA triad?

A

Type 1
Urticaria and /or angioedema:

aspirin sensitivity 
asthma
nasal polyps 
(small doses: 20-30mg)
*in asthma pts*

foods with salicylate–>hypersn

31
Q

ASA ped cautions (also teenagers)

symptoms ??

A

varicella infections (chicken pox) or influenza-like illnesses is reportedly associated with an increased risk of developing Reye’s syndrome

sudden vomiting, violent headaches and belligerence that may progress to delirium and coma

32
Q

what to use in peds for an anti-pyretic instead of ASA?

A

ACETAMINOPHEN

33
Q

ASA Pregnancy, fertility, lactation

A

safe use has not been established

can diffuse thru placenta and BBB

could be teratogenic, congenital abnormality associations, use only when potential benefits>possible risks to fetus

caution to nursing mothers

maternal and fetal hemorrhagic complication

34
Q

ASA intoxication

A

Chronic salicylate intoxication is also known as salicylism

> than 100 mg/kg daily for 2 days or longer

Acute salicylate OD results from ingestion of a single toxic dose
lethal:
10-30g adults
4g kiddos

35
Q

ASA intox manifests

A

Tinnitus and hearing loss

Hyperventilation and CNS effects (kiddos)

metabolic acidosis and respiratory alkalosis

CNS stimulation (salicylate jag), then CNS depression–>resp. failure or CV collapse–>coma/death

principal: acid-base and electrolyte disturbances, dehydration, hyperpyrexia, and either hyperglycemia or hypoglycemia

36
Q

ASA OD tx

A

immediately!
symptomatic and supportive

enhance salicylate elimination: lavage

prevent further absorption: activated charcoal (2hr)

correct fluid, e-lyt, A/B disturbances

alkalinize urine to
pH 7.5 or greater enhances salicylate excretion (will be neg. charged): IV sodium bicarbonate:

37
Q

ASA drug interactions

A

Protein-bound drugs: compete for binding site

don’t use with anticoagulants/thrombolytic agents–>inc. risk bleeding

corticosteroids inc. clearance of ASA

NSAIDs DON’T used in conjunction with other NSAIDs: synergy (GI effects)

38
Q

ASA dosage for RA, OA, etc

A

2.4-3.6 g daily

gram-level! at risk for toxicity

39
Q

NSAIDs adverse effects: CV

A

HTN: dose-dependent, from inhibition of COX-2 in the kidney

(use w. caution in HTN, dec. cardiac function pts)

fluid retetion and peripherial edema

40
Q

NSAIDs adverse effects: CNS

A

diffuse thru BBB and placenta

dizziness, ha (indomethacin, fenoprofen, ketorolac)
psych
somnolence/drowiness

41
Q

NSAIDs adverse effects: dermatologic

A

rashes

42
Q

NSAIDs adverse effects: elderly

A

ulcers

spontaneous bleeding

43
Q

NSAIDs adverse effects: GI

A

gastric/duodenal ulcers
inhib. PG production (gastric cells have COX1)

*can occur anytime, with or without warning symptoms in patients receiving NSAID therapy chronically

44
Q

factors assoc. with inc. risk GI ulcer

A

smoking, etOH

bleeding

45
Q

NSAIDs adverse effects: hematologic

A

autoimmune hemolytic anemia (Type II drug allergy)-IgG, IgM with Tolmetin, *reversible
-remove offending drug, tx with corticosteroids

platelet (COX1) aggregation less and dec. duration than with ASA
*reversible

NSAIDs may prolong bleeding time-affect coagulation cascade

46
Q

NSAIDs hypersn. rxns

A

rare in ASA (3 hrs after)

manifests as asthma, anaphylaxix, acute resp. distress, rapid fall in BP- shock-like, angioedema, dyspnea, angiitis

47
Q

NSAIDs adverse effects: lactation

A

DON’T use NSAIDS in nursing mothers because the potential effects on the infant’s cardiovascular system

48
Q

NSAIDs adverse effects: renal

A

COX 2 constitutively expressed
NSAIDs inhibit COX-2–>inhibit renal PG synthesis:

progressive renal impairment

Acute renal insufficiency

Interstitial nephritis

hyper Na+, K+

Papillary necrosis (chronic renal injury)

49
Q

NSAIDs adverse effects: pregnancy

A
  • inhibit prostaglandin E2 synthesis may induce the closure of the fetal ductus arteriosus
  • can prolong labor (avoid, esp during 3rd trimester)

use: FDA-labelled NSAIDS for closure of patent ductus arteriosus in
premature infants, are either indomethacin (ha) or ibuprofen

50
Q

NSAIDs drug interaxns

A

All NSAIDs bind to plasma proteins

51
Q

Celecoxib, last COX-2 standing

A

inhibition of prostaglandin synthesis, via inhibition of cyclooxygenase-2 (COX-2)

Metabolism is via cytochrome P450 2C9 (drug interactions)
Elim by hepatic metabolism

52
Q

celecoxib CIs

A

not for pts who have allergic-type reactions to sulfonamides

OR experience asthma, urticaria or allergic-type reactions after taking aspirin or other NSAIDs

53
Q

celecoxib adverse effects

A 
GI: less since not COX 1 inhib, but still some GI
CNS
resp
skin
psych
54
Q

endothelial cells have

A

COX-1 and COX-2–>PGI2

vasodilaiton and declumping

55
Q

platelets have

A

COX-1–>TXA2
vasoconstriction and aggregation (via TXA2)

*not inhib. by selective COX-2 inhibitors, had to remove from market exc. celecoxib (milder)

56
Q

acetaminophen affects

A

paracetamol

affect on fever by action on hypothalamic
heat-reg center

weakly inhibits COX1, 2, 3? (spliced)

57
Q

acetaminophen pharmkin

A

metabolized by the hepatic microsomal
enzymes to acetaminophen sulfate and acetaminophen glucuronide (typ. excreted)

  • small amount metab by cytP450 to N-acetyl-p-benzoquinoneimine, which is highly reactive to cellular proteins and thus becomes toxic to both liver and kidney (norm. detox by glutathione)
  • toxicity in large amounts*
58
Q

acetamin SEs

A

hepatotoxicity*** (reversible) potentially fatal hepatic centrilobular necrosis

nephrotoxicity

59
Q

acetominophen OD

antidote?

A

gastric lavage

oral N-acetylcystein (Mucomyst)- restores glutathione levels-neutralizes toxic metabolites

use w.in 8 hrs post-ingestion

60
Q

ASA used for

A

mild-mod pain, fever, inflamm. disease

also: prevention of arterial and venous thrombosis

61
Q

NSAIDs

A

mostly used as anti-inflammatory agents

both analgesic and antipyretic properties

reversible inhibition of COX 1 and 2

absorbed rapidly and completely, pKa 3.5-6.3 (acidic)
protein bound, variable half life

62
Q

NSAIDs for RA

A

all except Ketorolac, Meloxicam, Mefenamic acid

63
Q

NSAIDs for OA

A

all except Ketorolac and Mefenamic acid

64
Q

JRA tx

A

Tolmetin and naproxen

65
Q

Ibuprofen hypersensitivity

A

severe rxns w. fever, rash, abd pain, ha, N/V, liver damage and meningitis in pts w. SLE or other collagen diseases

may not start immediately

66
Q

celecoxib uses

A

OA, RA, acute pain, dysmenorrhea, familial adenomatous polyposis

67
Q

why other selective COX 2 drugs were taken off the market

A

CV problems from uninhibited COX-1–>platelets–>prod. TXA2–>vasoconstriction and aggregation

68
Q

COX-1 inhibitor:

ibuprofen–>inhib COX1–>prevents TXA2 release–>inhibits platelet aggregation and vasoconstriction

A

endothelium cells (COX-2) NOT inhibited by ibuprofen–>still releases PGI2–>unopposed vasodilation and declumping

69
Q

COX-2 inhibitors: celecoxib

affects endothelial cells (COX-2)–>NO release PGI2–>inhibits vasodilation and decamping

A 
BUT
platelets (COX-1) still release TXA2-->*vasoconstriction and aggregation UNOPPOSED*-->CV problems

all COX-2s removed except celecoxib: milder effects

70
Q

don’t take more than ?? g acetaminophen/day

alcoholics?

A
71
Q

acetominophen uses

A

analgesic
antipyretic
weaker anti-inflammatory than ASA

mild-mod pain
OA

Pharm (45 decks)

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