Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

(71 cards)

Start Studying
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)

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

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

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

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

Etodolac

A

Acetic Acid Derivative

more COX-2 selectivity

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

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

Diclofenac

A

Acetic Acid Derivative

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

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

Tolmetin

A

Acetic Acid Derivative

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

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

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

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

Naproxen [AnaproxR, NaprosynR, AleveR]

A

Propionic Acid Derivative

rev. inhib COX 1 and 2
tox: GI

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

Ketoprofen

A

Propionic Acid Derivative

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

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

Oxaprozin [DayproR]

A

Propionic Acid Derivative

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

tox: GI
use: RA, OA

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

Piroxicam (FeldeneR)

A

Enolic Acid Derivative: Oxicam

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

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

Meloxicam (MobicR)

A

Enolic Acid Derivative: Oxicam

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

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

Nabumetone

A

Non acidic compound (Alkanones)

rev. inhib COX 2 > 1
activated by liver

tox: GI, CNS
use: RA, OA

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

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

platelets only have..

A

COX-1 (not COX-2)

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

Celecoxib (CelebrexR)

A

COX-2 INHIBITOR

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acetyl Salicylic Acid [Aspirin] pharmkin

A

widely distributed through tissues, binds plasma proteins

can diffuse through placenta and BBB–>CNS effects

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Misoprostol (Cytotec®)

A

prostaglandin E1 analogue

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
ASA otic effects
tinnitus and hearing loss- *reversible 200-300 μg/mL for anti-inflammatory effects, appearance of tinnitus indicates adequate plasma concentrations have been reached
26
ASA hepatic effects
reversible, particularly with previous hepatic impairment and high dose salicylates -must monitor
27
ASA renal effects
renal medullary ischemia as a result of inhibition of renal prostaglandin synthesis
28
ASA CV effects
noncardiogenic pulmonary edema, HTN | CI: CHF pts (esp. w. Na)
29
ASA hematologic effects
(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
ASA hypersensitivity rxns ASA triad?
*Type 1* Urticaria and /or angioedema: ``` aspirin sensitivity asthma nasal polyps (small doses: 20-30mg) *in asthma pts* ``` foods with salicylate-->hypersn
31
ASA ped cautions (also teenagers) symptoms ??
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
what to use in peds for an anti-pyretic instead of ASA?
ACETAMINOPHEN
33
ASA Pregnancy, fertility, lactation
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
ASA intoxication
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
ASA intox manifests
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
ASA OD tx
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
ASA drug interactions
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
ASA dosage for RA, OA, etc
2.4-3.6 g daily | gram-level! at risk for toxicity
39
NSAIDs adverse effects: CV
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
NSAIDs adverse effects: CNS
diffuse thru BBB and placenta dizziness, ha (indomethacin, fenoprofen, ketorolac) psych somnolence/drowiness
41
NSAIDs adverse effects: dermatologic
rashes
42
NSAIDs adverse effects: elderly
ulcers | spontaneous bleeding
43
NSAIDs adverse effects: GI
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
factors assoc. with inc. risk GI ulcer
smoking, etOH | bleeding
45
NSAIDs adverse effects: hematologic
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
NSAIDs hypersn. rxns
rare in ASA (3 hrs after) | manifests as asthma, anaphylaxix, acute resp. distress, rapid fall in BP- shock-like, angioedema, dyspnea, angiitis
47
NSAIDs adverse effects: lactation
DON'T use NSAIDS in nursing mothers because the potential effects on the infant's cardiovascular system
48
NSAIDs adverse effects: renal
*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
NSAIDs adverse effects: pregnancy
- 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
NSAIDs drug interaxns
All NSAIDs bind to plasma proteins
51
Celecoxib, last COX-2 standing
inhibition of prostaglandin synthesis, via inhibition of cyclooxygenase-2 (COX-2) *Metabolism is via cytochrome P450 2C9* (drug interactions) Elim by hepatic metabolism
52
celecoxib CIs
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
celecoxib adverse effects
``` GI: less since not COX 1 inhib, but still some GI CNS resp skin psych ```
54
endothelial cells have
COX-1 and *COX-2*-->PGI2 | vasodilaiton and declumping
55
platelets have
COX-1-->TXA2 vasoconstriction and aggregation (via TXA2) *not inhib. by selective COX-2 inhibitors, had to remove from market exc. celecoxib (milder)
56
acetaminophen affects
paracetamol affect on fever by action on hypothalamic heat-reg center weakly inhibits COX1, 2, 3? (spliced)
57
acetaminophen pharmkin
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
acetamin SEs
hepatotoxicity*** (reversible) potentially fatal hepatic centrilobular necrosis nephrotoxicity
59
acetominophen OD antidote?
gastric lavage oral N-acetylcystein (Mucomyst)- restores glutathione levels-neutralizes toxic metabolites use w.in 8 hrs post-ingestion
60
ASA used for
mild-mod pain, fever, inflamm. disease also: prevention of arterial and venous thrombosis
61
NSAIDs
*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
NSAIDs for RA
all except Ketorolac, Meloxicam, Mefenamic acid
63
NSAIDs for OA
all except Ketorolac and Mefenamic acid
64
JRA tx
Tolmetin and naproxen
65
Ibuprofen hypersensitivity
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
celecoxib uses
OA, RA, acute pain, dysmenorrhea, familial adenomatous polyposis
67
why other selective COX 2 drugs were taken off the market
CV problems from uninhibited COX-1-->platelets-->prod. TXA2-->vasoconstriction and aggregation
68
COX-1 inhibitor: | ibuprofen-->inhib COX1-->prevents TXA2 release-->inhibits platelet aggregation and vasoconstriction
endothelium cells (COX-2) NOT inhibited by ibuprofen-->still releases PGI2-->unopposed vasodilation and declumping
69
COX-2 inhibitors: celecoxib | affects endothelial cells (COX-2)-->NO release PGI2-->inhibits vasodilation and decamping
``` BUT platelets (COX-1) still release TXA2-->*vasoconstriction and aggregation UNOPPOSED*-->CV problems ``` all COX-2s removed except celecoxib: milder effects
70
don't take more than ?? g acetaminophen/day | alcoholics?
71
acetominophen uses
analgesic antipyretic weaker anti-inflammatory than ASA mild-mod pain OA

Pharm (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions