Bone & Skin Drugs

Bone and skin look like the quiet parts of the body — scaffolding and wrapping paper. They are neither. Bone is a living, constantly rebuilt mineral bank that the body raids whenever blood calcium dips, and skin is a barrier that fails loudly and expensively when it is burned, inflamed, or broken. The drugs in this chapter are unusually dependent on you: a bisphosphonate swallowed the wrong way can burn a hole in an esophagus, methotrexate taken daily instead of weekly can kill, and a burn cream chosen carelessly can tip a patient into metabolic acidosis. Almost nothing here is about the pill itself. It is about how it is given, what you watch, and what you teach.

Section 1Bone, calcium & vitamin D

Bone is never finished

The skeleton you have today is not the skeleton you had ten years ago. Bone is torn down and rebuilt continuously in a process called remodeling, carried out by two cell crews working in opposition. Osteoclasts are the demolition crew: they attach to a patch of bone, acidify it, and dissolve the mineral, releasing calcium into the blood. Osteoblasts are the construction crew: they lay down new collagen matrix and mineralize it. In a healthy adult the two are balanced. Tip the balance toward the clasts and bone thins; tip it toward the blasts and bone thickens.

The signal that decides the balance is worth memorizing because half the drugs in the next section act on it. Osteoblasts secrete a protein called RANK ligand (RANKL), which binds RANK receptors on osteoclast precursors and tells them to mature and start resorbing. Osteoblasts also secrete a decoy, osteoprotegerin, that mops up RANKL and shuts resorption down. Estrogen restrains RANKL — which is precisely why bone loss accelerates after menopause, when estrogen falls and the demolition crew works unsupervised.

The calcium thermostat

Serum calcium is defended within a narrow band (roughly 8.5–10.5 mg/dL total) because so much depends on it: nerve conduction, muscle contraction, clotting, and cardiac rhythm. Three hormones do the defending.

Parathyroid hormone (PTH) is the emergency responder. When calcium falls, the parathyroid glands release PTH, which pulls calcium out of bone, tells the kidney to reabsorb calcium (while dumping phosphate), and switches on the enzyme that activates vitamin D. Everything PTH does raises calcium. Vitamin D, once activated, is the absorber — it makes the gut take calcium in from food. Calcitonin, from the thyroid, is the brake: it "tones down" calcium by blocking osteoclasts. A simple way to hold it: PTH pulls calcium up, calcitonin tones it down.

Vitamin D deserves a moment because it is not really a vitamin — it is a hormone made in two steps. Skin makes cholecalciferol from sunlight, or the patient swallows cholecalciferol (D₃) or ergocalciferol (D₂). The liver then hydroxylates it to 25-hydroxyvitamin D — the storage form, and the one the lab measures when someone orders a "vitamin D level." Finally the kidney performs the activating step, producing calcitriol (1,25-dihydroxyvitamin D). That last step is the clinical punchline: a patient with advanced kidney disease cannot activate ordinary vitamin D no matter how much you give, so they are prescribed calcitriol or a related activated analog instead.

Giving calcium and vitamin D without causing harm

Calcium supplements are labeled by salt weight, but only part of that weight is usable elemental calcium. Calcium carbonate is about 40% elemental calcium — the most calcium per tablet, and cheap — but it needs stomach acid to dissolve, so it must be taken with food and it works poorly in patients on proton pump inhibitors or H₂ blockers, or after gastric surgery. Calcium citrate is only about 21% elemental (more tablets), but it dissolves without acid, so it can be taken with or without food and is the right choice for the acid-suppressed patient. Either way, the gut can only absorb roughly 500–600 mg of elemental calcium at one time, so a 1,200 mg daily target must be split into two or three doses. Constipation is the near-universal side effect; fluids, fiber, and activity are part of the teaching, not an afterthought.

Two clinical pictures should be automatic. Hypocalcemia makes nerves twitchy: numbness and tingling around the mouth and fingers, muscle cramps, positive Chvostek (facial tap) and Trousseau (cuff-induced carpal spasm) signs, tetany, laryngospasm, seizures, and a prolonged QT. Hypercalcemia makes everything sluggish — "stones, bones, groans, thrones, and psychiatric overtones": kidney stones, bone pain, nausea and constipation, polyuria, lethargy and confusion, and a shortened QT.

Section 2Osteoporosis drugs

Bisphosphonates: the first-line drugs, and the fussiest

Bisphosphonates — alendronate, risedronate, ibandronate, and IV zoledronic acid — are antiresorptive drugs. They bind tightly to the hydroxyapatite mineral of bone and sit there. When an osteoclast comes along and dissolves that patch, it swallows the drug, which poisons an enzyme (farnesyl pyrophosphate synthase) the osteoclast needs to survive. The osteoclast undergoes apoptosis. Demolition slows, the blasts keep building, and bone density climbs.

The problem is that oral bisphosphonates are absorbed miserably — well under 1% of the dose — and they are corrosive to the esophagus. That combination generates the most heavily tested administration rules in all of pharmacology, and they are not negotiable:

• Take first thing in the morning, on a completely empty stomach, before any other food, drink, or medication.
• Swallow with a full glass (6–8 oz) of plain water — not coffee, juice, mineral water, or milk. Calcium, iron, magnesium, and antacids block absorption entirely.
• Remain fully upright — sitting or standing, never lying down — for at least 30 minutes (a full 60 minutes for ibandronate).
• Wait that same interval before eating, drinking anything else, or taking other drugs.
• Do not give to a patient who cannot sit or stand upright for that long, or who has esophageal stricture, achalasia, or delayed emptying.
• Correct hypocalcemia and vitamin D deficiency first — an antiresorptive given to a calcium-depleted patient drives calcium lower.

Two rarer adverse effects earn their own teaching. Osteonecrosis of the jaw (ONJ) is exposed, non-healing jaw bone, most often after a dental extraction; the risk is highest with IV, high-dose, oncology-level therapy, and the nursing action is to arrange a dental exam and any needed extractions before therapy starts, then reinforce meticulous oral hygiene. Atypical femoral fracture is a transverse fracture of the femoral shaft after years of therapy, and it announces itself first: teach every patient that new, dull, aching thigh or groin pain must be reported immediately, because that prodrome is the window to catch it before the bone snaps.

IV zoledronic acid is once yearly, which solves adherence, but check renal function first (generally avoid if creatinine clearance is under about 35 mL/min), hydrate the patient well, and warn them about the acute phase reaction — a flu-like day or two of fever, myalgia, and headache after the first infusion, blunted by acetaminophen and unlikely to recur.

When a bisphosphonate is not the answer

Denosumab is a monoclonal antibody against RANKL — a manufactured osteoprotegerin. Given subcutaneously every 6 months, it is not cleared by the kidney, so it can be used at renal function where bisphosphonates are contraindicated — but that convenience comes with a warning. It carries a boxed warning for severe hypocalcemia in patients with advanced chronic kidney disease (including those on dialysis), so calcium and vitamin D must be repleted and serum calcium checked before each injection and monitored closely afterward in those patients. It also carries a rule that patients under-appreciate: it must not be stopped or delayed without a replacement antiresorptive, because withdrawal triggers a rebound surge of bone resorption and multiple vertebral fractures. ONJ occurs here too.

Raloxifene is a selective estrogen receptor modulator (SERM): an estrogen agonist at bone (density up) and an antagonist at breast (invasive breast cancer risk down), while sparing the uterus. Its price is estrogen's thrombotic risk — a boxed warning for venous thromboembolism and fatal stroke in women at risk. Teach that it should be stopped 72 hours before prolonged immobilization (surgery, long travel) and restarted only when fully mobile. Hot flashes and leg cramps are common.

Everything above slows demolition. Two drug groups actually build bone. Teriparatide and abaloparatide are PTH-pathway analogs, given as a daily subcutaneous injection; the trick is that intermittent PTH exposure stimulates osteoblasts, whereas the continuous exposure of hyperparathyroidism destroys bone. Watch for hypercalcemia, and warn about orthostatic hypotension with the first several doses — the patient should inject where they can sit or lie down immediately. Avoid in patients at baseline increased risk of osteosarcoma (Paget disease, prior skeletal radiation, unexplained elevated alkaline phosphatase). Romosozumab inhibits sclerostin, building bone while also slowing resorption, given monthly for 12 months only — but it carries a boxed warning for myocardial infarction, stroke, and cardiovascular death and must not be used in anyone who has had an MI or stroke within the past year.

Section 3Gout & antiarthritis drugs

Gout: put out the fire, then lower the fuel

Gout is uric acid crystallizing in a joint. Two entirely separate jobs follow, and mixing them up is the classic error. Job one is stopping the acute flare — an anti-inflammatory problem. Job two is lowering serum urate for the long run, which does nothing for today's pain and can even provoke a flare when it starts.

For the flare, three options: an NSAID (naproxen, indomethacin), a corticosteroid (oral, or injected into a single hot joint), or colchicine. Colchicine is the interesting one. It binds tubulin, wrecking the microtubules that neutrophils need in order to crawl into the joint and unleash inflammation. It has no analgesic and no urate-lowering effect at all — it simply keeps the neutrophils away. Modern dosing is low: 1.2 mg at the first hint of a flare, then 0.6 mg one hour later. The signature toxicity is gastrointestinal — nausea, vomiting, and diarrhea are the first sign of toxicity, and the instruction is to stop the drug, not push through. Colchicine is cleared by CYP3A4 and P-glycoprotein, so combining it with clarithromycin, verapamil, diltiazem, cyclosporine, or a strong azole in a patient with kidney impairment has caused fatal marrow suppression and myopathy. Note also that aspirin is avoided in gout: low doses raise urate.

For the long run, allopurinol is the anchor. It inhibits xanthine oxidase, the enzyme that manufactures uric acid, so less is produced. Start low (100 mg, less in kidney disease) and titrate slowly to a serum urate under 6 mg/dL; encourage 2–3 L of fluid daily. Because starting it mobilizes urate and can set off a flare, patients are covered with low-dose colchicine or an NSAID for the first several months. Two allopurinol facts must be reflexes: any rash means stop the drug and call immediately (allopurinol is a leading cause of Stevens–Johnson syndrome, toxic epidermal necrolysis, and DRESS), and allopurinol blocks the metabolism of azathioprine and mercaptopurine, causing life-threatening bone marrow suppression unless those doses are slashed. Febuxostat is an alternative xanthine oxidase inhibitor for allopurinol-intolerant patients, but it carries a boxed warning for cardiovascular death and is second-line. Probenecid takes the other route — it is a uricosuric, blocking urate reabsorption in the renal tubule so more is excreted; it needs decent kidney function and generous fluids, and it is avoided if the patient has a history of stones. Pegloticase, an IV enzyme that dissolves urate directly, is reserved for refractory tophaceous gout: boxed warning for anaphylaxis, and it must never be given in G6PD deficiency (hemolysis, methemoglobinemia) — so screening comes first.

DMARDs: changing the disease, not just the symptoms

Rheumatoid arthritis is not gout and it is not wear-and-tear osteoarthritis — it is an autoimmune attack on the synovium that erodes joints permanently. NSAIDs and steroids make an RA patient feel better while the joints quietly dissolve. Disease-modifying antirheumatic drugs (DMARDs) slow the disease itself, and the guiding principle is to start them early, within weeks of diagnosis, before erosion is done. They work slowly — weeks to months — which is a teaching point, because a patient who expects ibuprofen-speed relief will stop taking them.

Methotrexate is the anchor DMARD and the single most dangerous prescribing error in this chapter. At RA doses it is given once weekly. Taken daily by mistake — and this has happened, and patients have died — it produces catastrophic mucositis and pancytopenia. Confirm the weekly schedule out loud with the patient and with anyone taking a verbal order, and check that the pill bottle and the MAR say weekly. Daily folic acid (usually 1 mg, not on the methotrexate day in some regimens) blunts the mouth sores, GI upset, and marrow effects without blocking the benefit. Methotrexate carries boxed warnings for bone marrow suppression, hepatotoxicity, pulmonary toxicity, and embryo-fetal toxicity — it is contraindicated in pregnancy, and effective contraception is required for both partners. Monitor CBC, LFTs, and creatinine. Teach no alcohol, report a persistent dry cough or dyspnea (pneumonitis) and mouth ulcers (the earliest toxicity sign). Avoid trimethoprim/sulfamethoxazole, which is an additive antifolate and can produce pancytopenia. Leucovorin is the rescue agent.

Among the other conventional DMARDs, hydroxychloroquine is the gentlest — and the one with a memorable rule: it can deposit in the retina, so patients need a baseline and annual eye exam and must report changes in vision or color perception. Sulfasalazine is avoided in sulfa allergy and G6PD deficiency and turns urine orange-yellow (harmless, but tell them). Leflunomide is hepatotoxic and a potent teratogen with a very long half-life, requiring a cholestyramine washout if pregnancy occurs or is planned.

The biologic DMARDs — TNF inhibitors (etanercept, adalimumab, infliximab), plus IL-6, T-cell, and B-cell agents — are extraordinarily effective and share one governing safety idea: they take the brakes off infection. Every patient is screened for latent tuberculosis and hepatitis B before the first dose, boxed warnings cover serious infections and malignancy including lymphoma, live vaccines are contraindicated during therapy, and the drug is held during any active infection and usually around surgery. The oral JAK inhibitors (tofacitinib, baricitinib, upadacitinib) add boxed warnings for major adverse cardiovascular events, thrombosis, malignancy, and mortality.

Section 4Skin drugs

Acne: four problems, four drug jobs

Acne is not dirt. Four things go wrong in a follicle: sebum production rises (androgen-driven), the follicle lining sheds abnormally and plugs the pore, Cutibacterium acnes multiplies behind the plug, and inflammation follows. Every acne drug attacks one of those four, which is exactly why combinations work better than any single agent.

Benzoyl peroxide kills the bacteria by releasing free radicals — and crucially, bacteria do not develop resistance to it. Teach that it bleaches fabric: white towels and pillowcases, or ruined ones. Topical retinoids (tretinoin, adapalene, tazarotene) fix the plugging by normalizing follicular shedding; apply a pea-sized amount at bedtime to dry skin, expect an initial worsening and peeling for several weeks, use non-comedogenic moisturizer, and use sunscreen because they cause photosensitivity. Topical antibiotics (clindamycin, erythromycin) should essentially never be used alone — always pair with benzoyl peroxide to prevent resistance. Oral antibiotics for moderate inflammatory acne are usually doxycycline or minocycline: photosensitivity again, pill-induced esophagitis (full glass of water, stay upright), and contraindicated in pregnancy and in children under 8 (tooth staining). Hormonal options — combined oral contraceptives, spironolactone (monitor potassium) — target the androgen driver.

Isotretinoin is the only drug that hits all four mechanisms, and it is the most tightly controlled drug most nurses will ever handle. It is a severe teratogen, and dispensing runs through the iPLEDGE risk management program: patients who can become pregnant must use two forms of contraception beginning one month before, throughout, and for one month after therapy, with monthly negative pregnancy tests and monthly program authorization. There is no blood donation during therapy or for a month afterward, because a transfused unit could reach a pregnant recipient. Expected effects: cheilitis in nearly everyone (dry cracked lips), dry eyes and nose, epistaxis, myalgia, night-vision changes, elevated triglycerides, and hepatotoxicity — so monitor lipids and LFTs and teach no alcohol. Mood changes should be reported. And a hard rule: never combine isotretinoin with a tetracycline — the pair raises intracranial pressure (pseudotumor cerebri, presenting as headache, visual changes, and nausea).

Psoriasis: turning down an overdriven immune system

Psoriasis is immune-driven hyperproliferation — keratinocytes turning over in days instead of weeks, producing thick silvery plaques. Mild disease is topical: corticosteroids (the workhorse), vitamin D analogs like calcipotriene (do not exceed the weekly maximum — systemic absorption causes hypercalcemia; it is inactivated by salicylic acid, so do not layer them), tazarotene, coal tar, and calcineurin inhibitors (tacrolimus, pimecrolimus ointment) for the face and skin folds where steroids thin the skin. Moderate to severe disease escalates to phototherapy (narrowband UVB; or PUVA, where oral methoxsalen plus UVA requires UV-blocking eyewear for 24 hours after the dose) and systemic drugs: methotrexate, cyclosporine, acitretin (a retinoid, and a teratogen so persistent that pregnancy must be avoided for 3 years after and alcohol is forbidden because it regenerates a long-lived metabolite), apremilast, and the biologics — TNF inhibitors, IL-17 blockers (secukinumab, ixekizumab), and IL-23 blockers (guselkumab, risankizumab). All of the biologics carry the same TB-screening and infection precautions as in rheumatoid arthritis.

Topical corticosteroids: potency, vehicle, quantity, and time

Topical steroids are the most used and most misused drugs in dermatology, and the nursing content is four variables. Potency is ranked in classes from 1 (superpotent, e.g., clobetasol) to 7 (low, e.g., hydrocortisone 1%). Vehicle changes potency for the same molecule: ointments are the most potent because they occlude and hydrate (best for thick, dry, scaly skin), creams are middle-ground and cosmetically acceptable, and lotions, gels, solutions, and foams are for hairy areas and the scalp. Quantity is measured in the fingertip unit — the ribbon squeezed from the tip of an adult index finger to the first crease, about 0.5 g, which covers an area equal to two adult palms. Time matters because effects accumulate.

The adverse effects follow directly from what steroids do. Locally: skin atrophy, striae, telangiectasia, hypopigmentation, acneiform eruption, and tachyphylaxis (the drug stops working, so patients use more, which is the trap). Systemically, absorption is greatest where skin is thin (face, eyelids, genitals), where skin is inflamed and barrier-broken, where the surface area is large, and wherever the site is occluded. Children absorb disproportionately more because their body-surface-to-weight ratio is high. The rule set is short: lowest potency that works, thin layer, shortest duration, no occlusion unless it is ordered, and do not put a potent steroid on the face or in a skin fold.

Section 5Burns & wound agents

Why burns get topical drugs instead of IV antibiotics

A deep burn produces eschar — dead, leathery, and, most importantly, avascular. No blood supply means no delivery: an IV antibiotic cannot reach the bacteria colonizing that surface, because the drug travels in blood and the blood does not go there. So the antimicrobial is put on the wound. Systemic antibiotics in burn care are reserved for documented invasive infection or sepsis, not prophylaxis — prophylactic systemic antibiotics simply select for resistant organisms while the wound surface stays untouched.

Three classic topical agents divide the work, and each has one toxicity that defines it.

Silver sulfadiazine is the traditional workhorse: broad-spectrum, soothing, painless to apply, spread about 1/16 inch thick with a sterile gloved hand. Its defining problem is transient leukopenia, typically appearing two to three days in — so the WBC count gets checked, and a dip is usually self-limiting. It is a sulfonamide, so it is contraindicated in sulfa allergy, and it is contraindicated in infants under 2 months and in near-term pregnancy because it displaces bilirubin and risks kernicterus. It does not penetrate eschar well, and it forms a gray pseudo-eschar that must be cleaned off before reapplication.

Mafenide acetate is the one that penetrates eschar and cartilage, which makes it the agent for burned ears and noses where cartilage is at risk. Two things follow. It hurts — a real burning pain on application, so premedicate. And it is a carbonic anhydrase inhibitor, so it causes metabolic acidosis; the patient compensates by hyperventilating, and a burn patient who becomes tachypneic on mafenide is telling you their pH is falling. Monitor acid-base status and watch the respiratory rate.

Silver nitrate 0.5% solution is applied on wet dressings that must be kept continuously moist (drying concentrates it into a caustic). It stains everything — skin, linens, walls — black or gray, which is alarming but harmless. Its real hazard is that it leaches electrolytes out of the wound: hyponatremia and hypochloremia, plus a risk of methemoglobinemia. Monitor electrolytes.

Getting the dead tissue off

Nothing granulates under slough. Debridement is the removal of nonviable tissue, and it comes in flavors. Autolytic debridement uses the body's own enzymes trapped under a moisture-retentive dressing (hydrogel, hydrocolloid) — painless and selective, but slow, and not for infected wounds. Enzymatic debridement uses collagenase, applied daily; remember it is destroyed by silver and iodine products, so those two cannot share a wound bed. Mechanical debridement — the old wet-to-dry gauze — is nonselective and painful: it rips out healthy granulation along with the slough, and it has largely been abandoned for exactly that reason. Sharp/surgical debridement is fastest and is the standard for extensive burns. Biologic (larval) debridement is a real, occasionally used option for chronic wounds.

What actually heals a wound

The single most important idea in modern wound care is that a moist wound heals faster than a dry one. Old teaching let wounds "air out" and form a scab; we now know epithelial cells migrate across a moist bed and stall at a dry crust. The dressing's job is to hold moisture at the wound while wicking away excess — hence the working shorthand: if it's dry, moisten it; if it's wet, absorb it. Antiseptics deserve the same skepticism you would apply to any drug: full-strength povidone-iodine and hydrogen peroxide are cytotoxic to fibroblasts and have no place being poured routinely into a healing granulating wound.

The nursing work around these agents is as consequential as the agents themselves. Premedicate for pain 30 minutes before a dressing change — burn dressing changes are among the most painful procedures in the hospital, and in the acute phase with massive fluid shifts, analgesia must be given IV, because IM and subcutaneous absorption is unreliable and doses stack up unabsorbed until perfusion returns. Maintain strict aseptic technique, since the burn patient's greatest threat after the first 48 hours is infection. Verify tetanus status on every wound. Support nutrition aggressively — protein and calories are literally the raw material for granulation, and healing fails without them.

ReferenceWords worth knowing

A quick reference for the terms in this chapter — skim it now, or circle back whenever a word trips you up.

Antiresorptive

A drug that slows bone breakdown by suppressing osteoclasts; bisphosphonates, denosumab, raloxifene, and calcitonin. Contrast with anabolic drugs, which build new bone.

Atypical femoral fracture

A transverse fracture of the femoral shaft associated with long-term antiresorptive therapy, typically preceded for weeks by dull thigh or groin pain — a symptom patients must be taught to report.

Bisphosphonate

A drug that binds bone mineral and triggers osteoclast apoptosis when the cell resorbs it; first-line for osteoporosis, and requiring strict upright, empty-stomach, plain-water administration.

Calcitriol

1,25-dihydroxyvitamin D — the fully activated hormone form of vitamin D, produced by the kidney. Given directly when the kidney can no longer perform that step.

Debridement

Removal of nonviable tissue from a wound; may be autolytic, enzymatic, mechanical, sharp/surgical, or biologic.

Disease-modifying antirheumatic drug (DMARD)

A drug that slows the underlying autoimmune joint destruction of rheumatoid arthritis rather than only relieving symptoms; works over weeks to months and is started early.

Elemental calcium

The amount of usable calcium in a supplement, as opposed to the total salt weight — roughly 40% for calcium carbonate and 21% for calcium citrate.

Eschar

Dead, leathery, avascular tissue over a deep burn; because no blood reaches it, systemic antibiotics cannot treat its surface bacteria.

Fingertip unit

The ribbon of topical medication from an adult fingertip to the first crease (about 0.5 g), which covers an area equal to two adult palms — the standard way to teach quantity.

Hypercalcemia

Serum calcium above the normal range, producing "stones, bones, groans, thrones, and psychiatric overtones," constipation, lethargy, and a shortened QT interval.

Osteoblast

The bone-building cell that lays down and mineralizes new matrix, and that also secretes RANKL and osteoprotegerin to regulate osteoclasts.

Osteoclast

The bone-resorbing cell that dissolves mineral and releases calcium into the blood; the target of every antiresorptive drug.

Osteonecrosis of the jaw (ONJ)

Exposed, non-healing jaw bone associated with bisphosphonates and denosumab, most often triggered by dental extraction — hence dental clearance before therapy.

Parathyroid hormone (PTH)

The hormone that raises serum calcium by resorbing bone, increasing renal calcium reabsorption, and activating vitamin D; its analogs, given intermittently, build bone.

Photosensitivity

Exaggerated sunburn response caused by a drug; expected with retinoids, tetracyclines, and several other agents in this chapter, and managed with sunscreen and covering clothing.

RANK ligand (RANKL)

The signal from osteoblasts that drives osteoclast maturation and bone resorption; blocked naturally by osteoprotegerin and pharmacologically by denosumab.

Retinoid

A vitamin A derivative that normalizes epithelial turnover; topical (tretinoin, adapalene) or systemic (isotretinoin, acitretin). All are photosensitizing and the systemic ones are potent teratogens.

Selective estrogen receptor modulator (SERM)

A drug that acts as an estrogen agonist in some tissues and an antagonist in others; raloxifene builds bone and blocks breast tissue while carrying estrogen's clot risk.

Teratogen

A substance that causes fetal malformation. Isotretinoin, acitretin, methotrexate, and leflunomide are among the most dangerous teratogens a nurse will handle.

Tophus

A visible deposit of urate crystals in soft tissue, seen in chronic untreated gout; its presence signals long-standing hyperuricemia needing urate-lowering therapy.

Uricosuric

A drug that lowers serum urate by increasing renal excretion rather than reducing production; probenecid is the prototype, and it requires adequate kidney function and generous fluids.

Xanthine oxidase inhibitor

A drug that blocks the enzyme making uric acid, lowering urate at the source; allopurinol is the prototype and febuxostat the alternative.