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Compare and Contrast Aspirin and Morphine

Paper Type: Free Essay Subject: Biology
Wordcount: 2065 words Published: 29th May 2018

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Morphine is class of drugs called opioid which potentially cause change in mood, physical dependence, tolerance and rewarding effects which would eventually cause drug dependence. Oipoid drugs have effect on both the central and peripheral nervous systems. In central nervous systm opioids have effects on spinal cord and other parts of CNS. In peripheral nervous system opioid have effects of nerve tissue under lining muscles within oesophagus and submucous plexus in the wall of gud which causes constipation. Within pheriphral nervous system, opioids reduce the inflammation.

Opioid receptors

The main effects of opioids are on neurons where they act 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 which 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 comparatively greater affinity for mu receptor. Analgesic effect is produced when opioid binds to any of 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 resting state guanosine diphosphate (GDP) are in contact with alpha subunit. When the opioids binds with receptor the guanosine diphosphate (GDP) changes to guanosine triphosphate (GTP). This as a result 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 cellular responce. This cause dissociation of alpha subunit from guanosine triphosphate (GTP), alpha subunit binds back with beta and gamma and form the complex. guanosine triphosphate (GTP) convert back to guanosine diphosphate (GDP).

There are many different type of G-proteins found but the G-protein to which the opioid receptors coupled 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 main action of opioids on presynaptic neuron will be inhibiting the release of neurotransmitter and that is the main effect 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. For example the inhibition of presynoptic nuron may cause excitatory effects in the next neuron if the neurotransmitter normally produce the inhibitory effects however the inhibition of post synaptic neuron cause these excitatory effect not to occur. Therefore the location of and density of opioid receptor on the target neuron describe the overall effect of opioids on the neuron.

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There are many diffrent type of nurons with in nervous system which are diffrent in size, shape, function and the chemical nature of the neurotransmitters released from their terminals to carry information to other neurons. Howeven morphine by acting on mu receptors cause inhibition in release of of many diffrent type of nurotransmitters such as noradrenaline, acetylcholine and the neuropeptide, substance P.

It has been shown that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream.

Pain pathways

Pain is linked with stimulation in primary sensory neurons caused by strong mechanical or thermal stimuli, or the relese of chemicals by damaged tissues or inflammation. In event of pain the primary sesory neurons release substance 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 activate descending pathways, from the midbrain periaqueductal grey area, which exert an inhibitory control over the dorsal horn.

The opioid receptor are located in diffrent parts of the pain transmission pathway and have contron over primary afferent neurons, spinal cord, midbrain and thalamus. The analgesic effects of opioid drugs is caused by their effects on at diffrent levels of nervous system specially inhibition of neurotransmitter release from the primary afferent terminals in the spinal cord and activation of descending inhibitory controls in the midbrain.

The mechanism of pain pathway involve ongoing activity in nociceptive pathways will cause changes in the levels of neurotransmitters in primary afferent neurons and to changes in sensitivity to opioid analgesia. The nuropathic pain is mainly caused by reduction in opioid sensitivity, where as inflammatory pain is caused by increase in sensitivity of opioids.

Inhibition of neurotransmitter releasese

The nerotransmitter are released by depolarisation of presynoptic nerve terminal. This is caused by Ca++ ion entery via voltage-sensitive Ca++ channels. The nurotransmitter release could be reduced by direct inhibition of these voltage gated chennels. Another way to inhibit nerotransmitter release is to increasing the outward K + current which as a result cause shortening repolarisation time and the duration of the action potential. Opioids create both these effects as the receptors are coupled with G-protien directly to K+ channels and voltage-sensitive Ca++ channels. 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 indicated for the relief of pain 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 debate. Until recently the opoids were only been used for acute pain and cancer pain syndromes. The use of opioids in less severe persistent pain was thought to be less effective with too many risks. The main fears were development of tolerance to drug, medical abuse etc. how ever recent studies have shown that prescribing of opioids for long term in these group of patients is common. Open label clinical trials and different surveys have shown safety and effectiveness of opioids in patients with less severe persistent pain

Up to recently many surveys and controlled trail have shown usefulness of opioids in the treatment of less severe persistent pain such as back pain, post-herpetic neuralgia, and painful peripheral neuropathy. The studies have shown the direct analgesic actions of opioids to reduce the unpleasantness of pain. In the treatment of chronic low back pain, transdermal fentanyl significantly decreased pain and improved functional disability.

Controlled-release oral 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 inflammation. These findings suggest a role for opioids in the treatment of chronic inflammatory diseases such as rheumatoid arthritis and connective tissue disorders.

The effects of opioids in treatment of non-inflammatory musculoskeletal conditions were studied. Oral controlled release morphine was performed in patients with chronic regional, soft tissue musculosketal pain conditions that were resistant to codeine, anti-inflammatory agents and anti-depressants. Although patients experienced a decrease in pain, they did not experience significant psychological or functional improvement

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

  • Morphine
  • Aspirin

 Include precise details of the action of these agents, the nature of the disease and how the drug’s effect leads to 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 responsible for production of Prostaglandins and Thromboxanes which are potent mediators of inflammation. There are two main type 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 different part of body

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Main role of Prostaglandins in hypothalamus of brain is temperature regulation where as in stomach the main role is to protection the gastrointestinal tract. Main function of COX 1 involves production of prostaglandin which controls the release of mucus from stomach lining and protect stomach wall from acid environment of stomach. Whereas COX 2 enzymes are mainly involve in production of inflammation due to action of prostaglandin by increasing sensitivity of pain receptor in skin and alteration of body temperature due to effects at hypothalamus.

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

Aspirin have active ingredient salicylates. The main function of aspirin is to block the COX1 and COX2 enzymes and therefore inhibit the production of prostaglandin and thromboxanes. This is achieved by acetilation of a serine residue within the active site of enzymes. As action of aspirin on COX enzymes is reversible there for the duration of action mainly depend on the re-synthesis of COX enzymes by body.

The main function of COX 1 enzyme is to catalysis the production of prostaglandin which leads to blood clot. Therefore the inhibiting effect of COX1 enzymes leads to reduction in blood clot formation. The inhibition of COX1 enzymes also lead to reduce in protective prostaglandin, which protect stomach lining from acid environment. This would cause the gastrointestinal side effects.

The beneficial effects are mainly achieved by inhibition of COX2 enzymes which leads to reduces production of prostaglandins which are mainly responsible for inflammation and swelling. The effect also involves reduction in mild pain due to inflammation. The prostaglandin produced by COX2 enzymes also have effects temperature regulatory centre in the hypothalamus of brain. Beneficial effects involve bringing the high body temperature of body back to normal.

Clinical benefits

Aspirin is one of the most widely used over the counter analgesic. The main uses include reduction in mild pain of skeletal, muscular and post operative pain. It has advantages over opioid drugs which cause drug dependency.

Small doses of aspirin are often used in patients with high risk of following conditions:

  • Formation of blood clot due to thrombus which eventually cause blockage of blood vessels and may also break of and travel in blood to block smaller blood vessels which is called embolism.
  • Cardiovascular disease angina which involve reduction of blood supply to heart muscle and which ultimately cause death of that muscle of heart. Therefore reduction in blood clotting will reduce the risk.
  • Ischemic strokes which will mainly caused by embolism. The small blood vessels in brain will be blocked there oxygen supply to that part of brain will be reduced. This will ultimately have effect on motor function.
  • These problems are associated with high risks as they involve major organs of body heart and brain. Therefore if left untreated there will be a severe reduction in supply of nutrients which leads to death tissue.


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