For example, when one takes aspirin or ibuprofen does the chemical get dispersed to all pain receptor? My question really is, how does the chemical know where to target in the body? I figure wherever there is pain in the body that a certain signal is being produced; which possibly acts as a chaperone to direct the medication chemical where to bind and inhibit.
No, orally taken painkillers act systemically.
Taking a painkiller orally results in the drug being taken up into the bloodstream by the digestive system. From there it can potentially reach all tissues.
In other words, a pain response does not act as a chaperone. A hypothetical drug that would home in on tissues with a pain response, while avoiding unaffected tissues would be the ultimate painkiller, if it existed.
EDIT: To emphasize that painkillers act systemically I will elaborate on aspirine's pharmacokinetics. Notably, aspirine's actions are not restricted to the pain centers in the brain, and I quote the following excerpt from Wiley's interactive Concepts in Biochemistry]1:
Aspirin's analgesic and anti-inflammatory effects are due to the drug's ability to stop the production of prostaglandins that cause tissue swelling and pain.
Aspirin's antipyretic (fever-reducing) effect is due to its direct action on the hypothalamus gland, which results in vasodilation of peripheral blood vessels and sweating.
Prostaglandins are also the key mediators of platelet aggregation. By modifying the COX enzymes within platelets, aspirin causes platelets to lose the "stickiness" that is needed to stimulate blood clotting.
Hence, by these examples it can be seen that aspirine works in the periphery (wound swelling and pain), centrally (brain's hypothalamus) as well as in the bloodstream. Hence, aspirine (and other orally administered painkillers) do not target specific areas in the body, and most certainly not only the brain.
There are such targeted drugs, however. An interesting one is carbamezipine, an anti-epileptic that blocks Na+ channels. It blocks Na+ channels only when they are in an active conformation, however (i.e., engaged in action potential firing). Epileptic activity is basically paroxysmal (massive), synchronous over-activity in the brain that is accompanied by massive Na+ channel activity. Hence, epileptic activity will in effect trigger the drug into action.
Most NSAIDs derive their analgesic effects from inhibit the cyclooxygenase (COX) enzymes that produce the prostaglandin-H2 precursor to the prostaglandins that sensitize neurons to pain.
Edit: With respect to where this takes place, the COX enzymes are expressed in inflamed tissues as well as constitutively in the stomach and kidney. The prostaglandins whose production they block act on the spinal nerves and can diffuse across the blood-brain barrier.