Compare and Compare Aspirin and Morphine

Morphine is class of drugs called opioid which possibly cause change in feeling, physical dependence, tolerance and worthwhile results which would eventually cause medicine dependence. Oipoid drugs have influence on both central and peripheral nervous systems. In central anxious systm opioids have results on spinal-cord and other parts of CNS. In peripheral anxious system opioid have ramifications of nerve structure under coating muscles within oesophagus and submucous plexus in the wall structure of gud which causes constipation. Within pheriphral anxious system, opioids decrease the inflammation.

Opioid receptors

The main ramifications of opioids are on neurons where they react on receptors present on neuronal cell membranes. The main opioids receptors are mu, delta and kappa. These receptors are part of large family of receptors that have 7 transmembrane-spanning domains of amino acids.

The naturally occurring ligands for opioid receptors are; b endorphin binds with mu receptor, the enkephalins binds with delta receptor and dynorphin binds with kappa receptors. Morphine has relatively increased affinity for mu receptor. Analgesic result is produced when opioid binds to the above 3 receptors.

All three opioid receptors are coupled with G-proteins. The G-protein consists of three subunits alpha, beta and gamma. At relaxing talk about guanosine diphosphate (GDP) are in contact with alpha subunit. If the opioids binds with receptor the guanosine diphosphate (GDP) changes to guanosine triphosphate (GTP). This consequently causes conformational changes which dissociate the opioid from receptor. At the same time alpha subunit attached with guanosine triphosphate (GTP) dissociate from beta and gamma subunits and binds to the effectors, which produce mobile responce. This cause dissociation of alpha subunit from guanosine triphosphate (GTP), alpha subunit binds again with beta and gamma and form the complex. guanosine triphosphate (GTP) convert back to guanosine diphosphate (GDP).

There a wide range of different type of G-proteins found but the G-protein to which the opioid receptors combined mainly produce inhibitory effects in neurons.

Sites of action of opioids on neurons

The main action of opioids is at pre and postsynaptic neurons. The effect of opioids on postsynaptic neuron is mainly being inhibitory. Whereas the primary action of opioids on presynaptic neuron will be inhibiting the discharge of neurotransmitter and that is the main influence on nervous system. However the overall effect of opioids in brain is depend on both presynaptic neurons on both excitatory and inhibitory neurons and its post synoptic effect. Including the inhibition of presynoptic nuron may cause excitatory effects in the next neuron if the neurotransmitter normally produce the inhibitory results nevertheless the inhibition of post synaptic neuron cause these excitatory result not to take place. Which means location of and density of opioid receptor on the target neuron describe the overall effect of opioids on the neuron.

There are many diffrent kind of nurons with in nervous system which can be diffrent in proportions, condition, function and the chemical mother nature of the neurotransmitters released from other terminals to carry information to other neurons. Howeven morphine by functioning on mu receptors cause inhibition in release of of several diffrent type of nurotransmitters such as noradrenaline, acetylcholine and the neuropeptide, material P.

It has been proven that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory impulses, pain modulation can carry on downstream.

Pain pathways

Pain is associated with stimulation in principal sensory neurons triggered by strong mechanised or thermal stimuli, or the relese of chemicals by broken tissues or swelling. In event of pain the principal sesory neurons release element P and glutamate in the dorsal horn of the spinal-cord. The impulses are then send to brain by the spinothalamic tracts. This ascending information can trigger descending pathways, from the midbrain periaqueductal greyish area, which exert an inhibitory control over the dorsal horn.

The opioid receptor are situated in diffrent parts of the pain transmitting pathway and have contron over most important afferent neurons, spinal-cord, midbrain and thalamus. The analgesic ramifications of opioid drugs is brought on by their effects on at diffrent degrees of anxious system specially inhibition of neurotransmitter release from the primary afferent terminals in the spinal-cord and activation of descending inhibitory handles in the midbrain.

The device of pain pathway involve ongoing activity in nociceptive pathways may cause changes in the degrees of neurotransmitters in main afferent neurons and changes in awareness to opioid analgesia. The nuropathic pain is mainly caused by decrease in opioid sensitivity, while inflammatory pain is induced by increase in level of sensitivity of opioids.

Inhibition of neurotransmitter releasese

The nerotransmitter are released by depolarisation of presynoptic nerve terminal. This is triggered by Ca++ ion entery via voltage-sensitive Ca++ programs. The nurotransmitter release could be reduced by immediate inhibition of the voltage gated chennels. Another way to inhibit nerotransmitter release is to increasing the outward K + current which therefore cause shortening repolarisation time and the duration of the action probable. Opioids create both these results as the receptors are in conjunction with G-protien directly to K+ stations and voltage-sensitive Ca++ programs. or by inhibiting adenylate cyclase (AC), the enzyme which converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP).

Clinical benefits

Morphine is a narcotic pain management agent suggested for the pain relief in patients who require opioid analgesics for more than a few days.

However use of morphine for less severe persistent pain is a subject of considerable argument. Until just lately the opoids were only been used for acute pain and malignancy pain syndromes. The use of opioids in less severe prolonged pain was regarded as less effective with too many risks. The primary anxieties were development of tolerance to drug, medical misuse etc. how ever recent studies show that prescribing of opioids for permanent in these band of patients is common. Open up label clinical studies and different surveys have shown security and efficiency of opioids in patients with less severe persistent pain

Up to recently many research and controlled trail have shown effectiveness of opioids in the treatment of less severe continual pain such as rear pain, post-herpetic neuralgia, and unpleasant peripheral neuropathy. The studies have shown the direct analgesic activities of opioids to reduce the unpleasantness of pain. In the treating chronic low back again pain, transdermal fentanyl significantly decreased pain and upgraded functional impairment.

Controlled-release dental opioids were more effective than tricyclic antidepressants in decreasing the pain of post-herpetic neuralgia. Other studies have documented the presence of opioid receptors in the peripheral tissues activated by irritation. These studies suggest a job for opioids in the treatment of persistent inflammatory diseases such as rheumatoid arthritis and connective tissue disorders.

The effects of opioids in treatment of non-inflammatory musculoskeletal conditions were researched. Oral handled release morphine was performed in patients with serious regional, soft structure musculosketal pain conditions which were protected to codeine, anti-inflammatory agencies and anti-depressants. Although patients experienced a decrease in pain, they didn't experience significant subconscious or practical improvement

For the following TWO drugs illustrate the mechanism of action and exactly how these agents are being used therapeutically.

  • Morphine
  • Aspirin

Include specific information on the action of these agents, the nature of the disease and how the drug's effect causes clinical benefits.


Aspirin belongs to class of drugs called Non Steroidal Anti Inflammatory Drugs (NSAIDs) which work by blocking to normal activity of a type of enzymes called Cyclo-Oxygenase (COX) enzymes. These enzymes are in charge of production of Prostaglandins and Thromboxanes that are effective mediators of infection. A couple of two main kind of COX enzymes COX1 and COX2 which convert a substrate known as arachidonic acid in to Prostaglandins and Thromboxanes. Each Prostaglandins and Thromboxanes have different role in various part of body

Main role of Prostaglandins in hypothalamus of brain is temperature regulation where as in stomach the key role is to protection the gastrointestinal tract. Main function of COX 1 consists of development of prostaglandin which handles the discharge of mucus from abdominal coating and protect belly wall membrane from acid environment of belly. Whereas COX 2 enzymes are mainly involve in development of inflammation due to action of prostaglandin by increasing sensitivity of pain receptor in pores and skin and alteration of body's temperature due to effects at hypothalamus.

The healing goals are attained by blocking these enzymes include anti-inflammatory, analgesic and antipyretic. Each kind of NSAID differs in their function both chemically and structurally. Drugs such as aspirin stop activity of both COx1 and COX 2 enzyme where as the celecoxib would only block activity of COX1 enzymes. The connections with COX enzyme for every single type of NSAID is also different for example aspirin bind with the COX enzyme irreversibly while the ibuprofen bind reversibly.

Aspirin have active component salicylates. The main function of aspirin is to block the COX1 and COX2 enzymes and therefore inhibit the development of prostaglandin and thromboxanes. That is achieved by acetilation of any serine residue within the active site of enzymes. As action of aspirin on COX enzymes is reversible there throughout action mainly rely upon the re-synthesis of COX enzymes by body.

The main function of COX 1 enzyme is to catalysis the creation of prostaglandin which causes blood clot. Therefore the inhibiting effect of COX1 enzymes contributes to reduction in blood clot formation. The inhibition of COX1 enzymes also lead to lessen in protecting prostaglandin, which protect abdominal coating from acid environment. This might cause the gastrointestinal part effects.

The beneficial effects are mainly achieved by inhibition of COX2 enzymes which brings about reduces development of prostaglandins which are mainly accountable for inflammation and swelling. The effect also involves decrease in mild pain due to swelling. The prostaglandin made by COX2 enzymes also have results temperature regulatory centre in the hypothalamus of brain. Beneficial results involve providing the high body temperature of body back again to normal.

Clinical benefits

Aspirin is one of the most widely used over the counter analgesic. The primary uses include decrease in slight pain of skeletal, muscular and post operative pain. They have advantages over opioid drugs which cause medication dependency.

Small doses of aspirin tend to be used in patients with risky of following conditions:

  • Formation of blood clot anticipated to thrombus which eventually cause blockage of blood vessels and could also break of and travel in blood to obstruct smaller blood vessels to create embolism.
  • Cardiovascular disease angina which entail reduction of blood circulation to heart and soul muscle and which finally cause death of this muscle of heart. Therefore decrease in blood clotting will reduce the risk.
  • Ischemic strokes that will mainly induced by embolism. The tiny arteries in brain will be obstructed there oxygen supply compared to that part of brain will be reduced. This can ultimately have effect on motor unit function.
  • These problems are associated with high hazards as they involve major organs of body center and brain. Therefore if left untreated you will see a severe reduction in supply of nutrients which contributes to death tissue.

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