NSAIDs

The most commonly used treatment for phantom pain. "NSAIDs/Tylenol are the most commonly used treatment for PLP." NHS lists NSAIDs such as ibuprofen for stump and phantom pain.

[Bell’s palsy] Pain relief — NINDS: "aspirin, acetaminophen, or ibuprofen," checking interactions first. [Trigeminal neuralgia] Not usually helpful — "Common pain-relieving medications (such as aspirin and ibuprofen)" and opioids "are not usually helpful in treating TN."

NSAID eye drops, with steroid drops, treat cystoid macular edema after surgery; the NHS lists ibuprofen for post-op ache.

The first-line analgesic for biliary colic — and the answer that replaced a generation of opioid folklore. Cochrane 2016 (12 trials, 828 participants): patients given NSAIDs were far less likely to be left without complete pain relief than on placebo (RR 0.27) and did better than spasmolytics, with pain relief equal to opioids and fewer disease-related complications. Pooled data suggest NSAIDs may reduce short-term complications such as progression to acute cholecystitis — teach "may reduce," not "prevents," because that effect was not confirmed by trial sequential analysis and the trials excluded elderly, comorbid patients. After laparoscopic surgery, pain is usually modest — non-opioid analgesics first, opioids as backup.

A risk to avoid. "NSAIDs may increase the chance of diverticulitis complications," and NSAIDs are on the risk-factor list. The AGA advises patients with a history of diverticulitis to "avoid regular use (≥ 2 times per week) of nonsteroidal anti-inflammatory drugs except aspirin prescribed for secondary prevention of cardiovascular disease."

The caveat class here, not the go-to: "Nonsteroidal anti-inflammatory drugs can contribute to delayed union through cyclooxygenase enzyme inhibition." Fracture healing depends on the inflammatory cascade the COX enzymes drive, so NSAID use joins smoking and diabetes on the list of healing saboteurs — a teaching point for patients reaching for ibuprofen on their own.

One of three equally STRONG first-line options for the flare, and the page does not rank them. ACR 2020: "we STRONGLY recommend using ORAL COLCHICINE, NSAIDs, OR GLUCOCORTICOIDS (ORAL, INTRAARTICULAR, OR INTRAMUSCULAR) as appropriate FIRST-LINE therapy for gout flares over IL-1 inhibitors or ACTH (THE CHOICE OF COLCHICINE, NSAIDs, OR GLUCOCORTICOIDS SHOULD BE MADE BASED ON PATIENT FACTORS AND PREFERENCES)." So the examinable content is the choosing, not a ranking — and on a gout page the patient factors that decide it are the comorbidities gout travels with. Chronic kidney disease, heart failure, hypertension and diabetes are all on gout’s own risk list, and every one of them bears on whether an NSAID is safe. The practical framing the patient needs is speed: attacks "are usually treated with a non-steroidal anti-inflammatory (NSAID), like ibuprofen," taken "as soon as possible." NSAIDs are also one of the three named prophylaxis agents for the 3-to-6-month window after urate-lowering therapy starts. The class page owns the renal, gastrointestinal, bleeding and cardiovascular adverse effects; this page teaches that the gout patient is disproportionately likely to have the contraindications.

AVOID. NHS: "do not take aspirin, ibuprofen or other non-steroidal anti-inflammatory drugs (NSAIDs)." In VWD, NSAIDs also "can worsen hyponatremia" with desmopressin.

One enzyme, four effects — and the mechanism is already drawn on this page. "Non-steroidal anti-inflammatory drugs like NAPROXEN, IBUPROFEN, and ASPIRIN act by inhibiting an enzyme CYCLOOXYGENASE (COX) that contributes to inflammation," and the class has "ANALGESIC, ANTIPYRETIC, ANTIPLATELET, and ANTI-INFLAMMATORY effects," being "among the world’s most used or prescribed medications." COX sits in the arachidonic acid cascade, which is why blocking one enzyme produces four different clinical effects — and why the same block lowers a fever: PGE2, made through exactly that COX step, is what shifts the hypothalamic set-point, so "medications that inhibit COX are a mainstay of treatment for fevers, as it halts the conversion of [arachidonic acid] into PGE2." On the two isoforms: "lumiracoxib is a SELECTIVE inhibitor of COX-2, the INDUCIBLE form of COX, whereas naproxen is a NONSELECTIVE COX inhibitor, inhibiting COX-2 and COX-1, the CONSTITUTIVELY EXPRESSED form. The COX-2 selective inhibitors are collectively called COXIBS." A finding that complicates the tidy story, and is worth teaching for that reason: "the effects of NSAIDs on CRP levels are MIXED… naproxen was associated with a decreased CRP, whereas lumiracoxib was associated with an increased CRP… the MORE SELECTIVE an NSAID is for COX-2, the GREATER the effect on INCREASING CRP. Due to the increased risk of severe cardiovascular events, celecoxib is the only coxib available in the American market," and "the cardiovascular risks posed by NSAIDs are an area of active research and are an UNDER-RECOGNIZED issue." Two disorder-side cautions belong here rather than on the class page. NSAIDs are named among the medications that "can adversely affect healing" — which matters in any patient with a fresh incision or a non-healing wound. The full list puts the class in company worth noticing: "medications that can adversely affect healing include anticonvulsants, steroids, antibiotics, angiogenesis inhibitors, and NSAIDs." So the drug that makes the inflamed joint usable is also on the list of things delaying the wound next to it — which is a conversation to have, not a reason to withhold analgesia. The class page owns the gastrointestinal, renal and bleeding adverse-effect profile.

First-line analgesia for renal colic, and the reason is mechanistic: the pain comes from prostaglandin-driven ureteral and capsular pressure, which is exactly what an NSAID reduces. Stated plainly by the sources: "NSAIDs are typically the first-line treatment for pain relief, as they are often as effective as, or even more effective than, opioids, while avoiding the complications associated with opioid usage." Parenteral options include ketorolac 15–30 mg IV or IM, or diclofenac 37.5 mg IV; ketorolac may also run as a continuous infusion at 3–5 mg/h. Two limits belong with the dose: ketorolac is for short-term use of under 5 days regardless of formulation, and the oral form is indicated only as a continuation of IV or IM therapy — it is not a stand-alone oral starter. An NSAID is also given immediately before shockwave lithotripsy to "minimize postoperative patient discomfort and decrease the requirement for post-procedure analgesics."

The first-line drug — when medicine is wanted after nonpharmacologic measures. ACP 2017, acute or subacute pain: "If pharmacologic treatment is desired, clinicians and patients should select nonsteroidal anti-inflammatory drugs or skeletal muscle relaxants." Chronic pain: "consider pharmacologic treatment with nonsteroidal anti-inflammatory drugs as first-line therapy." For radiculopathy, management "may include NSAID therapy, exercise, traction, or spinal manipulation."

First step for mild-to-moderate attacks without nausea or vomiting (ibuprofen, naproxen, diclofenac, aspirin); caution with bleeding risk. Also a medication-overuse culprit. Indomethacin is the diagnostic response in hemicrania continua.

NSAIDs are the pharmacologic backbone of osteoarthritis treatment in the 2019 ACR and Arthritis Foundation guideline. Oral NSAIDs are strongly recommended for hand, knee and hip — one of only a handful of strong recommendations in the whole document — with the practical rider to use "the lowest effective dose." Topical NSAIDs are strongly recommended for the knee and only conditionally for the hand, and the asymmetry has a disorder-side explanation worth teaching: the knee is superficial enough for a topical agent to reach the joint, so the same analgesia is achieved without the systemic gastrointestinal, renal and cardiovascular exposure. The guideline makes no topical recommendation for the hip, which is too deep for the route to work — state that absence rather than extrapolating a hip recommendation from the knee one. The practical sequence this produces at the knee is topical first, then oral at the lowest effective dose, with the systemic-risk profile of the patient deciding how far up that ladder to go. When an NSAID is unsafe — anticoagulation, renal impairment, peptic ulcer disease, significant cardiovascular risk — the guideline does not leave the patient with nothing, because acetaminophen and tramadol both carry conditional recommendations. NSAID adverse-effect profile, renal and gastrointestinal risk, and the interaction with anticoagulants belong to the class page.

Nonopioid for mild to moderate pain that also reduces fever and inflammation by blocking prostaglandin production. Watch older adults and patients on warfarin or corticosteroids for GI bleeding (melena); renal failure and, except with aspirin, heart attack, heart failure and stroke are risks.

The mainstay of acute pericarditis: aspirin or an NSAID, always paired with colchicine, continued until symptoms resolve — typically 3 days to 2 weeks — at full dose for 7–10 days and then tapered over 3–4 weeks guided by CRP, with a PPI for gastroprotection. Aspirin is preferred after an MI or in patients on antiplatelet therapy (Dressler, post-ACS, recent stent). Use the lowest dose and shortest duration with heart failure, CKD, peptic ulcer disease, bleeding risk or concurrent diuretics, ACE inhibitors or ARBs; keep doses minimal in myopericarditis; in uremic pericarditis NSAIDs give little relief and severe renal impairment limits them — intensified dialysis is the treatment. Abrupt or rapid tapering frequently precipitates a flare.

NSAIDs such as ibuprofen help reduce pleuritic pain and inflammation (NHLBI).

Endometriosis pain — part of the first-line group with combined hormonal contraceptives and progestins; the NHS names ibuprofen.

Avoid for chronic pain. KDIGO: "Acetaminophen is the first-line drug for chronic pain control. Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is discouraged for treatment of chronic pain, but these may be used short-term for acute pain in people with stable kidney function." StatPearls lists "avoidance of NSAIDs" among the lifestyle measures; NIDDK warns that "Sometimes AKI is caused by using OTC painkillers for a long time."

Indomethacin is the tocolytic below 32 weeks, and the disorder-side reason is mechanistic: the inflammatory pathway that starts preterm labor runs through prostaglandins, and "COX inhibitors prevent the conversion of arachidonic acid to prostaglandins, which stimulate contractions." The hard limit is the fact to carry: it is "contraindicated after 32 weeks of gestational age," because the ductus arteriosus becomes prostaglandin-sensitive later in gestation and the drug can close it prematurely. Its use is limited to 48 hours in any case. The fetal adverse effects are specific and named — "premature closure of the ductus arteriosus," and "Other fetal effects from indomethacin include oligohydramnios, gastric perforation, and pulmonary hypertension" — and the maternal ones are gastrointestinal: it increases "the rate of ulcer formation," and prostaglandin loss "increases the prevalence of mucosal injury and gastrointestinal bleeding." Contraindications are "bleeding disorders, gastritis, aspirin hypersensitivity, and hepatic impairment." The gestational-age split with nifedipine is the whole teaching point, and continuing indomethacin past 32 weeks is listed as an iatrogenic precipitant of deterioration rather than a minor protocol drift. General NSAID pharmacology belongs to the class page.

IVIG premedication option — StatPearls lists "non-steroidal anti-inflammatory drugs" among premedications; weigh against the IVIG renal-failure warning.

Symptom relief only — they "do not have any disease-modifying effects." Meloxicam, naproxen, celecoxib and nabumetone are named, and the class carries a cardiovascular black-box warning, which bites harder here because rheumatoid arthritis is itself an independent cardiovascular risk factor. The disorder-specific interaction is the one most often forgotten: NSAIDs "increase the risk of MTX toxicity" — and methotrexate is the anchor drug nearly every RA patient is taking. Trimethoprim-sulfamethoxazole and proton pump inhibitors raise methotrexate toxicity the same way, and all three are commonly co-prescribed. Note also what the current guideline says about NSAIDs in RA: nothing at all — its "recommendations are limited to DMARDs approved by the US FDA for treatment of RA" (ACR 2021). Present them as symptomatic adjuncts with the methotrexate interaction front and centre; the gastrointestinal and renal cautions belong to the class page.

[Scleroderma] Scoped. Mild arthralgias "respond well to nonsteroidal anti-inflammatory drugs (NSAIDs)," but in gastrointestinal involvement "NSAIDs should be avoided."

First-line pain relief for medical or surgical management. WHO: "Recommend that pain management should be offered routinely (e.g. non-steroidal anti-inflammatory drugs [NSAIDs])." "Women who received NSAIDs had lower mean pain scores and fewer women from that group required additional analgesic medication, based on high-certainty evidence." "Pain management should always be available and it should be administered in advance, in anticipation of the onset of pain, or provided to the woman in case it is needed for later use at home."

Culprit — NSAIDs (oxicams; celecoxib). Celebrex: patients should "stop taking CELEBREX immediately if they develop any type of rash or fever"; it "is contraindicated in patients with previous serious skin reactions to NSAIDs." FDA: NSAIDs such as ibuprofen and naproxen "also carry the risk of causing serious skin reactions."

The symptom-control tool for the mild end only — "For minor arthralgias, NSAIDs may be used" — and one component of pleuropericarditis management alongside colchicine or moderate-dose corticosteroids, with escalation to hydroxychloroquine, mycophenolate or azathioprine when pericarditis recurs despite them. The disorder-specific caution is not a stated contraindication but an intersection the nurse must hold in mind: roughly 40% to 50% of these patients develop nephritis, often silently, and lupus drives accelerated atherosclerosis — so NSAIDs are given against a background of renal and cardiovascular vulnerability. Monitor renal function and blood pressure rather than assuming an over-the-counter analgesic is a neutral choice here.

Ease muscle spasm and spasticity — mostly by sedating the CNS. The defining risks are drowsiness/falls and additive depression with opioids, benzodiazepines, and alcohol.

Slow osteoclast bone breakdown to build bone density in osteoporosis. The exacting oral-administration protocol is central to nursing care — it protects the esophagus and rescues a <1% absorption.

Beyond the bisphosphonates, three kinds of drug treat bone and calcium. Teriparatide, abaloparatide and romosozumab build bone. Denosumab, raloxifene and calcitonin slow bone loss in other ways. Cinacalcet and calcitriol reset the calcium–parathyroid balance. Serum calcium runs through the nursing care of nearly all of them, and three carry boxed warnings: denosumab (Prolia) for severe hypocalcemia in advanced kidney disease, romosozumab for heart attack and stroke, and raloxifene for blood clots and death from stroke.

Two different jobs: stop an acute attack vs lower uric acid long-term. Don’t stop urate-lowering therapy for a flare.