NSAIDS Flashcards
What are the 4 shared properties of NSAIDS?
Analgesics
Anti-inflammatory
Antipyretic
Platelet Inhibition (aspirin)
What are 7 NSAID Selected indications?
___itis
Headaches
Myalgia
Neuralgia
Arthralgia
Post-op pain
Gout
What is the primary MOA of NSAIDs?
What do they effect to a lesser degree?
Inhibition of prostaglandin synthesis
Leukotriene pathway
Which enzymes convert arachidonic acid into prostaglandins?
How do NSAIDS get involved?
COX 1 and COX 2
NSAIDS inhibit these enzymes to prevent conversion into prostaglandins
Explain COX-1
-present where?
-maintains?
-involved in 2 things:
Beneficial body effects
Maintains GI mucosa
Blood clotting
Renal blood flow
Explain COX-2
-when is it active?
-what 2 effects?
Only active in inflammation
-inflammation
-pain
most NSAIDS block ____ COX enzymes
Blocking COX-___ causes more serious AEs
both
COX-1
NSAID Contraindications
-documented….
-2 conditions causing bleeding risk
-_____ disease
-?
Documented aspirin allergy
-Vitamin K deficiency
-Peptic ulcer disease
-renal disease
-pregnancy
Explain the pregnancy considerations for NSAIDS
1-2 Trimester: Cat. C- benefits outweigh risks
3rd Trimester: Cat. D: risks outweigh benefits
Which NSAID does not have a BBW?
Aspirin
What is the NSAID BBW?
NSAIDS may counteract the ________ effects of _____
Increased risk of cardiovascular thrombotic AEs: fatal MI, stroke
Counteract the cardioprotective effects of aspirin
T or F:
Aspirin should never be taken with another NSAID
True
NSAID Key AE
Bleeding
GI: pain or ulcers
Acute renal failure
Cardio: MI/stroke risk
Disruption of prostaglandin function by NSAIDS cause cause acute or chronic _________
Renal failure
What can happen if a patient takes NSAIDS when they have dehydration, HF, liver dysfunction, take diuretics or ACE inhibitors?
Renal toxicity
What are 3 less common AEs for NSAIDS?
Hepatotoxicity
Hypersensitivity rxns
Tinnitus/hearing loss
What are the 2 Propionic Acid Derivative NSAIDS?
Ibuprofen
-most commonly used NSAID
Naproxen
-2nd most commonly used NSAID
-somewhat better AE profile than ibuprofen
-fewer interactions w/ ACE inhibitors
Which NSAID is a COX-2 inhibitor?
-main benefit?
-little effect on?
-Contraindications?
Celecoxib (Celebrex)
-decreased risk of GI bleed
-platelet function
-known sulfa allergy
Why does Celecoxib decrease the GI bleed risk?
Prevents COX-2 from inhibiting GI mucosa
Which NSAID is an acetic acid derivative?
-Primary use?
-Duration limit?
-AEs?
-AE if taken for more than the time limit?
Ketorolac (Toradol)
-Powerful analgesic for acute moderate/severe pain
-5 days limit
-Renal impairment
Which NSAID is a salicylate?
-Inhibits?
-Reduces?
-Administered when?
-Other uses?
-Combo med?
-Risk w/ children?
Aspirin
-inhibits platelet aggregation
-Reduces cardiac death post-MI
-First sign of MI
-Headache, pain, fever
-Excedrin= aspirin+acetominophen+caffiene
-Reye’s Syndrome
Explain the MOA of Aspirin
Irreversible inhibitor of COX-1 receptors within platelets
Reduced formation of thromboxane A2
Explain Reye’s Syndrome
-related med?
-most common age?
-progressive ______
-can lead to?
-triggered by?
-Patient should?
Aspirin
4-12 years old
Progressive neurologic deficits
Coma, liver damage
Triggered by viral illness + aspirin use
Read labels on combo meds like pepto-bismol
What should a patient evaluate for themselves when taking NSAIDS?
Black/tar-like stool- GI bleed
