Non Opioid Pain Meds

What enzyme do NSAIDs inhibit?

Cyclooxygenase (COX).

What does the COX enzyme normally convert?

Arachidonic acid into prostaglandins.

What does COX-1 normally protect?

Stomach, kidneys, and platelets.

What happens when COX-1 is inhibited?

Gastric ulcers, bleeding, and renal impairment.

What beneficial effect results from COX-1 inhibition by aspirin?

Protection against MI and stroke through platelet inhibition.

What does COX-2 primarily produce?

Pain, fever, and inflammation.

What happens when COX-2 is inhibited?

Decreased pain, fever, and inflammation.

What are the three main therapeutic effects of NSAIDs?

Analgesic, antipyretic, and anti-inflammatory.

What are the major risks of NSAIDs?

GI ulceration, bleeding, and renal impairment.

Which medication is NOT an anti-inflammatory?

Acetaminophen.

Which drugs are first-generation NSAIDs?

Aspirin, Ibuprofen, Naproxen, and Ketorolac.

Which COX enzymes do first-generation NSAIDs inhibit?

Both COX-1 and COX-2.

What conditions are first-generation NSAIDs commonly used to treat?

RA, OA, bursitis, mild to moderate pain, and fever.

What is aspirin's mechanism of action?

Irreversible nonselective COX inhibitor.

What are the therapeutic uses of aspirin?

Analgesia, antipyretic, anti-inflammatory, prevention of platelet aggregation, MI/stroke prevention, dysmenorrhea, and cancer prevention.

What are the major adverse effects of aspirin?

GI irritation, bleeding, renal impairment, salicylism, Reye syndrome, pregnancy complications, and hypersensitivity.

What are the classic signs of salicylism?

Tinnitus, sweating, headache, and dizziness.

Which syndrome can aspirin cause in children with viral illnesses?

Reye syndrome.

Which medications increase bleeding risk when taken with aspirin?

Warfarin, heparin, glucocorticoids, alcohol, NSAIDs, ACE inhibitors, and ARBs.

What are the major concerns with aspirin overdose?

Respiratory depression, hyperthermia, dehydration, and metabolic acidosis.

How is aspirin overdose treated?

Supportive care.

How do non-aspirin NSAIDs differ from aspirin?

Their COX inhibition is reversible.

Do non-aspirin NSAIDs protect against MI or stroke?

No.

What is the major safety warning for first-generation NSAIDs?

Increased risk of GI bleeding.

What are the common uses of ibuprofen?

Fever, mild to moderate pain, and arthritis.

Which drug is the prototype second-generation NSAID?

Celecoxib.

Which COX enzyme does celecoxib selectively inhibit?

COX-2.

What is the major benefit of celecoxib over first-generation NSAIDs?

Lower GI toxicity.

What major cardiovascular risks are associated with celecoxib?

MI and stroke.

What are the therapeutic uses of celecoxib?

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

What are the major adverse effects of celecoxib?

Dyspepsia, abdominal pain, renal impairment, sulfa allergy, MI, and stroke.

Which medications interact with celecoxib?

Warfarin, furosemide, ACE inhibitors, lithium, and fluconazole.

What is another name for acetaminophen?

Paracetamol.

What IV formulation of acetaminophen should you know?

Ofirmev.

Where does acetaminophen primarily inhibit COX?

In the CNS (brain).

Does acetaminophen have anti-inflammatory properties?

No.

What are the therapeutic effects of acetaminophen?

Analgesic and antipyretic.

What is the major adverse effect of acetaminophen?

Hepatotoxicity.

What is the maximum daily dose of acetaminophen?

4 grams (4000 mg).

What is the recommended maximum daily dose of acetaminophen for chronic alcohol users?

Less than 2000 mg/day.

What severe skin reactions are associated with acetaminophen?

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).

What are the early symptoms of acetaminophen overdose?

Nausea, vomiting, diarrhea, sweating, and abdominal pain.

What can acetaminophen overdose progress to?

Liver failure, coma, and death.

What is the antidote for acetaminophen overdose?

Acetylcysteine (Mucomyst).

Which headaches have identifiable underlying causes?

Headaches due to hypertension, hyperthyroidism, tumors, infections, or sinus disease.

What are the two goals of migraine therapy?

Abort an acute attack and prevent future attacks.

Which medication is the prototype triptan?

Sumatriptan (Imitrex).

How does sumatriptan work?

Causes cranial vasoconstriction and decreases inflammation.

Is sumatriptan used to prevent migraines?

No, it aborts active migraine attacks.

What routes can sumatriptan be administered?

Oral and intranasal.

What are the major adverse effects of sumatriptan?

Chest pressure, heavy arms, coronary vasospasm, angina, vertigo, fatigue, tingling, and bad taste with nasal use.

When is ergotamine used?

When triptans fail (second-line therapy).

What is the probable mechanism of ergotamine?

Serotonin receptor activation.

What are the major adverse effects of ergotamine?

Nausea, vomiting, and dependence.

What food should patients avoid while taking ergotamine?

Grapefruit juice.

Which medication is first-line for migraine prevention?

Propranolol.

Is propranolol used to treat an acute migraine?

No.

When do propranolol's benefits usually begin?

After several weeks.

Which supplements may help prevent migraines?

Vitamin B2, CoQ10, and Butterbur.

What serious adverse effect is associated with Butterbur?

Liver toxicity.

What causes gout?

Hyperuricemia leading to uric acid crystal deposition.

Where does gout most commonly occur?

The big toe.

What is the first-line treatment for an acute gout attack?

NSAIDs.

What medications may also be used for acute gout?

Glucocorticoids.

What is the goal of chronic gout therapy?

Lower uric acid levels.

What are the uses of colchicine?

Acute gout attacks and long-term prophylaxis.

What are the major adverse effects of colchicine?

Nausea, vomiting, diarrhea, and rhabdomyolysis.

Which patients are at higher risk for colchicine-induced rhabdomyolysis?

Patients taking statins or those with liver or kidney disease.

Is colchicine still first-line therapy?

No.

How does allopurinol work?

Inhibits xanthine oxidase to decrease uric acid production.

What is the most serious adverse effect of allopurinol?

Hypersensitivity syndrome.

What should be done immediately if a patient taking allopurinol develops a rash?

Stop the medication immediately.

How does febuxostat work?

Inhibits xanthine oxidase to decrease uric acid production.

How does probenecid work?

Increases uric acid excretion by the kidneys.

What are the major adverse effects of probenecid?

GI upset and kidney impairment.

What teaching should be given to patients taking probenecid?

Take with food, drink 2.5–3 L/day, and alkalinize the urine.

How does pegloticase work?

Converts uric acid into allantoin.

What is rasburicase primarily used for?

Cancer-related hyperuricemia.

What is the highest-yield difference between COX-1 and COX-2?

COX-1 protects the stomach and kidneys; COX-2 causes pain, fever, and inflammation.

Which NSAID irreversibly inhibits platelet aggregation to prevent MI and stroke?

Aspirin.

Which NSAIDs reversibly inhibit COX and do NOT prevent MI or stroke?

Non-aspirin NSAIDs (e.g., ibuprofen, naproxen).

What is the biggest cardiovascular concern with celecoxib?

Increased risk of MI and stroke.

What is the highest-yield fact about acetaminophen overdose?

It causes hepatotoxicity and is treated with acetylcysteine.

What is the highest-yield fact about sumatriptan?

It aborts active migraines but does NOT prevent them.

What is the highest-yield fact about propranolol?

It prevents migraines but does NOT abort acute attacks.

What is the first-line treatment for acute gout?

NSAIDs.

What medications lower uric acid in chronic gout?

Allopurinol, febuxostat, probenecid, and pegloticase.

What is the highest-yield nursing intervention for allopurinol?

If a rash develops, stop the medication immediately.