Pain

Ibuprofen — Has analgesic, antipyretic and anti-inflammatory effects. The selected label says the mechanism is not fully understood and may involve inhibition of prostaglandin synthesis.

Hydrocodone / Acetaminophen — Hydrocodone is a full opioid agonist with relative mu-receptor selectivity. Although its analgesia has no defined ceiling, respiratory and CNS adverse effects limit dosing. Acetaminophen has a separate analgesic action thought to involve central pathways; its precise mechanism is not established.

Oxycodone — A full opioid agonist with relative mu-receptor selectivity and analgesic activity. Although there is no defined ceiling for analgesia, respiratory and CNS adverse effects limit dosing.

Aspirin — Aspirin inhibits prostaglandin synthesis and platelet aggregation through cyclooxygenase acetylation; its irreversible platelet COX-1 inhibition reduces thromboxane A2 formation.

Tramadol — Binds mu-opioid receptors and weakly inhibits reuptake of norepinephrine and serotonin; metabolite M1 is a more potent mu agonist.

Acetaminophen — Precise mechanism not established; analgesic and antipyretic effects thought to involve mainly central actions.

Naproxen — Has analgesic, anti-inflammatory and antipyretic effects. The mechanism is not completely understood but involves COX-1 and COX-2 inhibition; reduced prostaglandin production may contribute.

Oxycodone / Acetaminophen — Oxycodone is a full opioid agonist with relative mu-receptor selectivity; its analgesic action involves CNS opioid receptors. Although analgesia has no fixed ceiling, clinical dosing is limited by toxicity including respiratory/CNS depression. Acetaminophen has an unestablished analgesic mechanism thought to involve central actions.

Celecoxib — Has analgesic, anti-inflammatory and antipyretic effects; its mechanism is believed to involve reduced prostaglandin synthesis, primarily through COX-2 inhibition.

Diclofenac — Has analgesic, anti-inflammatory and antipyretic effects. The mechanism is incompletely understood but involves COX-1/COX-2 inhibition and reduced prostaglandin synthesis.

Diclofenac — The mechanism is not completely understood but involves inhibition of COX-1 and COX-2. Diclofenac inhibits prostaglandin synthesis in vitro; reduced peripheral prostaglandins may contribute to its analgesic and anti-inflammatory effects.

Acetaminophen / Codeine — Codeine is a mu-opioid agonist with weaker receptor affinity than morphine. Conversion to morphine may explain its analgesia, but the exact mechanism is unknown. Acetaminophen’s analgesic mechanism is not established and is thought to involve central actions.

Butalbital / Acetaminophen / Caffeine — Fixed combination for tension headache; the role of each component is incompletely understood.

Morphine — Full opioid agonist relatively selective for mu receptors. There is no ceiling for analgesia, but respiratory and CNS depression limit dosing; the precise analgesic mechanism is unknown.

Ketorolac — NSAID analgesic with an incompletely understood mechanism that may involve prostaglandin-synthetase inhibition.

Lidocaine — Amide local anesthetic suggested to stabilize neuronal membranes by inhibiting ionic fluxes needed to initiate and conduct impulses.

Each summary is the mechanism line from the medicine’s study card.

Listed most often on cards in this body system

Used for

Primary dysmenorrhea · 3/16: Ibuprofen, Naproxen, Celecoxib

Same boxed-warning wording on: Naproxen, Celecoxib

An item counts as shared only when both cards use the same wording. If a card does not list an item, that is not a statement that the effect never occurs.

Pain

Drug classes in this body system

Nonsteroidal anti-inflammatory drugs

Opioid analgesics

How each medicine works

Listed most often on cards in this body system

Used for

Common side effects

Interactions

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