Pain Relief Drug List

Over-the-Counter Pain Relievers

Over-the-counter (OTC) pain relievers include:


Both acetaminophen and NSAIDs reduce fever and relieve pain caused by muscle aches and stiffness, but only NSAIDs can also reduce inflammation (swelling and irritation). Acetaminophen and NSAIDs also work differently. NSAIDs relieve pain by reducing the production of prostaglandins, which are hormone-like substances that cause pain. Acetaminophen works on the parts of the brainthat receive the “pain messages.” NSAIDs are also available in a prescription strength that can be prescribed by your physician.

Using NSAIDs increase the risk of heart attack or stroke and have also been known to cause stomach ulcers and bleeding. They can also cause kidney problems.

Topical pain relievers are also available without a doctor’s prescription. These products include creams, lotions, or sprays that are applied to the skin in order to relieve pain from sore muscles and arthritis. Some examples of topical pain relievers include Aspercreme, Ben-Gay, Icy Hot, and Capzasin-P.

Prescription Pain Relievers

Prescription pain relievers include:

  • Corticosteroids
  • Opioids
  • Antidepressants
  • Anticonvulsants (anti-seizure medications)
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Lidocaine patches

Prescription corticosteroids provide relief for inflamed areas of the body by easing swelling, redness, itching and allergic reactions. Corticosteroids can be used to treat allergies, asthma and arthritis. When used to control pain, they are generally given in the form of pills or injections that target a certain joint. Examples include: prednisone, prednisolone, and methylprednisolone.

Opioids are narcotic pain medications that contain natural, synthetic or semi-synthetic opiates. Opioids are often used for acute pain, such as short-term pain after surgery. Some examples of opioids include:


Opioids are effective for severe pain and do not cause bleeding in the stomach or other parts of the body, as can some other types of painrelievers. It is rare for people to become addicted to opioids if the drugs are used to treat pain for a short period of time.

Antidepressants are drugs that can treat pain and/or emotional conditions by adjusting levels of neurotransmitters (natural chemicals) in the brain. These medications can increase the availability of the body’s signals for well-being and relaxation, enabling pain control for some people with chronic pain conditions that do not completely respond to usual treatments. Research suggests antidepressants work best for neuropathic or nerve pain.

Chronic pain conditions treated by low-dose antidepressants include some types of headaches (like migraines) and menstrual pain. Some antidepressant medications include:

  • Selective serotonin reuptake inhibitors (SSRIs) such as citalopram(Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft)
  • Tricyclic antidepressants such as amitriptyline, desipramine(Norpramin), doxepin (Silenor), imipramine (Tofranil), and nortriptyline(Pamelor)
  • Serotonin and norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta)

Anticonvulsants are drugs typically used to treat seizure disorders. Some of these medications are shown to be effective in treating pain as well. The exact way in which these medicines control pain is unclear but it is thought that they minimize the effects of nerves that cause pain. Some examples include carbamazepine (Tegretol), gabapentin (Neurontin), and pregabalin (Lyrica).

Acetaminophen Mechanism of action

Paracetamol (acetaminophen) is generally considered to be a weak inhibitor of the synthesis of prostaglandins (PGs). However, the in vivo effects of paracetamol are similar to those of the selective cyclooxygenase-2 (COX-2) inhibitors.


Paracetamol also decreases PG concentrations in vivo, but, unlike the selective COX-2 inhibitors, paracetamol does not suppress the inflammation of rheumatoid arthritis. It does, however, decrease swelling after oral surgery in humans and suppresses inflammation in rats and mice.

Paracetamol is a weak inhibitor of PG synthesis of COX-1 and COX-2 in broken cell systems, but, by contrast, therapeutic concentrations of paracetamol inhibit PG synthesis in intact cells in vitro when the levels of the substrate arachidonic acid are low (less than about 5 mumol/L). When the levels of arachidonic acid are low, PGs are synthesized largely by COX-2 in cells that contain both COX-1 and COX-2.

Thus, the apparent selectivity of paracetamol may be due to inhibition of COX-2-dependent pathways that are proceeding at low rates. This hypothesis is consistent with the similar pharmacological effects of paracetamol and the selective COX-2 inhibitors. COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant.

There is considerable evidence that the analgesic effect of paracetamol is central and is due to activation of descending serotonergic pathways, but its primary site of action may still be inhibition of PG synthesis. The action of paracetamol at a molecular level is unclear but could be related to the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase.

Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects.

While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme’s active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2.

This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.

Acetaminophen Drug Interactions (5)

1 2 3 142