Pain killers - analgesics

[murulidhara]

I want to know how pain killers like analgin , stop pain. Do they really removel pain or work on our nervous system to block the sense of pain. ?

 

What is the diference between sedatives and analgesics?

[ecoli]

I don't think any two analgesic works the same why on our nervous systems. http://en.wikipedia.org/wiki/Analgesic

 

Sedatives, I believe work solely on the central nervous system and, generally, the effect is stronger than an analgesic. Unlike analgesics, they don't directly control pain, but rather control feelings of anxiety. I believe they're more easily addictive as well.

http://en.wikipedia.org/wiki/Sedative

[lucaspa]

Ecoli is right. Different analgesics work by different mechanisms. Aspirin belongs to a general group called "NSAIDS" and work by inhibiting the enzyme cyclooxygenase (Cox). Cox is necessary to make prostaglandins, which work at the level of the nerve endings. Without prostaglandins, the nerve endings don't sense pain.

 

Morphine and its derivatives work in the brain. They bind to the endorphin receptors, which trigger them and gives a sense of well-being, pleasure, and blocks pain perception. Runners do this by releasing endorphins as they run, which is why they have a "runner's high".

 

Other analgesics work by other mechanisms.

 

Sedatives render a patient unconscious.

[Revenged]

I want to know how pain killers like analgin , stop pain. Do they really removel pain or work on our nervous system to block the sense of pain.

 

Analgesics work by blocking the path pathways...

 

The major pain pathway is the spinothalamic tract... Nerve impulses travel via a sensory nerve to the spinal cord, then to the brain (first the thalamus then to the somatosensory cortex)...

 

Analgesics can work by inhibiting activation of sensory nerves or central nerves via different mechananisms...

 

What is the diference between sedatives and analgesics?

 

Analgesics stop pain whereas sedatives put you to sleep or make you calm...

 

Sedatives include benzodiazepines... short acting ones like diazepam (Valium) to reduce anxiety and long-acting ones like temazepam to put you to sleep... both works on GABA A receptors...

 

You also get major tranquillizers for schizophrenics... e.g. chlorprozamine...

 

Barbituates for induction of anasthesia... e.g. thiopentone...

 

Ecoli is right. Different analgesics work by different mechanisms. Aspirin belongs to a general group called "NSAIDS" and work by inhibiting the enzyme cyclooxygenase (Cox). Cox is necessary to make prostaglandins, which work at the level of the nerve endings. Without prostaglandins, the nerve endings don't sense pain.

 

Morphine and its derivatives work in the brain. They bind to the endorphin receptors, which trigger them and gives a sense of well-being, pleasure, and blocks pain perception. Runners do this by releasing endorphins as they run, which is why they have a "runner's high".

 

The mechanisms of action are complicated... Non-steroidal anti-inflammatories do inhibit the COX enzyme, they stop prostaglandin production but their main effect (as the name suggests) is to prevent inflammation... it's the inflammation that causes the activation of sensory nerve fibres... btw, i'm pretty sure that nerves sense pain without prostaglandins... NSAIDs are one of the least effect analgesic agents...

 

Morphine works on the central nervous system and acts on mu opioid receptors... Opioid receptors are inhibitory receptors that prevent activation of second order neurones within the spinothalamic tract, which is how they cause almost totaly analgesia... Morphine also causes release of endogenous opioids (such as endophins) that have an additive effect... it also causes release of other neurotransmitters e.g. the 'sense of well-being' is disinhibition of GABA neurones causing dopamine release within reward centres of the brain...

 

 

I would just like to point out that there are quite a lot of drugs that we don't fully know the mechanism for and some we have no idea how they work... This is especially true for drugs that have actions within the central nervous system...

[lucaspa]

The mechanisms of action are complicated... Non-steroidal anti-inflammatories do inhibit the COX enzyme, they stop prostaglandin production but their main effect (as the name suggests) is to prevent inflammation... it's the inflammation that causes the activation of sensory nerve fibres..

 

and what do you think the major stimulator of local inflammation is? Prostaglandin! Prostaglandins also stimulate substance P, which is a direct stimulator of peripheral sensory nerves. So, blocking prostaglandin also blocks stimulation of the nerves

 

Morphine works on the central nervous system and acts on mu opioid receptors.

 

Which are the receptors for endorphins! The reason the receptors were called "opioid" was because opioids were known long before endorphins were discovered. The natural ligands for the receptors are the endorphins. The names should have been "endorphin" receptors.

 

Morphine also causes release of endogenous opioids (such as endophins) that have an additive effect.

 

True. More molecules to bind to the same receptors.

 

it also causes release of other neurotransmitters e.g. the 'sense of well-being' is disinhibition of GABA neurones causing dopamine release within reward centres of the brain...

 

Very good. Altho your description is somewhat overly complex. ("disinhibition" is a somewhat awkward term. ) What happens is that morphine inhibits the release of GABA. Without GABA to inhibit the release of dopamine in dopaminergic neurons (those that use dopamine as a transmitter), the result is increased release of of dopamine.

http://www.portfolio.mvm.ed.ac.uk/studentwebs/session6/54/opioids.html

http://www.anesth.utmb.edu/cohen/DRUG%20HANDOUT.htm

[Revenged]

ok, sorry if i misunderstood you there... i've never heard of mu opioid receptors been called endophin receptors before but they are certainly the same thing... and prostaglandins are inflammatory mediators - they seem to do just about everything if i remember correctly...

 

i did a libary project on opioids last year and that's the reason i know about it... one thing i found particularly interesting is the research into polymorphisms of the mu opioid (endorphin) receptor... i thought it was quite interesting because resent research showed that people with different polymorphisms of the receptor required very different amounts of morphine to get total analgesia from cancer pain... the difference was quite dramatic... such research is important because it gives a physiological explanation behind why some people require more analgesia than others and it is not purely a psychological responce (as was previously assumed)... the eventual implication for practice may mean that may doctors will be able to adapt medication matched to their particular receptor

polymorphisms...

 

references...

 

Klepstad P., Rakvåg T.T., Kaasa S., Holthe M., Dale O., Borchgrevink P.C., Baar C., Vikan T., Krokan H.E., Skorpen F., The 118 A > G polymorphism in the human µ-opioid receptor gene may increase morphine requirements in patients with pain caused by malignant disease, Acta Anaesthesiologica Scandinavica, Vol. 48., (2004), pp. 1232.-1239.

 

Rakvag T.T., Klepstad P., Baar C., Kvam T.M., Dale O., Kaasa S., Krokan H.E., Skorpen F., The Val158Met polymorphism of the human catechol-O-methyltransferase (COMT) gene may influence morphine requirements in cancer pain patients., Pain, 1116, 2005, p 73.78.